Concepts in Atheism & Physicalism

Atheism, secularism & freethought etc.

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Re: Concepts in Atheism & Physicalism

#61  Postby Spearthrower » Feb 18, 2011 7:27 am

fade wrote:The default equation of anything atheistic with physicalism/materialism bothers me a great deal. It's all too common from the modern neo-atheist who worships at the alter of Dawkins and Dennett. It also acts to shut down any sort of interesting philosophical debate with a fundamentalist argument that is both baseless and borderline religious in itself (the external world is real).

I wonder, how does equating atheism, with say idealism, make one any less of an atheist? How does it make anyone less rational or logical? Many well regarded and well respected philosophers have held, and still do, to philosophies such as idealism.

How about some of you stop trying to shoehorn your pet philosophies like materialism or physicalism in with your theological positions? It's seriously amateur. If you want to talk about atheism then talk about atheism. Where in the definition of the word 'atheist', as 'non-believer in a deity' do you find room to fit a whole host of philosophical beliefs and positions as well such as materialism or physicalism? Enquiring minds would love to know.



Oh look!

Someone didn't read the fucking topic then went on a rant.

How clever.
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Re: Concepts in Atheism & Physicalism

#62  Postby Peter Brown » Feb 18, 2011 10:12 am

chriscase wrote:
Peter Brown wrote:One of the problems of free will is the body is not always able to allow it. For instance you can’t just decide to have your heart, breath, liver etc to stop working, there is no free will there. Also the spinal cord has nerves to react to situations before the brain knows what is occurring eg pain that causes you to pull your arm away. These involuntary reactions are real and go against the abstract concept of free will.

Then there are other aspects like the sex drive. You can’t help wanting sex but you can have free will to actually perform it. Expanding the free will of sex, what makes you pick whom you have sex with? You can’t watch sperm or eggs do push ups or run round the body to check how fit they are, which might be the best way if sex is to breed. So you have to look at cues from the mate and make the best guess if that mate gives the most favourable signs that their egg/sperm is right for you.

In a way sex tells us what free will is. The best choice in the light of the available information. That choice can be very random, externally or internally influenced or not at all, but the end product is a choice and QED demonstrates free will.


I don't see how any "choice", once made, demonstrates free will in the sense that a different choice can be shown to have been possible. Certainly, once the choice is in the past, no other can be demonstrated. Of course, the concept of choice implies that another course of action could have been taken at the time. But how could we demonstrate that's not an illusion? I don't see any way.

Other realities, such as our limited influence (i.e., the observation that our will does not extend particularly far into the objective world), and the limited knowledge upon which we base our decisions do not seem to me to be particularly relevant. As far as I can tell, "free will" is only potentially coherent in the case where a choice between one course of action and at least one other are both known and possible.

But even in this case, I don't see how the notion can be tested. Perhaps the dilemma is that, although we can imagine taking all of the possible actions (indeed, the imagination of them is neccesary to the perception of choice in the first place), only one can actually be chosen - only one can be made real. Yet the imagination of multiple choices might mislead us into the illusion that more than one can somehow be accessible.


I appreciate that dilemma and suppose the test would demonstrate the randomness of free will with blind luck.
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Re: Concepts in Atheism & Physicalism

#63  Postby logical bob » Feb 18, 2011 11:20 am

logical bob wrote:
hackenslash wrote:I would certainly be willing to stand by any assertion that mathematics is the language of philosophy, because it is the core of logic.

:picard: Sometimes wibble is the only word.

But I'll try to say something constructive about that, because I don't really want to resort to vitriol as readily as you do.

How can maths be the core of logic? Would you really say that Fourier analysis or the theory of noncommutative rings are part of the core of logic? Generally maths has looked to logic for support and not the other way around.

In the nineteenth and early twentieth centuries maths made huge progress by becoming systematic and rigourous, which it hadn't been for Newton and Leibniz (they couldn't define what their fluxions and infinitessimals were) or for Kant (no modern mathematician would call mathematical facts synthetic). In the process, however, it ran up against some logical paradoxes and also began to prove some results that some found troubling, such as that it's possible to draw an infinite line on the back of a stamp or cut a sphere into five pieces which can be reassembled like a jigsaw to five two spheres the same size as the original.

When intuition, or what seemed reasonable, could no longer be trusted the hope was to imbed maths into logic so that we could be as confident of mathematical statements as we are of logical ones. This was the goal of the Hilbert Programme from 1900 to 1931 and also took up much of the early career of Bertrand Russel.

Then in 1931 Godel proved that no logical system can prove all true statements about arithmetic with integers, let alone the whole of maths. Maths lies outside the scope of every possible logical system, so far from being the core of logic or used to support the application of logic to philosophy it is a distinct thing.

Had you said that maths is the discipline that best exemplifies the use of logic, or that philosophers would do well to learn some maths because it hones your logical skills then I would have totally agreed with you. To go on instead to claim that maths is the language of philosophy and geometry is metaphysics is just cheerleading for a romantic view of how you'd like things to be.

Making big and ill informed claims about a subject you don't understand properly and then heaping abuse on someone who points out that you don't understand it is unappealing when creationists do it in C&ID. It certainly does't suit a far more intelligent person like you.
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Re: Concepts in Atheism & Physicalism

#64  Postby fade » Feb 18, 2011 11:44 am

Spearthrower wrote:Oh look!

Someone didn't read the fucking topic then went on a rant.

How clever.


It's a sanity thing. If I kept reading junk like "Consciousness is to the brain as digestion is to the stomach. Consciousness is just as real as digestion is, it's just that it's a verb not a noun" my eyes are going to end up rolling around in my head without stopping, picking up speed in until my whole head implodes at the baseless assumptive illogicality of it all.

That would be problematic. So instead you got a rant.
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Re: Concepts in Atheism & Physicalism

#65  Postby Teuton » Feb 18, 2011 1:52 pm

fade wrote:The default equation of anything atheistic with physicalism/materialism bothers me a great deal. … Where in the definition of the word 'atheist', as 'non-believer in a deity' do you find room to fit a whole host of philosophical beliefs and positions as well such as materialism or physicalism? Enquiring minds would love to know.


You're right, an atheist need be neither a naturalist nor a materialist.
"Perception does not exhaust our contact with reality; we can think too." – Timothy Williamson
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Re: Concepts in Atheism & Physicalism

#66  Postby John P. M. » Feb 18, 2011 4:02 pm

These kinds of topics always makes me think that I'm either very dim and naive, or... :ask:

To me, the metaphysical, dualist stance seems to be based in an ideal answer; an answer that works like a 'deus ex machina', something 'out of the blue' that 'swoops down' and answers the question, and therefore doesn't really answer it.

What are the demonstrable properties of the metaphysical 'mind stuff' that makes it solve whatever problems physical matter may have when it comes to the mind? Is it only that it is unbound by the physical constraints of this universe? An ideal substance to solve this problem?

If, say, some external (to this universe) entity has given us consciousness via some metaphysical substance that only exists in that other realm, and that substance somehow works across realms to give us our consciousness here, in tandem with our material brain, how does that substance solve the consciousness of the entities in that other realm? Wouldn't this metaphysical substance be that realms' material substance? Shouldn't they then be arguing that their substance cannot account for their consciousness? What are the properties of this substance, so that it solves this universally? That it simply is consciousness? Is that really an Answer?

I think it's perfectly reasonable to ask questions about the materialist view, and seek to find answers, but this way of finding answers in the metaphysical reminds me of the Intelligent Design proponents' way of arguing; that if we can't immediately see a solution to a certain puzzling occurrence in nature, we should say "Halt your inquiry!" and solve it by saying it was intelligently designed. Instead of having patience and looking to see if there is a natural, material solution to the material problem.

Could it be that we don't yet fully understand the material world, and that there may lie an answer there instead, an answer that will be demonstrable and more parsimonious?

I guess you could say this all depends on one's presuppositions. I think most atheists (here at least) have a material world presupposition because they have a 'bottom up' way of discovering reality, through skepticism, parsimony and evidence.
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Re: Concepts in Atheism & Physicalism

#67  Postby Andrew4Handel » Feb 18, 2011 6:58 pm

Calilasseia wrote:
Andrew4Handel wrote:This excerpt from a conversation between Philosopher of science David Papineau and fellow philosoper Alex Barber highlights the problems of materialist, naturalist and physicalist positions.


This is only a "problem" for people who think that all they have to do is fabricate tinselly metaphysical holograms, and reality will magically rearrange itself to conform thereto. To those of us who start with REALITY as our basis for substantive postulates about the world, not invoking fabricated magic entities isn't a problem. Going to learn this elementary lesson sometime?



David Pappineau is not a theist and he is an avowed materialist. I wish you would stop waffling about magic entities unless you can quote me as mentioning any specific magic entities and their qualities?

You clearly do not understand then historical role of philosophy in science. Science itself used to be called natural philsophy. You give no indication that you understand anything about materialism, naturalism and the basis of scienticism or the logic of the scientific method.

You have not even clarified a logical position concerning what exactly science can say and what its potential boundaries or lack of boundaries are. You are doing as I have said to people on here before which is hiding behind the success of science without an understanding of the ramafications.

I don't see what you have mentioned about science that gives us a compelling picture of a self creating reality exhibiting the properties it does for a coherent reason. Just calling things people say magic and wibble because they don't accept the ability of the scientific method to fully explain reality is resorting to scorn over a compelling or logical argument. This makes alll that you are saying sound like rant rant rant!!

The reality THE REALITY is that science has not given a comprehensive explanation of reality which shows that reality is just inanimate matter that appeared from nowhere that just happenes to produce sentient life.

I don't care about your opinion on this. Science has not explained reality and in my opinion it will never. It is a successfull paradigm that has benefitted us and allowed us to manipulate reality but without given us any sense of finality or explanatory closure.

You seem hysterically adverse to the notion of creation preffering the equally loopy idea that an infinitely vast insentient universe creating itself is less silly..
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Re: Concepts in Atheism & Physicalism

#68  Postby Andrew4Handel » Feb 18, 2011 7:03 pm

Calilasseia wrote:
And similarly it sees to me, notions of representation would have seemed unproblematic if you thought of our mind as fragments of the divine mind, but once you take away the divine mind and its power to imbue physical bodies with intentionality then intentionality, representation becomes very problematic indeed.


Poppycock. Do I have to bring in the primate research literature and the evolution of ASPM into this in order to refute this tripe?



What does primate research have to tell us about the nature or representation and intentionality? Do you even understand the context of these terms?

I don't follow Papineaus above comment but it comes in the context of a university course book on how language can have meaning and how sounds can represent, what thought constitues and what an intentional stance is.

I suppose you have studied the philosophy of language?...maybe you were under the gross illussion that scientists and theorists had an explanation for language?
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Re: Concepts in Atheism & Physicalism

#69  Postby Andrew4Handel » Feb 18, 2011 7:14 pm

Calilasseia wrote: As I have stated elsewhere, science is in the business of testing assumptions and presuppositions to destruction.


And how exactly can you test theories about the long gone past to destruction? How can you test the Big bang to destruction or the idea that the brain evolved. If the brain evolved it already happened and the process can't be observed again anything else is speculation.

Has the multiverse theory /string theory been tested to destruction?

Here are some scientific critics of the big bang

http://www.cosmologystatement.org/

You appear to be suggesting in a metaphysical way that science is the only tool for investigating reality.

The actual best tool for investigating reality is human consciousness and intelligence. Science isn't an entity in itself, it is the manifestation of a human cognitive capacity. This human cognitive capacity which now has to be subjugated to materialist elimination.
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Re: Concepts in Atheism & Physicalism

#70  Postby paceetrate » Feb 18, 2011 7:42 pm

fade wrote:
Spearthrower wrote:Oh look!

Someone didn't read the fucking topic then went on a rant.

How clever.


It's a sanity thing. If I kept reading junk like "Consciousness is to the brain as digestion is to the stomach. Consciousness is just as real as digestion is, it's just that it's a verb not a noun" my eyes are going to end up rolling around in my head without stopping, picking up speed in until my whole head implodes at the baseless assumptive illogicality of it all.

That would be problematic. So instead you got a rant.


Oh, so do you mean to assert that consciousness is NOT something the brain does? That it somehow exists outside the brain? You have any evidence for that, sparky?

And forgive me if I treat your past post with the same reaction as you did mine. Anybody who can be both atheist AND dualist at the same time makes "my eyes end up rolling around in my head without stopping, picking up speed in until my whole head implodes at the baseless assumptive illogicality of it all."
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Re: Concepts in Atheism & Physicalism

#71  Postby Calilasseia » Feb 19, 2011 12:22 am

Oh dear. It seems that replying to the bullshit that's landed in my in tray requires me to split this post into two. This is Part One. Are you sitting comfortably, ladies and germs? :mrgreen:

Andrew4Handel wrote:
Calilasseia wrote:
Andrew4Handel wrote:This excerpt from a conversation between Philosopher of science David Papineau and fellow philosoper Alex Barber highlights the problems of materialist, naturalist and physicalist positions.


This is only a "problem" for people who think that all they have to do is fabricate tinselly metaphysical holograms, and reality will magically rearrange itself to conform thereto. To those of us who start with REALITY as our basis for substantive postulates about the world, not invoking fabricated magic entities isn't a problem. Going to learn this elementary lesson sometime?


David Pappineau is not a theist and he is an avowed materialist.


I didn't say he was if you had bothered to read my post properly. What I said was that he manifestly needed to learn some basic lessons, most notably the prime one of basing one's ideas upon reality instead of tinselly metaphysical holograms. Since he had trouble even defining naturalism at the start of his piece, I concluded that he hadn't given the matter proper thought. What part of this escaped you again?

Andrew4Handel wrote:I wish you would stop waffling about magic entities unless you can quote me as mentioning any specific magic entities and their qualities?


Excuse me, but YOU are the individual who has hopped from thread to thread, posting a range of tiresome and previously debunked supernaturalist canards, so YOU are the one who has set the relevant precedents. If you don't subscribe to the idea that fabricated magic entities are needed in order to keep the universe running, I'd like to know why you have set the aformentioned precedents? As a corollary thereof, if you don't subscribe to this view, what's your problem with me stating, clearly and explicitly, that naturalism consists of not assuming that such entities are needed?

Andrew4Handel wrote:You clearly do not understand then historical role of philosophy in science.


The big problem I have with all too many "philosophers" is that they behave like supernaturalist apologists. Namely, they erect grand metaphysical castles in the sky, then expect the rest of us to take up residence within them, without once asking the basic question "does REALITY agree with the foundational assertions upon which these castles are built?" Fortunately, Popper (who had rather a lot to say on the subject of philosophy in science) had the good sense to pay attention to REALITY, and retract his ridiculous assertion that evolution wasn't a scientific theory. But that's a subject for a separate thread.

The simple fact of the matter is, that all too often, the role of some "philosophers" has been to try and tell scientists that they should fit their theories to assorted metaphysical presuppositions instead of REALITY. Well, sadly, if you do that, you're no longer doing science, you're practising apologetics. Indeed, it's about time that assorted purveyors of tinselly metaphysical holograms woke up to the fact that it's game over for them, and that science is increasingly bringing into the remit of quantitative analysis entities and phenomena that were not only beyond the imagination of these "philosophers" to dream up, but whose observed behaviour falsifies a good number of metaphysical speculations. The Dalai Lama woke up to this after he was taken on a tour of the Large Hadron Collider - with one simple exclamatory remark, he realised that the game of fabricating fanciful fantasies, and then declaring that the world somehow magically rearranged itself to conform thereto, was well and truly over.

At bottom, hard empiricism WORKS, whilst armchair speculation and fantasising doesn't. It's about time a lot of people woke up to this basic fact, and you give me the impression in your posts of being one of the people who needs this wake up call.

Andrew4Handel wrote:Science itself used to be called natural philsophy. You give no indication that you understand anything about materialism, naturalism and the basis of scienticism or the logic of the scientific method.


Oh please, spare me your hubristic attempts to know me better than I know myself. I know these basic facts. This is something that formed a part of my junior school education.

Andrew4Handel wrote:You have not even clarified a logical position concerning what exactly science can say and what its potential boundaries or lack of boundaries are.


That's because I don't possess the arrogance required to tell scientists what they can and cannot learn through their research. Worked this elementary concept out yet?

The only limits upon what science can learn are the limits that REALITY imposes upon us. That is IT. If REALITY tells us we can go no further, then we have to suck on it. If, on the other hand, REALITY tells us that there's a lot more work to be done, and a lot more interesting things to investigate, then we can look forward to a nice roller coaster ride as that work is done. The idea that science is in any way "limited" by the fanciful erections of enthusiasts for made up shit is one of those nonsense notions you will have to learn to ditch.

Andrew4Handel wrote:You are doing as I have said to people on here before which is hiding behind the success of science without an understanding of the ramafications.


Oh, the hubris once again!

I understand the ramifications of that success all right, one of them being that every one of humanity's invented mythologies is WRONG. I suggest you learn that elementary lesson pretty quickly. And because all of those invented mythologies are WRONG, they are UNRELIABLE. Which means that with respect to the assorted pontifications of those mythologies, we should treat them ALL with suspicion, and look for evidentially supported postulates instead of accepting uncritically blind assertions just because assorted groups of ignorant, pre-scientific humans thought they were true. This, incidentally, applies beyond the realm of physical science as well - the lesson I for one have learned is that not only are all of these mythologies hopelessly wrong with respect to the physical universe and its contents, in some cases laughably, absurdly so, but that they are also wrong with respect to a number of important ethical issues, and consequently, we should be moving away from assertionist mythological ethics to a proper, scientific, evidence-based ethics. If that scares you, then it merely testifies to the palsying effects of supernaturalism on the mind, because I have no worries at all about basing ethics upon evidence with respect to what decisions result in gratuitous harm or not. Supernaturalists, of course, are scared shitless of this, because all too frequently it means taking a machine gun to their precious sacred cows.

Andrew4Handel wrote:I don't see what you have mentioned about science that gives us a compelling picture of a self creating reality exhibiting the properties it does for a coherent reason.


Oh, you mean you haven't bothered to learn about the relevant scientific discoveries? Start doing some of your own bloody homework, I've presented enough scientific papers here to establish that the scientific case is sound.

Andrew4Handel wrote:Just calling things people say magic and wibble because they don't accept the ability of the scientific method to fully explain reality is resorting to scorn over a compelling or logical argument.


When some of these people present evidence that they have a better way of learning about reality, I'll sit up and take notice., Until then, I'll treat made up shit with the scorn and derision it deserves. Learned this elementary concept yet?

Andrew4Handel wrote:This makes alll that you are saying sound like rant rant rant!!


As opposed to the droning from assorted supernaturalists I've been dealing with here and elsewhere for three years, much of which is based upon unsupported blind assertions, blatant fabrications, and in the case of creationism, outright lies. You might want to factor this into your assessment sometime.

Andrew4Handel wrote:The reality THE REALITY is that science has not given a comprehensive explanation of reality


It's given a damn sight more comprehensive an explanation of reality than any mythology. Or were you asleep in the classes that taught you this?

Science has alighted upon entities and phenomena that the authors of mythology were incapable of even fantasising about, and subjected those entities and phenomena to precise quantitative analysis. For example, quantum electrodynamics describes the behaviour of relevant systems of interaction to fifteen decimal places, and REALITY agrees with it. If you think this, alongside general relativity and a host of other developments, constitutes a "failure" to produce a comprehensive explanation for reality, then you really must have slept through all of your science classes.

Andrew4Handel wrote:which shows that reality is just inanimate matter that appeared from nowhere that just happenes to produce sentient life.


Oh for fuck's sake, here we go again with the fatuous strawman caricatures supernaturalists love so much ... YAWN, FUCKING YAWN.

Excuse me, but did you not bother to pay attention in the classes that were in the business of teaching you certain relevant elementary concepts? Such as the fact that scientists regard all real world observational phenomena as being ultimately the product of testable natural processes, even if they are not currently in a position to test some of the processes in question?

And the scientific picture doesn't erect the nonsense caricature you've presented above, that life just "happened", it postulates relevant testable mechanisms for the origin of life. Or do I have to carpet bomb you with my collection of scientific papers from the abiogenesis literature in order to drive this elementary concept into your skull?

For fuck's sake, the level of rampant ignorance you have demonstrated with your above crass caricature is breathtaking. YOU purport to castigate me for being allegedly "ignorant" about a whole range of topics, yet in the next breath erect one of the most singularly retarded caricatures of the scientific world view in existence, one that moreover is straight out of the duplicitous playbook of creationist apologetics? You have some fucking chuztpah.

Andrew4Handel wrote:I don't care about your opinion on this.


Ahem, my "opinion" is backed by hard empirical research. I suggest you go and read some of it. You can start with the 2,000 or so papers I have in my collection on evolutionary biology.

Andrew4Handel wrote:Science has not explained reality


It's done a damn sight better job than made up shit mythology. Or doesn't the fact that smallpox has been eradicated, manned spaceflight is an engineering reality, and the operation of subatomic particles is being probed routinely in laboratories around the world, ALL as a result of paying attention to REALITY instead of mythological made up shit, in any way, shape or form, tell you this?

Andrew4Handel wrote:and in my opinion it will never.


Oh, so you want to dismiss MY opinion, despite the fact that a large body of hard empirical scientific research backs it up, but now introduce YOUR opinion, and expect us to regard it as being more valid, despite lacking ANY empirical support whatsoever? This is the sort of hubris I've come to expect from supernaturalists.

Andrew4Handel wrote:It is a successfull paradigm that has benefitted us and allowed us to manipulate reality but without given us any sense of finality or explanatory closure.


Let's see ... in 300 years, science has explained more classes of real world phenomena than made up shit mythology has in 5,000 ... I wonder what science will achieve when it's had the same amount of time as supernaturalism? Only a fool says "never", as numerous real world precedents have informed us.

Andrew4Handel wrote:You seem hysterically adverse to the notion of creation


There's nothing "hysterical" about my aversion to made up shit. My aversion to made up shit is the same aversion that everyone should have to made up shit, namely that because it's made up shit, it bears no connection to REALITY. Worked this elementary concept out yet?

Plus, the mere fact that enthusiasts for "creation" have to LIE about valid science in order to propagandise on behalf of a manifest ideological masturbation fantasy should be telling you the same thing it tells me, namely that their ideas are worthless. I don't have to lie in order to present the scientific case, all I have to do is present the relevant empirical research honestly (as opposed to quote mining it the way creationists do) and let REALITY do the talking for me. If you think I should not be averse to ideas that require people to LIE on their behalf, then I really hope you never achieve a position of political power, because such an attitude is dangerous.

Andrew4Handel wrote:preffering the equally loopy idea that an infinitely vast insentient universe creating itself is less silly..


Oh dear, do I have to hit you with a brace of cosmology papers containing the evidence for modern cosmological ideas? Once again, what part of the words "HARD EVIDENCE FROM THE REAL WORLD" do you not understand?

Let's get something straight once and for all. When it comes to a contest between made up shit, and HARD EVIDENCE FROM REALITY, then the hard evidence from reality wins every time. If you don't understand why, then you really are in need of going back to school. Here's a clue for you: any idiot can make shit up and assert that his made up shit governs how the world behaves, but it takes rather more diligent effort to come up with ideas that WORK, and are SUPPORTED BY REALITY. It's why mythology fails, and science succeeds. Learn this lesson quickly.

Andrew4Handel wrote:
Calilasseia wrote:
And similarly it sees to me, notions of representation would have seemed unproblematic if you thought of our mind as fragments of the divine mind, but once you take away the divine mind and its power to imbue physical bodies with intentionality then intentionality, representation becomes very problematic indeed.


Poppycock. Do I have to bring in the primate research literature and the evolution of ASPM into this in order to refute this tripe?


What does primate research have to tell us about the nature or representation and intentionality? Do you even understand the context of these terms?


Yes. And guess what? We don't need an invisible fucking magic man in order to possess them. Looks like I'm going to have to carpet bomb you with this ... this is a little something that I wrote some time ago in order to refute the fatuous "you need my magic man to be moral" assertion, and it's apposite here, because the ability to represent concepts in a mental model, and the ability to act upon ideas arising therefrom, is central to our ethical functioning. Are you sitting comfortably? Here we go ...

The Evolutionary And Biological Basis For Altruism, Ethics And Abstract Thought

I said I would cover some relevant scientific papers dealing with the evolutionary and biological basis for altruism, empathy and ethical behaviour, and so, I shall do that. Before doing so, however, I shall open with some pertinent remarks.

All morality is a human invention. The only evidence we have, of creatures producing an abstract concept of ethics and devising conceptual frameworks within an intellectual field of endeavour devoted to these, centres upon humans. We have evidence that humans have written treatises on ethics - everything from Urukagina's laws and Hammurabi's laws through to, for example, the works of Immanuel Kant. We have NO evidence that any other entity has produced treatises on ethics or formulated ethical ideas. Any statement that an invisible magic man is responsible for our ethical constructs is mere blind assertion, not least because the postulate that this invisible magic man even exists is a blind assertion. As a direct consequence, the observational evidence supports the notion that morality is a human invention.

Oh, and one of the more interesting developments from neuroscience that supernaturalists have apparently missed out on is this. Humans (and indeed other primates) possess a part of the brain known as the ventromedial pre-frontal cortex. It has been demonstrated experimentally, courtesy of cases of brain injury to this region, that this part of the brain is the very part of the brain responsible for our capacity to engage in ethical decision making. When that part of the brain is damaged, ethical decision making is manifestly impaired. In other words, we have an organic and biological basis for our capacity to act as moral beings. An interesting and relevant paper is this one:

Characterisation Of Empathy Deficits Following Prefrontal Brain Damage: The Role Of The Right Ventromedial Prefrontal Cortex by S.G. Shamay-Tsoory, R. Tomer B.D. Berger and J. Aharon-Peretz, Journal of Cognitive Neuroscience, 15: 324-337 (2003)

Here's the abstract:

Shamay-Tsoory et al, 2003 wrote:Impaired empathic response has been described in patients following brain injury, suggesting that empathy may be a fundamental aspect of the social behavior disturbed by brain damage. However, the neuroanatomical basis of impaired empathy has not been studied in detail. The empathic response of patients with localized lesions in the prefrontal cortex (n = 25) was compared to responses of patients with posterior (n = 17) and healthy control subjects (n = 19). To examine the cognitive processes that underlie the empathic ability, the relationships between empathy scores and the performance on tasks that assess processes of cognitive flexibility, affect recognition, and theory of mind (TOM) were also examined. Patients with prefrontal lesions, particularly when their damage included the ventromedial prefrontal cortex, were significantly impaired in empathy as compared to patients with posterior lesions and healthy controls. However, among patients with posterior lesions, those with damage to the right hemisphere were impaired, whereas those with left posterior lesions displayed empathy levels similar to healthy controls. Seven of nine patients with the most profound empathy deficit had a right ventromedial lesion. A differential pattern regarding the relationships between empathy and cognitive performance was also found: Whereas among patients with dorsolateral prefrontal damage empathy was related to cognitive flexibility but not to TOM and affect recognition, empathy scores in patients with ventromedial lesions were related to TOM but not to cognitive flexibility. Our findings suggest that prefrontal structures play an important part in a network mediating the empathic response and specifically that the right ventromedial cortex has a unique role in integrating cognition and affect to produce the empathic response.


Another apposite paper is this one:

The Role Of The Ventromedial Prefrontal Cortex In Abstract State-Based Inference During Decision Making In Humans by Alan N. Hampton, Peter Bossaerts and John. P. O'Doherty, The Journal of Neuroscience, 26(32):, 8360-8367 (9th August 2006) (full paper downloadable from here)

Here's the abstract:

Hampton et al, 2006 wrote:Many real-life decision-making problems incorporate higher-order structure, involving interdependencies between different stimuli, actions, and subsequent rewards. It is not known whether brain regions implicated in decision making, such as the ventromedial prefrontal cortex (vmPFC), use a stored model of the task structure to guide choice (model-based decision making) or merely learn action or state values without assuming higher-order structure as in standard reinforcement learning. To discriminate between these possibilities, we scanned human subjects with functional magnetic resonance imaging while they performed a simple decision-making task with higher-order structure, probabilistic reversal learning. We found that neural activity in a key decision-making region, the vmPFC, was more consistent with a computational model that exploits higher-order structure than with simple reinforcement learning. These results suggest that brain regions, such as the vmPFC, use an abstract model of task structure to guide behavioral choice, computations that may underlie the human capacity for complex social interactions and abstract strategizing.


Likewise we have this paper:

Another apposite paper is this one:

Characterisation Of The Decision-Making Deficit Of Patients With Ventromedial Prefrontal Cortex Lesions by Antione Bechara, Daniel Tranel and Hanna Damasio, Brain, 123: 2189-2202 (2000)

and also this one:

Ventromedial Prefrontal Cortex Activation Is Critical For Preference Judgements by Martin P. Paulus and Lawrence R. Frank, NeuroReport, 14(10): 1311-1315 (28th March 2003)

However, the one I'd really like to concentrate upon from here on is this one:

Impairment Of Social And Moral Behaviour Related To Early Damage In Human Prefrontal Cortex by Steven W. Anderson, Antoine Bechara, Hanna Damasio, Daniel Tranel and Antonio R. Damasio, Nature Neuroscience, 2(11): 1032-1037 (November 1999)

Here's what this paper says:

Anderson et al, 1999 wrote:The long-term consequences of early prefrontal cortex lesions occurring before 16 months were investigated in two adults. As is the case when such damage occurs in adulthood, the two early-onset patients had severely impaired social behavior despite normal basic cognitive abilities, and showed insensitivity to future consequences of decisions, defective autonomic responses to punishment contingencies and failure to respond to behavioral interventions. Unlike adult-onset patients, however, the two patients had defective social and moral reasoning, suggesting that the acquisition of complex social conventions and moral rules had been impaired. Thus early-onset prefrontal damage resulted in a syndrome resembling psychopathy.


Indeed, further research in this area has established an interesting fact: if the pre-frontal cortex is damaged in childhood, before a child has begun to learn basic ethical precepts, that child becomes a sociopathic adult, incapable of responding to any impulse other than instant gratification of wants and desires, regardless of the cost to that person or others affected by said behaviour. If the damage occurs in adulthood, the behaviour is still antisocial, but is accompanied by feelings of guilt because ethical precepts have already been learned, and knowledge of this affects the individual adversely in terms of guilt feelings after the fact. Plus, when subjected to testing in a clinical environment, adults with pre-frontal cortex damage can give appropriate responses to questions about appropriate behaviour in social settings, but are unable to act upon this knowledge, and continue to be driven by immediate gratification, even when they know that this behaviour is self-defeating. The pre-frontal cortex has also been implicated as the origin of fear memories in normal individuals, as of 2006 (courtesy of researchers at the University of Toronto). Modern data with respect to this relies upon functional MRI scanning, which can track brain activity in real time, and those brain imaging systems have found a startling correlation between reduced activity, reduced volume and reduced interconnections with other brain subsystems, and individuals falling into the following categories:

[1] Sufferers of unipolar depression;

[2] Persons subjected to repeated high-intensity stress (e.g., battlefield shock cases);

[3] Incarcerated criminals;

[4] Diagnosed sociopaths;

[5] Drug addicts;

[6] Suicide victims (survivors of suicide attempts have been imaged via fMRI: successful suicide victims have had the pre-frontal cortex directly measured by dissection).

Therefore there is a biological basis for ethical behaviour in humans, and work on the great apes is being performed in anticipation of finding corollary brain activity related to socialisation and the establishment of behavioural 'norms' within great ape social groupings.

The pre-frontal cortex is regarded as being implicated in the presence of empathy not just in humans, but on other mammals too, though this work is in its infancy and detailed, robust findings have yet to be published. However, given what has been verified empirically in cases of pre-frontal cortex injury, scientists anticipate that empathy will also be found to be correlated with healthy functioning of the pre-frontal cortex.

Additionally, I have since found that pre-frontal cortex damage is implicated in schizophrenia, courtesy of this page from the Society for Neuroscience. Again, it refers to brain imaging studies, this time in humans and other primates.

A letter to Nature is also apposite here (link), viz:

The psychological and neurobiological processes underlying moral judgement have been the focus of many recent empirical studies1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11. Of central interest is whether emotions play a causal role in moral judgement, and, in parallel, how emotion-related areas of the brain contribute to moral judgement. Here we show that six patients with focal bilateral damage to the ventromedial prefrontal cortex (VMPC), a brain region necessary for the normal generation of emotions and, in particular, social emotions12, 13, 14, produce an abnormally 'utilitarian' pattern of judgements on moral dilemmas that pit compelling considerations of aggregate welfare against highly emotionally aversive behaviours (for example, having to sacrifice one person's life to save a number of other lives)7, 8. In contrast, the VMPC patients' judgements were normal in other classes of moral dilemmas. These findings indicate that, for a selective set of moral dilemmas, the VMPC is critical for normal judgements of right and wrong. The findings support a necessary role for emotion in the generation of those judgements.


Indeed the pre-frontal cortex appears to be involved in a surprising amount of decision making. This page on depression covers this in some detail. This page also reports a study from the British Journal of Psychiatry, which notes structural differences in the pre-frontal cortex that are observed between socially well-adjusted individuals and pathological liars, and a parallel reversal of those differences in persons with autistic spectrum conditions (who have been observed for many years as possessing a considerably reduced capacity to lie and fabricate - there are numerous peer reviewed studies with respect to this, from researchers such as Professor Uta Frith and Dr Simon Baron-Cohen).

A peer reviewed paper that can be accessed that discusses several of these findings in detail is this one, in which the connection between pre-frontal cortex damage and increased pursuit of immediate gratification is experimentally verified. This article from the American Journal of Psychiatry also covers the relation between pre-frontal cortex damage and schizophrenia.

So, the evidence the basis for morality is organic, and has precious little to do with any invisible magic men. In the case of humans, our accelerated brain evolution (courtesy of ASPM and FOXP2, two genes critical to the development of a large cerebral cortex and language capability, papers on which I have presented elsewhere) has also led to an expansion of the size of the ventromedial pre-frontal cortex, and the forging of connections between that brain region and the cerebral cortex proper, facilitating the coupling of our empathic capabilities, which are also seen in other primates. The following scientific papers, authored or co-authored by primate researcher Frans de Waal, are apposite here:

Empathy: Its Ultimate And Proximate Bases by Stephanie D. Preston and Frans de Waal, Behavioural and Brain Sciences, 25: 1-20 (2001)

Mechanisms Of Social Reciprocity In Three Primate Species: Symmetrical Relationship Characteristics Or Cognition? by Frans B. M. de Waal and Lesleigh M. Luttrell, Ethology and Sociobiology, 9(2-4): 101-118 (1988)

Monkeys Reject Unequal Pay by Sarah F. Brosnan & Frans B. M. de Waal, Nature, 425: 297-299 (18th September 2003)

Primates—A Natural Heritage Of Conflict Resolution by Frans B. M. de Waal, Science, 289: 586-590 (28th July 2000)

Reconciliation And Consolation Among Chimpanzees by Frans B. M. de Waal and Angeline van Roosmalen, Behavioural Ecology & Sociobiology, 5(1): 55-66 (March 1979)

I'll now set about covering these papers in some detail. First,

Empathy: Its Ultimate And Proximate Bases by Stephanie D. Preston and Frans de Waal, Behavioural and Brain Sciences, 25: 1-20 (2001). The full paper is downloadable from here. Here is the abstract, with appropriate sections highlighted in bold:

Preston & de Waal, 2001 wrote:There is disagreement in the literature about the exact nature of the phenomenon of empathy. There are emotional, cognitive, and conditioning views, applying in varying degrees across species. An adequate description of the ultimate and proximate mechanism can integrate these views. Proximately, the perception of an object's state activates the subject's corresponding representations, which in turn activate somatic and autonomic responses. This mechanism supports basic behaviors (e.g., alarm, social facilitation, vicariousness of emotions, mother-infant responsiveness, and the modeling of competitors and predators) that are crucial for the reproductive success of animals living in groups. The Perception-Action Model (PAM), together with an understanding of how representations change with experience, can explain the major empirical effects in the literature (similarity, familiarity, past experience, explicit teaching, and salience). It can also predict a variety of empathy disorders. The interaction between the PAM and prefrontal functioning can also explain different levels of empathy across species and age groups. This view can advance our evolutionary understanding of empathy beyond inclusive fitness and reciprocal altruism and can explain different levels of empathy across individuals, species, stages of development, and situations.


So already we have a paper that discusses evolutionary explanations for altruism. Let's take a further look at this, shall we?

Preston & de Waal, 2001 wrote:In an experiment with rhesus monkeys, subjects were trained to pull two chains that delivered different amounts of food. The experimenters then altered the situation so that pulling the chain with the larger reward caused a monkey in sight of the subject to be shocked. After the subjects witnessed the shock of the conspecific, two-thirds preferred the nonshock chain even though it resulted in half as many rewards. Of the remaining third, one stopped pulling the chains altogether for 5 days and another for 12 days after witnessing the shock of the object. These monkeys were literally starving themselves to prevent the shock to the conspecific. Starvation was induced more by visual than auditory cues, was more likely in animals that had experienced shock themselves, and was enhanced by familiarity with the shocked individual (Masserman et al. 1964).


So we have hard experimental evidence that rhesus macaques will suffer privation rather than see fellow members of their species endure pain. Which means that these organisms possess empathy for each other that is directly observable, and reflects the sort of empathic responses that used to be thought to be exclusive to humans.

Continuing, the authors write:

Preston & de Waal, 2001 wrote:These examples, all from empirical reports, show that individuals of many species are distressed by the distress of a conspecific and will act to terminate the object’s distress, even incurring risk to themselves. Humans and other animals exhibit the same robust effects of familiarity, past experience, and cue salience (Table 1), and parallels exist between the development of empathy in young humans and the phylogenetic emergence of empathy (de Waal 1996; Hoffman 1990, respectively). These facts suggest that empathy is a phylogenetically continuous phenomenon, as suggested by Charles Darwin more than a century ago (1871/1982).


So the notion that empathy, and as a consequence, altruistic behaviour, is a natural consequence of evolutionary processes can be traced in the scientific literature all the way back to Darwin. Which means tht an evolutionary explanation for altruism is anything but a recent development.

The paper concludes with:

Preston & de Waal, 2001 wrote:The complex social world of primates requires the central nervous system to perceive the facial expressions, body postures, gestures, and voices of conspecifics accurately and quickly in order to generate a response (Brothers 1990; Byrne & Whiten 1988). Parsimoniously, the same nervous system link between perception and action that helps us to navigate the physical environment helps us navigate the social environment. The perception-action link allows for facile motor skill acquisition as well as facile social interaction, as we perceive external conditions and incorporate them into our current plan of action. In this way, the proximate model is intricately linked with the ultimate model. While natural selection acts on phenotypes, these phenotypes reflect the underlying physiology. Thus, the general design of the nervous system, created through millions of years of evolution, should be considered a factor in the evolution of emotional processes like empathy and overt behaviors like helping. In this way, the proximate and ultimate levels of analysis are intimately related.


So, the authors conclude that in order to act in an altruistic manner, what is needed is:

[1] An ability to relate perceptions to actions within an internal mental model of some sort (and the model in question doesn't have to be anywhere near as intricate as ours);

[2] An ability to relate responses of other organisms of the same species to a given external action, to our own likely actions to those same external actions (in short, "putting oneself in the shoes of the other");

[3] An ability to make judgements, with respect to future actions to take, that maximise shared benefit and minimise shared suffering.

Since the papers on the ventromedial pre-frontal cortex and human brain development mediated by ASPM cover the development of the relevant hardware required for this, it should not be surprising to conclude, as a result of observing empirically that rhesus macaques possess the necessary hardware to act in this manner, that our own hardware supporting this behaviour arises from the familiar process of common descent with modification, and indeed, the ASPM papers provide evidence with respect to the modifications that took place in our lineage.

Next, we have this:

Monkeys Reject Unequal Pay by Sarah F. Brosnan & Frans B. M. de Waal, Nature, 425: 297-299 (18th September 2003). The abstract reads as follows:

Brosnan & de Waal, 2003 wrote:During the evolution of cooperation it may have become critical for individuals to compare their own efforts and pay-offs with those of others. Negative reactions may occur when expectations are violated. One theory proposes that aversion to inequity can explain human cooperation within the bounds of the rational choice model1, and may in fact be more inclusive than previous explanations2, 3, 4, 5, 6, 7, 8. Although there exists substantial cultural variation in its particulars, this 'sense of fairness' is probably a human universal9, 10 that has been shown to prevail in a wide variety of circumstances11, 12, 13. However, we are not the only cooperative animals14, hence inequity aversion may not be uniquely human. Many highly cooperative nonhuman species seem guided by a set of expectations about the outcome of cooperation and the division of resources15, 16. Here we demonstrate that a nonhuman primate, the brown capuchin monkey (Cebus apella), responds negatively to unequal reward distribution in exchanges with a human experimenter. Monkeys refused to participate if they witnessed a conspecific obtain a more attractive reward for equal effort, an effect amplified if the partner received such a reward without any effort at all. These reactions support an early evolutionary origin of inequity aversion.


Oh dear, that evidence that evolution can produce such behaviour is starting to pile up. So, even capuchin monkeys possess what might be termed "a sense of fair play". Sadly, I don't have access to the full paper, but I suspect it will make very interesting reading for those who do have full access. :)

Let's see another paper, shall we? Namely:

Reconciliation And Consolation Among Chimpanzees by Frans B. M. de Waal and Angeline van Roosmalen, Behavioural Ecology & Sociobiology, 5(1): 55-66 (March 1979). Abstract quoted yet again below:

de Waal and van Roosmalen, 1979 wrote:Summary 1. After agonistic interactions among chimpanzees, former opponents often come into non-violent body contact. The present paper gives a quantitative description of such contacts among the chimpanzees of a large semi-free-living colony at the Arnhem Zoo, in order to establish whether these post-conflict contacts are of a specific nature.

2. Our data indicate that former opponents preferentially make body contact with each other rather than with third partners. They tend to contact each other shortly after the conflict and show special behaviour patterns during these first contacts. Data on contacts of the aggressed party with third animals indicate that such contacts are characterized by the same special behaviour patterns as first interopponent contacts. These patterns are: 'kiss', 'embrace', 'hold-out-hand', 'submissive vocalization' and 'touch'.

3. Such interactions apparently serve an important socially homeostatic function and we termed them 'reconciliation' (i.e. contact between former opponents) and 'consolation' (i.e. contact of the aggressed party with a third animal). According to our data, 'kissing' is characteristic of reconciliation and 'embracing' of consolation.


This was a paper that performed a quantitative analysis of the requisite behaviours back in 1979. And which, moreover, contains what appears to be a direct empirical observation of chimpanzees acting socially to mitigate the results of violent conflict, and seek to minimise the occurrences thereof amongst their number. Which once again demonstrates that we are not unique in this vein by any stretch of the imagination.

Let's see what else is in the literature shall we?

Mechanisms Of Social Reciprocity In Three Primate Species: Symmetrical Relationship Characteristics Or Cognition? by Frans B. M. de Waal and Lesleigh M. Luttrell, Ethology and Sociobiology, 9(2-4): 101-118 (1988). Again, here's the abstract:

de Waal and Luttrell, 1988 wrote:Agonistic intervention behavior was observed in 23 chimpanzees, 50-60 rhesus monkeys, and 25 stumptail monkeys. Reciprocity correlations of interventions were determined while removing the effects of matrilineal kinship, proximity relations, and same-sex combination. It was considered likely that if significant reciprocity persisted, it was based on cognitive mechanisms. All 3 species exhibited significant reciprocity with regard to beneficial interventions, even after controlling for symmetrical traits. Harmful interventions were reciprocal among chimpanzees only. Both macaque species showed significantly inversed reciprocity in harmful interventions. Macaques rarely intervened against higher-ranking group members.


Next, we have:

Primates—A Natural Heritage Of Conflict Resolution by Frans B. M. de Waal, Science, 289: 586-590 (28th July 2000) (full paper downloadable from here). Once again ...

de Waal, 2000 wrote: The traditional notion of aggression as an antisocial instinct is being replaced by a framework that considers it a tool of competition and negotiation. When survival depends on mutual assistance, the expression of aggression is constrained by the need to maintain beneficial relationships. Moreover, evolution has produced ways of countering its disruptive consequences. For example, chimpanzees kiss and embrace after fights, and other nonhuman primates engage in similar “reconciliations.” Theoretical developments in this field carry implications for human aggression research. From families to high schools, aggressive conflict is subject to the same constraints known of cooperative animal societies. It is only when social relationships are valued that one can expect the full complement of natural checks and balances.


Well, I think that more or less wraps that up, don't you?

Basic empathy for others of our species, and to a varying extent, individuals of other species as well, is an integral part of us as human beings, and it has its origins in our primate social ancestry. Indeed, examples of that ancestry coming to the fore in other modern primates are well documented - the gorilla Binti Jua, who, in her zoo enclosure, rescued a three year old boy who fell into it, carried him to a place of safety, and guarded him from the other gorillas, until the zookeepers could carry the boy to a waiting ambulance. You can read more about this here, here and here. Presumably, Binti Jua knows nothing about an invisible magic man, and certainly not the invisible magic man that numerous supernaturalists contend is supposedly "necessary" for altruistic or ethical behaviour. That last link I just provided, incidentally, highlights the fact that scientists are increasingly aware of the presence of behaviours in other species that can be classified as 'ethical', and indeed, much of the primate research of Frans de Waal and others has brought this into sharp relief in recent years, as I documented above.

Incidentally, one of the papers above also cites the instance of Binti Jua (described briefly on page 19 of the paper, with a reference to an earlier paper describing the incident more comprehensively).

I think that should deal effectively with the "you need my magic man to be moral" canard, don't you? :)

Now, having dropped that little lot in your lap, the ability to construct mental models of relevant concepts, derive conclusions from those mental models, and act upon those conclusions, is central to the business of representation and intentionality. I therefore conclude that I've dealt with your fatuous assertion that I am unfamiliar with these concepts with the above.

Andrew4Handel wrote:I don't follow Papineaus above comment but it comes in the context of a university course book on how language can have meaning and how sounds can represent, what thought constitues and what an intentional stance is.

I suppose you have studied the philosophy of language?...maybe you were under the gross illussion that scientists and theorists had an explanation for language?


I'm sure that Noam Chomsky and every compiler writer on the planet is so grateful to you for telling them that they don't know anything about their core disciplines. You might also want to look this up. Before you're tempted to dismiss that link, I suggest you get in touch with anyone who takes part in natural language research in any decent computer science department, and spend a couple of hours learning about his research. It should prove highly educational.

Oh, and while you're at it, stay tuned, because I'm going to hit you with something interesting with respect to the evolution of language capability in humans. Don't go away now ...

Andrew4Handel wrote:
Calilasseia wrote: As I have stated elsewhere, science is in the business of testing assumptions and presuppositions to destruction.


And how exactly can you test theories about the long gone past to destruction?


HA HA HA HA HA HA!

YOU were the one who purported to be in a position to tell ME that I was ignorant of the scientific method earlier?

HA HA HA HA HA HA!

Let me give you a crash course in how it's done, shall we?

One of the central ideas in science is that the laws of physics have remained largely unchanged in 13.6 billion years or so. Now, how do we test this? Simple. We find instances of well defined physical phenomena, that we can reproduce here in the laboratory, and which occurred in the past. If the laws of physics underwent any substantive change over that time, then the outcomes of those two instances of the relevant phenomena will be substantively different. If the laws of physics haven't changed substantively, then the outcomes of those two instance of the relevant phenomena will be the same.

Now, one useful set of phenomena is the class of phenomena known as radioactive decays. Thousands of different decay processes have been observed in the laboratory, quantfied in detail with respect to such matters as half-life, isotopic ratios etc., and consequently, the behaviour of various radionuclide decays is known to an exquisite degree. If you have any doubts about this, then go and look up the [utl=http://www.kayelaby.npl.co.uk/atomic_and_nuclear_physics/4_6/4_6_1.html]Table of the Nuclides[/url] in Kaye & Laby's Tables of Physical & Chemical Constants, which contains vast swathes of relevant data - indeed, due to the sheer volume of data, they've had to split the table into 11 parts. Scroll down that page, and learn just how much we know about radionuclides and their decay behaviour.

Now, armed with that information, we can look around for instances of naturally occuring radionuclide decays that took place a long time ago, and see if those instances yield data consistent with the data for present day observed decay sequences. One source of such data is known as SN1987A. This is a supernova remnant, the star generating it was observed in telescopes to have detonated back in 1987, and since it was the first such observed supernova detonation of the year, it was given the the designation I've just cited. However, because the star in question was located in the Large Magellanic Cloud, it was some distance from Earth. 169,000 light years, to be precise. Which means that the light reaching us from that supernova took 169,000 years to reach us. Which means that any spectroscopic data obtained from that supernova pertains to events that took place 169,000 years ago. As a consequence, given that scientists have constructed a detailed and fairly elegant theory about the behaviour of supernovae, and the formation of various elements by supernovae and supernova remnants, this event, being the first to be observed in detail by modern space-based instrumentation, gave scientists the perfect opportunity not only to test their ideas about supernova behaviour, but also provided a neat test of the notion that the laws of physics haven't changed substantively over a long period of time.

This was achieved by observing the appearance of different elements in the supernova remnant over time. Now, scientists have theorised that in the aftermath of a supernova, elements are formed in a specific sequence, via a process known as the r-process, which involves new nuclear species being formed from absorption of neutrons in the dense neutron flux around a supernova, followed by decay along what is termed the 'neutron drip line'. As a consequence thereof, scientists had before them the perfect opportunity to test these ideas. Which could be tested courtesy of the fact that when those new nuclear species were formed, they would not only be bathed in a neutron flux, but a flux of electromagnetic radiation, which would result in the generation of characterisitc absorption and emission spectra for each of the elements in question. Cosnequently, by analysing the light emitted from SN1987A over a long period of time, the emergence of new nuclear species could be observed, and relevant isotopic ratios computed from the data, to determine if the theory matched observations.

And guess what? The data and theory match precisely.

Now, the key point here, is not just that the scientists got it right (courtesy, once again, of paying attention to reality instead of made up shit), but that their observations provide evidence that the laws of physics haven't changed in 169,000 years. Any substantive change in those laws would have resulted in significant, observable changes in the spectra being analysed. That no such changes have been observed leads to the conclusion that the laws of physics haven't changed substantively in 169,000 years.

Oh, and before you try erecting the tiresome creationist assertions about changes in the speed of light, apart from the fact that this apologetic fabrication effectively turns creationists' god into a cosmic liar, there's the little matter of the fact that SN1987A has been subject to measurements allowing the size of the outermost features to be determined via trigonometric parallax, which means that for creationists to be right, not only does the whole of physics have to be wrong, but trigonometry has to be wrong as well. I contend that the most parsimonious explanation is that it's the creationists that have got it wrong.

Therefore, the above is a direct test of any assertion that the laws of physics were substantively different in the past, and the data derived therefrom falsifies that assertion.

There, that's how it's done. I can cite relevant scientific papers if needed.

Now, do I have to bludgeon you with the Oklo natural nuclear reactor as well, a system that allows us to push back the boundaries even further, to 1.5 billion years before present?

Part 2 follows shortly.
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Re: Concepts in Atheism & Physicalism

#72  Postby Calilasseia » Feb 19, 2011 12:26 am

Welcome to Part 2.

Andrew4Handel wrote:How can you test the Big bang to destruction


Oh dear, it's time to reprise this ...

Testing The Braneworld Collision Theory for the Big Bang

Allow me to present two scientific papers by Neil Turok, one of the world's leading theoretical physicists, which contain the exposition of a testable naturalistic mechanism for the instantiation of the observable universe:

Colliding Branes In Heterotic M-Theory by Jean-Luc Jehners, Paul McFadden and Neil Turok, arXiv.org (12 February 2007) [Download from here]

Generating Ekpyrotic Curvature Perturbations Before The Big Bang by Jean-Luc Lehners, Paul McFadden, Neil Turok & Paul J. Steinhardt, arXiv.org, 19th February 2007 [Download from here]

Let's look at the first of the above two scientific papers. The abstract reads as follows:

Turok et al, 2007 wrote:We study the collision of two flat, parallel end-of-the-world branes in heterotic M-theory. By insisting that there is no divergence in the Riemann curvature as the collision approaches, we are able to single out a unique solution possessing the local geometry of (2d compactified Milne)/Z[sub[2[/sub] × R3, times a finite-volume Calabi-Yau manifold in the vicinity of the collision. At a finite time before and after the collision, a second type of singularity appears momentarily on the negative-tension brane, representing its bouncing off a zero of the bulk warp factor. We find this singularity to be remarkably mild and easily regularised. The various different cosmological solutions to heterotic M-theory previously found by other authors are shown to merely represent different portions of a unique flat cosmological solution to heterotic M-theory.


The paper goes on to state as its conclusions:

Turok et al, 2007 wrote:We have presented a cosmological solution describing the collision of the two flat boundary branes in heterotic M-theory. This solution is a significant step towards our goal of describing the cosmic singularity as a brane collision within the well-motivated framework of Horava-Witten theory. Requiring the collision to be the ‘least singular’ possible, i.e., that the metric tends towards (2d compactified Milne)/Z2 × R3 times a finite-volume Calabi-Yau, has two important consequences. First, it selects a single solution to the equations of motion. Second, it shifts the singularity in the Calabi-Yau volume that one might have naively expected at the brane collision to two spacetime events before and after the brane collision. We have shown these two events to be very mild singularities, which are easily removed by including an arbitrarily small amount of matter (for example scalar field kinetic energy) on the negative-tension brane. Before the initial bounce of the negative-tension brane, and after the final bounce, the solution presented here can be identified with that described by Chen et al. [11].

When the branes move at a small velocity, we expect to be able to accurately describe the solution using a four-dimensional effective theory (see e.g. [18–22] and also [12]). We shall present such a description in a companion publication [23]. If our colliding brane solution is to successfully describe the universe, we must also add potentials capable of stabilising the moduli; in particular the volume of the Calabi-Yau manifold, which determines the value of gauge couplings, and the distance between the branes, which determines Newton’s constant of gravitation. These potentials also permit us to generate an interesting spectrum of cosmological perturbations. Although the required potentials cannot yet be derived from first principles, we can study the consequences of various simple assumed forms. The results will be presented elsewhere [24].


Reference [24] cited above is the second paper I listed earlier, which was described as being "in press" at the time of the publication of the first paper. This second paper opens with the following:

Turok et al, 2007 wrote:We analyze a general mechanism for producing a nearly scale-invariant spectrum of cosmological curvature perturbations during a contracting phase preceding a big bang, that can be entirely described using 4d effective field theory. The mechanism, based on first producing entropic perturbations and then converting them to curvature perturbations, can be naturally incorporated in cyclic and ekpyrotic models in which the big bang is modelled as a brane collision, as well as other types of cosmological models with a pre-big bang phase. We show that the correct perturbation amplitude can be obtained and that the spectral tilt ns tends to range from slightly blue to red, with 0.97 < ns < 1.02 for the simplest models, a range compatible with current observations but shifted by a few per cent towards the blue compared to the prediction of the simplest, large-field inflationary models.


The conclusions of this paper are as follows:

Turok et al, 2007 wrote:The entropic mechanism for generating approximately scale-invariant curvature perturbations in a contracting universe has two appealing features. First, it can be analyzed entirely within the context of 4d effective theory. For those who were skeptical about the ekpyrotic and cyclic models because of their apparent reliance on 5d effects to create curvature perturbations, this work shows that there is another, more prosaic mechanism that can be totally understood in familiar terms. This should terminate the debate on whether it is possible, in principle, to generate curvature perturbations in a pre-big bang phase.

The second attractive feature is that the essential elements occur quite naturally in extra-dimensional theories like string and M-theory. There is no shortage of scalar field moduli, and, quite generically, these fields can possess negative and steeply decreasing potentials of the ekpyrotic form. In this situation, approximate scaling solutions exist in which several fields undergo ekpyrosis simultaneously so that nearly scale-invariant entropy perturbations are naturally generated. Furthermore, if the relevant scalar field trajectory encounters a boundary in moduli space (like that described in Ref. [15]), then as the trajectory reflects off the boundary, entropy perturbations are naturally converted into curvature perturbations with the identical large-scale power spectrum. We hasten to add that, although we have only presented here the concrete example of heterotic M-theory, it is clear that the present formalism is generic and can be applied to other types of pre-big bang models, including those that do not rely on there being extra dimensions.

We have also seen that the entropic mechanism has an interesting signature. Because of the gravitational contribution to the spectral tilt of the entropically-induced perturbations, the spectrum is typically a few per cent bluer than the time-delay (Newtonian potential) perturbations or the density perturbation in inflation. To push the inflationary perturbations into this bluer range requires adding extra degrees of otherwise unnecessary fine-tuning, as delineated in Ref. [21]. In particular, Ref. [21] shows that the natural range for inflationary models is 0.93 < ns < 0.97, whereas entropically-induced spectra tend to lie in a range that is a few per cent bluer, roughly 0.97 < ns < 1.02 by our estimates. Hence, a highly precise measure of the spectral tilt at the one per cent level or better could serve as an indicator of which mechanism is responsible. For example, a value of ns = 0.99 is awkward to obtain with inflation but right in the middle of the predicted range for pre-big bang entropically-induced perturbations.


In other words, the two papers, taken together, provide not only a mechanism for the formation of the universe using a pre-Big-Bang physics that is consistent with the known physics of our universe, but also provides a means of testing experimentally whether or not the conclusions of the authors are correct, namely by analysing the spectrum of gravitational waves passing through the universe. If that spectrum of waves is observed to be shifted toward shorter wavelengths, then this provides confirmation that the authors have alighted upon a mechanism that is consistent with observational reality. Which, needless to say, is why research and development money is now being devoted to the matter of gravitational wave detection, so that this question can be answered either way. Therefore we have a real world phenomenon to observe that will provide an answer as to whether Turok et al have alighted upon a consistent mechanism that is in accord with observational reality for the formation of the known universe, a mechanism moreover that allows the formation of other, causally separated universes and which may even, in the fullness of time, allow us to experimentally form new universes via laboratory means.

Note how I ended the above paragraph. Build a sufficiently sophisticated particle accelerator that would be capable of reproducing the requisite conditions, and that particle accelerator could spawn a new universe by fostering an appropriate braneworld collision. Of course, getting to the point where this is an engineering reality is the hard part, but the above papers make it theoretically possible. All we would need to be able to do is generate a positive-tension brane and a negative-tension brane by appropriate means in a suitable piece of experimental apparatus, collide them, and a new universe would be the result. Of course, that new universe would become causally separated from ours in a very short space of time (around 10-35 seconds), so we would have to devise means of detecting events upon such a tiny time scale to allow us to confirm that we had indeed succeeded in doing this in a laboratory experiment, but the fact that we would be able to do so by the simple expedient of harnessing natural processes would make any supernatural "creator" utterly irrelevant. After all, if we could construct a machine that could perform this function, using nothing more than an application of physics, the idea that some magical entity was a necessary requirement would be dead in the water.

Oh look. A testable mechanism for the instantiation of the universe, and all the matter contained therein, that doesn't need an invisible Magic Man. Game Over.

Andrew4Handel wrote:or the idea that the brain evolved.


Oh dear, you REALLY are a sucker for punishment tonight, aren't you? If the papers I presented above on the ventromedial pre-frontal cortex aren't enough, then it's time to reprise this, which was written to deal with another creationist's fatuous assertions that evolution never took place:

ASPM and FOXP2 : Evolution Of Genes Implicated In Brain Size, Advanced Cognition And Language Development

The relevant papers I'm going to bring here are these:

Accelerated Evolution of the ASPM Gene Controlling Brain Size Begins Prior to Human Brain Expansion by Natalay Kouprina, Adam Pavlicek, Ganeshwaran H. Mochida, Gregory Solomon, William Gersch, Young-Ho Yoon, Randall Collura, Maryellen Ruvolo, J. Carl Barrett, C. Geoffrey Woods, Christopher A. Walsh, Jerzy Jurka and Vladimir Larionov, Public Library of Science Biology, 2(5): e126 (23rd March 2004)

Evolution of the Human ASPM Gene, A Major Determinant Of Brain Size by Jianzhi Ziang, Genetics, 165: 2063-2070 (December 2003)

Molecular Evolution Of Microcephalin, A Gene Determining Human Brain Size by Yin-Qiu Wang and Bing Su, Human Molecular Genetics, 13(11): 1131-1137 (1st June 2004)

Molecular Evolution of FOXP2, A Gene Involved In Speech And Language by Wolfgang Enard, Molly Przeworski, Simon E. Fisher, Cecilia S. L. Lai, Victor Wiebe, Takashi Kitano Anthony P. Monaco and Svante Pääbo, Nature, 418: 869-872 (22 August 2002)

Let's take a look at these papers shall we?

First, the papers on ASPM:

Kouprina et al, 2004 wrote:Primary microcephaly (MCPH) is a neurodevelopmental disorder characterized by global reduction in cerebral cortical volume. The microcephalic brain has a volume comparable to that of early hominids, raising the possibility that some MCPH genes may have been evolutionary targets in the expansion of the cerebral cortex in mammals and especially primates. Mutations in ASPM, which encodes the human homologue of a fly protein essential for spindle function, are the most common known cause of MCPH. Here we have isolated large genomic clones containing the complete ASPM gene, including promoter regions and introns, from chimpanzee, gorilla, orangutan, and rhesus macaque by transformation-associated recombination cloning in yeast. We have sequenced these clones and show that whereas much of the sequence of ASPM is substantially conserved among primates, specific segments are subject to high Ka/Ks ratios (nonsynonymous/synonymous DNA changes) consistent with strong positive selection for evolutionary change. The ASPM gene sequence shows accelerated evolution in the African hominoid clade, and this precedes hominid brain expansion by several million years. Gorilla and human lineages show particularly accelerated evolution in the IQ domain of ASPM. Moreover, ASPM regions under positive selection in primates are also the most highly diverged regions between primates and nonprimate mammals. We report the first direct application of TAR cloning technology to the study of human evolution. Our data suggest that evolutionary selection of specific segments of the ASPM sequence strongly relates to differences in cerebral cortical size.


So, one of the genes that acts as a determinant of brain size, and as a consequence brain complexity in primates, has been found to have been subject to strong positive selection courtesy of the relevant Ka/Ks ratios (which are used to differentiate between purifying selection, neutral drift and positive selection for any given gene). A gene that plays an important role in human brain development has now been determined to contain within its sequence evidence for positive selection in precisely those areas that are most divergent between primates and other lineages, and the divergence in those areas increases in humans compared to other primates. Moreover, mutations in the human ASPM gene are directly correlated with primary microcephaly, a brain disorder in which the brain size is severely reduced compared to a typical human brain, and in one of those serendipitous correspondences of observed data with evolutionary theory that creationists like to say don't exist, the brain size in individuals exhibiting primary microcephaly is comparable to that of early hominds.

The authors continue as follows:

Kouprina et al, 2004 wrote:Introduction

The human brain, particularly the cerebral cortex, has undergone a dramatic increase in its volume during the course of primate evolution, but the underlying molecular mechanisms that caused this expansion are not known. One approach shedding light on the molecular mechanisms of brain evolution is the analysis of the gene mutations that lead to defects in brain development. Among the best examples of such defects is the human primary microcephaly syndrome. Primary microcephaly (MCPH) is an autosomal recessive neurodevelopmental disorder in which the brain fails to achieve normal growth. The affected individuals have severe reduction in brain size; however, the gyral pattern is relatively well preserved, with no major abnormality in cortical architecture (McCreary et al. 1996; Mochida and Walsh 2001). Moreover, there are no recognizable abnormalities in the organs other than the central nervous system. The most common cause of MCPH appears to be mutations in the ASPM gene (Roberts et al. 2002).

The ASPM gene encodes a 10,434-bp-long coding sequence (CDS) with 28 exons, and spans 65 kb of genomic DNA at 1q31. ASPM contains four distinguishable regions: a putative N-terminal microtubule-binding domain, a calponin-homology domain, an IQ repeat domain containing multiple IQ repeats (calmodulin-binding motifs), and a C-terminal region (Bond et al. 2002). Though the exact function of the human ASPM in the brain needs to be clarified, the homologue in the fruit fly, Drosophila melanogaster, abnormal spindle (asp), is localized in the mitotic centrosome and is known to be essential for both the organization of the microtubules at the spindle poles and the formation of the central mitotic spindle during mitosis and meiosis. Mutations in asp cause dividing neuroblasts to arrest in metaphase, resulting in reduced central nervous system development (Ripoll et al. 1985; do Carmo Avides et al. 2001; Riparbelli et al. 2001). In the mouse (Mus musculus) brain, the Aspm gene is expressed specifically in the sites of active neurogenesis. Expression in the embryonic brain was found to be greatest in the ventricular zone, which is the site of cerebral cortical neurogenesis (Bond et al. 2002). This expression profile suggests a potential role for Aspm in regulating neurogenesis.

Interspecies comparisons of ASPM orthologs have shown their overall conservation, but also a consistent correlation of greater protein size with larger brain size (Bond et al. 2002). The increase in protein size across species is due mainly to the increased number of IQ repeats, suggesting that specific changes in ASPM may be critical for evolution of the central nervous system.

In an attempt to reconstruct the evolutionary history of the ASPM gene, we isolated large genomic clones containing the entire ASPM gene in several nonhuman primate species. Sequence analysis of these clones revealed a high conservation in both coding and noncoding regions, and showed that evolution of the ASPM gene might have been under positive selection in hominoids. These clones could also provide important reagents for the future study of ASPM gene regulation in its native sequence context.


So, we have a gene that is known to exist in a wide variety of taxa, and in one of those taxa, has been demonstrated experimentally to be responsible for proper development of central nervous system components, with mutations in that gene resulting in reduced central nervous system development because of mitotic arrest in metaphase that takes place in affected central nervous system neuroblasts. Moreover, experimental work has alighted upon no anomalies arising in systems other than the central nervous system as a result of mutations in this gene. So already we have strong evidence that this gene plays a major role in central nervous system development, which is augmented by the finding that mutations in human ASPM are associated with a well understood diagnosable anomaly of brain development.

Moving on, the authors state their results:

Kouprina et al, 2004 wrote:Results

Comparison of Genomic Organization of the ASPM Genes in Primates

Homologues from chimpanzee (Pan troglodytes), gorilla ([/i]Gorilla gorilla[/i]), orangutan (Pongo pygmaeus), and rhesus macaque (Macaca mulatta) were isolated by transformation-associated recombination (TAR) cloning in yeast (Saccharomyces cerevisiae), the technique allowing direct isolation of a desirable chromosomal region or gene from a complex genome without constructing its genomic library (Kouprina and Larionov 2003). The method exploits a high level of recombination between homologous DNA sequences during transformation in the yeast. Since up to 15% divergence in DNA sequences does not prevent selective gene isolation by in vivo recombination in yeast (Noskov et al. 2003), for cloning purposes, a TAR vector was designed containing short human ASPM-gene-specific targeting hooks specific to the exon 1 and 39 noncoding regions (see ‘‘Materials and Methods’’). The TAR cloning scheme for isolating the ASPM gene homologues from nonhuman primates is shown in Figure 1. The yield of ASPM-positive clones from chimpanzee, gorilla, orangutan, and rhesus macaque was the same as that from the human DNA, suggesting that most homologous regions from nonhuman primates can be efficiently cloned by in vivo recombination in yeast using targeting hooks developed from human sequences.

We have compared complete gene sequences from primate species with a 65-kb, full-size human ASPM gene. All the analyzed genes are organized into 28 exons encoding a 3,470–3,479-amino-acid-long protein. ASPM genes start with an approximately 800-bp-long CpG island, that harbors promoter sequences, 59 untranslated regions, and the first exon (Figure 2). ASPM sequences share a high degree of conservation (Figure 2H), and pairwise DNA identity ranges from 94.5% for macaque and gorilla to 99.3% for the human–chimpanzee comparison (Table 1). Multiple alignment of the genes revealed a low proportion of indels. Only ten insertions/deletions equal to or longer than 50 bp have been found, all of them located within introns (Figure 2B). Seven detected insertions were mainly associated with repetitive DNA: two (AT)n microsatellite expansions, three Alu insertions, including retroposition of AluYi9 in the orangutan–gorilla–chimpanzee–human clade, and retroposition of a new macaque-specific AluY subfamily similar to human AluYd2. Analysis of eight different macaque individuals showed that this particular insertion is polymorphic in the macaque population (data not shown), and thus the insertion appears to be very recent. One macaque-specific 245-bp-long insertion is linked to expansion of a 49-bp-long, minisatellitelike array. The remaining macaque-specific insertion (50 bp) is nonrepetitive. A closer analysis suggests that the insert is not a processed pseudogene of known genes (data not shown).

Of the two detected deletions, the macaque-specific 72-bp long deletion appears to be associated with nonrepetitve DNA. The second one, an 818-bp-long deletion in orangutan, was probably caused by homologous Alu–Alu recombination (see below and Figure S1). The remaining indels are related to expansion/contraction of a short minisatellite array. It was caused either by a 53-bp expansion in the gorilla–chimpanzee–human clade or by two independent deletions/contractions in the macaque and orangutan lineages.

An approximately 3-kb-long intronic segment between exons 4 and 5 is present in several copies in the genome (Figure 2E; Figure S2). Closer analysis of the human genome confirmed that copies of this region are homologous to 24 segmental duplications located mainly in telomeric regions of Chromosomes 1–8, 10, 11, 16, 19, 20, and Y. Based on the sequence similarity and the presence of an L1P4 LINE insertion at the 5' end, the most closely related are three duplications at 7q11–13. The most similar copy is located on Chromosome 7 and shares 93% identity with the ASPM intronic segment. Five duplications are located on Chromosome 1; the closest copy is found 27 Mb away from the ASPM gene.

We looked for several common motifs associated with genomic breakpoints in cancers (Abeysinghe et al. 2003). Figure 2F shows the positions of such potentially unstable oligonucleotides. Interestingly, the orangutan-specific deletion (Figure 2B) has its 5' breakpoint located just 1 bp upstream of a sequence 100% identical to the chi-like consensus motif GCWGGWGG (see Figure S1). The chi motif is recognized by the RecBCD-mediated recombination pathway in prokaryotes and seems to be associated with rearrangements in the human genome (Dewyse and Bradley 1991; Chuzhanova et al. 2003). Both deletion breakpoints in the orangutan deletion are located within 5' parts of two Alu sequences, suggesting that the deletion was created by homologous Alu–Alu recombination. Similar homologous recombinations with breakpoints located near chi-like motifs in 5' regions of Alu sequences were described previously (Chen et al. 1989; Rudiger et al. 1995).

In summary, despite the presence of a few indels, coding and noncoding regions of ASPM homologues show a marked degree of conservation.


Note how differences between human/chimpanzee and other primate lineages, when located, are accompanied by specification of appropriate mechanisms for the generation of those differences in the respective lineages, and whilst the exact mechanism applicable remains to be determined in some cases, the fact that the observed data are consistent with known mutational mechanisms once again reinforces our confidence in the results.

The authors move on to state the following:

Kouprina et al, 2004 wrote:Evolution of the ASPM Protein

We have analyzed ASPM CDSs from six primate species: human, chimpanzee, gorilla, orangutan, rhesus macaque, and African green monkey (Cercopithecus aethiops). Except for orangutan and rhesus macaque, two or more ASPM CDSs were used for analysis. ASPM proteins showed the same overall length and domain structure (Figure 3A). The IQ repeat domain contains the same number of repeats, suggesting that their expansion occurred in early primate evolution. The CDSs are, as expected, more conserved than the complete gene sequences with promoter and intronic regions (Table 2; Table 3). Only six short indels were identified (Figure 3B).

From the DNA and protein conservation profiles (Figure 3I), ASPM segments evolve differently along the length of the CDS. N- and C-terminal regions and the region corresponding to exons 5–15 are conserved. In contrast, exons 3 and 4 and the complete IQ repeat domain (positions 1,267–3,225) are more variable. Indeed, nonsynonymous substitutions in hominoid primates (Figure 3C) and in ancestral lineages (Figure 3D) and nonsynonymous polymorphism (Figure 3E) are nearly absent in the conserved central (exons 5–15) and C-terminal regions. This pattern indicates different rates of evolution along the ASPM protein, visualized by plots of synonymous Ks and nonsynonymous Ka rates (Figure 3H) and supported by phylogenetic analysis (see below and Figure 4). It is notable that the comparison of the primate and mouse proteins also revealed the same pattern of conservative and nonconservative regions along ASPM protein (Figure S3).

Analysis of the nonsynonymous/synonymous substitution ratio (x = Ka/Ks) revealed an elevated value in the human branch (Figure 4A). According to the likelihood ratio test, the human x rate is significantly different from the rate in the rest of the tree (p < 0.05). Also the model that the complete gorilla–chimpanzee–human clade is evolving at one x rate different from that in the rest of the tree is well supported (p < 0.01). Because ASPM consists of regions with different degrees of sequence conservation (see Figure 3), we separately analyzed a conserved region (exons 5–15 plus a small part of exon 16) and a variable IQ repeat domain. As can be seen (Figure 4B) the conserved region has all branches shorter, indicating overall a slower rate of evolution. In the human lineage, the x ratio equals zero; however, the test for whether the human branch has a different (lower) x rate than the rest did not yield significant values. In contrast, the tree based on the variable IQ repeat domain exhibits x values greater than one for the human and gorilla branches (Figure 4C). The likelihood ratio test supports the model in which human and gorilla lineages evolved under a significantly higher x ratio than the rest of the tree. Similar results were obtained for exon 18 with additional sequences from two New World monkeys (Figure 4D). As seen from Figure 4A–4D, different sequences from African green monkey, gorilla, and chimpanzee individuals result in different x values for their corresponding terminal branches. One chimpanzee sequence also produced an x ratio greater than one for exon 18 (Figure 4D). It is worth noting that neither codon bias nor selection on third codon positions seemed to influence the synonymous rate Ks strongly (Table S1). Therefore, the high Ka/Ks ratios in human and gorilla are likely to be products of adaptive evolution.

Sequencing of two CDSs in African green monkey, three in gorilla, and three in chimpanzee allowed us to look for ASPM polymorphism in those species (see Figure 3E). Human polymorphism data from ASPM mutant haplotypes are not representative of wild-type variation so were not used in these comparisons. For African green monkey, five synonymous and five nonsynonymous changes were found between two sequences. The gorilla and chimpanzee CDSs in particular showed an apparently high degree of replacement polymorphism. Gorilla polymorphism included 35 point mutations (15 silent mutations and 21 replacements). Chimpanzee sequences differed in five synonymous and 11 nonsynonymous sites. In order to interpret this seemingly high level of observed polymorphism, intraspecific diversity was compared to interspecific diversity using the McDonald and Kreitman test (McDonald and Kreitman 1991). In the case of chimpanzee polymorphism compared to divergence with human, we could not reject the null hypothesis that polymorphism and divergence between species were significantly different (William’s adjusted G statistic = 0.083, chi-square with 1 d.f., not significant; values based on PAML-generated Ka and Ks values using the free ratio model). Gorilla polymorphism was compared to divergence between the gorilla common ancestor and the human–chimpanzee common ancestor. In this case we can reject the null hypothesis (William’s adjusted G statistic = 122.45, chi-square with 1 d.f., p < 0.001) to conclude that the pattern of gorilla polymorphism is therefore different from the divergence pattern. Indeed gorilla polymorphism is less than variation resulting from divergence: within species, the x ratio is 1.43 for gorillas compared to 2.2 for the divergence between the gorilla common ancestor and the human–chimpanzee common ancestor. Intraspecific variation, although seemingly unusual in showing so many replacement substitutions in both chimpanzee and gorilla, is less than or in line with what we have observed for ASPM divergence between species. Therefore, relaxation of selection cannot explain the high nonsynonymous/synonymous substitution ratios among African hominoids, further supporting the idea that adaptation has occurred in ASPM.


For those unfamiliar with Ka/Ks ratios, Ks is the number of synonymous mutations. These are mutations that result in a codon that codes for the same amino acid as the codon that existed prior to mutation - for example, the codons ATT and ATC both code for the amino acid isoleucine, so a change from an ATT codon to an ATC codon is a synonymous mutation. Ka is the number of non-synonymous mutations, for example a change from ATT (coding for isoleucine) to ATG (which codes for methionine, and also acts as a start codon). If the ratio Ka/Ks is less than one, then the gene in question is subject to purifying selection (in other words, most mutations in this gene are selected against because they are deleterious). If the Ka/Ks ratio is very close to 1, then the gene is subject to neutral drift. If the Ka/Ks ratio is greater than one, then the gene is subject to positive selection (mutations in the gene that have occurred have been beneficial and thus disseminated to future generations). The important tests performed upon the ASPM gene yield Ka/Ks ratios greater than one in those primate lineages closest to humans, with the human ASPM gene possessing the largest Ka/Ks ratio, indicating that positive selection took place on the ASPM gene leading to an increase in brain size.

Let's catch up with the authors again in the discussion section:

Kouprina et al, 2004 wrote:Discussion

In this study, we applied TAR cloning technology to investigate molecular evolution of the ASPM gene, which is involved in determining the size of the human brain and in which mutations lead to MCPH. The ASPM homologue in the fruit fly is essential for spindle function, suggesting a role for this gene in normal mitotic divisions of embryonic neuroblasts. Complete gene homologues from five primate species were isolated and sequenced. In agreement with the predicted critical role of ASPM in brain development, both coding and noncoding regions of ASPM homologues showed a marked degree of conservation in humans, other hominoids, and Old World monkeys. The differences found in noncoding regions were small insertions/deletions and lineage-specific insertions of evolutionarily young Alu elements into introns.

Analysis of nonsynonymous/synonymous substitution ratios indicates different rates of evolution along the ASPM protein: part of ASPM evolved under positive selection while other parts were under negative (purifying) selection in human and African ape lineages. Such ‘‘mosaic’’ selection has been previously described for other proteins (Endo et al. 1996; Crandall et al. 1999; Hughes 1999; Kreitman and Comeron 1999). When our work was completed, the paper by Zhang supporting accelerated evolution of the human ASPM was issued (Zhang 2003). However, because the author did not analyze the gorilla gene homologue, he concluded that accelerated sequence evolution is specific to the hominid lineage. Our finding that selection on ASPM begins well before brain expansion suggests that the molecular evolution of ASPM in hominoids may indeed be an example of a molecular ‘‘exaptation’’ (Gould and Vrba 1982), in that the originally selected function of ASPM was for something other than large brain size.

In the case of ASPM, rapidly evolving residues are mainly concentrated in the IQ repeat domain containing multiple IQ motifs, which are calmodulin-binding consensus sequences. While there is no direct evidence yet, it is likely that the function of human ASPM is modulated through calmodulin or calmodulinlike protein(s). Previous interspecies comparisons of ASPM proteins have shown a consistent correlation of greater protein size with larger brain size mainly because of the number of IQ repeats (Bond et al. 2002). For example, the asp homologue of the nematode Caenorhabditis elegans contains two IQ repeats, the fruit fly—24 IQ repeats, and the mouse—61 IQ repeats, and there are 74 IQ repeats in humans (Bond et al. 2002). ASPM homologues in the nonhuman primates examined here contain the same number of IQ repeats as human, supporting the idea that repeat expansion occurred prior to the anthropoid divergence (which gave rise to New World monkeys, Old World monkeys, and hominoids) and possibly even earlier in primate evolution. IQ motifs are seen in a wide variety of proteins, but the ASPM proteins in primates are unique, because they have the largest known number of IQ repeats. Given the proposed role of ASPM in regulating divisions of neuronal progenitors, both the number of repeats and the particular amino acid substitutions in the IQ repeats may be strongly related to brain evolution.

Human ASPM gene mutations which lead to MCPH provide a direct link between genotype and phenotype. ASPM is yet another example on the growing list of positively selected genes that show both accelerated evolution along the human lineage and involvement in simple Mendelian disorders (Clark et al, 2003). However, ASPM is unique because its distinctive pattern of accelerated protein evolution begins several million years prior to brain expansion in the hominid lineage. Absolute brain size in orangutans (430 g in males; 370 g in females) is barely different from that in gorillas (530 g in males; 460 g in females) and common chimpanzees (400 g in males; 370 g in females) (Tobias 1971), yet accelerated ASPM evolution began in the common ancestor of gorillas, chimpanzees, and humans, approximately 7–8 million years ago. Only much later did brain expansion begin in hominids, starting at 400–450 g roughly 2–2.5 million years ago and growing to its final current size of 1350–1450 g approximately 200,000–400,000 years ago (Wood and Collard 1999). Therefore genotypic changes in ASPM preceded marked phenotypic changes in hominoid brain evolution, at least at the level at which they have currently been studied. The molecular changes in ASPM may predict the existence of differences in early neurogenesis between orangutans, on the one hand, and gorillas, chimpanzees, and humans, on the other, which may manifest as more subtle differences in brain anatomy than gross changes in brain volume.

How might evolutionary changes in the ASPM protein affect cerebral cortical size? One potential mechanism might be that changes in ASPM induce changes in the orientation of the mitotic spindle of neuroblasts. Normally, neural precursor cells can have mitotic spindles oriented parallel to the ventricle or perpendicular to the ventricle. Mitoses in which daughter cells are oriented next to one another at the ventricular zone are typically ‘‘symmetric’’ in that a single progenitor cell generates two progenitor cells, causing exponential expansion of the progenitor pool. In contrast, mitoses that generate daughter cells that are vertically arranged are typically ‘‘asymmetric’’ so that one daughter cell becomes a postmitotic neuron, whereas the other daughter cell remains as a progenitor, causing only a linear increase in cell number. Control of this proliferative symmetry can cause dramatic alterations in cerebral cortical size (Chenn and Walsh 2002), and so changes in ASPM could regulate cortical size by making subtle changes in spindle orientation. Alternatively, evolutionary changes in ASPM may not themselves have led to increase in the size of the brain, but instead perhaps ASPM might be essential to insure faithful DNA replication and proper chromosome segregation. In rodents, a surprising number of cerebral cortical neurons are aneuploid (Rehen et al. 2001). Perhaps directed selection of specific domains of ASPM helps insure faithful chromosome segregation to allow a larger number of cerebral cortical neurons to be formed without an unduly high incidence of chromosome aneuploidy.

Functional genomics studies are clearly needed to elucidate the exact nature of the molecular mechanisms affected by ASPM gene evolution in hominoids. Here, we have demonstrated the utility of TAR cloning for evolutionary sequence comparisons among humans and other primates. In addition, the ASPM TAR clones isolated in these studies could provide valuable reagents for studying ASPM gene regulation in its natural sequence context. Overall, we anticipate this technology will be extremely useful in studying the evolution of other genes that may be responsible for uniquely human traits.

Note

The related paper by Evans et al. (2004) was published in Human Molecular Genetics shortly after this paper was submitted.


So, not only has a correlation between ASPM and human brain evolution been established, but a possible mechanism by which it affects brain size, courtesy of the orientation of the mitotic spindle in dividing brain cells, has been proposed, and will doubtless be the subject of further research in order to confirm or refute the hypothesis with respect to the known mitotic spindle role that this gene plays.

Moving on, let's now look at the other ASPM paper:

Ziang, 2003 wrote:ABSTRACT

The size of human brain tripled over a period of 2 million years (MY) that ended 0.2–0.4 MY ago. This evolutionary expansion is believed to be important to the emergence of human language and other high-order cognitive functions, yet its genetic basis remains unknown. An evolutionary analysis of genes controlling brain development may shed light on it. ASPM (abnormal spindle-like microcephaly associated) is one of such genes, as nonsense mutations lead to primary microcephaly, a human disease characterized by a 70% reduction in brain size. Here I provide evidence suggesting that human ASPM went through an episode of accelerated sequence evolution by positive Darwinian selection after the split of humans and chimpanzees but before the separation of modern non-Africans from Africans. Because positive selection acts on a gene only when the gene function is altered and the organismal fitness is increased, my results suggest that adaptive functional modifications occurred in human ASPM and that it may be a major genetic component underlying the evolution of the human brain.


And, appositely enough, the Kouprina et al paper cites this paper by Ziang in its list of references as one of the supporting papers providing additional confirmation of the results.

Ziang continues with:

Ziang, 2003 wrote:AMONG mammals, humans have an exceptionally big brain relative to their body size. For example, in comparison with chimpanzees, the brain weight of humans is 250% greater while the body is only 20% heavier (McHenry 1994). The dramatic evolutionary expansion of the human brain started from an average brain weight of 400–450 g ~2–2.5 million years (MY) ago and ended with a weight of ~1350–1450 g ~0.2–0.4 MY ago (McHenry 1994; Wood and Collard 1999). This process represents one of the most rapid morphological changes in evolution. It is generally believed that the brain expansion set the stage for the emergence of human language and other high-order cognitive functions and that it was caused by adaptive selection (Decan 1992), yet the genetic basis of the expansion remains elusive. A study of human mutations that result in unusally small brains may help identify the genetic modifications that contributed to the human brain expansion. In this regard, primary microcephaly (small head) is of particular interest (Mochida and Walsh 2001; Bond et al. 2002; Kumar et al. 2002). Microcephaly is an autosomal recessive genetic disease with an incidence of 4–40 per million live births in western countries (Mochida and Walsh 2001; Kumar et al. 2002). It is defined as a head circumference >3 standard deviations below the population age-related mean, but with no associated malfunctions other than mild-to-moderate mental retardation (Mochida and Walsh 2001; Kumar et al. 2002).

The reduction in head circumference correlates with a markedly reduced brain size. Microcephaly is genetically heterogeneous, associated with mutations in at least five loci (Mochida and Walsh 2001; Kumar et al. 2002), one of which was recently identified and named ASPM (abnormal spindle-like microcephaly associated; Bond et al. 2002). Four different homozygous mutations in ASPM introducing premature stop codons were found to cosegregate with the disease in four respective families, while none of these mutations were found in 200 normal human chromosomes (Bond et al. 2002). Because the brain size of a typical microcephaly patient (430 g; Mochida and Walsh 2001; Kumar et al. 2002) is comparable with those of early hominids such as the 2.3- to 3.0-MY-old Australopithecus africanus (420 g; McHenry 1994; Wood and Collard 1999), I hypothesize that ASPM may be one of the genetic components underlying the human brain expansion. Signatures of accelerated evolution of ASPM under positive selection during human origins would strongly support my hypothesis, because the action of positive selection indicates a modification in gene function resulting in elevated organismal fitness (Zhang et al. 2002). Below I provide population genetic and molecular evolutionary evidence for the operation of such adaptive selection on ASPM.


So, let's look at the results, shall we?

Ziang, 2003 wrote:RESULTS

Elevation of dN/dS in the human ASPM lineage:

Human ASPM has 28 coding exons, spanning 62 kb in chromosome 1p31 and encoding a huge protein of 3477 amino acids (Figure 1). I determined the entire coding sequences of ASPM from one human, one chimpanzee, and one orangutan, and compared them in the phylogenetic tree of the three species (Figure 2). The orangutan sequence is used as the outgroup for humans and chimpanzees so that nucleotide substitutions on the human and chimpanzee lineages can be separated. I did not sequence the gorilla because the gorilla sequence may not be appropriate as the outgroup due to incomplete lineage sorting (Satta et al. 2000). Use of orangutan, a slightly more distant outgroup, solves this problem. A commonly used indicator of natural selection at the DNA sequence level is the ratio of the rate of nonsynonymous nucleotide substitution (dN) to that of synonymous substitution (dS). Most functional genes show dN/dS < 1, because a substantial proportion of nonsynonymous mutations are deleterious and are removed by purifying selection, whereas synonymous mutations are more or less neutral and are generally uninfluenced by selection. A gene may occasionally exhibit dN/dS > 1 when a large fraction of nonsynonymous mutations are advantageous and are driven to fixation by positive selection (Li 1997; Nei and Kumar 2000). I estimated the dN/dS ratio for ASPM in each of the three tree branches (Figure 2), using a maximum-likelihood method, and found that dN/dS is lowest in the orangutan branch (0.43), higher in the chimpanzee branch (0.66), and highest in the human branch (1.03). The hypothesis of dN/dS = 1 is rejected for the orangutan branch (P < 0.001, likelihood-ratio test), but not for the other two branches, suggesting a difference in selection has occurred. Indeed, a test of the difference in dN/dS between the human and orangutan branches gives a marginally significant result (P = 0.064), but the difference between the chimpanzee and orangutan branches is not significant (P = 0.29), nor is the difference between human and chimpanzee branches (P = 0.45). Because the dN/dS ratio between the orangutan and mouse (Mus musculus) is also low (0.29), an increase of dN/dS in humans is more likely than a decrease in orangutans. The mouse sequence (GenBank accession no. AF533752) was not included in the phylogeny-based analysis as it is relatively distantly related to the ape sequences and contains multiple insertions and deletions, which would make the inference less reliable. Similar results are obtained when I first infer the ASPM sequence for the common ancestor of humans and chimpanzees and then estimate the dN/dS ratio by counting the numbers of synonymous and non- synonymous nucleotide substitutions on each branch. For instance, this approach gives dN/dS = 1.13, 0.84, and 0.52, respectively, for the human, chimpanzee, and orangutan branches.

Complete functional relaxation does not adequately explain the elevation of dN/dS:

Two hypotheses may explain the increase in dN/dS to 1.03 during the evolution of human ASPM. First, the functional constraints and purifying selection on ASPM may have been completely relaxed and many deleterious nonsynonymous mutations were fixed by random genetic drift. Alternatively, advantageous nonsynonymous substitutions under positive selection occurred at some sites, while purifying selection acted at some other sites, resulting in an average dN/dS of ~ 1. Under the first hypothesis, ASPM has been under pure neutral evolution since the human-chimpanzee separation ~6–7 MY ago (Brunet et al. 2002). Using rates of single-nucleotide mutations and insertion/deletion mutations estimated from human-chimpanzee genomic comparisons (Britten 2002; Yi et al. 2002), I conducted a computer simulation of neutral evolution of ASPM (see materials and methods). I found that the probability that ASPM retains its open reading frame after 6 MY of neutral evolution is extremely low (1.7 × 10-4). Even when the above two mutation rates are both halved, the probability is still very small (0.014), suggesting that ASPM must have been under purifying selection. The fact that nonsense mutations in ASPM lead to microcephaly also demonstrates the presence of functional constraints on the gene. Thus, the hypothesis of complete relaxation of functional constraints and lack of purifying selection for the past 6–7 MY of human evolution is inconsistent with the data, and some sites in ASPM must have been subject to purifying selection (dN/dS < 1). This result would imply, although not prove, that some other sites are under positive selection (dN/dS > 1), so that the average dN/dS across the entire protein is ~1. However, it is difficult to rule out the possibility of an incomplete functional relaxation in human ASPM, which can lead to a dN/dS ratio of ~1 when the number of substitutions is relatively small. A population genetic study may help resolve this question.

Signatures of purifying selection from population genetic data:

The entire coding sequence of ASPM is determined from 14 human individuals of different geographic origins. A total of 33 single-nucleotide polymorphisms are found (Tables 1 and 2). The derived and ancestral alleles are inferred using the chimpanzee and orangutan sequences as outgroups. Tajima’s (1989) and Fu and Li’s (1993) tests reveal slight departure of the data from the Wright-Fisher model of neutrality (D = -1.29, P =0.081; F = -1.76, P = 0.074; Table 2). But Fay and Wu’s (2000) test, which is designed to detect recent selective sweeps, does not show a significant result (H = -2.08, P = 0.21). Thus, the negative D and F likely reflect recent population expansions and/or purifying background selection. A recent study suggested that negative D values may also be found under certain sampling schemes if there is fine-scale population differentiation (Ptak and Przeworski 2002). When the synonymous and nonsynonymous sites were analyzed separately, I detected significant negative D and F values at nonsynonymous sites (P < 0.05; Table 2), but not at synonymous sites. H is not significant at either type of site. These results suggest that the nonsynonymous sites in human ASPM are subject to purifying selection. It should be mentioned that the recombination rate in the ASPM region is ~1.8 cM/106 nucleotides (Kong et al. 2002), which translates into 1.1 × 10-3 recombination/meiosis for the sequences analyzed here. This relatively high recombination rate localizes signatures of selection to a small region surrounding the selected sites. This might in part explain the above differences in the test results between synonymous and nonsynonymous sites.

Population genetic theory predicts that deleterious mutations do not reach high frequencies in populations, while neutral and advantageous mutations do. A comparison between rare and common polymorphisms may detect purifying selection of deleterious mutations (Fay et al. 2001). Fay et al. recommended a frequency of ~10% for the derived allele as a cutoff between rare and common polymorphisms (Fay et al. 2001, 2002). In the present sample of 28 chromosomes, derived alleles that appear one or two times are regarded as rare polymorphisms, and the rest are common. Because of the limited sample size, a truly rare allele may inadvertently appear more than twice in our sample and a truly common allele may inadvertently be regarded as rare. Using probability theory, I computed that the probability of the former error is <5% for an allele with frequency <3% and the probability of the latter error is <5% for an allele with frequency >20%. Thus, the present classification of rare and common alleles is expected to be relatively accurate. I observed that nR =15 nonsynonymous and sR = 5 synonymous rare polymorphisms and nC = 5 nonsynonymous and sC = 8 synonymous common polymorphisms from the present data (Table 2; Figure 1). The ratio of nC to nR (5/15 = 0.333) is significantly lower than that of sC to sR (8/5 = 1.6; [cvhr]967[/chr]2 = 4.41, P < 0.05; Table 2). Since synonymous mutations are more or less neutral, the observed deficit of common nonsynonymous polymorphisms suggests that purifying selection has prevented the spread of nonsynonymous deleterious mutations. It is estimated by the likelihood method that there areN=7459 and S=2972 potentially nonsynonymous and synonymous sites in ASPM, respectively. Thus, for rare polymorphisms, there are nR/N = 15/7459 = 2.01 × 10-3 polymorphisms/nonsynonymous site and sR/S = 5/2972 = 1.68 × 10-3/synonymous site. Their difference is statistically insignificant (χ2 = 0.09, P > 0.5). In contrast, for common polymorphisms, the number is significantly smaller per nonsynonymous site (nC/N = 5/7459 = 0.67 × 10-3) than per synonymous site (sC/S = 8/2972 = 2.69 × 10-3; χ2 = 6.98, P < 0.01), confirming that purifying selection has reduced the number of common nonsynonymous polymorphisms. This result also suggests the absence or rareness of advantageous nonsynonymous polymorphisms of ASPM that are currently segregating in humans, as such polymorphisms would predominantly show up as common polymorphisms and render nC/N higher. This is consistent with the above result from Fay and Wu’s test. The proportion of nonsynonymous polymorphisms not under purifying selection may be estimated by (nC/N)/(sC/S) = (0.67 × 10-3)/(2.69 × 10-3) = 0.25 or by (nC/sC)/(nR/sR) = (5/8)/(15/5) = 0.21. The two estimates are close to each other and to the dN/dS ratio between the mouse and orangutan (0.29). This indicates that human ASPM is currently under relatively strong purifying selection, and the strength of selection is comparable to or even greater than that in the long-term evolution of mammalian ASPM.

Comparison of polymorphism and divergence suggests past positive selection:

Because both the synonymous and nonsynonymous common polymorphisms are largely neutral, comparing them with the fixed substitutions between humans and chimpanzees can reveal the signature of selection that has influenced the substitution processes (McDonald and Kreitman 1991; Fay et al. 2001, 2002; Smith and Eyre-Walker 2002). This comparison shows a significant excess of fixed nonsynonymous substitutions (χ2 = 3.88, P < 0.05, Table 2), suggesting that some nonsynonymous substitutions were fixed by positive selection. Because the expansion of brain size occurred in the human lineage after the human-chimpanzee split, it is more relevant to examine whether the human branch exhibits an excess of nonsynonymous substitutions. For this, the ASPM sequence of the common ancestor of humans and chimpanzees was inferred by the Bayesian method. Because the sequences considered are closely related, this inference is reliable, with the average posterior probability >0.999. Comparing the ancestral sequence with the polymorphic human sequences, I identified 16 nonsynonymous and 6 synonymous mutations that have been fixed in the human lineage (Table 2; Figure 1). Their ratio (16/6 = 2.67) is significantly greater than that for common polymorphisms (nC/sC = 5/8 = 0.63; χ2 = 4.00, P < 0.05). The number of neutral nonsynonymous substitutions may be estimated from the number of synonymous substitutions multiplied by nC/sC, which yielded 6 × (5/8) = 3.75 (Fay et al. 2001, 2002; Smith and Eyre-Walker 2002). The number of nonsynonymous substitutions unexplainable by neutral evolution is 16 - 3.75 = 12, which may have been fixed by positive selection. It should be noted that a recent population expansion can cause an overestimate of the number of adaptive substitutions when slightly deleterious mutations are present. However, such overestimation is unlikely in the present case because the current effective population size of humans, even after the recent expansion, is still smaller than the long-term effective population size separating humans and chimpanzees and the effective population size of the common ancestor of humans and chimpanzees (Takahata et al. 1995; Chen and Li 2001; Kaessmann et al. 2001; Eyre-Walker 2002). It is interesting that there is no significant excess of nonsynonymous substitutions for either the chimpanzee or orangutan branches when the common polymorphisms and substitutions are compared (P > 0.05).

IQ repeats and brain size variation:

Human ASPM contains multiple calmodulin-binding IQ repeats (Bond et al. 2002). In a comparison of putative orthologous ASPM genes from the human, mouse, fruit fly (Drosophila melanogaster), and nematode (Caenorhabditis elegans), Bond et al. (2002) noticed that organisms with larger brains have more IQ repeats, implying a possible relation of IQ repeats and brain size. In particular, the predominant difference between the human and mouse ASPM genes is a large IQ-repeat-encoding insertion of 867 nucleotides at the end of exon 18. However, my data showed no difference in the number of IQ repeats between human and chimpanzee ASPM sequences. To trace the origin of the large insertion in human ASPM, I amplified and sequenced from several mammals two DNA segments that cover most of the insertion (Figure 1). Segment I is of 212 nucleotides and segment II is of 706 nucleotides. One or both segments were obtained from species belonging to primates, Cetartiodactyla, Carnivora, and Hyracoidea, but not from mouse or hamster (Figure 3). Phylogenetic analyses were conducted to confirm that the obtained sequences are orthologous to the human sequence (Figure 4). While nonamplification of a sequence does not prove its nonexistence, the amplification of the orthologous sequence indicates its presence. From the recently established mammalian phylogeny (Murphy et al. 2001), it can be inferred that the large human insertion was already present in the common ancestor of most placental mammals, but was deleted in mouse and possibly in other rodents (Figure 3). Thus, this IQ-repeat-containing sequence does not explain the brain size variation among many nonrodent mammals.


Yes, a lot of statistical work in there. Basically, the above is a fairly involved calculation intended to extract from the data the likely number of sites that were subject to purifying selection, and the number likely to have been subject to positive selection, with a view to elucidating which sites were subject in each case to each selection process, then comparing that theoretical calculation with the observed data in order to verify the robustness of the underlying theory.

Now, at last, the discussion section!

Ziang, 2003 wrote:DISCUSSION

In the above, I provided evidence that advantageous amino acid substitutions unrelated to IQ repeats have been fixed by adaptive selection in human ASPM after the human-chimpanzee split, which strongly suggests that ASPM might be an important genetic component in the evolutionary expansion of human brain. The episode of positive selection on ASPM appears to have ended some time ago, as there is no evidence for positive selection on ASPM in current human populations; rather, relatively strong purifying selection is detected. Roughly, selective sweeps occurring in the past 0.5N generations may be detected (Fay and Wu 2000), where N is the effective population size of humans and is thought to be ~10,000 (Takahata et al. 1995; Harpending et al. 1998). That is, the positive selection detected in ASPM occurred some time between 6–7 and 0.1 MY ago (0.5 × 10,000 generations × 20 years/generation). The latter date coincides with the suggested time of migration of modern humans out of Africa (reviewed in Cavalli-Sforza and Feldman 2003). It is also interesting to note that although the precise time when positive selection acted on ASPM is difficult to pinpoint, my estimate is consistent with the current understanding that the human brain expansion took place between 2–2.5 and 0.2–0.4 MY ago (McHenry 1994; Wood and Collard 1999). Furthermore, a selective sweep in human FOXP2, a gene involved in speech and language development, has been detected (Enard et al. 2002; Zhang et al. 2002). This sweep was estimated to have occurred no earlier than 0.1–0.2 MY ago (Enard et al. 2002; Zhang et al. 2002). That is, the adaptive evolution of FOXP2 postdated that of ASPM, consistent with the common belief that a big brain may be a prerequisite for language (Decan 1992).

Studies of ASPM in model organisms can help us understand how it impacts brain size. The mouse Aspm is highly expressed in the embryonic brain, particularly during cerebral cortical neurogenesis (Bond et al. 2002). The fruit fly ortholog asp is involved in organizing and binding together microtubules at the spindle poles and in forming the central mitotic spindle (Gonzalez et al. 1990; Wakefield et al. 2001). Mutations in asp cause dividing neuroblasts to arrest in metaphase, resulting in reduced central nervous system development (Wakefield et al. 2001). The amino acid substitutions in human ASPM are located in exons 3, 18, 20, 21, and 22 (Figure 1), which encode a putative microtubule-binding domain and an IQ calmodulin-binding domain (Bond et al. 2002). These features suggest that the adaptive substitutions in human ASPM might be related to the regulation of mitosis in the nervous system, which can be tested in the future by functional assays of human ASPM as well as a laboratory-reconstructed ASPM protein of the common ancestor of humans and chimpanzees.


Oh look. Ziang mentions one of the other papers in my above list of citations, namely the Enard et al paper on FOXP2! Another one of those serendipitous happenstances. :)

Basically, Ziang presents evidence that ASPM mutations were positively selected for at an early stage in human evolution, which then led to brain expansion, and this was then followed by mutations in FOXP2 facilitating language development (more on this in a moment!).

I'll leave the microcephalin paper to one side at this juncture, except to quote the abstract (I can provide the full paper via E-Mail to anyone who wants it):

Wang & Su, 2004 wrote:Microcephalin gene is one of the major players in regulating human brain development. It was reported that truncated mutations in this gene can cause primary microcephaly in humans with a brain size comparable with that of early hominids. We studied the molecular evolution of microcephalin by sequencing the coding region of microcephalin gene in humans and 12 representative non-human primate species covering great apes, lesser apes, Old World monkeys and New World monkeys. Our results showed that microcephalin is highly polymorphic in human populations. We observed 22 substitutions in the coding region of microcephalin gene in human populations, with 15 of them causing amino acid changes. The neutrality tests and phylogenetic analysis indicated that the rich sequence variations of microcephalin in humans are likely caused by the combination of recent population expansion and Darwinian positive selection. The synonymous/non-synonymous analyses in primates revealed positive selection on microcephalin during the origin of the last common ancestor of humans and great apes, which coincides with the drastic brain enlargement from lesser apes to great apes. The codon-based neutrality test also indicated the signal of positive selection on five individual amino acid sites of microcephalin, which may contribute to brain enlargement during primate evolution and human origin.


So, ASPM and microcephalin apparently act as a genetic tag team in human brain development, and mutations in either are associated with microcephaly-class conditions. Interesting.

But now, as promised, on to FOXP2. This is a gene that is implicated in several interesting developments, namely bird song, bat echolocation, and human speech and language. Here's the abstract:

Enard et al ,2002 wrote:Language is a uniquely human trait likely to have been a prerequisite for the development of human culture. The ability to develop articulate speech relies on capabilities, such as fine control of the larynx and mouth1, that are absent in chimpanzees and other great apes. FOXP2 is the first gene relevant to the human ability to develop language2. A point mutation in FOXP2 co-segregates with a disorder in a family in which half of the members have severe articulation difficulties accompanied by linguistic and grammatical impairment3. This gene is disrupted by translocation in an unrelated individual who has a similar disorder. Thus, two functional copies of FOXP2 seem to be required for acquisition of normal spoken language. We sequenced the complementary DNAs that encode the FOXP2 protein in the chimpanzee, gorilla, orang-utan, rhesus macaque and mouse, and compared them with the human cDNA. We also investigated intraspecific variation of the human FOXP2 gene. Here we show that human FOXP2 contains changes in aminoacid coding and a pattern of nucleotide polymorphism, which strongly suggest that this gene has been the target of selection during recent human evolution.


Oh look. Mutations in FOXP2 in humans are correlated strongly with speech and language deficits.

The authors continue with:

Enard et al, 2002 wrote:FOXP2 (forkhead box P2) is located on human chromosome 7q31, and its major splice form encodes a protein of 715 amino acids belonging to the forkhead class of transcription factors2. It contains a glutamine-rich region consisting of two adjacent polyglutamine tracts, encoded by mixtures of CAG and CAA repeats. Such repeats are known to have elevated mutation rates. In the case of FOXP2, the lengths of the polyglutamine stretches differed for all taxa studied. Variation in the second polyglutamine tract has been observed in a small family affected with speech and language impairment, but this did not co-segregate with disorder, suggesting that minor changes in length may not significantly alter the function of the protein4. If the polyglutamine stretches are disregarded, the human FOXP2 protein differs at only three amino-acid positions from its orthologue in the mouse (Fig. 1). When compared with a collection of 1,880 human–rodent gene pairs5, FOXP2 is among the 5% most-conserved proteins. The chimpanzee, gorilla and rhesus macaque FOXP2 proteins are all identical to each other and carry only one difference from the mouse and two differences from the human protein, whereas the orang-utan carries two differences from the mouse and three from humans (Fig. 1). Thus, although the FOXP2 protein is highly conserved, two of the three amino-acid differences between humans and mice occurred on the human lineage after the separation from the common ancestor with the chimpanzee. These two amino-acid differences are both found in exon 7 of the FOXP2 gene and are a threonine-to-asparagine and an asparagine-to-serine change at positions 303 and 325, respectively. Figure 2 shows the amino-acid changes, as well as the silent changes, mapped to a phylogeny of the relevant primates.

We compared the FOXP2 protein structures predicted by a variety of methods6 for humans, chimpanzees, orang-utans and mice. Whereas the chimpanzee and mouse structures were essentially identical and the orang-utan showed only a minor change in secondary structure, the human-specific change at position 325 creates a potential target site for phosphorylation by protein kinase C together with a minor change in predicted secondary structure. Several studies have shown that phosphorylation of forkhead transcription factors can be an important mechanism mediating transcriptional regulation7,8. Thus, although the FOXP2 protein is extremely conserved among mammals, it acquired two amino-acid changes on the human lineage, at least one of which may have functional consequences. This is an intriguing finding, because FOXP2 is the first gene known to be involved in the development of speech and language.


I hope you'll forgive me, after the above efforts, for truncating the presentation of the paper at this point, but those who are interested can contact me for copies of the full paper. Basically, the paper contains evidence that FOXP2 again was subject to positive selection in humans, and that nonsense mutations in the gene lead to diagnosable defects in speech and language that not only affect such features as motor control of the speech apparatus, but, intriguingly, also affect the ability to comprehend grammar and syntax.

So, in the light of the above, I hereby contend that the scientific evidence for evolution of brain size and language development is suitably solid.

Now, do you have anything resembling the above to support the idea that a magic man was needed?

Andrew4Handel wrote:If the brain evolved it already happened and the process can't be observed again anything else is speculation.


HA HA HA HA HA HA!

Read the above papers and weep. What part of the words "common descent with modification" do you not understand?

The whole point, in case you hadn't worked this out, is that because evolution is founded upon inheritance, and inheritance involves well understood mechanisms that have been elucidated in fine detail, we can trace ancestry back across different lineages, using not only genes, but such entities as endogenous retroviral insertions, which, I might add, pose a serious problem for creationist assertions about a magic man. Since scientists know what to expect from inheritance followed by relevant mutations, they can look for the relevant patterns appearing in organismal genomes. Oh, and the fact that in the above papers, mutations in the ASPM gene result in a cranial volume very similar to that of a chimpanzee, is rather telling, don't you think?

Oh dear, it seems I need to make this a three parter. Part 3 coming up soon ...
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Re: Concepts in Atheism & Physicalism

#73  Postby Calilasseia » Feb 19, 2011 12:26 am

Welcome to Part 3.

Andrew4Handel wrote:Has the multiverse theory /string theory been tested to destruction?


We're about to embark on that process. See those papers by Steinhardt & Turok I presented above? They're the start of this process.

Andrew4Handel wrote:Here are some scientific critics of the big bang


Oh let me guess ... it's a link to a creationist website?

Andrew4Handel wrote:http://www.cosmologystatement.org/


Oh look, it's that favourite chestnut of conspiracy theorists, the assertion that only one theory is getting a look in. Funny how Steinhardt & Turok, Lisa Randall, and Michio Kaku among others are being given free rein to publish a range of ideas in print going beyond the Standard Big Bang model. Oh, and does the fact that there exists evidence supporting much of Big Bang cosmology not play a part in this? Look up cosmic microwave background, which is one of the key pieces of evidence supporting Big Bang cosmology. If you don't understand why this is, you can find plenty of resources on the Internet from university physics departments explaining this.

Andrew4Handel wrote:You appear to be suggesting in a metaphysical way that science is the only tool for investigating reality.


No, what I'm suggesting is that so far, it's the only RELIABLE tool. It's the only tool that WORKS and DELIVERS RESULTS. Come up with a rival that works, and I'll pay attention.

Andrew4Handel wrote:The actual best tool for investigating reality is human consciousness and intelligence.


Except that human consciousness and intelligence has been known to MAKE SHIT UP. We have EVIDENCE for this. It's called fiction. Now, since we are beings that are capable of inventing fanciful stories, don't you think that the best tools for finding out about REALITY, are tools that exert some effort toward distinguisghing between made up shit and evidentially supported postulates? That's what science is. That's why it works. Learn this lesson quickly.

Andrew4Handel wrote:Science isn't an entity in itself, it is the manifestation of a human cognitive capacity.


So is made up shit. Does this mean that we have to give equal time to made up shit? If you think this, then please, allow me to point and laugh.

Andrew4Handel wrote:This human cognitive capacity which now has to be subjugated to materialist elimination.


Oh for fuck's sake. What part of SCIENCE IS ABOUT TELLING THE DIFFERENCE BETWEEN REALITY AND MADE UP SHIT do you not understand?

If you had brought this nonsense of yours to ANY of the classes I'd attended at just 12 years of age, you'd be nursing a sore pair of buttocks in one hand and an F grade in the other. Now, is there some chance you'll LEARN SOMETHING SUBSTANTIVE here, or are you going to continue boring us all shitless with fatuous apologetic excrement and ignorance-based whingeing?
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Re: Concepts in Atheism & Physicalism

#74  Postby Andrew4Handel » Feb 19, 2011 12:35 am

I am sorry to have to say this again Calilasseia but you are hiding behind scientific wiffle.

The issues confronting us are not scientific anyhow.

None of your papers on the brain are testing the theory of brain evolution to destruction as I pointed out earier its impossible as the past has eradicated each step of the process.
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Re: Concepts in Atheism & Physicalism

#75  Postby Andrew4Handel » Feb 19, 2011 12:40 am

Comparison of polymorphism and divergence suggests past positive selection:


Nuff said.
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Re: Concepts in Atheism & Physicalism

#76  Postby chriscase » Feb 19, 2011 12:49 am

Andrew4Handel wrote:
Comparison of polymorphism and divergence suggests past positive selection:


Nuff said.

An entire post to quibble about the word "suggests"? At this rate you will need to post dozens of these ridiculous responses before you will have posted anything that looks remotely like a response. And the timestamps as well as your own demeanor clearly indicate you have no intention of even reading the series of extremely detailed and substantial responses that were made to you. If you won't even pretend to attempt to understand the methods and results of scientific inquiry, you should stop posting on the subject.
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Re: Concepts in Atheism & Physicalism

#77  Postby Calilasseia » Feb 19, 2011 12:49 am

Andrew4Handel wrote:I am sorry to have to say this again Calilasseia but you are hiding behind scientific wiffle.


Bollocks. I'm presenting the HARD EVIDENCE FROM REALITY that says mythology is horseshit. What part of this don't you understand? Oh that's right, you dismiss as "wiffle" anything that's too much like hard work.

Andrew4Handel wrote:The issues confronting us are not scientific anyhow.


Some of them certainly aren't. Some of them are political. And I expend diligent effort dealing with those too.

Andrew4Handel wrote:None of your papers on the brain are testing the theory of brain evolution to destruction as I pointed out earier its impossible as the past has eradicated each step of the process.


Do us all a favour Andrew, go back to school and learn some real science, before posturing as being in a position to tell those of us who DID pay attention in science classes that we're wrong, let alone the actual research scientists that wrote the papers. Because that's what you're saying here, namely that the research scientists who wrote those papers and performed the relevant experiments aren't doing their job. You might like to reflect upon how hubristic it is for you to do so from a position of manifestly inferior knowledge, let alone defamatory with respect to the integrity of the scientists in question.
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Re: Concepts in Atheism & Physicalism

#78  Postby Andrew4Handel » Feb 19, 2011 12:54 am

chriscase wrote:
Andrew4Handel wrote:
Comparison of polymorphism and divergence suggests past positive selection:


Nuff said.

An entire post to quibble about the word "suggests"? At this rate you will need to post dozens of these ridiculous responses before you will have posted anything that looks remotely like a response. And the timestamps as well as your own demeanor clearly indicate you have no intention of even reading the series of extremely detailed and substantial responses that were made to you. If you won't even pretend to attempt to understand the methods and results of scientific enquiry, I think you should stop posting on the subject.



Calilasseia's responses are predictable hiding behind science that really doesn't answer any of the questions.. at hand

He claimed that science tested theories to destruction. So articles that claim the word "suggest" are suspect.


The universe exists because.????.Lets have a succinct answers not a barrage of scientific paper excerpts. I could post vast excerpts for the bible and Quran in chinese if you want. I don't usually answer questions people ask me by swishing around tedious excerpts from papers aimed at scholars.





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Re: Concepts in Atheism & Physicalism

#79  Postby Andrew4Handel » Feb 19, 2011 12:58 am

Calilasseia wrote:Bollocks. I'm presenting the HARD EVIDENCE FROM REALITY that says mythology is horseshit. What part of this don't you understand? Oh that's right, you dismiss as "wiffle" anything that's too much like hard work.
.



I am not promoting mythology I can just see patently that the scientific paradigm is not sufficient to explain reality.

It is the equivalent of you saying that you knew how I was feeling now.... that you had access to my first person experience.I can accept the limitations of knowledge in certain positions.

Turoks cyclical eternal universes..never ending reality..thats all I needed.

As mentioned earlier..naturalism tries to explain the universe without resorting to god.

The laws of physics make themselves.... Scientists are infallible.
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Re: Concepts in Atheism & Physicalism

#80  Postby LucidFlight » Feb 19, 2011 1:00 am

Andrew4Handel wrote:He claimed that science tested theories to destruction. So articles that claim the word "suggest" are suspect.

Have you been speaking to stevebee?

:ask:
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