Re: Teleology etc.

From: Dace (
Date: Fri Aug 17 2001 - 20:10:13 BST

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    Subject: Re: Teleology etc.
    Date: Fri, 17 Aug 2001 12:10:13 -0700
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    > > And who says you can cite molecular biology as an authority on life?
    > > has molecular biology ever explained about life? Description is not the
    > > same as explanation. We know all kinds of things that go on in our
    > > but we don't know why any of it happens. We still can't answer the
    > > question of what distinguishes a living cell from a dead cell. Why
    > > the living cell just stop and begin disintegrating? Molecular biology
    > > no answer to this question. The *science* of biology hasn't been
    > > yet. At least Sheldrake is actually trying to explain life on its own
    > > rather than calling it a machine and then trying to explain that
    > This isn't that hard to explain, the problems with defining life etc.
    > revolve more around conference politics than anything - we all know
    > roughly what we mean (at least for organic life anyway). The 'animate'
    > state of a piece of (organic) matter arises from the (temporarily)
    > third-law-defying dynamics, which are those of a driven system far from
    > equilibrium. Dead stuff is on a steady path to thermodynamic
    > equilibrium, living stuff is not as long as it is alive.

    You're not explaining anything. *Why* do living things defy the tendency
    towards equilibrium?

    > It's not a binary thing either. If you shot me, and I was 'dead' then in
    > some bits of my body, genes would be being expressed for maybe half an
    > hour, other metabolic stuff would be going on too. There is no magic
    > there (that wasn't meant to be a pejorative pun btw), just a set of
    > reactions that do some stuff, and rely on each other in a closed ntwork
    > of interactions.

    If living bodies followed the logic of determinism, they would do what dead
    bodies do, i.e., they would break down to their molecular components. This
    is why we have the concept of genetic instructions. Something has to be
    guiding these processes. What is it?

    > > > 2) Protein folding is rather complex -
    > >
    > > So complex in fact that we have absolutely no idea what's going on in
    > > You'd think by now we'd have some kind of model or map of how this
    > > is carried out. After all, we have very powerful computers than can
    > > extremely complex processes. But protein folding is so unimaginably
    > > that no one's ever been foolish enough to try to model it (though in
    > > the world's most powerful supercomputers could do the job if they worked
    > > it continuously for the next 100 years.)
    > 'In theory'? As in perfectly feasible given a decent computer (or the
    > real system)?

    According to Thomas Sterling of the Center for Advanced Computing Research
    at the California Institute of Technology, "It could take 100 years, for
    example, for the largest existing system to perform a complete
    protein-folding computation-- a long-sought capability." He claims we won't
    be in a position to really begin to model protein-folding until we have
    computers that process data at least 1000 times faster than today's top
    computers. It's a vastly complex process about which we know virtually
    nothing. We certainly can't claim to know that it proceeds

    > > many chaperones help out,
    > > > different cellular compartments are involved, as are timing effects to
    > > > allow local folding. You need a concept of an energy landscape, which
    > > > 'out there' in a sense(...), but you most emphatically do not need
    > > > mystery fields of force.
    > >
    > > It's all descriptive. We know these "chaperones" are involved, but they
    > > don't explain why it happens the way it does. It's just assumed that
    > > someday we'll have an explanation.
    > >
    > > The question is what controls this unbelievably complex process. If
    > > controlled from our genes, then our genes must be vastly more powerful
    > > any supercomputer ever devised. The only other option is that it's
    > > self-organized.
    > Nothing controls it. Proteins fold to reduce the overall free energy
    > (from hydrogen bonds) in the system (that's what keeps the two strands
    > of DNA together too). This is no more complex than oil drops joining up
    > on the surface of water - the system seeks its lowest energy
    > configuration by *randomly* exploring the space of all configurational
    > states. Chaperones guide the folding away from the wrong low energy
    > configurations (like the BSE disease form of the prion protein) along
    > with other tricks (like piping into the ER, codon adaptation index
    > exploitation and so on), but proteins would fold into something anyway,
    > it's just a question of what.

    As I've said, the contraints of physics and chemistry do not explain why a
    given chain of amino acids folds up into the correct protein as opposed to
    any number of equally feasible alternatives. If chaperones are guiding the
    process, then what's guiding the chaperones? It's all supposed to come back
    to DNA somehow, so where's the causal sequence that links the genetic
    "instructions" to the protein? It's just all up in the air. You act as if
    all these details have already been worked out. Perhaps you imagine there
    are wise, old men in lab coats and thick glasses puttering about in their
    ivory tower compiling the evidence and solving the relevant equations.
    These people are no more real than the supreme deity up in the heavens with
    his infinite knowledge and wisdom. There's a meme at work here. Call it
    the "authority" meme. We like to think someone, somewhere, knows what the
    hell is going on.

    > I snipped the complexity stuff about why ants are not like bees because
    > someone else took up the cudgels on that one (in case you thought I
    > ducked it).

    You asserted that the complexity of the organism can follow from a set of
    simple rules. Okay. But that doesn't explain why an ant egg becomes one
    particular complex structure (namely, an ant) and not another (for instance,
    a bee). Clearly we need something more to explain this, such as genetic
    instructions or morphic resonance. At least Sheldrake has presented
    evidence for morphic resonance. No one has ever bothered to present
    evidence for the existence of genetic instructions. The only "proof" we
    have is our belief that any alternative theory is inconceivable. So we
    don't have to prove it, any more than Christians have to prove the

    > > > > Memes not a product of genes, so must be from MR etc. etc.
    > > >
    > > > Uh-uh - the whole point of this group is the study of culturally
    > > > heritable patterns - heritable as in copyable. No need for any
    > > > templates. And again, where do the first ones come from? Evolution by
    > > > natural selection operating on variation explains this diversification
    > > > for me, what does MR have to say about it (genuine question)?
    > >
    > > MR offers a model of evolution that gives organisms an active role in
    > > shaping themselves. We know, for instance, that camels begin developing
    > > calluses on their kneepads when they're still in the womb. This would
    > > suggest that camels who developed calluses as a result of kneeling in
    > > desert passed this trait onto their offspring. Since behavior can't
    > > directly affect genes, the logical assumption is that the calluses are
    > > passed on non-genetically. Otherwise we must accept the colossal
    > > improbability that the genetic mutation for calluses on the kneepads
    > > happened to appear right when the camels needed it. You'd think they'd
    > > to have gone through a lot of useless mutations first, like calluses in
    > > other places, or the wrong alterations on kneepads before they'd hit on
    > > right mutation. How many millions of years should it have taken for
    them to
    > > get the right mutation? Now consider the fact that this applies many
    > > over for every species on earth, and you start to see just how high that
    > > mountain of improbability is. Sheldrake offers a more streamlined,
    > > model of evolution.
    > Baldwin effect. Guy kept developing drosophila at a high temperature,
    > and found that a particular pattern of wing venation occurred (but only
    > at the high temp). However after breeding several generations at this
    > high temperature the new venation pattern became fixed, even when at low
    > temp. This is because you are selecting out from the existing variety
    > (heterozygosity drops like a stone when you do this sort of thing),
    > combinations of genes that do the thing best (bear in mind that the
    > venation pattern is just the visible change for a shift in genotype
    > arising from the usual selective mass killing). This would involve (in
    > the simplest explanation) fixation of null alleles (duds basically) that
    > systemically turn on a particular pathway.

    Waddington found the same effect in his experiments. The wings of the fruit
    flies lacked cross-veins. He also exposed eggs of fruit flies to ether,
    which produced a bithorax mutation. He selected the abnormal flies to serve
    as the parents of the next generation, and this trait continued appearing
    even after the eggs were no longer subjected to the fumes. There's no
    reason why ether would affect genes. He accounted for this phonemenon with
    the term, "genetic assimilation," according to which acquired
    characteristics are somehow converted into inherited characteristics. But
    he refused to offer a strictly reductionist explanation, prefering to
    describe the process in terms of canalized pathways of development, i.e.
    chreodes. "Developmental proceses have some structural stability, so that
    once you have got a developmental process going in a certain direction it
    tends to go on there independently of changes in the environment." This is
    exactly what you would expect on the basis of morphic resonance. When lots
    of flies develop the abnormal characteristic, later flies will develop these
    same traits through resonance. This interpretation is supported by the
    findings of Mae-wan Ho, who replicated Waddington's experiment, but with one
    crucial difference. Instead of selecting abnormal flies as parents of the
    next generation, the flies were allowed to mate randomly. As long as the
    ether was applied to the eggs, the abnormal characteristics increased with
    each generation, from 2% in the first generation to 30% by the tenth. This
    occurred despite the fact that the altered flies were at a reproductive
    disadvantage compared to the normal flies. Ho even repeated the experiment
    with inbred flies having virtually no genetic variation, and the same thing
    occurred. Cearly, there was no subtle genetic selection at work. While Ho
    did not advocate a morphic interpretation of these results, she did assert
    that they could not be explained according to genetics theory.

    > Camels have selection pressure for really decent Doc Marten's kneepads
    > (apparently, who thinks of these examples?). But once the trait is fixed
    > in adults, why is it so hard to imagine that selection for building the
    > structures earlier in development could occur (timing changes are fairly
    > easy)?

    Because the trait isn't genetically fixed in adults. It's a function of
    behavior. The camel develops calluses after kneeling repeatedly on desert
    terrain. They're not genetically programmed to appear among adults, so it's
    not simply a matter of changing the timing.

    > What's the rat thing (genuine question)? If it's a 'too good to be
    > learned' thing his controls had better be damn good...

    Alright, here it is again, for all those who missed it the first time

    In 1920 William McDougall of Harvard began training rats to learn to escape
    from a water maze by choosing the correct exit. While the brightly lit exit
    would give them an electric shock, when they picked the dimly-lit exit, they
    got out undisturbed. McDougall found that the first generation of rats had
    to endure 165 shocks before getting the message. But by the 30th
    generation, only 20 transgressions were necessary to persuade the rats of
    the error in their way. (McDougall, 1938. British Journal of Psychology

    McDougall assumed the rats were passing on acquired characteristics.
    Wishing to disprove this "Lamarckian" (and Darwinian) interpretation of the
    data, F. A. E. Crew replicated the experiment in Edinburgh. Right from the
    get-go, Crew's rats needed only 25 errors to learn their lesson, as if
    picking up where the Harvard rats had left off. (Crew, 1936. Journal of
    Genetics 33:61-101.)

    In Melbourne, W. E. Agar found the same effect. His trials went on for over
    twenty years, and even when he tested control subjects that weren't
    descended from trained rats, they still showed improvement over the
    performance of previous generations. So it couldn't have been coming from
    their parents. (Agar, 1954. Journal of Experimental Biology 31:307-321.)
    In disproving the Lamarckian explanation, Agar inadvertantly demonstrated
    the existence of non-genetic, species-wide memory.



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