The Blind Watch Dropper

Here is one of the more essays I wrote based on discussions I’ve had hereon and on other sites like Pandas Thumb. I think this is one of the more appropriate essays for discussions here and it also happens to be one I feel is fully finished at this point. Well…I’m happy with it, but clearly I may edit it a bit given constructive criticism… 🙂

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I haven’t seen much press on this lately, but back in the late 1980s, Creationists – a slice of Christians who hold that the creation of the universe, Earth, and all living things on Earth were created by God exactly as described in the Christian Bible and that the Earth is roughly 10,000 years old…tops – tried an end around to the 1987 Supreme Court decision (Edwards v. Aguillard) barring the teaching of Creation Science in public schools. The attempted end-around was called Intelligent Design (ID).

ID, boiled down, is essentially a dressed up version of William Paley’s The Watch and The Watchmaker argument for the existence of God, or rather, a slightly gussied up Teleological Argument for the Existence of God. Paley’s argument goes like this: if you stumble upon a rock in the woods, you could reasonably surmise that it had been there, in that state, forever (keep in mind that Paley wrote his analogy in 1802 and was not familiar with what we now know about geology and in particular plate tectonics and erosion and similar forces. So, he can be forgiven for thinking that some items of the universe (like planets and stars) and the Earth (like soil, rocks, mountains, rivers, land masses, and so forth) exist unchanged forever) as a simple object of nature. By contrast, if you stumble upon a watch, you would not think that this item had been there forever, but rather you’d likely think that this item reflected the intent of a creator and, in particular given its complex parts working in intricate harmony, functions specifically for a purpose the creator designed it for. Given this, by analogy one can reasonably look at the universe and, seeing its complex interactions working in intricate harmony, infer it too must be designed and conclude, therefore, there is an ultimate Designer.

All Teleological Arguments rely on the same basic argument: certain features and functions of the world exhibit complexity that appears far too harmonious and intricate to have occurred by accident and thus must have been intelligently designed. Ergo…God.

It’s helpful to understand a bit about the history and use of the concept to better understand the application of teleology in theology, but it’s not absolutely necessary. That said, here are a definition and a brief summary:

Teleology comes from the Greek telos, meaning end (as in goal or purpose), and logos, meaning reason. So, teleology is about understanding the purpose of things. In its most basic form, teleology is the study of the purpose that phenomena serve rather than the cause by which they arise in order to provide an explanation for the phenomena. In other words, teleologists hold that the purpose for the sky being blue is more useful in understanding aspects of the world than studying and understanding optics and the Rayleigh Diffusion Effect. I admit, I’ve had no luck digging up a teleological explanation for the sky being blue, but apparently there used to be some popular ones back before modern science’s explanations. The point is, teleology attempts to address ‘why’ things occur, as opposed to scientific approaches that attempt to answer ‘how’ things occur. It’s also worth understanding that teleology, particularly as popularized by Aristotle and Plato in their day, was a reflection by analogy of the fact that nearly all human endeavors are goal-oriented and purpose driven. Thus by analogy, Aristotle saw the universe as rational and purposeful – analogous to human rational and purposeful behavior – and thus felt that all phenomena can only fully be understood when one considers and appreciates the purpose of the various phenomena.

There are a number of issues I have with teleological arguments and perspectives, but I’m going to focus on four main issues here.

First and foremost, technically there is no actual argument in the teleological approach to the existence of God as it’s simply a tautology and thus question begging. If your philosophy’s premise assumes that all things have purpose and goals, using that philosophy to argue for a goal-oriented and purpose-creating designer is simply restating your premise’s assumptions. It’s just arguing in a circle. Intelligent Design tries to dress the argument up a bit by focusing on complexity vs purpose and goals, but the issue remains the same. In ID, the argument is changed slightly to certain biological and informational features of living things are too complex to be the result of natural selection (or natural processes) and therefore must be the result of intentional and rational (intelligent) design requiring an intelligent designer. This, of course, suffers from the same tautological issue noted above: the first premise of ID is that living things are too complex to be the product of natural processes, but if the premise is that living things can’t come about from natural processes, what’s left? By premising that living things can’t be the product of natural processes, the premise implies something other than natural processes – i.e. design processes. To then conclude a designer is simply restating the premise. Yet again, a tautology.

Next, there’s the fallacy of the General Rule. The fallacy of the General Rule is a logical fallacy wherein someone assumes that something in general is true in all possible cases. A standard example is the claim that “all chairs have four legs”. But clearly rocking chairs have either no legs or two legs, depending on the design, and there are plenty of modern chair designs with three legs, and not a few bar stools that are essentially held up on a single pole. In the case of ID, the assumption is that complexity implies design and since biological objects are complex they must be designed. The thing is though, not all designed things – well, human designed things – are complex. Consider toothpicks, paper clips, floss, and Popsicle sticks as but a few examples. These objects are never used in teleological arguments for obvious reasons. And while it’s certainly possible that a toothpick could come about through natural processes, we know a human-designed toothpick when we see it and not because of the harmonious workings of its complex parts. No, it’s because of two things: man-made toothpicks have tell-tale evidence of being manufactured and they exist in greater collected numbers than nature could reasonably produce.

Another issue with ID that is related to the fallacy of the General Rule noted above is that it relies upon a false dichotomy. A false dichotomy is a logical fallacy wherein someone argues that some condition has only two alternatives when in fact there are more. An example would be someone who insists that the only alternative to driving a car is walking when clearly bicycles, skateboards, pogo sticks, and air travel all exist. In the case of ID, even if one were to agree that most, if not all, living organisms are too complex to have come about through evolutionary processes, it’s questionable at best whether a designer (and specifically God) is the only alternative. There are abundant natural processes that lead to complex organized structures (think snowflakes, tree rings, and the Giant’s Causeway). And even if we grant a necessitated designer, since there’s no way to assess or know anything about the supposed designer inferred by ID, the designer could very well be invisible pink unicorns or aliens. The bottom line is that it’s a rather large (and unrealistic) stretch to assume the only way to get biological complexity is either evolution or God.

Lastly, as noted above, we don’t infer design from complexity so much as we infer design from indications of manufacturing. This, for me, the primary failure of all forms of teleological arguments for the existence of God and ID in particular.  Designs are a very specific form of plan and planning. We make designs (usually written and drawn) to help us visualize how various components and processes will interact and work in a given environment in order to (hopefully) highlight problems and issues before we actually manufacture the object of design. So the truth is that looking at an object tells one very little about the actual activity that went into designing that object. And while looking at an object can indicate something about whether the object was designed, it’s really the indications that the object was manufactured through some tool use process that provides that inference. Manufacturing leaves evidence; design does not.

I’ve never found the ID arguments for the design of biological organisms all that compelling for a number of reasons. The dubious math, the fallacious arguments, the disingenuous bait and switch to Christian apologetics, and so forth. But even beyond that, there was something about the objects in nature – organisms themselves – that just don’t seem designed to me. There is something different about them compared to man-made objects, but I was not able to put my finger on what I felt the difference was. And then it hit me one night: replaceable parts.

All man-made objects – every single one – are either designed specifically to be replaced or have components that are designed specifically to be replaced. Why? Because tool users and manufacturers learn really quick that tools and/or certain parts of tools wear out. So as designers, we anticipate the need for maintenance.

No such anticipation or planning for maintenance can be found in nature. None. If something breaks in an organism, either that organism learns to live without it or it dies. Or, in the case of humans, that part gets replaced by human designed or human configured replacements (as in my case). But even in the later case, humans have to create a work-around, because biological parts actual resist being replaced. You can’t just replace human parts with other human parts willy-nilly. In most cases, the new parts just won’t work, or worse, they’ll be rejected by the body’s immune system. But of particular note, there’s no surplus of replacement parts anywhere; no storage unit somewhere with a bunch of eyes or hearts or toes or hair or kidneys or…anything. Not even bark or leaves or antennae or scales. Nothing.

Of course, this makes perfect sense given evolution and other similar natural processes. It makes no sense if there were an actual designer, particularly an omni-god Designer, behind it all.

601 thoughts on “The Blind Watch Dropper

  1. Allan Miller: So there is neither a teleological nor a non-teleological account, according to you?

    Heh. Seems like Charlie hasn’t completely thought this one through. An explanation that doesn’t invoke any purpose or goals for / of organisms is not teleological of course. I also wonder about those no-purpose “inner drives” that motivate marine flatworms to have penis duels. What intellectually satisfying explanations Goethean-science-style teleological thinking brings us!

    But if I am not mistaken, Charlie has always been arguing that the purpose of the whole show was to bring forth “individual self-consciousness” and that all non-human lineages operate in the service of achieving that goal in our lineage. Hence, I assume flatworm penis fencing can be explained in the context of this lofty goal. I really, really, really like to hear this explanation.

  2. Corneel:
    CharlieM: The concept of quantitative trait loci is not hard to understand. My mistake with that example was that I chose the wrong example. I should have been more careful and researched mice coat colour which I now believe to be a strongly Mendelian trait.

    Corneel: Don’t worry about that: Coat colour can be easily recoded as a continuous trait. But could you please explain what you meant by “genetic regulatory changes associated with areas such as quantitative trait loci” producing mice with exceptionally dark coats? Does it involve genetic mutations at multiple genomic positions affecting coat colour, perchance?

    For a quantitative trait, multiple genes from these regions are involved in determining how the trait is expressed in the individual. And, yes, genetic differences between individuals at particular locations will play their part in the production of various coat colours.

  3. Allan Miller:
    CharlieM: But the answer only satisfies those who already believe in the orthodox account of evolution.

    Allan Miller: Not strictly true. The fact of sex, and the role of males, have been a puzzle on the ‘orthodox’ account for a long while. Largely, I think, due to a ‘diplocentric’ bias.

    I’m talking about the orthodox view of evolution not the orthodox view of the origin of sex.

    Whether one’s view is ‘diplocentric’ or ‘haplocentric’, both these positions fall within the orthodox view of evolution in general. By this view chemicals in motion are what ultimately produces life.

  4. Corneel:
    CharlieM: Are specialized cells able to revert to pluripotency without the insertion of foreign genes by artificial means?

    Corneel: Oh yes, most plant cells for example.

    Excellent point.

    Plants retain a strong life force down to their cells. They have marvelous powers of regeneration.

    We humans have gained our consciousness at the expense of retaining powers of growth and regeneration. Consciousness is destructive to this life force. This is why we cannot maintain our waking level of consciousness 24 hours a day seven days a week. Without regular intervals of sleep to compensate for this destruction we would not have the level of consciousness that is ours to appreciate.

    In general, as living organisms develop higher stages of consciousness they begin to lose their powers of regeneration.

  5. Allan Miller:
    CharlieM,

    Yes Allan’s opus magnum does address these issues. But only with regard to the interaction of molecules. 

    Not quite true, old bean! I may have a reductionist bias, but I’m not that reductionist!

    As regards what it leaves out on sexual dimorphism, it was 54 pages long already…

    Fair enough. It would have been more accurate if I had said your main focus was on the molecular aspects of the origins of sex.

  6. DNA_Jock:
    CharlieM: Isn’t it the case that non-pregnant women benefit from having the lining of there uteri destroyed every month?

    DNA_Jock: No, not really. That’s something of a marketing ploy.

    I should have been more specific. I meant they benefit in that their ability to produce offspring is under constant renewal. And if the name of the game is in passing on one’s genes then what benefit is there to being fit and healthy if it means she cannot conceive.

  7. Allan Miller:
    CharlieM: From haploid to diploid. From an original unity life becomes polarized. I can agree with that.

    Allan Miller: It goes back to haploid every generation. With a few exceptions.

    Are you walking back your contention that non-teleological explanations for sex fail?

    When did I claim that?

  8. Corneel:
    CharlieM: Yes, life is very complicated. And because within it there is a tangled mess of multilayered, convoluted, interactions, it cannot be disentangled into meaningful linear causal laws in the way that mechanical systems can. And Goethe was trying to develop a science of life with its own laws and rules that were not just borrowed from the physics of matter. The idea of the typus is something that could be developed further in relation to life as a compliment to the ways that formulae and equations are used in physics. Another aspect of viewing the living world in this way is in coming to an understanding of how the polarities of life and death, expansion and contraction, growth and decay, cooperation and conflict, and such like, are all necessary contributors to the evolution of life on earth.

    Corneel: Rubbish!

    It saddens me that you have bought into the idea that biology is so “very complicated” that it “cannot be disentangled” and I forcefully reject the idea that complementing the findings of decades of meticulous research with soothing stories adds something of scientific value.

    I did not say that it cannot be disentangled. We can follow the threads, but they don’t end up in nice simple relationships of cause and effect. We see multiple causes, feedback loops, various levels of activity interpenetrating each other.

    Kick a football and the trajectory can be neatly worked out mathematically when all the forces are taken into account. Kick a dog and things do not turn out so neatly. Vectors of forces will not help in predicting the outcome.

    I’m not sure where the soothing comes into play in believing that we have responsibilities to fulfil and that suffering is a fact of life.

  9. Kantian Naturalist:
    Corneel: It saddens me that you have bought into the idea that biology is so “very complicated” that it “cannot be disentangled” and I forcefully reject the idea that complementing the findings of decades of meticulous research with soothing stories adds something of scientific value.

    Kantian Naturalist: Agreed.

    You are agreeing with a misinterpretation.

  10. Allan Miller:
    to Corneel,

    Allan Miller: Even the attempt to disentangle it brings the charge of dread ‘reductionism’.

    Show us the ends of the threads? Phrases such as “life cycle”, “Krebs cycle”, “cardiac cycle”, “Calvin cycle”, “nitrogen cycle”, “menstrual cycle”, to name but a few biological processes are so named for a reason.

    I have no objection to investigating biology in a reductionist way. Focusing on the details helps us to understand the whole. But when we delve down in search of causes we end up like the ouroboros catching our tails.

  11. Allan Miller:
    CharlieM,

    Allan Miller: So there is neither a teleological nor a non-teleological account, according to you? Seems a bit empty, then. If Steiner and Goethe taught us anything … well, they didn’t. Seems science got a lot further without Goethe’s urgings than if it had noted them. What has been achieved by dispensing with ‘the methods of inorganic science’ (whatever they may be)?

    There is plenty of teleology. For instance, a pigeon grows wings so that it can fly. Birds build nests for the purpose of having somewhere to raise chicks. But knowing what wings are used for tells us little about the pentadactyl limb in general. Its existence is meaningless without the whole organism. And pigeons only have meaning as part of vertebrates in general. And vertebrates as part of earthly life.

    Inorganic science uses mathematics and formulae to make predictions with great effect. Biology requires an understanding that mathematics and formulae cannot give it. Looking at all the various life forms we can see that they are just specific instances of an infinite potential. Goethe came to understand this with his archetypal plant which connects all plants.

  12. CharlieM: CharlieM: The concept of quantitative trait loci is not hard to understand. My mistake with that example was that I chose the wrong example. I should have been more careful and researched mice coat colour which I now believe to be a strongly Mendelian trait.

    Corneel: Don’t worry about that: Coat colour can be easily recoded as a continuous trait. But could you please explain what you meant by “genetic regulatory changes associated with areas such as quantitative trait loci” producing mice with exceptionally dark coats? Does it involve genetic mutations at multiple genomic positions affecting coat colour, perchance?

    Charlie: For a quantitative trait, multiple genes from these regions are involved in determining how the trait is expressed in the individual. And, yes, genetic differences between individuals at particular locations will play their part in the production of various coat colours.

    Excellent. So here is the comment that set off this exchange:

    I suspect the appearance of mice with exceptionally dark coats was due to genetic regulatory changes associated with areas such as quantitative trait loci having the effect of producing these colours. Only when these appear will natural selection come into effect.

    This comment led me to doubt that you have a proper understanding of what quantitative trait loci are and how they affect the phenotype, which of course you denied. So that is why I asked:

    Does it involve genetic mutations at multiple genomic positions affecting coat colour, perchance?

    … which you kindly confirmed.
    So, let us assume that these genetic mutations are all responsible for a “genetic regulatory change” that increases pigmentation. The important thing to realise here is that each and every one of these genetic mutations in isolation only has a small effect. However, combining multiple mutations into a single genotype will give a cumulative effect that results in a darker phenotype than can be achieved by a single mutation. But what are the chances these mutations get combined into a single individual, without natural selection?

    When a novel mutation is introduced into the population, it starts off at a frequency of 1/2N (for diploids) where N is the population census size. So suppose we have a modestly large population of 100 individuals and suppose that variation in coat color is conditioned by 10 loci. At each of those 10 loci we have recently had a mutation event that introduced a “dark” allele. What is the chance that a single individual acquired all these “dark” alleles? Well, the chance of being homozygous for (having 2 copies of) the “light” allele at a single locus, which I will call P, is simply the chance of not being the individual carrying the only “dark” allele, which is P = 1-(1/N). Further, the chance of observing all 10 “dark” alleles in a single individual is (1 - P)^{9}. A little back-of-the-envelope calculation tells us that is an astronomically slim chance of one in 10^{18}!

    Is this the darkest phenotype possible? Well, unless the mutations are all dominant, it is not. Chances are that an individual that is homozygous for the “dark” alleles expresses an even darker phenotype. But this is impossible with only a single copy of a mutation circulating at every locus. It looks like it is nigh impossible to achieve mice with “exceptionally dark coats”, doesn’t it?

    And yet, when directional selection for darker coats starts operating and the frequency of the “dark” alleles starts rising, quantitative genetics tells us that, without input of any further mutations, we can be certain that the population will eventually fix all “dark” alleles and that we will observe the new “exceptionally dark coat” phenotype. Evolutionary novelty produced by natural selection!

    So despite your insistence that natural selection can only work on the existing phenotypic variation, the fact remains that most novel phenotypes would never have been produced if it were not for natural selection.

  13. CharlieM: Excellent point.

    Thanks. It appears you forgot to withdraw the comment that started off this particular exchange though, to wit:

    When a kind or a species takes on physical form the limits of archetypal expression is set. This is similar to what we see with pluripotent stem cells. The line of specialist cells that they give rise to will not normally produce cells with the potential of the former pluripotent cells they developed from.

    Cells in living organisms quite frequently engage in dedifferentiation. So, following your analogy of evolution as development, there is no reason whatsoever to suppose that “the limits of archetypal expression is [sic!] set”.

  14. CharlieM: I did not say that it cannot be disentangled. We can follow the threads, but they don’t end up in nice simple relationships of cause and effect. We see multiple causes, feedback loops, various levels of activity interpenetrating each other.

    All of which are also observed in non-biological disciplines, like geophysics or meteorology. You are just making up excuses.

    CharlieM: I’m not sure where the soothing comes into play in believing that we have responsibilities to fulfil and that suffering is a fact of life.

    .. and soul qualities! Do not forget soul qualities.

    CharlieM to Allan: There is plenty of teleology. For instance, a pigeon grows wings so that it can fly. Birds build nests for the purpose of having somewhere to raise chicks.

    And of course marine flatworms have penises so they can fence.

    GOETHEAN SCIENCE! It works b*tches!

  15. CharlieM: You are agreeing with a misinterpretation.

    I can’t speak for Corneel’s understanding, but I understand your position perfectly well. I share his opinion about its merits.

  16. CharlieM: Fair enough. It would have been more accurate if I had said your main focus was on the molecular aspects of the origins of sex.

    Not even that. That’s like saying endosymbiosis focusses on the molecular aspects of the origin of mitochondria. There aren’t just the 2 levels at which things can be understood.

  17. CharlieM,

    Goethe came to understand this with his archetypal plant which connects all plants.

    The bulk of your output seems to be about what Steiner thought or what Goethe thought. There doesn’t seem to be much ‘there’ there. If everything is simply labelled ‘archetypal’, and nothing is not, what insight is gained by doing that?

  18. CharlieM: There is plenty of teleology. For instance, a pigeon grows wings so that it can fly. Birds build nests for the purpose of having somewhere to raise chicks.

    And sexual eukaryotes reduce to the haploid state for the purpose of … what?

  19. Robin:
    CharlieM: We are in agreement that machines with parts which break and have to be replaced by humans is a long long way from living organisms that maintain their viability by constantly replacing their own material constituents.

    Regarding kidney regeneration I also found this: “Origin and fate of the regenerating cells of the kidney” Here is the abstract:

    But within organisms turnover of material takes place at many levels, regenerating cells is just one example. By eating, drinking and breathing we are constantly exchanging material with our environment. Cells do the same. An active cell is constantly exchanging materials with the extracellular environment through such processes as osmosis, excretion and ingestion via vesicles, and active transport through pores. We metabolize, cells metabolize. The message of “the ship of Theseus” applies equally to individual cells as it does to us as individuals. The whole reflected in the parts.

    Robin: I think you’re engaging in a little overemphasis here, Charlie. I know the story of the “Ship of Theseus”, but the fact is, replacing iron with iron in the body or replacing calcium with calcium is not really either mechanical part replacement or renewal in any real sense. At least to my understanding.

    If any complex machine is to remain operative for any length of time it will require the replacement of parts. Any organism will require a constant renewal of substances to maintain viability. So in what way do I think they differ? Organisms are whole functioning units throughout their life even when they might initially lack parts which they are capable of self-generating when required. Before they can function as intended, machines need to have all their parts put in place by an external agent.

    CharlieM: We all experience reality in our own limited ways.

    Corneel: Fair enough…

    CharlieM: From what I could tell you thought of this as evidence that machines are in some way superior to organisms. I believe it shows the opposite.

    Corneel: No, I don’t think that at all. I was noting that (I’m assuming you’re referring to my response concerning James Watt) to Phoodoo because that was what James Watt was attempting to imply to see his steam engine.

    I simply don’t see organisms and machines as equivalent at all.

    Sorry for my misunderstanding. So we agree that they are not equivalent. Dawkins was wrong to encourage others to think of us as “gigantic lumbering robots” and “survival machines”. Biology teaching aids should rid themselves of the machine metaphor which is rife throughout the subject.

    CharlieM: I’m not looking at models, I would say I’m looking at how things are in actuality.

    Robin: As you note above, “we all experience reality in our own limited ways.” There is no way to experience “actual” reality (whatever that might be); all we can do is experience some variation of some model of reality we can interact with and believe in.

    Well I don’t believe we have to grasp reality in its fullness in order to be able to experience it in the parts that are available to us. I see kidneys and roses and planets and rivers as real although never isolated. They are real within the context of the whole. My sense perception alone will not give me this reality, but I am not limited to sense perception alone.

  20. Corneel:
    Allan Miller: So there is neither a teleological nor a non-teleological account, according to you?

    Corneel: Heh. Seems like Charlie hasn’t completely thought this one through. An explanation that doesn’t invoke any purpose or goals for / of organisms is not teleological of course. I also wonder about those no-purpose “inner drives” that motivate marine flatworms to have penis duels. What intellectually satisfying explanations Goethean-science-style teleological thinking brings us!

    But if I am not mistaken, Charlie has always been arguing that the purpose of the whole show was to bring forth “individual self-consciousness” and that all non-human lineages operate in the service of achieving that goal in our lineage. Hence, I assume flatworm penis fencing can be explained in the context of this lofty goal. I really, really, really like to hear this explanation.

    I find that asking about purposes is very counter productive in trying toi figure out what life is all about.. What is the purpose of wheat seeds? What purpose do cows serve? Is it to produce more cows? Or to provide milk for humans? Or to provide meat? Or to fertilize the ground? Or to keep fields well trimmed? Purposes vary according to who is asking.

    Everything from the entire cosmos, to planetary systems, to biomes, to the smallest organism, is in a state of evolution. The presence of self-aware living beings is an undeniable fact of evolution. Living systems begin with potential, and I do not know in advance what they will make of this potential. But I do know that consciousness is a consequence of the evolution of life on earth. And I do not envision evolution suddenly coming to a halt at the stage we believe it to be at.

  21. Corneel
    So here is the comment that set off this exchange:

    CharlieM: “I suspect the appearance of mice with exceptionally dark coats was due to genetic regulatory changes associated with areas such as quantitative trait loci having the effect of producing these colours. Only when these appear will natural selection come into effect.”

    Corneel: This comment led me to doubt that you have a proper understanding of what quantitative trait loci are and how they affect the phenotype, which of course you denied. So that is why I asked:

    Does it involve genetic mutations at multiple genomic positions affecting coat colour, perchance?

    … which you kindly confirmed.

    I will confirm that I believe genetic differences at quantitative trait loci (QTL) are involved in the production of a variety of hair colour. But there are other factors to consider.

    Corneel: So, let us assume that these genetic mutations are all responsible for a “genetic regulatory change” that increases pigmentation. The important thing to realise here is that each and every one of these genetic mutations in isolation only has a small effect. However, combining multiple mutations into a single genotype will give a cumulative effect that results in a darker phenotype than can be achieved by a single mutation. But what are the chances these mutations get combined into a single individual, without natural selection?

    When a novel mutation is introduced into the population, it starts off at a frequency of (for diploids) where is the population census size. So suppose we have a modestly large population of 100 individuals and suppose that variation in coat color is conditioned by 10 loci. At each of those 10 loci we have recently had a mutation event that introduced a “dark” allele. What is the chance that a single individual acquired all these “dark” alleles? Well, the chance of being homozygous for (having 2 copies of) the “light” allele at a single locus, which I will call , is simply the chance of not being the individual carrying the only “dark” allele, which is . Further, the chance of observing all 10 “dark” alleles in a single individual is . A little back-of-the-envelope calculation tells us that is an astronomically slim chance of one in !

    Is this the darkest phenotype possible? Well, unless the mutations are all dominant, it is not. Chances are that an individual that is homozygous for the “dark” alleles expresses an even darker phenotype. But this is impossible with only a single copy of a mutation circulating at every locus. It looks like it is nigh impossible to achieve mice with “exceptionally dark coats”, doesn’t it?

    And yet, when directional selection for darker coats starts operating and the frequency of the “dark” alleles starts rising, quantitative genetics tells us that, without input of any further mutations, we can be certain that the population will eventually fix all “dark” alleles and that we will observe the new “exceptionally dark coat” phenotype. Evolutionary novelty produced by natural selection!

    So despite your insistence that natural selection can only work on the existing phenotypic variation, the fact remains that most novel phenotypes would never have been produced if it were not for natural selection.

    Natural selection acting on variety, yes. Genetic mutations are not the only source of variation. The very same genes can be manipulated in a multitude of ways during the processes of expression. It is not as simple as each gene from a specific QTL having a set effect on hair colour. These genes are not isolated, independent units. We do not know how their combined expression and interactions will affect the phenotype under the various conditions in which they are active. The fact that individual black and white mice have been bred tells us that the same genotype can produce these opposite colours. The Agouti gene is important in mouse hair colouration and it’s an example of the complexities of gene expression.

    Your vastly simplified model above make many assumptions, but it doesn’t counter the fact that natural selection needs something to work on.

    Pet mice have been bred in various colours from pure white to jet black. The house mouse that I am familiar with is a mottled, brownish colour. And I sure that populations could become darker due to external conditions and then they could do a U-turn and become lighter if conditions changed accordingly.

  22. CharlieM: I find that asking about purposes is very counter productive in trying [to] figure out what life is all about..

    Perhaps you meant something different from what you wrote? As it stands now this is self contradicting

  23. CharlieM: Your vastly simplified model above make many assumptions, but it doesn’t counter the fact that natural selection needs something to work on.

    I never denied that natural selection needs something to work on.

    So what assumptions do you question and why would that invalidate my argument that novel phenotypes can arise as a consequence of natural selection? None of the things you brought up are remotely relevant, as far as I can tell.

  24. Corneel: novel phenotypes can arise as a consequence of natural selection

    Maybe this statement requires too much unpacking? It kind of assumes the role of mutations, and doesn’t really address questions like how novel a phenotype should be to count as “new”, how many generations to produce how much novelty, etc. Selective breeding can produce a mind-boggling amount of phenotypic variation without any mutations, but how much of that is already lurking in a genome, how much results from recombination, how much from copying errors (and are such errors considered mutations?), and so on. These are questions that interest me, anyway.

  25. Flint: Maybe this statement requires too much unpacking?

    Perhaps this warrants some OP to explain the basics. Maybe, someday, I will find the time to write that.

    Flint: It kind of assumes the role of mutations, and doesn’t really address questions like how novel a phenotype should be to count as “new”, how many generations to produce how much novelty, etc. Selective breeding can produce a mind-boggling amount of phenotypic variation without any mutations, but how much of that is already lurking in a genome, how much results from recombination, how much from copying errors (and are such errors considered mutations?), and so on. These are questions that interest me, anyway.

    It is quite saddening that in an online community that has been discussing evolution for years this needs introduction at all; What I am trying fruitlessly to get across to Charlie here is actually the core idea of the modern synthesis, which demonstrated how Mendelian inheritance undergirds the evolution of continuously varying characters. This provided a satisfactory account for evolutionary change many years before the discovery of the molecular nature of genetic mutations. In species with long generation times (like us), the response to a newly imposed selection pressure will almost certainly be fueled predominantly by standing (= pre-existing) heritable variation.

    As to your other questions: Copying errors resulting from unfaithful base pairing by the DNA polymerase definitely count as mutations. In fact, this is the main source of new mutations. The focus on genetic mutations is understandable, but IMO diverts attention from the fact that most species already harbour what you rightfully refer to as a “mind-boggling amount of phenotypic variation”. Once you see this, it is only a small step to realize that between-species variation is simply an extension of within-species variation. Not surprisingly, Charles Darwin was well aware of the large variation within species and this led him to make his case for common descent resulting from ongoing splitting of lineages. Also unsurprisingly, this is why creationists cannot let go of thinking in terms of fixed “types” and why Charlie is continuously trying to trivialize within-species variation.

    We have discussed “new” many times here and the main tactic of creationists appears to consist of restricting the definition of “new” to “instant creation of novel species”. As far as I am concerned, “new” just means “not observed before”. Moreover, I consider this discussion to be a red herring. All evolutionary theory is required to do is provide a plausibe explanation for the current biodiversity, which it easily can.

    Finally, the earliest description of genetic recombination of linked traits I am aware of is by Thomas Hunt Morgan in 1911 during his work on Drosophila melanogaster. His research led to a major breakthrough in chromosome theory. Morgan hypothesized that recombination was associated with crossing over of chromosomes during meiosis, which we now know to be correct. Recombination does not necessarily increase phenotypic variation, although in specific scenario’s it can. That, in itself, deserves a complete OP of its own 😀

  26. Corneel:
    CharlieM: Excellent point.

    Corneel: Thanks. It appears you forgot to withdraw the comment that started off this particular exchange though, to wit:

    CharlieM “When a kind or a species takes on physical form the limits of archetypal expression is set. This is similar to what we see with pluripotent stem cells. The line of specialist cells that they give rise to will not normally produce cells with the potential of the former pluripotent cells they developed from.”

    Corneel: Cells in living organisms quite frequently engage in dedifferentiation. So, following your analogy of evolution as development, there is no reason whatsoever to suppose that “the limits of archetypal expression is [sic!] set”.

    It is true that many plants can be grown by taking cuttings from, say, the stem or the leaf. But as the plant develops, the more derived types of tissue tends to lose the life force than is retained in the primitive tissue. The formation of corollas or petals exhausts the life force and no further regeneration will result from these structures.

    The general pattern is that the more derived tissue lose the powers of regeneration observed in the primitive tissue.

  27. Biology has come a long way since it was believed that the human genome must consist of at least 100 000 genes and it was generally believed that one gene was responsible for one trait. Of course with the complication of alternative splicing it is no longer believed that one gene coding for one enzyme is the norm.

    Up steps quantitative genetics to figure out how to deal with traits that can have a multitude of genes spread throughout the genome. We come across single genes associated with multiple traits and a multitude of genes associated with single traits. Oh what a tangled web life weaves!

    And now an omnigenic model is being proposed to replace the polygenic model.

    From the link:

    The one gene-one trait idea was succeeded long ago by the polygenic model, the idea that many traits, such as height, are complex and controlled by many genes. Now, as bewildering findings accumulate from genome-wide association studies, the polygenic model is starting to show the strain.

    It goes on:

    Any given trait, it seems, is not controlled by a small set of genes. Instead, nearly every gene in the genome influences everything about us. The effects may be tiny, but they add up…

    In any cell, there might be 50 to 100 core genes with direct effects on a given trait, as well as easily another 10,000 peripheral genes that are expressed in the same cell with indirect effects on that trait, noted Dr. Pritchard.

    Regarding complex traits, one result that surprised them was that, “essentially the entire genome influenced height”. At the end he admits that, “it’s telling us something profound about how cells work that we don’t really understand very well”.

    We will never understand the story of life if we are focused solely on the composition of its alphabet. The creative principle is found in understanding the whole, not in analyzing the letters.

    Biology is moving from talk about genes, to polygenes and now to omnigenes. This is progress.

  28. CharlieM: But as the plant develops, the more derived types of tissue tends to lose the life force than is retained in the primitive tissue. The formation of corollas or petals exhausts the life force and no further regeneration will result from these structures.

    Oh, Charlie. Your view of biodiversity is so delightfully simplistic. Corolla’s and petals are parts of flowering plants (angiosperms). You appear to have binned all the greeny stuff into a single catch-all. What about ferns, what about mosses, what about horsetails, what about cycads, what about conifers, what about liverworts? Do they all consist in large part of highly differentiated cells that are incapable of reverting to pluripotency? Indeed, is this even true for the non-reproductive structures of angiosperms? I don’t think you have shown this to be the case.

    CharlieM: The general pattern is that the more derived tissue lose the powers of regeneration observed in the primitive tissue.

    Alas, plant cells were just an example. You have not shown this to be “the general pattern” at all. I suspect that, outside of a few select metazoan lineages, irreversible differentiation is not quite that wide spread as you believe it to be . But to be fair, I haven’t investigated this issue very deeply. So now is your chance to prove me wrong.

    And of course, given that dedifferentiation exists in some cell lineages, by analogy some species should be capable of wholesale reversal to a primitive state and re-evolution down another evolutionary path. I don’t believe we have ever observed something like that, did we now?

  29. CharlieM: Biology has come a long way since it was believed that the human genome must consist of at least 100 000 genes and it was generally believed that one gene was responsible for one trait. Of course with the complication of alternative splicing it is no longer believed that one gene coding for one enzyme is the norm.

    Up steps quantitative genetics to figure out how to deal with traits that can have a multitude of genes spread throughout the genome. We come across single genes associated with multiple traits and a multitude of genes associated with single traits. Oh what a tangled web life weaves!

    Charlie, you are all over the place again. Please tell me that you do not actually believe that quantitative genetics originated after the discovery of alternative splicing. Even without that goof-up, this comment is a veritable mess. I appreciate that you are trying to learn quantitative genetics in a hurry, but it works better if you lay off the “everything-is-so-complicated” stance, bypass the sensationalist news story and read the primary source. It is quite accessible for laymen and does a decent job of introducing the historical background.

    CharlieM: The one gene-one trait idea

    That’s funny. I once tried to hunt down the primary reference for “one gene-one trait” quote but did not succeed. I believe it is a corruption of the “one gene-one enzyme hypothesis” title of the paper by Norman Horowitz referring to the work of Beadle and Tatum. We are talking 1948 here, folks. Polygenic inheritance for quantitative traits was already proposed by George Shull, E. M. East and H. Nilsson-Ehle in the multiple-factor hypothesis 40 (!) years earlier. Once again, it turns out geneticists, even those living 100 years ago, were not incompetent fools.

    CharlieM: We will never understand the story of life if we are focused solely on the composition of its alphabet. The creative principle is found in understanding the whole, not in analyzing the letters.

    Biology is moving from talk about genes, to polygenes and now to omnigenes. This is progress.

    Quantative genetics and the concept of polygenic inheritance was developed many years before James Watson and Francis Crick elucidated the structure of DNA. Learning about the “alphabet” did not displace quantitative genetics; it complemented it. What you fail to understand is that biologists are already trying to understand the whole and the details and everything in between.

    The “creative principle” was abandoned a long time ago. Until you learn the reasons why, you will, as you say, never understand the story of life.

  30. Corneel:
    CharlieM: I did not say that it cannot be disentangled. We can follow the threads, but they don’t end up in nice simple relationships of cause and effect. We see multiple causes, feedback loops, various levels of activity interpenetrating each other.

    Corneel: All of which are also observed in non-biological disciplines, like geophysics or meteorology. You are just making up excuses.

    Geophysics and meteorology are disciplines in the study of the living earth. 🙂

    CharlieM: I’m not sure where the soothing comes into play in believing that we have responsibilities to fulfil and that suffering is a fact of life.

    Corneel: .. and soul qualities! Do not forget soul qualities.

    Suffering is an example of a soul quality. Call it what you will, but I can observe higher animals and discern soul qualities in their behaviour and in the way they can communicate their inner feelings through sound. A dog will let you know when it is happy and excited through its actions and it will whimper when it is unhappy.

    CharlieM to Allan: There is plenty of teleology. For instance, a pigeon grows wings so that it can fly. Birds build nests for the purpose of having somewhere to raise chicks.

    Corneel: And of course marine flatworms have penises so they can fence.

    GOETHEAN SCIENCE! It works b*tches!

    And of course we all know that we humans liberated our forelimbs from being tied to their locomotive duties so that we could experience the pleasure of masterbation. And the shortcomings of T. Rex is the reason it was such a short tempered brute. Males cry out in frustration, “Either give me longer arms or a longer penis!” 🙂 Mother nature can be cruel. 🙁

    Back to reality:

    Martin Wagenschein had some thoughts on education that aligned well with Goethe’s way of thinking. In the article Teaching to Understand he says:

    Hermann Heimpel says that “the universal is contained in the particular and can be found: Mundus in gutta (the world in a drop),” and that it is possible “within the framework of a general survey to come face-to-face with history in particular places, and … to apply this to other areas.” Wilhelm Weischedel speaks of the “presence of the whole in the parts” and says that “something of the essence of history only really lights up in a particular event.”

    The concept of the exemplary is the opposite of specialization. It doesn’t want to get stuck in particulars, it looks for the whole in the particular. “Impossible!” will be the response of the person who only knows addition.

    Further he says:

    But there is something decidedly more important that analytical research can show us. When we slap our leg, we are basically all convinced we are touching the same old body we have always lived in. But we now know from chemical isotope research, as Butenandt reports, that all structures of living organisms, including bones and teeth, are constantly being built up and destroyed. So we cannot think of our body in mechanistic terms, because it is in flux equilibrium.

    So the body of an organism is not what the physicist calls a body, but it is a process. We would recognize our mistake sooner if the process were to run more quickly. If we want to compare a human body to something physical, we shouldn’t think of a stone or statue but — and even this would not yet be exhaustive — of a whirlwind that sucks up and again drops dust as it moves along, or a cumulus cloud, a fountain, a flame, or a river.

    By treating the living world analytically and mathematically we gain a great deal of practical knowledge, but we also lose a great deal by focusing on this method. We ignore the living world and relace it with dead mechanical systems.

    More translations of Martin Wagenschein’s works can be found here and I think they are worth reading.

  31. Kantian Naturalist: CharlieM: You are agreeing with a misinterpretation.

    Kantian Naturalist: I can’t speak for Corneel’s understanding, but I understand your position perfectly well. I share his opinion about its merits.

    Well my participation here wouldn’t be worth the effort if we all agreed with each other. I appreciate my views being challenged here.

  32. Allan Miller: CharlieM: Fair enough. It would have been more accurate if I had said your main focus was on the molecular aspects of the origins of sex.

    Alan Miller: Not even that. That’s like saying endosymbiosis focusses on the molecular aspects of the origin of mitochondria. There aren’t just the 2 levels at which things can be understood.

    True enough, and we should always keep in mind the context when delving into the molecular activities. And it doesn’t matter whether there is a reduction to haploid or diploid or whatever, living systems are never viable outwith the cell in which they function.

  33. Allan Miller: CharlieM: Goethe came to understand this with his archetypal plant which connects all plants.

    Alan Miller: The bulk of your output seems to be about what Steiner thought or what Goethe thought. There doesn’t seem to be much ‘there’ there. If everything is simply labelled ‘archetypal’, and nothing is not, what insight is gained by doing that?

    I follow their ways of enquiry because I see in their examples, a way of looking at nature with a means of understanding processes in their relationships to each other and their connections to the whole. This has to be a personal experience for each person. Without this mere explanations will not suffice.

    There have been a host of enlightened minds throughout history who I believe have experienced what I am talking about only in much greater clarity than my meagre glimpses.

  34. Allan Miller: CharlieM: There is plenty of teleology. For instance, a pigeon grows wings so that it can fly. Birds build nests for the purpose of having somewhere to raise chicks.

    Allan Miller: And sexual eukaryotes reduce to the haploid state for the purpose of … what?

    Purposes only tell us about individual cases. We have to look to the general for a deeper understanding. A knife can have many purposes: to make its maker a profit, to cut up food, to whittle sticks, to murder someone, and so on. But looking at knives in general we see them as the product of human creativity. The purpose a knife has been put to can tell us only one aspect of its existence. Knowing how it came to exist and its history will give us a much fuller picture.

    Organisms are subject to growth and decay, expansion and contraction. Reduction to a haploid state is just one instance of this cyclic process which is a common theme throughout the natural world.

  35. CharlieM: I appreciate my views being challenged here.

    I know you believe that about yourself, but that’s not how I see you.

    I see you as someone who evades and avoids responding to any challenges presented: either we’re told that we just need to read more of the stuff that you’ve read, you repeat the point to which someone else has already objected, or criticisms are simply ignored.

  36. Kantian Naturalist: I know you believe that about yourself, but that’s not how I see you.

    I see you as someone who evades and avoids responding to any challenges presented: either we’re told that we just need to read more of the stuff that you’ve read, you repeat the point to which someone else has already objected, or criticisms are simply ignored.

    I agree. Charlie serves but he never volleys.

  37. CharlieM: Purposes only tell us about individual cases. We have to look to the general for a deeper understanding. A knife can have many purposes: to make its maker a profit, to cut up food, to whittle sticks, to murder someone, and so on.But looking at knives in general we see them as the product of human creativity. The purpose a knife has been put to can tell us only one aspect of its existence. Knowing how it came to exist and its history will give us a much fuller picture.

    OK… but my interest is precisely in how it (sex) came to exist. But you are disinterested in that fuller picture, and retreat to Goethe or Steiner’s vague waffle.

    Once, there was no haploid/diploid cycle, now there is, with a significant clade performing this reduction, and even the ones that don’t have ancestors who did. Their ‘cycle’ is repetition of the diploid.

    Organisms are subject to growth and decay, expansion and contraction. Reduction to a haploid state is just one instance of this cyclic process which is a common theme throughout the natural world.

    Yebbut why? I don’t know how describing life in such a vague way provides any insight. Yes, life is cyclic. Even bacteria undergo a cell cycle. But how is something so vaguely descriptive meant to be illuminative?

  38. Corneel:
    CharlieM: I find that asking about purposes is very counter productive in trying [to] figure out what life is all about..

    Corneel: Perhaps you meant something different from what you wrote? As it stands now this is self contradicting

    Can you clarify? What have I said that is self contradictory?

  39. Corneel:
    CharlieM: Your vastly simplified model above make many assumptions, but it doesn’t counter the fact that natural selection needs something to work on.

    Corneel: I never denied that natural selection needs something to work on.

    So what assumptions do you question and why would that invalidate my argument that novel phenotypes can arise as a consequence of natural selection? None of the things you brought up are remotely relevant, as far as I can tell.

    How do you know that black fur is novel? How do you that, with regards to their evolution, the first mice did not have black fur?

  40. Flint:
    Corneel: novel phenotypes can arise as a consequence of natural selection

    Flint: Maybe this statement requires too much unpacking? It kind of assumes the role of mutations, and doesn’t really address questions like how novel a phenotype should be to count as “new”, how many generations to produce how much novelty, etc. Selective breeding can produce a mind-boggling amount of phenotypic variation without any mutations, but how much of that is already lurking in a genome, how much results from recombination, how much from copying errors (and are such errors considered mutations?), and so on. These are questions that interest me, anyway.

    In my opinion, all expressed novelty is already contained within the etheric archetype.

  41. Corneel to Flint: It is quite saddening that in an online community that has been discussing evolution for years this needs introduction at all; What I am trying fruitlessly to get across to Charlie here is actually the core idea of the modern synthesis, which demonstrated how Mendelian inheritance undergirds the evolution of continuously varying characters. This provided a satisfactory account for evolutionary change many years before the discovery of the molecular nature of genetic mutations.

    I am happy to accept the laws of Mendelian inheritance from genes influencing pea colour to genes involved in height or hair colour.

    But what does this tell us? it tells us that organisms have a vast array of options in how they organize their genetic makeup. Not that I think there is any consciousness of this on the part of the organism. It is only humans who have begun to make a tenuous attempt at doing this.

  42. I was sitting in the sun and I felt something on my arm. I looked down and I could barely see the tiniest of flies moving around. I pondered that this minute creature had the same basic organs as a creature many orders of magnitude bigger. The smallest mammal has the same basic organs as a blue whale.

    Consider vehicles with internal combustion engines and think what range of sizes could humans build with the same basic components. Wisdom is deep-rooted in nature.

  43. CharlieM: I was sitting in the sun and I felt something on my arm. I looked down and I could barely see the tiniest of flies moving around. I pondered that this minute creature had the same basic organs as a creature many orders of magnitude bigger. The smallest mammal has the same basic organs as a blue whale.

    Not sure what the point of the last sentence is, since flies aren’t mammals — and in fact, there are pretty strict constraints on how big insects can be and how small mammals can be, though there’s some overlap.

    There’s also the question of what exactly you mean by “basic organs”. Insects have ganglia, not brains like ours, their nervous system runs down their ventral side (not dorsal like ours), their hearts are long open cylinders (not pumps), they don’t have lungs, and they don’t have kidneys (though they have similar organs for excreting waste products).

    Sure, insects and mammals are bilateral metazoans, so in some very broad sense they are variations on a worm-like body-plan — though we don’t really know what the last common ancestor of insects and mammals looked like, since it must have predated the split between protostomes and deuterostomes, and soft-bodied animals before the Cambrian are exceedingly rare.

  44. Corneel:
    CharlieM: But as the plant develops, the more derived types of tissue tends to lose the life force than is retained in the primitive tissue. The formation of corollas or petals exhausts the life force and no further regeneration will result from these structures.

    Corneel: Oh, Charlie. Your view of biodiversity is so delightfully simplistic. Corolla’s and petals are parts of flowering plants (angiosperms). You appear to have binned all the greeny stuff into a single catch-all. What about ferns, what about mosses, what about horsetails, what about cycads, what about conifers, what about liverworts? Do they all consist in large part of highly differentiated cells that are incapable of reverting to pluripotency? Indeed, is this even true for the non-reproductive structures of angiosperms? I don’t think you have shown this to be the case.

    I’m not trying to show this to be the case. I was giving a specific example, looking at structures, and determining their powers of regeneration. Greenery tends to have good powers of regeneration.

    Vegetative propagation is common in the plant world but not in animals. This leads me to question what should be classed as an individual. Plants are not individuals to the same extent that humans are. I believe that individualization of organisms is a later product of evolution compared to clonal growth. And it is the same with the development of each one of us. The whole reflected in the parts.

    CharlieM: The general pattern is that the more derived tissue lose the powers of regeneration observed in the primitive tissue.

    Corneel: Alas, plant cells were just an example. You have not shown this to be “the general pattern” at all. I suspect that, outside of a few select metazoan lineages, irreversible differentiation is not quite that wide spread as you believe it to be . But to be fair, I haven’t investigated this issue very deeply. So now is your chance to prove me wrong.

    And of course, given that dedifferentiation exists in some cell lineages, by analogy some species should be capable of wholesale reversal to a primitive state and re-evolution down another evolutionary path. I don’t believe we have ever observed something like that, did we now?

    Some species do lose attributes that have existed in their ancestors. Blind cave fish are an example. But any one-sided specialization limits and further evolution in any meaningful sense.

    Life in general will not and cannot return to its starting point. Like planets revolving round stars and stars round galaxies, Earthly life is on a helical course.

  45. Corneel:
    CharlieM: Biology has come a long way since it was believed that the human genome must consist of at least 100 000 genes and it was generally believed that one gene was responsible for one trait. Of course with the complication of alternative splicing it is no longer believed that one gene coding for one enzyme is the norm.

    Up steps quantitative genetics to figure out how to deal with traits that can have a multitude of genes spread throughout the genome. We come across single genes associated with multiple traits and a multitude of genes associated with single traits. Oh what a tangled web life weaves!

    Corneel: Charlie, you are all over the place again. Please tell me that you do not actually believe that quantitative genetics originated after the discovery of alternative splicing. Even without that goof-up, this comment is a veritable mess. I appreciate that you are trying to learn quantitative genetics in a hurry, but it works better if you lay off the “everything-is-so-complicated” stance, bypass the sensationalist news story and read the primary source. It is quite accessible for laymen and does a decent job of introducing the historical background.

    And from “Cell” comes the question, “Are genome-wide association studies fundamentally flawed?”.

    It is only in recent times that researchers have had the tools to look at the actual DNA sequences involved in quantitative genetics. And things are far from being as straight forward as they would have hoped.

    Stephen Talbott wrote an interesting piece on this subject with some references I’d like to have a look at.

    I’m in the middle of reading the contents of the link you provided, so thank you for that.

    Linking genes with various phenotypic features is one thing, but as we all know correlation does not equal causation.

  46. CharlieM: And from “Cell” comes the question, “Are genome-wide association studies fundamentally flawed?”.

    False.
    We have tried on previous occasions to explain to you the difference between the article in the primary literature and some rando journalist’s sensationalizing the same.
    You link to a journalist writing in MedCity News, and to a self-published polemic. The article under discussion, that Corneel linked to, does not contain your quote. You need to read (and understand…) the underlying literature.

  47. CharlieM:
    CharlieM: I find that asking about purposes is very counter productive in trying [to] figure out what life is all about..

    Corneel: Perhaps you meant something different from what you wrote? As it stands now this is self contradicting

    Charlie: Can you clarify? What have I said that is self contradictory?

    Trying to figure out what life is all about IS asking about its purpose.

  48. CharlieM: Corneel: I never denied that natural selection needs something to work on.

    Corneel: So what assumptions do you question and why would that invalidate my argument that novel phenotypes can arise as a consequence of natural selection? None of the things you brought up are remotely relevant, as far as I can tell.

    Charlie: How do you know that black fur is novel? How do you that, with regards to their evolution, the first mice did not have black fur?

    How does “the first mice” possibly having black fur invalidate my argument above?

    And why are you suddenly fascinated by the fur colour of mice? I thought you liked “to look to the general for a deeper understanding.”

  49. Kantian Naturalist to CharlieM: There’s also the question of what exactly you mean by “basic organs”.

    Charlie means whatever organs humans and flies have in common, since if they didn’t have them in common they wouldn’t be “basic organs”.

    GOETHEAN SCIENCE BABY!!

  50. CharlieM: I’m not trying to show this to be the case.

    Yes, you are. Otherwise, this statement remains unsupported:

    When a kind or a species takes on physical form the limits of archetypal expression is set. This is similar to what we see with pluripotent stem cells. The line of specialist cells that they give rise to will not normally produce cells with the potential of the former pluripotent cells they developed from.

    CharlieM: Some species do lose attributes that have existed in their ancestors. Blind cave fish are an example.

    Hence the “wholesale” in my comment. Blind cave fish do not resemble the vertebrate ancestors. Such wholesale reversal is required to support anything beyond a superficial resemblance between cell differentiation and anagenesis, as suggested by your initial comment above.

    Let me also point out that the above exchange is highly supportive of KN’s statement that you are somebody “who evades and avoids responding to any challenges presented”. In your comment you are clearly trying to trivialize vegetative propagation instead of wondering why your statement is vulnerable to such an obvious counter example. If your approach were truly scientific, it would be you, not me, who had first come up with it.

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