Intelligent Design explains Sex!

A thread for ID proponents to explain their alternative theory for biological phenomena.

Allan Miller has written an article on sex, proposing an evolutionary explanation for why almost all Eukaryota indulge in sex. In response to comments from evolution skeptics questioning his explanation, he challenges them:

OK, you ID types, what’s the Design explanation for sex? You need to explain why all eukaryotes have genes that are involved in meiosis, though some never actually perform meiosis, and in some, the genes are ‘broken’. And you need to explain the taxonomic distribution of asexuality – absent in mammals and birds, but increasingly found as one descends your imagined scala naturae – though intermittent sex remains the norm, even in single celled organisms.

Why? What purpose does it serve that is common to single celled protists and our favourite organism, the chimp? Why wasn’t everything designed to just reproduce asexually?

In response, commenter phoodoo writes:

Why are there legs? Wouldn’t it be better if we just moved like water? Why ten fingers instead of thirty? Why skin? Evolution doesn’t answer these questions any better or worse than ID.

Now, for evolution to have a better or worse explanation than ID, there must be an explanation for sex according to the theory of “Intelligent Design”.

I don’t know of any Intelligent Design theory that attempts to explain biological observations such as sexual reproduction. So I invite those who do know of such a theory to correct my ignorance.

How does the theory of Intelligent Design explain sex?

PS: please feel free to use this thread as a peanut gallery WRT Allan’s article.

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402 thoughts on “Intelligent Design explains Sex!

  1. phoodoo: DNA_Jock,

    Let’s be clear, here is what keiths said:

    It’s already been explained to you. Nothing in evolutionary theory requires a one-to-one mapping between traits and genes. There are traits that are influenced by more than one gene — this is known as polygeny. And there are genes that influence multiple traits, which is known as pleiotropy.

    But this is not really very accurate now is it? The real truth is that there is virtually NO one to one mapping, perhaps literally NONE.

    Slow down and pay attention, phoodoo. What keiths wrote is entirely accurate. And if there were zero one-to-one gene-trait mappings, then it would still be entirely accurate.

    So how does this help your theory, about genes are selected? That makes the whole notion of natural selection EVEN MORE PREPOSTEROUS, if that was ever possible. Systems being built upon genes which account for all kinds of unrelated, mixed up, partial, and quite likely contradictory traits.

    All this has been explained to you multiple times. Here you are, quoting a five-year-old excerpt from someone explaining this to you, and demonstrably missing the point. These days, we have given up on your education.

    Did you even listen to the example he gave, a gene which could affect you being easily scared, politically liberal, and prone to adultery. And natural selection is going to select for this-amongst other things it does!

    Well, I don’t know if selection is going on, but there is evidently variation in the human population associated with different DRD4 alleles.
    The facts are stoically unmoved by how ridiculous phoodoo thinks they are. Are we any closer to an ID explanation for sex?

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  2. I’m watching Rutherford’s talk now. He said that most geneticists at the time the human genome project was about to publish it’s results predicted that there would be many more genes in our genome than the actual 21K found. I’m guessing Larry Moran would have a thing or two to say about that, right?

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  3. colewd:
    newton,

    Based on what standard?

    Standard is that is a designer is the most important component of the hypothesis,Intelligent Design, if one is making a positive argument about the nature of a design. Just as natural processes are the most important component for evolution.

    No capable natural processes, no evolution . No capable intelligent designer, no intelligent design.

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  4. newton,

    Standard is that is a designer is the most important component of the hypothesis,Intelligent Design, if one is making a positive argument about the nature of a design. Just as natural processes are the most important component for evolution.

    No capable natural processes, no evolution . No capable intelligent designer, no intelligent design.

    This is not a an argument that establishes a standard. Processes are not part of the scientific method. Causes and mechanisms are. Processes can be used to help identify causes.

    What evolution does not explain is the mechanistic cause of certain complex biological structures. It attempted to explain this through natural selection. Many scientists now believe this is insufficient.

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  5. colewd: What evolution does not explain is the mechanistic cause of certain complex biological structures. It attempted to explain this through natural selection. Many scientists now believe this is insufficient.

    And it took you only three posts to go from the “positive argument for ID” to “What evolution does not explain is …”.

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  6. colewd to newton,
    This is not a an argument that establishes a standard. Processes are not part of the scientific method. Causes and mechanisms are.Processes can be used to help identify causes.

    Are you serious? A process cannot be a “cause”? A process cannot be a mechanism? Oh they can? Then WTF?

    colewd to newton,
    What evolution does not explain is the mechanistic cause of certain complex biological structures.

    Certain … structures? Do you mean to say that not every complex biological structure has been studied profoundly enough to have a full explanation? Well, of course. The number of scientists is limited as is the amount of funding. So what? We do understand how these structures arise, and we do understand the kinds of mechanisms involved. That you don’t know any of it, or that you won’t accept any of it is a very different issue. So, stop it already with this bullshit. Repeating it won’t make it true.

    colewd to newton,
    It attempted to explain this through natural selection.

    Not just natural selection. Natural selection is but one component. To fully understand you have to gather and follow the evidence of the historical accumulation of successful traits. The evolutionary histories if the components, the existence of different “versions” of the complex feature you care about, the use of some of those components in other features that you didn’t care to check, etc. To understand, to have a profound explanation, it’s not just a matter of thinking of one, single, process, like natural selection, it’s a matter of putting the evolutionary history together too. Checking the role of pseudo neutral drift in allowing some variants to emerge later on, etc.

    colewd to newton,
    Many scientists now believe this is insufficient.

    Of course it’s insufficient. Just look at what I wrote. It’s not just natural selection. That just means that you don’t understand how science works, what it takes to obtain more profound explanations (scientists, laboratories and money, for example), and that, of course, there will always be some features that have not been studied, or for which the evidence might be hard to gather. One step at a time Bill. But we advance despite the stupidly simple-minded scientific denialism of the IDiots’ movement.

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  7. Entropy,

    Are you serious? A process cannot be a “cause”? A process cannot be a mechanism? Oh they can? Then WTF?

    I don’t know how you landed here but let me rephrase. Hypothesis is looking to explain an effect by an assigned cause. Yes a process does cause something or an output but we are looking for a cause specifically and not necessarily a process.

    Certain … structures? Do you mean to say that not every complex biological structure has been studied profoundly enough to have a full explanation? Well, of course. The number of scientists is limited as is the amount of funding. So what? We do understand how these structures arise, and we do understand the kinds of mechanisms involved. That you don’t know any of it, or that you won’t accept any of it is a very different issue. So, stop it already with this bullshit. Repeating it won’t make it true.

    Whats missing is a clearly identified cause powerful enough to explain the observed effect such as a bacterial flagellum.

    Of course it’s insufficient. Just look at what I wrote. It’s not just natural selection. That just means that you don’t understand how science works, what it takes to obtain more profound explanations (scientists, laboratories and money, for example), and that, of course, there will always be some features that have not been studied, or for which the evidence might be hard to gather. One step at a time Bill. But we advance despite the stupidly simple-minded scientific denialism of the IDiots’ movement.

    You mean the evotards will defeat the idiots given enough time 🙂

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  8. phoodoo: Because it would make Lamarckism right, not Darwinism (and I think this is probably true).That scares the hell out of evolutionists.It means that evolution is no longer accidental and purposeless.

    The Rutherford talk that you yourself linked expresses a skepticism of the importance of intergenerational epigenetic inheritance, which I share. Yet you – more of a contrarian than a skeptic, I’d say – think your own expert source is wrong.

    He also comes up with a couple of examples of 1:1 mapping. It’s not the norm (I never thought it was, heh heh) but nor is it non-existent. Mendel caught a break with his peas.

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  9. One thing Rutherford said had me disagreeing. He wondered how a gene ‘for’ transsexual inclinations could work, in a Darwinian sense. But, a transsexual of my acquaintance has a transitioned biological daughter. While the genetics may not be straightforward, nor even involved at all, that certainly suggests how it is possible for the genes to persist.

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  10. colewd: Whats missing is a clearly identified cause powerful enough to explain the observed effect such as a bacterial flagellum.

    It’s only missing to the willfully ignorant who refuse to read the scientific literature on the subject. That would be you Bill.

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  11. Allan Miller: He also comes up with a couple of examples of 1:1 mapping.

    In humans?

    Rutherford talked about examples of transgenerational epigenetic traits, but the only thing he did after that was hand wave it away by saying, but….but nothing. Just that he wasn’t convinced. And the reason he isn’t convinced is because he knows how devastating it would be to the theory.

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  12. colewd:

    Whats missing is a clearly identified cause powerful enough to explain the observed effect such as a bacterial flagellum.

    Has your hypothetical designer been “clearly identified” ?

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  13. DNA_Jock: And if there were zero one-to-one gene-trait mappings, then it would still be entirely accurate.

    And preposterous for a theory that thinks the gene is what is selected (which of course it isn’t, the individual is).

    DNA_Jock: Well, I don’t know if selection is going on,

    That is for sure.

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  14. DNA_Jock,

    I love this:

    In a study of 920 Swedish twin pairs, including 141 DZ twins and 319 MZ twins, most (80%) of whom were female, Cesarini et al. (2009) estimated that approximately 20% of individual variation in economic preferences for financial giving and risk-taking can be explained by genetic differences.

    That’s fucking hilarious. Oh, its 20% then is it? Not approximately 23? I was thinking its was 32.6 approximately, but, well, its science, so who could question it.

    Man is there anything you guys won’t believe.

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  15. DNA_Jock,

    More gems:

    Kluger et al. (2002) conducted a metaanalysis of 20 studies, with a total of 3,907 individuals, involving the association between DRD4 polymorphisms and novelty seeking. Thirteen reports suggested that the presence of longer alleles is associated with higher novelty seeking scores and 7 reports suggested the opposite. Kluger et al. (2002) concluded that, on average, there was no association between DRD4 polymorphism and novelty seeking

    Ha!

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  16. phoodoo,

    And:

    Pogue-Geile et al. (1998) administered personality questionnaires measuring novelty-seeking and positive emotional experience to 306 male and female young adult twins (92 monozygotic pairs; 61 dizygotic pairs) from the general population, 281 of whom were genotyped for DRD4 exon 1 and 3 polymorphisms. They found no significant association between novelty-seeking or positive emotional experience and the DRD4 polymorphisms. The statistical power of their study reduced confidence in the generality of the positive findings in earlier studies.

    And Jock thinks its hard to debunk studies, funny. No need, just read them and have some tea and laugh.

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  17. phoodoo: And the reason he isn’t convinced is because he knows how devastating it would be to the theory.

    Could you provide a link to the mm:ss in the video where he says that?

    You state that like it’s a fact, when actually it’s your opinion about what’s going on in somebody else’s mind. And this is basically the problem that colewd, J-Mac has as well.

    It’s not that your arguments are unconvincing, you think, it’s that they have reasons to reject my arguments no matter how solid they are. It’s not that my arguments are poor it’s they will never accept them because reasons.

    You get so close, so very close, but then fail at the final hurdle.

    phoodoo: And the reason he isn’t convinced is because he knows how devastating it would be to the theory.

    Could you provide a link to the mm:ss in the video where he says that?

    If not, please consider withdrawing that claim. If you want to be thought of has having honour, anyway.

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  18. phoodoo: Ha!

    And yet when confronted with meta-analysis of PSI studies showing PSI is not real you reject them outright.

    It’s called hypocrisy. When it suits you meta studies are valuable evidence, when it does not they are to be discarded and are irrelevant. I would go back and quote you but we both know it’ll shame you not as you are basically shameless.

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  19. phoodoo: Man is there anything you guys won’t believe.

    I’d make a distinction between coincidence and causality. A study may show that some phenomenon is coincident with certain facts or observations. Scientists may then remark “that’s interesting” and proceed to hypothesize a link – a mechanism. The next step is to look for that link using observation and controlled experiments.

    Some correlations might be dismissed as coincidences.

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  20. phoodoo: And Jock thinks its hard to debunk studies, funny. No need, just read them and have some tea and laugh.

    And the problem with further study of a proposed correlation showing it to be non-existent (or rather statistically insignificant) is what, exactly?

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  21. phoodoo: In humans?

    Yes. Did you watch it?

    Rutherford talked about examples of transgenerational epigenetic traits, but the only thing he did after that was hand wave it away by saying, but….but nothing.Just that he wasn’t convinced.And the reason he isn’t convinced is because he knows how devastating it would be to the theory.

    Is that why you are so eager to swallow it whole?

    It wouldn’t be devastating anyway. As he says, it’s not been shown to be non-Darwinian, and even if real affects a tiny handful of traits out of the many that we are sure follow the ‘Mendelian’ path.

    There’s a fundamental mechanistic problem with multigenerational inheritance: dilution. You supposedly inherit the epigenetic settings of parents, grandparents, great-grandparents etc – 2^n individuals, where n is number of generations. Which ones produce the phenotype, and how? Or, going forward, how do your epigenetic marks survive in the future descendants, against a stream of others?

    Mendelian genetics, we now know, gets round this by chucking away an entire haploid genome’s worth of genes from each parent, per offspring, at random. I can’t conceptualize an ‘epigenetic’ mechanism that can do the same thing non-genetically.

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  22. phoodoo: And preposterous for a theory that thinks the gene is what is selected (which of course it isn’t, the individual is).

    No, it’s more complicated than that, and it’s (finally!) relevant to the discussion on sex. In an asexual lineage, ‘the individual’ and its genome are tightly coupled through the generations. Selection of an individual selects its entire genome, and that’s what passes down the generations.

    In a sexual species, conversely, there are two phases to consider: haploid and diploid. Selection can take place in both phases. Then, because the haploid/diploid cycle automatically gives independent segregation of chromosomes, their futures become independent. So even though selection continues to target whole-genome packages (haploid or diploid), the result in a sexual species is to increase or decrease the frequency of the chromosomes that do better or worse in this milieu. Even though never encountered ‘naked’, selection in sexual species causes this assortment.

    Adding crossover adds an even lower level of segmentation, and the same argument applies.

    I realise this will inspire another round of phoodoo performance-art; it’s more for interested readers than him.

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  23. 127 posts and still no ID explanation for sex. As usual on any subject it devolves into phoodoo crying about “sceptics”.

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  24. phoodoo:
    Allan Miller,
    You had suggested you can think of some one to one gene mapping of traits.Can you name one in humans?

    Ear wax. It’s in the talk. Also (familiar to genetics students of the 70’s) the (in)ability to taste phenylthiourea. I can’t. It’s recessive.

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  25. Allan Miller: Ear wax. It’s in the talk. Also (familiar to genetics students of the 70’s) the (in)ability to taste phenylthiourea. I can’t. It’s recessive.

    Do you honestly believe that if you were to remove that gene, all that would happen is that you wouldn’t get earwax? No other adverse effects? Its essentially unnecessary?

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  26. Allan Miller,

    Furthermore, if you do believe this, you have to actually think that whoever got this gene for earwax had some terrific survival advantage, so they just out-competed the poor saps who never got it. Sexual selection perhaps?

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  27. phoodoo: Do you honestly believe that if you were to remove that gene, all that would happen is that you wouldn’t get earwax?No other adverse effects?Its essentially unnecessary?

    No; it affects whether the wax is ‘wet’ or ‘dry’. This is in the video, which I thought you’d watched.

    Having Mendelian inheritance of alleles of a gene is not a guide to the consequences of eliminating it entirely. One could view ‘absence’ as a third allele, with untested phenotypic consequences. Same goes for PTU tasting. The polymorphism in the population leads to just 2 states, taster and not-taster (1 in 4, so recessive). But if there was a deletion, who knows? Because it’s probably not a gene ‘for’ not-tasting PTU; that just acts as an assay.

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  28. phoodoo:
    Allan Miller,
    Furthermore, if you do believe this, you have to actually think that whoever got this gene for earwax had some terrific survival advantage, so they just out-competed the poor saps who never got it.Sexual selection perhaps?

    Like I said, performance art. Watch the video. Mendelian inheritance of a trait says nothing about its advantage or otherwise. You get Mendelian inheritance of many disease phenotypes.

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  29. Allan Miller: Having Mendelian inheritance of alleles of a gene is not a guide to the consequences of eliminating it entirely.

    Because that is not all it does, it is just all we know about. if you really believed that was all it does, why would you think eliminating it would be a problem?

    Next you are saying that things like earwax, although convenient might not be so convenient as so cause a survival advantage, its just a fortunate plus. Just like eyebrows, and eyelashes, and every other thing you can think of in the human body that is good to have, but it would be hard to say its so good that you are going to reproduce better because of it.

    I would say to that, that is a theory that is just dying to force conclusions. All these traits, NOT selected, just not bad to have. Don’t you see that this is all just more having to find solutions to inconvenient facts?

    Its the same thing that happens when we realize that genes aren’t one to one maps to traits. When we believed that was the case, before the genome was ever mapped, it could possibly sounded a little more believable to suggest that one mutation to a gene, causes one small phenotype change, and in this way you could slowly build up a working system (I say slightly more believable, but still fairy tale fodder). You know, that is how we got the whole eye from scratch story, one small mutation, one little light sensitive patch, another mutation, and it form a small indentation, and so on. To me, I say still ridiculous, but to the faithful evolutionist, Ok, well, at least it eliminates God for them.

    But NOW, we can’t just get those small little mutations that make nice little light spots, and then another that dents the light spot just right. No, no, that is far too easy. Instead, the gene that is mutating, it also does MANY other things! So we are not just denting the light spot, we have a cascade of effects going on. You have now been forced to shoehorn a far fetched idea, into a completely mind-blowingly unlikely story.

    But what choice do you have. You are stuck with the story, and no matter how matter changes to the facts come along, you have to stay with the same story. You can’t abandon it now.

    So you are also stuck with saying, well, earwax isn’t a reproductive advantage, but its benefit. Lucky benefit. Lots of lucky benefits. But not so lucky as to be selected lucky. Just lucky anyway.

    That’s isn’t performance art Allan, that is just telling your sides story. Spare me the, oh no one believes that refrain.

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  30. colewd: This is not a an argument that establishes a standard.

    So the standard is that an hypothesis that claims to be a better explanation for a material object does not need to explain what the explanation is? Is that just for design?

    Processes are not part of the scientific method. Causes and mechanisms are. Processes can be used to help identify causes.

    If you are saying that a process is a grouping of related causes and mechanisms , I agree. However , geology is science and it definitely studies geological processes.

    What evolution does not explain is the mechanistic cause of certain complex biological structures.

    Is that the standard that it must explain mechanistic causes? It cannot assert that since those structures exist there must be some natural process that caused it somehow back in deep time? Or does that only work as a positive argument for design?

    It attempted to explain this through natural selection. Many scientists now believe this is insufficient.

    Do these same scientists believe that an unknown and possibly unknowable designer somehow did something , sometime ,for some reason that caused these structures to become substance is a sufficient explanation?

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  31. phoodoo,

    That’s isn’t performance art Allan, that is just telling your sides story.

    No, you’re gibbering, and getting it wrong. That’s the ‘performance art’ part: long-winded riffs that show nothing other than your own ignorance. The more excitable Creationists put me in mind of a kid going into a fight, arms pinwheeling and eyes tight shut.

    God forbid you should learn anything. The Mendelian trait is not presence or absence of earwax, nor presence or absence of the gene of which ‘wet’ or ‘dry’ are alleles. It is not known whether ‘wet’ or ‘dry’ alleles are adaptive wrt each other. Probably not, I would say. But despite several corrections you’re still yammering about the presence or absence of earwax. That isn’t the 1:1 trait.

    Spare me the, oh no one believes that refrain

    Well, I would but for the fact that no-one believes that. I have never thought that one gene generally maps to just one trait, nor vice versa, so you can keep me out of that ‘we’.

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  32. My memory may be faulty, but I distinctly remember hearing in a lecture that Mendel struck lucky with his wrinkly/smooth peas; most genes aren’t like that. I can’t imagine where I might have attended such a lecture but at University, which would put it as 1975 or 6.

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  33. Allan Miller:
    My memory may be faulty, but I distinctly remember hearing in a lecture that Mendel struck lucky with his wrinkly/smooth peas; most genes aren’t like that. I can’t imagine where I might have attended such a lecture but at University, which would put it as 1975 or 6.

    I saw it on TV, maybe Bronowski’s Ascent of Man. Each of the seven trait alleles studied by Mendel occurs on a different chromosome. Good luck, or just brilliant observation before he started the formal experiment.

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  34. Allan Miller,

    You have said absolutely zero with respect to refuting the problems I raised for evolution theory. Do I need to number it so you can stop trying to squirm out of the problems?

    1. If the gene was only for determining if one’s earwax was either wet or dry, then there couldn’t possibly be any harm to deleting that gene could there? But you don’t believe it only does that, so of course you know it would cause harm.

    2. Secondly, are you telling me that YOU believe that nature packs all of these complicated interactions into some genes, and then some genes it just wastes time with ONE gene, for the type of earwax you have, because, you know that was selected for. Or even funnier still, NOT selected for, just drift. OH brother.

    3. YOU may never have thought that ONE gene mapped for ONE trait, but are you telling me that wasn’t at one time the expected paradigm? Come on Allan. And are you telling me that one gene for one trait isn’t much, much easier to make the argument for small mutations to ONE thing adding up to complex features? Stop hand-waving as this is not a problem for evolution, because you want to pretend no one in evolution believes anything they say they do.

    One gene for one trait is MUCH MUCH easier (though not easy!) to try to play the just so stories game of building an eye. Are you really going to say, whether its one gene for one trait or one gene for 40 traits, its just as easy to explain natural selection??? Its just as easier to explain, small, accidental mutations adding up to intricate sophistication? Are you honestly going to try to say that? With a straight face? Even when one mutations can affect 40 systems?

    For fuckssakes.

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  35. There is virtually nothing, NOTHING, that comes along and complicates and muddies up the whole small mutations, selection, more small mutations …stories, that evolutionists won’t say, …”not a problem” to. Nothing!

    Epigentics, no problem! Junk DNA great! No junk DNA, even better! Map one to one, map one to 100. So what, what’s the difference! Drift-no problem! Neutral theory? Ok, sure. Natural genetic engineering? We predicted it! Bananas having more genes than humans? Where’s the problem, of course they do!

    Performance art, my ass.

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  36. Hey, if there were a clear cut grammar and syntax to genomes — one gene, one trait — we could design stuff and wouldn’t need evolution.

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  37. petrushka,

    Then why do you think, before the human genome project, that EVERYONE predicted the number of genes would be much much more than it turned out to be.

    And why did not one single person on the planet predict that rice would have more genes than humans. Not one. Why do you think that is?

    But not a problem! Its great. What’s the issue? We predicted it!

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  38. phoodoo:
    Allan Miller,
    You have said absolutely zero with respect to refuting the problems I raised for evolution theory.Do I need to number it so you can stop trying to squirm out of the problems?

    If you were looking for engagement, less drama would certainly have helped.

    1.If the gene was only for determining if one’s earwax was either wet or dry, then there couldn’t possibly be any harm to deleting that gene could there?But you don’t believe it only does that, so of course you know it would cause harm.

    The gene itself isn’t ‘for’ determinining whether earwax is wet or dry. One allele is the gene ‘for’ wet. The other is the gene ‘for’ dry. But if you remove the locus altogether, that may have a catastrophic effect on the organism, even if the alleles are distinguishable by something mundane. That locus isn’t the gene for wet/dry, the 2 alleles are.

    2.Secondly, are you telling me that YOU believe that nature packs all of these complicated interactions into some genes, and then some genes it just wastes time with ONE gene, for the type of earwax you have, because, you know that was selected for.Or even funnier still, NOT selected for, just drift.OH brother.

    I have made no statement on selection of earwax.

    3. YOU may never have thought that ONE gene mapped for ONE trait, but are you telling me that wasn’t at one time the expected paradigm?Come on Allan.And are you telling me that one gene for one trait isn’t much, much easier to make the argument for small mutations to ONE thing adding up to complex features?Stop hand-waving as this is not a problem for evolution, because you want to pretend no one in evolution believes anything they say they do.

    I don’t think it’s any harder to make the argument using polygenic traits than monogenic, so I don’t accept that slur on scientists’ integrity. And, no-one challenges scientists harder than other scientists. I know you don’t believe that, but there you go.

    Are you really going to say, whether its one gene for one trait or one gene for 40 traits, its just as easy to explain natural selection??? Its just as easier to explain, small, accidental mutations adding up to intricate sophistication?Are you honestly going to try to say that?With a straight face?Even when one mutations can affect 40 systems?

    Here, you’re mixing up polygenic and pleiotropic genes. The latter have more than one effect, and yes, they may be harder to change – although they weren’t necessarily pleiotropic throughout their evolutionary history. But polygenic traits really aren’t a problem. After all, an organism is effectively one enormous ‘polygenic trait’. Think about it.

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  39. phoodoo: Its the same thing that happens when we realize that genes aren’t one to one maps to traits. When we believed that was the case, before the genome was ever mapped,

    Thursday, veal, waitress.

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  40. phoodoo: 10,000 years and still no evolutionary explanation for consciousness.

    Good point, ID doesn’t have an explanation for that either. Of all the things IDiots whine about not being explained by evolution, they’re also not being explained by ID. No models, no predictions, no experiments, no observations. Nothing. IDiots have nothing.

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  41. phoodoo: Then why do you think, before the human genome project, that EVERYONE predicted the number of genes would be much much more than it turned out to be.

    That is historically false. There were several well-informed evolutionary biochemists that predicted the number of genes accurately to within a few percent.

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  42. In an attempt to return to the topic of this thread, I will note that, phoodoo’s incredulity notwithstanding, polygenic traits and pleiotropy do NOT present a problem for goal-free evolution. They do, however, present an enormous problem for Design.
    phoodoo’s performance art is thus an on-topic critique of any Design explanation for sex. Unintentional, perhaps.

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