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Is There Enough Time For Humans to Have Evolved From Apes? Dr. Ann Gauger Answers

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153 Responses to Is There Enough Time For Humans to Have Evolved From Apes? Dr. Ann Gauger Answers

  1. Dr. Ann Gauger makes me proud to be a proponent of Intelligent Design.

  2. Dear Ann,

    We share a common ancestor with chimps so obvioulsy it happened and therefor the probability of it happening is one. Evolution(ism) works in mysterious ways and just because we cannot go into the past to see what happened does not change the fact that it did happen.

    We have it on good authority that only common descent and common descent only can explain the pattern of ERVs, pseudogenes, morphology, fossils and geological distribution that we observe. Human embryos have a tail and most evolutionists are direct proof of transitional forms. Heck I am sure you could line up the evos on most evo forums to match the early stages of the alleged human lineage.

    So why are you in denial?

    :)

  3. Based on the numbers Dr. Noor gave us in the Coursera Genetics course (approximately 65 point mutations per generation in humans), I did just a simple back-of-the-envelope calculation, and it looks to me like you can’t even explain the number of mutations in the time available from the alleged chimp-human split.

    And that is assuming all the mutations are additive and are fully preserved in the next generation.

    And that is completely ignoring the kind of mutations needed.

    And is completely ignoring whether any of the mutations actually do anything significant.

    And is completely ignoring whether any of the changes would actually confer a survival advantage.

    And is completely ignoring whether any survival advantage would actually get fixed in the population.

    And is completely ignoring the need for coordinated changes (as Ann rightly points out).

    —–

    I don’t know. I keep hearing about all the great evidence for chimp-human ancestry — even from many ID proponents. I acknowledge there are some interesting bits and pieces of evidence that could hint at a historical relationship. But I just can’t make the bits and pieces add up . . .

  4. 4
    Kantian Naturalist

    If evolutionary biologists and paleontologists thought that hominid evolution as Gauger believes that they do, she’d be right. But they don’t, and she isn’t.

    Particularly, her argument as presented above trades on an equivocation: she takes up Behe’s work on point mutations and acts as if all other kinds of mutations are subject to the same constraints. That’s just not so.

    I’m specifically appalled by her insinuation that different mutations would need to be specified independently for different parts of the body. It suggests that she’s largely ignorant of developmental biology. There’s no reason I can think of for why it’s implausible to think that minor, biochemically realistic changes in regulatory genes that coordinate the development of pelvis and brain, under the selective pressures that make those mutations advantageous in those ancestral environments, account for the proliferation of hominids.

  5. You can look at the oldest fossil of almost anything (bats, sharks, spiders, trilobites, ferns, whatever) and they can clearly be identified as being no different or little different from today’s life-forms. And this stability has supposedly lasted hundreds of millions of years in many cases.

    To get two humans from two ape-like critters in a few million years shows gullibility of the highest order.

  6. 6
    Kantian Naturalist

    To get two humans from two ape-like critters in a few million years shows gullibility of the highest order.

    I’m all in favor of criticisms of evolution, but that’s not what the theory or the evidence suggest. If one is going to criticize the theory, one should take the time to understand it.

    The question is whether it’s plausible that some mutations in regulatory genes, plus selective pressures, could have accounted for the evolution of australopithecines from some population of Miocene apes, of early Homo from australopithecines, of Homo sapiens from early Homo species — within about six or seven million years.

  7. as to: “The question is whether it’s plausible that some mutations in regulatory genes, plus selective pressures, could have accounted for the evolution of australopithecines from some population of Miocene apes, of early Homo from australopithecines, of Homo sapiens from early Homo species — within about six or seven million years.”

    More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012
    Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population.
    You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.
    Facing Facts
    But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes.
    http://www.uncommondescent.com.....rwin-said/

  8. Kantian naturalist,

    “It suggests that she’s largely ignorant of developmental biology”

    Well, Ann Gauger received a PhD in developmental biology from the University of Washington, so I think its more likely that your understanding developmental biology is wrong rather than hers.

  9. Kantian naturalist,

    “It suggests that she’s largely ignorant of developmental biology”

    Well, Ann Gauger received a PhD in developmental biology from the University of Washington, so I think its more likely that your understanding of developmental biology is wrong rather than hers.

  10. Based upon the behavior evidenced over at TSZ, I think a better question is, has there been enough time for apes to have evolved from humans.

  11. KN, I love your statement. It just needs a little tweak:

    “There’s no reason I can think of for why it’s plausible to think that minor, biochemically realistic changes in regulatory genes that coordinate the development of pelvis and brain, under the selective pressures that make those mutations advantageous in those ancestral environments, account for the proliferation of hominids.”

    There, that’s better.

    Your point about point mutations is well taken. However, Gauger was making a point about likelihood of a change plus getting the change fixed in a population. Other kinds of mutations are also subject to these issues. Whatever merit there may be to control mechanism mutations (and there may be merit), you still have to argue for an absurdly low number of mutations to even get close to the available time allotment. And that is ignoring the fact that there also happen to be tens of millions of base-pair differences between chimps and humans, which must have come from somewhere after all . . .

    Of course the willingness to believe unproven things was a hallmark of Darwin’s. He often argued for his theory in the following vein: “We can imagine that [fill in the blank] . . .” So you’re in good company.

  12. I did just a simple back-of-the-envelope calculation, and it looks to me like you can’t even explain the number of mutations in the time available

    Well, since the time is mainly estimated from the mutations you might want to try again…

    Back of an envelope

    6.5 million years is 450 000 15yr generations
    65 mutations * 450 000 gens * 2 lineages = 56 million fixed differences
    56 million positions in a 3.2 billion base genome is ~ 1.7% divergence (actually greater than the observed difference).

    Gauger is just playing the silly “over specify the target” game creationists of all ilks enjoy. It’s true that waiting for co-ordinated mutations in a very small specified region would take a long time if the first didn’t have a selective advantage. That might be a problem if you thought humanity was the goal of evolution and only very narrowly defined pathways could lead to us. But that’s not evolutionary biology’s position, so it doesn’t really matter.

  13. I can imagine Max Planck and Wolfgang Pauli smiling wrily at each other: Planck, for his remark about science progressing one funeral at a time – but, since their day, surely at a far slower rate than he could have imagined possible in his most disillusioned moments; and Pauli, for his astonishment that the biologists had made no probability computations whatsoever.

    And perhaps atheists, Crick and Watson, in ‘the other place’, wondering if they really had been so much brighter than their confreres, as Watson had sneered.

  14. 14

    How long do we have to wait for the required material conditions of recorded information transfer to arise?

    I’ve seen mud.

  15. I’ve seen mud.

    ok. Did you measure the information content?

    I hear if you fling enough mud you can get 500 bits of Shannon Information rather easily.

  16. Thanks, wd400. Brain cramp on the math — I was using the wrong timeframe. My bad. I need a new envelope. :) As you say, of course the basic number of differences lines up, because the stated date for the common ancestor depends on the assumption that the lineages did come from a common ancestor. (Although the % of difference between humans and chimps has arguably been regularly understated; but leaving that question aside for a separate interesting discussion.)

    —–

    I disagree, however, with your assessment of Gauger’s point as a silly creationist game. She is not saying that other mutation events (copies, splices, deletions, neutral changes, etc.) don’t occur. Just pointing out that for the simplest area where we have some decent observed data, it isn’t getting us anywhere. Of course, one could assume, that biology isn’t constrained by narrow pathways and that selective advantage is regularly and powerfully present, but those are huge assumptions — required for the storyline, rather than an objective assessment of what we actually see happening.

  17. Creationism is served well by sharp women like this. We need more.
    She’s right on about the impossibility of genes evolving in cohesion to make glorious biology.
    it’s against common sense or better sense of careful thinkers.

    I don’t agree that the fossil record is indicative of any evidence for or against evolution.
    its just snapshots of a critter at a moment.
    its only geology that says there is connections and not biological research.
    ID people need to learn from YEC people on this point.
    It’s illogical to base assertions or criticisms of biology on data from none biological evidence.
    The fossil record is not a BIOLOGICAL record of creatures changing even if it did indicate this.
    It’s only a line of reasoning from geological presumptions that connects data points into a relationship.

  18. This is an excellent question that needs further development! I think that especially with the differences between chimps and humans that are sure to come out in the “junk DNA” section of our genome which the evolutionists had conveniently not included in their calculation of a 98% similarity figure, it will become more and more clear that this is indeed an impossibility.

    So even if they are right that the figure is really 98%, just a 2% difference is still insurmountably huge because of the vast amount of information that is encoded in our DNA. (my opinion)

    But, again, when you include the differences that the ENCODE project has brought to light, I think we will find the differences are far more than just 2%. The 98% figure served evolutionists well for a while, but I think that figure is going to fall as more research is done.

  19. wd400:

    Well, since the time is mainly estimated from the mutations you might want to try again…

    Back of an envelope

    6.5 million years is 450 000 15yr generations
    65 mutations * 450 000 gens * 2 lineages = 56 million fixed differences
    56 million positions in a 3.2 billion base genome is ~ 1.7% divergence (actually greater than the observed difference).

    Whoa, wait a minute- how does that translate into 56 million FIXED differences?

    Also no one knows just how genetically different we are from chimps wd400- no one has ever done a complete side-by-side comparison of the two genomes.

    Ya see wd400, when scientists were seeing how similar the two genomes were they used DNA sequences that were similar. That is how they came up with the 1.x% difference.

    So, no, your math does not work.

  20. Joe, the problem is not with the math, but with the envelope.

  21. Joe,

    Whoa, wait a minute- how does that translate into 56 million FIXED differences?

    Entry level population genetics. For neutrally evolving variants the individual mutation rate is equal to the substitution rate.

    You’re ust wrong on the “no one knows” business. The ~1.1% figure is for regions that align and describes single nucleotide differences (arising from point mutations). There are, of course, stuctural differences too. They are subject to the same evolutionary forces, and since you need less of them to explain the observed differences (each makes a big difference) that don’t pose a problem.

    TJGuy,

    Again, the date is estimates from the observed differences, so it can’t be true that there isn’t enough time for the observed differences to have arrived! I don’t know how ENCODE contributes to pairwises differences between humans and chimps, but I sure would like to hear you try and explain it

  22. Joe, wd400 and I were just talking about aggregate mutation numbers over the 6M+- years. You are of course correct, that this does not address any of the other issues, including getting those mutations fixed in the population.

    —–

    wd400:

    The ~1.1% figure is for regions that align and describes single nucleotide differences (arising from point mutations).

    So I take it that it wasn’t so outrageous for Ann Gauger to be talking about point mutations after all? Maybe it wasn’t just a creationist talking point. :) And having a certain number of mutations occur over the course of generations is very different from having those mutations fixed in the population, which is what I think Ann was talking about in the short video segment.

    There are, of course, stuctural differences too. They are subject to the same evolutionary forces, and since you need less of them to explain the observed differences (each makes a big difference) that don’t pose a problem.

    Well, given that really big changes (chromosome duplication, deletion, etc.) almost invariably cause death (or in less severe cases things like Down’s, Klinefelter’s, etc.), there doesn’t seem to be a lot of evidence for the idea that big changes “don’t pose a problem.” On the other hand, if all you mean to say is that deleting or fusing or duplicating a huge chunk of DNA makes the math easier to get to the human-chimp % difference, then sure. But there is precious little evidence to believe that such changes would not be a problem in actual biology — indeed, what evidence we do have seems to point strongly in the opposite direction.

  23. KN, do you agree with wd400′s post? Just curious.

    I didn’t see any rebuttal or correction from you so I’m assuming you agree. Am I right?

    tj

  24. I’m sorry. I was unclear. I meant to copy the post that I was referring to. I’ll try again.

    Kantian Naturalist, do you agree with post number 12 by wd400?

    Do you agree with his figures? Here they are for easy reference:

    Back of an envelope

    6.5 million years is 450 000 15yr generations
    65 mutations * 450 000 gens * 2 lineages = 56 million fixed differences
    56 million positions in a 3.2 billion base genome is ~ 1.7% divergence (actually greater than the observed difference).

    Gauger is just playing the silly “over specify the target” game creationists of all ilks enjoy. It’s true that waiting for co-ordinated mutations in a very small specified region would take a long time if the first didn’t have a selective advantage. That might be a problem if you thought humanity was the goal of evolution and only very narrowly defined pathways could lead to us. But that’s not evolutionary biology’s position, so it doesn’t really matter.

    I saw no corrections/clarifications coming from you so I’m assuming you do.

    Am I right?

  25. wd400 @ #20

    In reference to your figures, I think Eric A made some key points:

    Eric: “And having a certain number of mutations occur over the course of generations is very different from having those mutations fixed in the population, which is what I think Ann was talking about in the short video segment.”

    This exactly right. I’m surprised you missed that as I thought she made that quite clear.

    So, tell us, are you claiming that all 56 million of these mutations were beneficial and were therefore fixed in the population? That sounds outrageous to me and I find it hard to believe that any scientist would dare to put forth such an idea as even remotely possible.

    Eric: And, “The ~1.1% figure is for regions that align and describes single nucleotide differences (arising from point mutations).”

    Good point. So what we want to know to get a less biased picture of the differences, is what the figure is when you include regions that do not align and that include more than just single nucleotide differences.

    wd400: “Again, the date is estimates from the observed differences, so it can’t be true that there isn’t enough time for the observed differences to have arrived!”

    I’m sorry, I don’t really follow what you are saying here. The date – what date? What does “estimates from the observed differences” mean?

    Are you trying to us the existence of the observed differences as proof that there was enough time for the differences to evolve?

    I don’t take evolution as a given so that line of evidence doesn’t work with me. I thought that is what we are debating. If you don’t show us how it is possible for it to happen in the allotted time frame, then how do we know it happened like you claim? You are just assuming it did. How scientific is that?

    wd400: “I don’t know how ENCODE contributes to pairwises differences between humans and chimps, but I sure would like to hear you try and explain it.”

    Sir, are you familiar with how scientists came up with the figure of 98% similarity? Here is a paper that explains the thinking behind scientists and the methods they used to come up with such figures. Here is the beginning excerpt:

    A review of the common claim that the human and chimpanzee (chimp) genomes are nearly identical was found to be highly questionable solely by an analysis of the methodology and data outlined in an assortment of key research publications. Reported high DNA sequence similarity estimates are primarily based on pre-screened biological samples and/or data. Data too dissimilar to be conveniently aligned was typically omitted, masked and/or not reported. Furthermore, gap data from final alignments was also often discarded, further inflating final similarity estimates. It is these highly selective data-omission processes, driven by Darwinian dogma, that produce the commonly touted 98% similarity figure for human–chimp DNA comparisons. Based on the analysis of data provided in various publications, including the often cited 2005 chimpanzee genome report, it is safe to conclude that human–chimp genome similarity is not more than ~87% identical, and possibly not higher than 81%. These revised estimates are based on relevant data omitted from the final similarity estimates typically presented.

    For details, please read the paper, but the important thing is what they chose to include and not to include in their comparison.

    creation.com/human-chimp-dna-similarity-re-evaluated

    Once you understand what they included and did not include in their comparisons, then I’m sure you can imagine the implications for the figures once you include everything including the junk dna that was assumed not to have function and therefore left out of the data that was compared.

    Here is a response in the Q&A section after the article I just referenced that relates to this:

    “There are about 35 million single-letter differences, tens of thousands of rearrangements, many duplications, many deletions, entire gene families missing from one or the other lineage, etc. And, that is after using the human genome as a scaffold upon which to construct that of the chimpanzee. It is very difficult indeed to create all those differences between the respective species in the time evolutionists give to our supposed common ancestor (commonly seen today as greater than 6 million years ago), and it will become even more different when they reconstruct a chimpanzee genome without using the human genome as a guide.”

    So I’m curious as to what you think about why certain things were included in the comparison data and why others were not.

    Does this show bias or is it just good science?

    Here is even more information. Britten’s study is mentioned in the above article. It came up with a difference of 5% between the two genomes and even this is absoluty huge because even just 5% represents 150 million DNA base pair differences! Surely this is way beyond the power of evolution in 6 million years?!

    The Britten study looked at 779 kilobase pairs to carefully examine differences between chimpanzees and humans. He found that 1.4% of the bases had been substituted, which was in agreement with previous studies (98.6% similarity). However, he found a much larger number of indels. Most of these were only 1 to 4 nucleotides in length, although there were a few that were > 1000 base pairs long. Surprisingly, the indels added an additional 3.4 % of base pairs that were different.

    While previous studies have focused on base substitutions, they have missed perhaps the greatest contribution to the genetic differences between chimps and humans. Missing nucleotides from one or the other appear to account for more than twice the number of substituted nucleotides.

    Although the number of substitutions is about ten times higher than the number of indels, the number of nucleotides involved in indels is greater. These indels were reported to be equally represented in the chimp and human sequences. Therefore, the insertions or deletions were not occurring only in the chimp or only in the human and could also be interpreted as intrinsic differences.

    http://www.answersingenesis.or.....v17/n1/dna

  26. Guys,

    People are getting a bit side tracked here.

    If we want to know how many differnces we expect to see between “species A” and “species B” 6.5 million years after they diverge we need to know the rate of substitution (fixation of mutations) in each lineage (and double it, since both are evolving).

    It turns, the neutral expectation is that population substitution rate is equal to the individual mutation rate. This make sense when you think about it, as the probability of a new mutation fixing is the inverse of the (effective) population size (one gene will ancestor of all others) and the rate at which they come into the population is the mutation rate per individual * population size. Do the math and you end up with the substituion rate equal to individual mutation rate ( and not effected by population size).

    What gauger is doing is pre-specifying changes and saying they are (under particular assumptions) unlikely. Which is extreme question-begging, since no one pre-specified anything.

    As for chromosomal rearrangements, well, we need to account for precisely one, and given the number of people walking around with Robertsonian translocations today I don’t think that will be a challenge.

  27. “If we want to know how many differnces we expect to see between “species A” and “species B” 6.5 million years after they diverge we need to know the rate of substitution (fixation of mutations) in each lineage (and double it, since both are evolving).”

    Can someone better explain this to me please “(and double it, since both are evolving.”?

    Why would you double it for both species? Would one species not evolve at a rate independant of the other?

    Also, and this may sound a little daft, but why would one species evolve (into us), when living amongst them, exposed to the same environmental pressures, another species simply stays almost unchanged (chimpanzee)?

    After all people and chimpanzees can still be found living side by side.

    Just a thought.

  28. Whoa, wait a minute- how does that translate into 56 million FIXED differences?

    wd400:

    Entry level population genetics. For neutrally evolving variants the individual mutation rate is equal to the substitution rate.

    Except no one has ever verified that the equations are correct.

    You’re ust wrong on the “no one knows” business.

    Nope, I am quite correct. No one has ever done a complete side-by-side comparison. No one.

    The ~1.1% figure is for regions that align and describes single nucleotide differences (arising from point mutations).

    That is incorrect as it only applies to some regions, not all. Also there are reports that including indels there is a 5% difference and possibly even more.

    IOW, wd400, you have no evidence to support any of your claims, as usual.

  29. And the fact remains that no one knows if any amount of mutational accumulation can account for all the physiological and anatomical DIFFERENCES observed between chimps and humans. We have no idea what makes a chimp a chimp nor what makes a human a human.

  30. wd400,

    The figures you give in #26, that’s if there is no evolution going on?

  31. Oh Boy,

    Peter,

    It’s the substitution rate * 2 because both species have evolved apart from a common ancestor. Substituions in either linegae will create a difference between the two. If you are really asking “why are their still monkeys” google can help you.

    Joe,

    If your position requires you to deny basic math then I think you need to take a long look at your position (c.f. all those idiots slagging off Nate Silver for the last few weeks)

    Mung,

    I don’t understand the question. Evolution is an unavoidable consequence of finite populations and mutations.

  32. wd400:

    If your position requires you to deny basic math then I think you need to take a long look at your position

    Except I do NOT dny basic math and you don’t have any basic math that supports your claims.

    So again I ask- who has verified the equations wrt to humans or any other sexually reproducing populations?

    My bet, the SAFE bet, is no one has.

  33. What do you mean by verified? They are very straight forward equations, grounded on very simple observations.

  34. No one has ever seen if the equations actually work in the real world. No one has ever observed a neutral mutation becoming fixed in a large population (over 1000 individuals).

    IOW the only thing “simple” about the equations are the people who just blindly accept them as fact.

  35. I’ve got a question. Do negative or harmful changes ever take hold in a population? Perhaps an organism has good genes that allow reproductive success but at the same time it carries one or two negative changes. It seems like negative genes get established in populations sometimes.

    Then there is the problem of people who are carriers of a bad gene but don’t have the disease because they also have one good gene inherited from on of their parents. But since natural selection cannot get rid of the bad genes in this case since it doesn’t result in any problems, the bad genes get spread around and the probability of someone marrying a partner with the same bad genes increases over time. For instance, my wife and i are both carriers of MCADD, but we don’t have the problem because we have one good gene. But our three kids got both bad genes and so they have the problem. It is not a life threatening disease so they’ll be ok, but it shows that mutations can also get established in our genome even if they are neutral or have harmful potential. In fact we are all mutants and the amount of mutations in our genome is growing each generation. Unfortunately, these types of mutations are not the desirable type and have potential for harm. How long can these mutations build up in our genome before it starts taking a real toll on our species? So there are some things that seem beyond the reach of natural selection. That would also seem to indicate that the long term trend is not necessarily up up and away to new and greater heights, but more likely a downward trend.

  36. Joe @34:

    Actually they have. That is what Ann is talking about — real-world data of what it takes for a mutation to become fixed in a population. And the result appears to be that it doesn’t even come close.

  37. tjguy @35:

    This is absolutely a relevant and critical issue. Any rational view of the data suggests that, on average, we run into serious genetic entropy and breakdown long before novel new beneficial mutations arise. If anything, the human genome is degrading, not evolving more functionality.

    The idea that we can mutate our way to novel function in a sophisticated, functionally-integrated, information-dense medium, is a joke of the highest order. Any rational person should laugh at the idea. The only thing that saves the idea from being completely dismissed is the tag-along assertion that: “Yeah, but we’re talking about lots of time and lots of individuals, so eventually something beneficial will arise.” Unfortunately, the math just doesn’t work.

  38. Eric,

    So what you and Ann are saying is that the data does not support the equations.

    However if you accept that common ancestry is true and work backwards from that, then perhaps the equations work. But only if you get the number of differences correct. And we just don’t know what that is yet…

  39. Joe,

    Mutations have gone to fixation many times. Even if that hadn’t been observed you’d still be denying math to claim that they somehow couldn’t.

    Eric,

    Nah, what Gauger is saying (which is based on math by they way) is that if you prespecify two mutations are required for a particular phenotype and those mutations have to fall within the same pre-speficied region of DNA, and the first one has no fitness effect (i.e. three assumptions) then you have to wait so long it would probably only happen once in the time allowed for human-chimp evolution. But the no one pre-specified humanity, so I don’t see how that matters.

    TJ,

    Two things. One, in the specific case that you are talking about the “disease” allele would fall into “mutation selection balance” a scenario in which the weak effect of selection (removing the allele) is balanced by the rate at which the allele is made anew by mutation. JBS Haldane was the first to predict this from the math, and amazingly used the theory to predict the human mutation rate very accurately before we even knew what DNA was (pretty good evidence that these models work).

    It is possible for weakly deleterious (bad) mutations to become fixed in a population, especially small populations which don’t expereince selection as strongly as larger ones. There are some very interesting theories as to how the “slakcening” of slection, which mainly acts to keep things as they are on a molecular level, might facilitate the evolution of complexity. As a rule, creationists hate this idea, I think because they are wedded to the idea that our apparent complexity is really really important, rather than a side of effect of another process.

  40. wd400:

    Mutations have gone to fixation many times.

    I call this the Law of Fixation.

    Even if that hadn’t been observed you’d still be denying math to claim that they somehow couldn’t.

    So it’s math that causes evolution?

  41. wd400:
    But then no one pre-specified humanity, so I don’t see how that matters.

    It matters because humanity is here, and so are chimps, and other primates, and people claim they all share a common ancestor, but they can’t say with any certainty what that ancestor looked like, genetically, or what specifically occurred in each lineage to get to the modern primates of today. But they call it science.

    So we’re encouraging you to put forth testable claims.

  42. I just went to random.org and picked a number between 1 and 100000000. I got 22166740. That’s a 1 in hundred million chance!

    I didn’t pre-specify it or anything. But it matters, because 22166740 is there.

  43. Well gee, wd400.

    It’s nice to see what committed evolutionists are reduced to in defending their commitment to junk science.

    Does 22166740 represent the human genome, the chimp genome, some other genome, or nothing at all relevant?

    What numbers did you obtain to represent the other players?

    What was the [alleged] common ancestor?

    How many steps did it take to get from the common ancestor to the current manifestation?

    How many mutations?

    How many generations?

    How much time?

    According to which model?

    Where are your testable claims?

    You claim to have a model (see your response to Joe @21)

    Now, take that model and plug in the numbers.

    Then compare the expected values to the actual values.

    You know, science.

  44. Evolutionary theory. Science, without the science.

  45. Mung,

    You are playing the gish gallop now.

    Do you think Gauger’s pre-specified mutations are relevent to human evolution? Who pre-specified them?

    In terms of the number of differences between humans and chimps I’ve shown you the neutral expectation for a 6.5 million year divergence, a data that fits nicely within the fossil evidence (and with phylogenetic methods that allow us to place dates on particular speciations)

  46. wd400:

    Mutations have gone to fixation many times.

    If so they did so either by design or via a severe bottle-neck.

    Even if that hadn’t been observed you’d still be denying math to claim that they somehow couldn’t.

    Look YOU made an unsupportable claim, not me. And don’t blame be because you cannot support your tripe.

    Also pre-specified just means they had to happen in some order to produce some benefit. Without that benefit all you have is evolution via sheer dumb luck.

  47. wd400 wrote:

    But the no one pre-specified humanity, so I don’t see how that matters.

    I just went to random.org and picked a number between 1 and 100000000. I got 22166740. That’s a 1 in hundred million chance!

    I didn’t pre-specify it or anything. But it matters, because 22166740 is there.

    Do you think Gauger’s pre-specified mutations are relevent to human evolution? Who pre-specified them?

    To all the onlookers, this highlights an absolutely critical point.

    wd400′s comments are a prime example of the Darwinist mindset as it relates to probabilities and their willingness to consider the design argument. Here is what is going on:

    If an ID proponent looks at an existing biological system (the eye, the Krebs cycle, an entire human being) and asks, “What is the most reasonable explanation for the existence of this system?” The ID proponent then analyzes the system, does the probability calculations, identifies complex functional specified information, and determines that the most reasonable explanation for the system’s existence is that it was designed.

    The Darwinist disputes this. In most cases they don’t bother carefully examining the system, don’t do the calculations, refuse to recognize complex specified information when it is staring them in the face and so on. Then they claim that the existence of the system isn’t really unlikely, or there isn’t any information worth talking about, or that the information can easily be generated (Elizabeth Liddle & Co’s laughable “Look! I can create Shannon Information with an algorithm!” proclamations, and the like). We’re all familiar with this kind of debate tactic and have seen many examples recently.

    However — and this is key — there is another, almost more insidious, approach, as exhibited by wd400 in the above quotes.

    The mindset exhibited by this approach is as follows: evolution could have produced anything, everything could have turned out differently. And because essentially anything goes, there is nothing to explain. That we see the biological systems we see today is nothing but a cosmic fluke. Having a complex functionally specified integrated system with digital code, information storage mechanisms, top-down software protocol hierarchies, etc., is no more unusual than picking out a random number from a hat. Such a system may look incredibly improbable, but, hey, anything goes and we just happen to be looking at one particular role of the dice, so there is nothing that we need to explain. Case [and mind] closed!

    Now at some superficial level this thinking seems seductively logical. After all, no-one is saying that organisms have to possess exactly all the characteristics that they do. We can see this fact simply by looking at the great variety of organisms that exist.

    However, this thinking is fatally flawed, both because (i) it ignores the fact that we do see certain systems in existence, which means they have a real, historical origin that needs to be explained, and (ii) it is based on a simplistic, naive, head-in-the-sand view of biological systems that thinks nearly anything can work; we just mutate a couple of things here and there and, poof, we have a new working system; anything goes and anything could have happened, you see, so there really is nothing that we need to explain!

    —–

    In contrast, those who have a more realistic understanding of the search space and the unimaginably small islands of function within that near infinite space sit up and take notice when they see systems exhibiting these incredibly unique characteristics.

    The reality is there is something that needs to be explained. And chance, or chance plus some culling process over time, doesn’t cut it.

  48. wd400:

    Do you, or anyone else, believe that neutral evolution is the answer to what makes humans and other primates different from their shared ancestors?

  49. Eric,

    And let’s not mention the design of random.org

  50. Eric,

    That’s really not it at all. Creationists of all types massively over-specify the target, calculate exact probabilities for that target and end up being woefully wrong.

    The exact probability that, say, the kreb cycle could evolve is completely unknowable. Evolution is a contingent process, and a chancy one at that. I’m very happy to say a random walk through the space of all sequences would never find a kreps cycle, or cellular division or whatever else you want to name. That’s because the parts of sequence space that are biologically viable are certainly very small. But selection can navigate them, we’ve seen that in the field and in the lab (and, in fact, in computational models).

    But, I’ve now said this three times, what does the paper Gauger is talking about, with its three narrow assumptions, have to do with human evolution? It tells us if particular sorts of changes were absolutely required to create humanity we’d probably only have enough time for one such. But noone prespecified humanity, and no one has shown those sorts of mutations would be required.

  51. Wd400 – You have been thumb sucking since post 1. I ask a very simple question. How does natural selection, a “force” as you call it, with very specific limitations that has been documented, with the help of random mutation another “force” as you call it that very seldom has beneficial mutations, sometimes neutral ones and mostly deadly ones somehow combine to make the “force” called genetic drift? So against all possible odds that you can possibly imagine, a purposeless process with no goals and that was completely random has somehow conspired to accidentally create a conscious being that can ask the very question… How?

    I’m not from America but let’s do as they say in Minnesota… Show me!

  52. 52

    Jeez — if you guys didn’t want to talk about neutral evolution, you shouldn’t have made this claim in the first place:

    Based on the numbers Dr. Noor gave us in the Coursera Genetics course (approximately 65 point mutations per generation in humans), I did just a simple back-of-the-envelope calculation, and it looks to me like you can’t even explain the number of mutations in the time available from the alleged chimp-human split.

    Just admit that this claim was wrong and move on! Don’t bash wd400 for answering this poorly-thought-out-and-can’t-be-bothered-to-do-the-basic-introductory-research question, on the basis of random other poorly-thought-out-and-can’t-be-bothered-to-do-the-basic-introductory-research question.

    In this thread the ID guys have:

    - shown the inability to admit the conclusions of very simple, basic math

    - shown that they don’t understand the difference between the definitions of “mutation” and “substitution”

    - confused point mutations with other sorts of mutations (insertions/deletions, duplications, etc.)

    - mixed all of this into some bizarre stew and randomly lashed out at anyone who tries to correct any piece of their misunderstandings.

    This kind of junk is why IDists will never be taken seriously by real scientists with actual basic coursework in the field, and why they will deserve this fate. You might as well try arguing with doctors that bleeding is a good medical treatment because the heart doesn’t pump blood.

  53. LoL@Nick Matzke-

    Nick, you cannot show that the math applies to the real world and the evidence says that it doesn’t.

    As for research, well your position lacks the research that says that any amount of mutational accumualtion can do what is required. And that is why your position isn’t taken seriously even though it is the reigning paradigm.

  54. 54
    Kantian Naturalist

    I was asked above if I agreed with wd400′s back-of-the-envelope calculations. I don’t disagree with them. And I don’t endorse them. I think that there’s just not enough evidence to play with, all things considered. We’ve got a few really outstanding fossils, and some bits and pieces, and how it all fits together is itself up for grabs. (Notice, for example, the debate between “lumpers” and “splitters” amongst paleontologists.) Then we’ve got the genetic data, and that’s problematic for all sorts of reasons — as was pointed out here a few months ago, if the molecular clock doesn’t have a fixed rate, everything’s up in the air until we’ve built a better model that take variability into account.

    So in the meantime, all we really have to go on is intuitions, assumptions, and prejudices. Suppose we assume that the last common ancestor (LCA) of chimps and humans was some sort of Miocene ape that lived around seven million years ago. In light of that assumption, if the question is asked, “is seven million years enough time for humans to have evolved from the LCA?”, then the best I can do (for now) is turn the question around and ask, “well, why wouldn’t it be?”

  55. Folks, the only reason wd400 gave us some numbers is because I was thinking out loud and tossed out the question whether the mutation rate would give us enough mutations to account for the human-chimp DNA differences (just on a simple raw # of mutations times # of generations basis).

    wd400 — correctly — answered me on the numbers and I promptly acknowledged that I had used the wrong timeframe. To that extent (i.e., raw # of mutations over x # generations) I don’t think there is much to dispute — largely because it is a circular issue (meaning, the timeframe is built on the mutation rate). So no point in questioning that.

    Nick @52 — incorrectly — misses the fact that I have already acknowledged to wd400 that his raw number matches up with the alleged human-chimp split and thanked him for pointing it out. This relates only to the simple basic question of whether there could even be enough mutations over the timeframe to account for the DNA difference.

    However, this basic initial calculation, as I and others have noted, tells us nothing about a whole host of other more critical issues: how long would it take to get mutations fixed in a population, what kinds of mutations would be required, whether there is a biologically realistic chain of changes from the alleged ancestor to humans and chimps, and on and on. It also does not address the question of whether the supposed 98% (97%, 99%, take your pick) similarity between human/chimp DNA will hold up to scrutiny. By every early indication, that number is wildly inaccurate and is going to have to come down significantly as we learn more.

    All of these are real and significant issues with the alleged human-chimp ancestry. These are legitimate questions that deserve real scrutiny.

    wd400′s attempt to argue that stuff can happen because no-one specified it beforehand doesn’t address these questions.

    Nick’s pretends the answers are all out there in the holy literature and we would all immediately jump on board if we just weren’t so stupid (his usual bluff, often accompanied by an irrelevant literature bluff — mercifully absent in this case). Finally, neutral evolution, while certainly of some relevance in explaining raw #s of changes between the species, is of little help in understanding the many functional differences between humans and chimps and whether those differences could have come about through evolutionary mechanisms.

  56. 56
    Kantian Naturalist

    Fair enough, Eric.

    My hunch, or prejudice, or whatever you want to call it, is that the more we learn about how genomes are organized and expressed, the more plausible it will seem that small changes in the nucleotide sequences (whatever the final data turn out to be in the human-chimp case) are consistent with the differences in anatomy and physiology, especially neuroanatomy and neurophysiology, and that the more we learn about neuroanatomy and neurophysiology, the more plausible it will seem that the differences in that regard are consistent with considerable differences between us and chimps with regards to cognition, culture, and morality.

  57. wd400 @50:

    Creationists of all types massively over-specify the target, calculate exact probabilities for that target and end up being woefully wrong.

    The exact probability that, say, the kreb cycle could evolve is completely unknowable. . . .

    So, in other words, you don’t know that the “creationists” are calculating it wrong. :)

    Furthermore, you are on the wrong side of history. Nearly every time we learn something more about a specific biological system we learn that we have underestimated the specification requirement, not overestimated it. Indeed, the only way your statement could be logically true is if: (i) we knew all parameters of the system in full detail, and (ii) we knew we were adding in extraneous stuff. Absent these two, which we clearly don’t have, your statement simply cannot be true. ID people who look at these probabilities almost always oversimplify and underestimate what is required. Typically they are looking at the minimal specification that would be required, based on current knowledge of the system in question.

    Evolution is a contingent process, and a chancy one at that. I’m very happy to say a random walk through the space of all sequences would never find a kreps cycle, or cellular division or whatever else you want to name. That’s because the parts of sequence space that are biologically viable are certainly very small. But selection can navigate them, we’ve seen that in the field and in the lab (and, in fact, in computational models).

    I was going to call BS on this last sentence, but before doing so, perhaps you can clarify. Are you saying that we have several documented instances of complex functional biological features (like the Krebs cycle) arising in the field and in the lab? I would be most interested in seeing any such examples (and I think you know we aren’t talking about finch beaks or bacteria resistance here).

    But, I’ve now said this three times, what does the paper Gauger is talking about, with its three narrow assumptions, have to do with human evolution? It tells us if particular sorts of changes were absolutely required to create humanity we’d probably only have enough time for one such. But noone prespecified humanity, and no one has shown those sorts of mutations would be required.

    Are you suggesting that no point mutations would need to be fixed in the population in order to get to humans? Or are you simply falling back on the “anything-can-happen-so-we-don’t-need-to-explain-what-actually-did-happen” argument? And you certainly haven’t shown that no point mutations would be required to get to humans. Gauger is not claiming that she has answered everything about the alleged human-chimp relationship; she is just giving us a reason to sit up and take notice and starting asking some questions about the facile evolutionary assumptions.

  58. Are you suggesting that no point mutations would need to be fixed in the population in order to get to humans?

    ??

    Have you read anything up there? We’d expect 50 million or so point mutations to get fixed without invoking selection. Gauger is talking about something very different (as I’ve explained).

    The extreme difficulty required to get this simple idea into some heads is really something.

  59. WD400 I forgot to add, your idea of random and undirected needs revision….

  60. wd400:

    We’d expect 50 million or so point mutations to get fixed without invoking selection.

    Only in a design scenario or via severe bottlenecks. There still isn’t any evidence that neutral mutations can become fixed in a sexually reproducing population over 1000

  61. wd400:

    We’d expect 50 million or so point mutations to get fixed without invoking selection.

    Which, in YOUR scenario, means the very unscientific sheer dumb luck didit.

  62. wd400:

    But selection can navigate them, we’ve seen that in the field and in the lab (and, in fact, in computational models).

    Except you’re not appealing to selection, you’re appealing to random genetic drift.

    wd400:

    Have you read anything up there? We’d expect 50 million or so point mutations to get fixed without invoking selection.

  63. wd400:

    I apologize, but it is a little unclear what you are arguing. You insist that Gauger’s comments have nothing to do with human-chimp evolution, which seems to be your primary position on this thread. Here is her statement: “. . . [given the population sizes and reproduction rates] it takes 6 million for 1 mutation in a DNA binding site to arise . . .”

    Now, obviously she is talking about a point mutation becoming fixed in the population. (As a follow-up matter, she then goes on to point out that if you need a series of coordinated mutations, the story is even worse.)

    You said:

    It tells us if particular sorts of changes were absolutely required to create humanity we’d probably only have enough time for one such. But noone prespecified humanity, and no one has shown those sorts of mutations would be required.

    So, you seem to acknowledge the time required for a specific point mutation to become fixed in the population, but, again, you seem to be falling back to the “it-wasn’t-specified-beforehand-by-someone-so-it-isn’t-a-problem” argument.

    Please clarify. Are you disputing her statement and arguing that a pre-specified change doesn’t in fact take that long to arise? Are you arguing that not a single point mutation would have to have been involved in the human-chimp evolutionary changes? Are you arguing that because evolution is contingent there is no specification?

    Why do you think the question of how long it takes for a point mutation to get fixed in a population is irrelevant to the question of human-chimp origins? Is discussing point mutations in the context of human-chimp origins off limits because, as you seem to be saying, it is irrelevant?

    What is it exactly that you are arguing?

  64. This really shouldn’t be this hard.

    First. You seem to still not understand the difference between mutation and substituion. The calculations above show you you’d expect 50 million fixed differences in SNPS (in the ballpark of the observed data) over 6 million years. That’s because the substituion rate is expected to equal the per individual mutation rate under neutrality. So the idea that somehow you’d wait 6 million years for one fixation (with selection!) is obviously woefully wrong.

    Now you think Gauger is saying it will take millions of years to get one mutation to arise she is just bizarrely wrong. Even if you specified to muation down to a single site the population mutation rate is Effective population size * per-site mutation rate. Back of an envelope that’s 10e4 * 10e-8 = 10e-4. The expected waiting time for a process like this is from the exponential distribution, giving 10,000 generations as teh waiting time for any specific mutation.

    What Gauger is persumably actually talking about is co-ordinated mutations (http://www.genetics.org/content/180/3/1501.full). But, again, this paper has some very narrow assumptions and, most importantly, it starts by prespecifying a particular combination of mutations and asking how likely that combination is to arise. But evolution is a contingent process, there was never a pre-specification for evolutoin to aim at.

    Is that clear enough.

  65. I love the you don’t understand argument because wd400 you do not understand. There is not even the slightest possibility that you could be right. Understand?

  66. There is not even the slightest possibility that you could be right. Understand?

    No, but then you haven’t yet explained…. care to?

  67. wd400:

    The calculations above show you you’d expect 50 million fixed differences in SNPS (in the ballpark of the observed data) over 6 million years.

    The equations that have never been verified to reflect reality? Why should anyone care about them?

    That’s because the substituion rate is expected to equal the per individual mutation rate under neutrality.

    Why? Has anyone ever confirmed that?

    Ya see wd400, when you use equations that no one knows if they work or not, there is a problem. So perhaps you should focus on that but I am sure that you won’t.

  68. wd400 @64:

    You seem to still not understand the difference between mutation and substituion.

    Hmmm . . . This is how the NIH’s National Human Genome Research Institute website defines a “substitution”:

    “Substitution is a type of mutation where one base pair is replaced by a different base pair. The term also refers to the replacement of one amino acid in a protein with a different amino acid.”

    Anyway, moving on . . .

    —-

    Now you think Gauger is saying it will take millions of years to get one mutation to arise she is just bizarrely wrong.

    She is not saying it takes that long for the mutation to arise, and you know it. She is saying it will take that long for the mutation to become fixed in a population. And by fixed in a population, she isn’t talking about some random person today having the mutation (which is how you seem to be approaching your calculation). She is talking about the population getting to the point where the mutational change is seen in essentially all organisms in the population. I presume you acknowledge that there are changes in the human-chimp genome of that category (namely, seen in all humans and not in chimps), so they must have become fixed in the entire population over time. We’re not just talking about adding up a bunch of random changes in multiple (human) lineages over time. Whatever key differences exist between humans and chimps must have become fixed in the entire human population at some point.

    But, again, this paper has some very narrow assumptions and, most importantly, it starts by prespecifying a particular combination of mutations and asking how likely that combination is to arise. But evolution is a contingent process, there was never a pre-specification for evolutoin to aim at.

    Is that clear enough.

    Oh, it is quite clear. And your statement is now Exhibit B in demonstrating precisely what I was saying about the Darwinist mindset way back in #47. Rather than repeating what I wrote, I will therefore just refer everyone back to #47.

  69. Eric.

    This is ridiculous.

    In pop. gen. substitution means the replacement of an existing allele by a new one. That is, fixed differences between humans and chimps. Of course lots of differences have taken over the human population – the first calculation I gave here shows that more than 50 million would be expected to be fixed in the ~6 million year window!

    The simplest reading of
    : “. . . [given the population sizes and reproduction rates] it takes 6 million for 1 mutation in a DNA binding site to arise

    would the time it takes for a mutation to turn up. I’ve shown the mean waiting time for a super-specified mutation is ~ 10 000 generations. The time it would then take to fix depends on selection pressure.

  70. Eric and wd400-

    The word “substitution” wrt biology is used to mean both a mutation and fixation

    the first calculation I gave here shows that more than 50 million would be expected to be fixed in the ~6 million year window!

    But no one can confirm/ verify that your calculation is correct, which means it is meaningless.

  71. wd400:

    This is ridiculous.

    Well, I’ll have to let NIH know! Anyway, I’m not that exercised about definitions. Gauger was talking about “one mutation in a DNA binding site.” Whether we want to think about point mutations, insertions, deletions, substitutions, whatever, the principle is the same.

    In pop. gen. substitution means the replacement of an existing allele by a new one. That is, fixed differences between humans and chimps. Of course lots of differences have taken over the human population – the first calculation I gave here shows that more than 50 million would be expected to be fixed in the ~6 million year window!

    Your numbers showed that a certain number of mutations could occur, in aggregate, over 6M years down a lineage line. Agreed. That is not at issue. However, having a mutation show up is very different from having the mutation become fixed across the population. (BTW, the 65 mutations/generation was based primarily on point mutations, but, again, the principle holds for other kinds of mutations, so we don’t need to get hung up on that.)

    I’ve shown the mean waiting time for a super-specified mutation is ~ 10 000 generations. The time it would then take to fix depends on selection pressure.

    Let me make sure I’m understanding you. It sounds like you are saying that Gauger is off by a factor of 40 (plus or minus) in terms of how long it will take for a pre-specified mutation to show up in the population? (10,000 generations x 15 years = 150,000 years; 150,000 x 40 = 6M years)

    Would you have a different view if you understood Gauger’s statement to be referring to the time necessary for the mutation to get fixed in the population (as you mention, and as I agree, it would be dependent significantly on the relevant selection pressure)?

  72. You still don’t get this first calculation! That’s the expected number of fixed differences, not the aggregate number of mutations (which would be much bigger,65 per individual * 10e4 individuals per generation * 45000 generations giving ~300 billion!)

    As for the other half, I think it’s very likely Gauger is mis-remembering the “waiting for two mutations” paper linked above. Otherwise it’s very hard to make sense of her statement.

  73. wd400 @72:

    Nobody is talking about the total number of mutations in the entire population. The calculation is talking about getting from point A organism at year 0 to point B organism 6M years later. Over 6M years, we can use your 15/years/generation = 400,000 generations *65 mutations per generation, gives the 28M number you indicated. That is perfectly clear. That is the total number of mutations that have arisen across the generations in the line leading to this particular individual.

    What is not clear is why you are calling these “fixed” mutations. That is not at all what we are talking about. We’re talking about a particular mutation becoming fixed throughout the population. I thought you agreed with this, as you said “the time to fix depends on selection pressure.”

    I am using “fixed” in the sense of population genetics, in which the new mutation spreads through the entire population. I’m now wondering if you are using the word the same way.

    Certainly there are not 65 new mutations that become fixed in the entire human population every generation. There are roughly 65 mutations per generation from one set of parents to a particular child. That has nothing to do with said mutations becoming fixed in the population. When you put out your calculation at the start of this thread I agreed that it was a reasonable number, based on the number of mutations to get to a particular individual. However, if you are now claiming that in each generation we get 65 mutations “fixed” throughout the population (in the sense the term is used in population genetics), then I will certainly have to disagree with the numbers.

    Bottom line: getting a certain number of mutations (a) in a single line leading to a particular individual, is vastly different from (b) getting those mutations to become fixed in the population.

  74. This is unbelievable.

    The number I calculated really is the expected number of fixed differences, in the population genetics, spreading through the population and taking over, sense.

    If you want to be a critic of evolutionary theory you might start by learning something about it.

  75. FWIW, here’s how I try to teach this to undergrads.

    For any gene in a population, you can trace back a lineage. Eventually all those lineages will coalesce to a shared common ancestor. If we disregard selection then the particular variant that becomes the common ancestor of the whole population is ‘chosen’ at random. So the probability that it’s a gene called “A” is just the freqency of “A” over the population size (N). Shorter version: the probability that an allele (a gene variant) gets fixed is equal to the frequency of the allele.

    How often to new mutants get fixed? For that we need the rate at which they enter the population, and the proportion of them make it to fixation.

    The mutation rate is obviosly the individual mutation rate (u) * the population size = Nu. When a new mutation enters the population it is fairly obviously at frequency 1/N. So the substituion rate (k) = N * u * 1/u = u.

    (as I say, this is in every intro to pop. gen. course, you can verify it easily enough)

  76. @wd400

    “There are some very interesting theories as to how the “slakcening” of slection, which mainly acts to keep things as they are on a molecular level, might facilitate the evolution of complexity.”

    How are you using the word theory here? In the scientific sense such as the theory of gravity or in the non scientific sense of “idea” or “speculation?”

    Creationists don’t hate these types of ideas. To be honest, we laugh at them. It is amazing what evolutionists are willing to consider to try and save their ideas and desired beliefs.

  77. @wd400

    “I just went to random.org and picked a number between 1 and 100000000. I got 22166740. That’s a 1 in hundred million chance!

    I didn’t pre-specify it or anything. But it matters, because 22166740 is there.”

    wd, you don’t see any fallacy here with this reasoning?

    In this case, you were guaranteed to get an outcome between your numbers, but with evolution, there is no such guarantee there will be any outcome. Life didn’t have to evolve, but in your example, you were guaranteed to get a number and for your purposes, any number would do.

    Let’s say you had to have this particular number in order to succeed in the evolutionary story. Then what are the chances of getting the desired number? Fantastically small!

    So two problems with this illustration. You guaranteed yourself an outcome and it was not specified. Any outcome was fine for your purposes.

  78. @wd400

    The exact probability that, say, the kreb cycle could evolve is completely unknowable. Evolution is a contingent process, and a chancy one at that. I’m very happy to say a random walk through the space of all sequences would never find a kreps cycle, or cellular division or whatever else you want to name. That’s because the parts of sequence space that are biologically viable are certainly very small. But selection can navigate them, we’ve seen that in the field and in the lab (and, in fact, in computational models).

    I admit the exact probability is probably unknowable, but we need to start from what we do know and not rely on what may or may not exist out there to bolster our faith. We know what does work and we know that a heck of a lot of other combinations do not work. These things are delicately balanced and fantastically designed. I think that just saying “Well, there might be other combinations that also would have worked.” is a cop out. Everything we know would seem to mitigate against that. It seems like a desperate attempt to try and nullify the obvious improbability problem that is staring us in the face.

    “But selection can navigate them…”

    That sir, is a statement of faith. you are assuming that there exists an incremental step from one thing to the next in which each successive step would provide enough of a benefit to the organism for selection to kick in. But we don’t know this. If such a path does indeed exist, then we would have to admit that it is possible, but even then being possible does not mean it happened like that. Possible means “maybe” not “certainty”.

    We do know that selection misses slightly negative changes and recessive genes that can later cause problems. So how could it select for slightly positive and recessive genes that might later on be beneficial to have?

  79. wd400-

    Neither YOU nor anyone else knows if the equations are valid. So why do you insist on using them?

  80. Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory – 2008
    Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue.
    Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person.
    http://www.icr.org/i/pdf/techn.....Theory.pdf

    Here is a short sweet overview of Mendel’s Accountant:

    When macro-evolution takes a final, it gets an “F” – Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory (Mendel’s Accountant)
    Excerpt of Conclusion: This (computer) program (Mendel’s Accountant) is a powerful teaching and research tool. It reveals that all of the traditional theoretical problems that have been raised about evolutionary genetic theory are in fact very real and are empirically verifiable in a scientifically rigorous manner. As a consequence, evolutionary genetic theory now has no theoretical support—it is an indefensible scientific model. Rigorous analysis of evolutionary genetic theory consistently indicates that the entire enterprise is actually bankrupt.
    http://radaractive.blogspot.co.....ution.html

    Oxford University Admits Darwinism’s Shaky Math Foundation – May 2011
    Excerpt: However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is. – On a 2011 Job Description for a Mathematician, at Oxford, to ‘fix’ the persistent mathematical problems with neo-Darwinism within two years.
    http://www.evolutionnews.org/2.....46351.html

    The next evolutionary synthesis: from Lamarck and Darwin to genomic variation and systems biology
    Excerpt: If more than about three genes (nature unspecified) underpin a phenotype, the mathematics of population genetics, while qualitatively analyzable, requires too many unknown parameters to make quantitatively testable predictions [6]. The inadequacy of this approach is demonstrated by illustrations of the molecular pathways that generates traits [7]: the network underpinning something as simple as growth may have forty or fifty participating proteins whose production involves perhaps twice as many DNA sequences, if one includes enhancers, splice variants etc. Theoretical genetics simply cannot handle this level of complexity, let alone analyse the effects of mutation..
    http://www.biosignaling.com/co.....X-9-30.pdf

  81. Gauger was talking about “one mutation in a DNA binding site.”

    A specific mutation. One that’s probably required before a DNA sequence can even be expressed. So we’re not just talking about any mutation to any stretch of DNA. We’re talking about mutation with an effect.

    Appealing to a vast number of mutations that do nothing in order to explain differences between humans and their alleged ancestors somehow seems wrong to me.

    Now, how do we know the human and chimp mutation rates? We have to know that before we can calculate the substitution rate, correct? Please tell me we don’t know it by looking at the differences between humans and chimps

  82. Mung, the pre-specified mutation would take 10 000 generations to occur (ignoring standing variation for now). Neutral mutations can have an effect, of course.

    Joe,

    If it isn’t entirely clear to you know, I’m ignoring you because you are a math denier. What possible reason is there to talk to someone who won’t even accept the most basic findings of the field we’re meant to be discussing?

  83. Mung @81:

    We do have at least some information on current rates of mutation in humans. That is the 65 point mutations (SNP’s essentially) per generation number wd400 and I have been using for purposes of discussion. This is a rough number for simplicity, but corresponds reasonably well to some studies looking at mutations across several generations of a single family line. According to the data Dr. Noor used for his class, this number varies considerably, depending primarily on the age of the father (i.e., older father at time of conception means more mutations, on average). However, for purposes of discussion, I think this number gives us a decent start.

    I should add that this rate is almost certainly too high if we are using a small generation time of, say, 15 years, as wd400 has been doing, because fewer mutations would be expected with more youthful parents (we probably should be using something more like 40 or 45 point mutations per generation). That would change wd400′s numbers by about 1/3, but it is not an order of magnitude thing (at least as long as we are doing simple additive mutation calculations and not exponential calculations). Again, for purposes of discussion I’ve been willing to concede 65 mutations/generation, as it corresponds reasonably well with current known rates for somewhat older parents.

    As to the time of divergence between humans and chimps, my understanding of what wd400 is saying is that the timeframe is calculated based on known mutation rates (I don’t know the current chimp mutation rate offhand, but presumably that figure is out there).

    —–

    So we’re not just talking about any mutation to any stretch of DNA. We’re talking about mutation with an effect.

    Appealing to a vast number of mutations that do nothing in order to explain differences between humans and their alleged ancestors somehow seems wrong to me.

    Indeed.

  84. wd400 @75:

    Thanks for your patience. Perhaps you can help me clarify one more thing, based on a very simple example.

    If we have a population of 5 organisms and they have each experienced 10 mutations randomly in the genome, you appear to be saying that the population has now “fixed” 10 new mutations in the population. While that may be true as some kind of abstract average across the population, it is unlikely that any particular mutation in one organism (call it organism ‘A’) even shows up in any of the other organisms. So in that sense, the new alleles of A are not fixed across the population, correct? It would only be unless and until the mutations experienced by A provided a survival advantage under sufficient selection pressure over time that the alleles of A would become pervasive in the population and supplant the corresponding non-mutated alleles.

    I’m wondering if we are back to the issue of (i) the abstract number of overall unspecified mutations vs. (ii) actual specific mutations that have become pervasive in the population.

  85. It a probabilistic argument, and we all know how fau;lty those are. ;)

  86. Eric,

    In you hypothetical population each generation would see (on average) 10 new fixations. That’s because each of the 50 new mutations arising in each generation would have a 1/5 chance of eventually fixing (note, it wouldn’t be the 50 mutations entering the population today that get fixed, the average time to fixation is 4Ne = 20 generations in this case). This is the actual number of fixations that will occur over time. The substitution rate is equal to the mutation rate, not the same thing as the mutation rate.

    Mung,

    Call be a Bayesian, but pretty much all interesting arguments are probabilistic.

  87. wd400:

    If it isn’t entirely clear to you know, I’m ignoring you because you are a math denier.

    You are a false accuser as I do NOT deny any math. I say that you have never shown that your math is correct. Huge differnce but one that proves that you are an intellectual coward.

    So ignore me all you want I will still be here making sure that people see you for what you are.

    What possible reason is there to talk to someone who won’t even accept the most basic findings of the field we’re meant to be discussing?

    Except there aren’t any findings. Population genetics works backwards- that is how the equations were formulated- Ann goes over that in the book “Scuence & Human Origins”.

  88. Joe.

    Tell me how the substitution rate could not be equal to the mutation rate for neutrally evolving variants. Until you can do that I’ll keep you in them mental killfile.

  89. wd400:

    Call be a Bayesian, but pretty much all interesting arguments are probabilistic.

    Nah, not name calling.

    I’m talking about the mathematics behind fixation (substitution) that you’ve been referring to.

    A given mutation in a population of size x which continues to reproduce at rate y with the population size remaining constant reaches fixation with probability z…

    The probability that a new mutation will disappear from the population in the first generation after it first appeared is d…

    Even a beneficial mutation will be lost with probability b…

    All that stuff.

    The mathematics don’t cause a mutation to become fixed, they merely describe the probabilities given certain assumptions.

    Or am I full of it? ;)

    Probably.

  90. p.s. If it is a probabilistic argument, then 1 > p > 0

    right?

    So you’re not saying something must happen, only that it will probably happen, with frequency f.

  91. wd400 proves that it does NOT understand science:

    Tell me how the substitution rate could not be equal to the mutation rate for neutrally evolving variants.

    Umm it is up to YOU to demonstrate that it is. There isn’t any “proving a negative”, YOU need POSITIVE evidence to support YOUR claims and you don’t have any.

    I keep asking for positive evidence and instead of producing any all you do is repeat yourself. That is a sure sign of dishonesty or insanity.

  92. wd400:

    In you hypothetical population each generation would see (on average) 10 new fixations. That’s because each of the 50 new mutations arising in each generation would have a 1/5 chance of eventually fixing (note, it wouldn’t be the 50 mutations entering the population today that get fixed, the average time to fixation is 4Ne = 20 generations in this case). This is the actual number of fixations that will occur over time. The substitution rate is equal to the mutation rate, not the same thing as the mutation rate.

    Thanks. I understand where you’re coming from on the raw calculation. I think I also understand now how you are using the term “fixed.” I believe you are saying that because humans can theoretically be traced back to a single individual in any given generation, then by definition, whatever mutations that individual had at the time will later be included in the entire later population because, again by definition, that individual was the ancestor of the final generation of organisms we are currently looking at.

    That means, of course, that we are really looking at the mutations along a single family line, so to speak, correct? We define the line after-the-fact, based on whatever organism in each generation happens to have been the progenitor of the now-existing population. We could perhaps probe this in more depth to see how it holds up in specific instances, but I think I understand the approach and it should suffice for the present discussion.

    (I presume we are also in agreement that this form of becoming “fixed” in a lineal descent simply by virtue of a particular organism being the progenitor of a later population is different from the concept of a mutation becoming “fixed” in a relatively contemporaneous population of multiple organisms?)

    So that brings us back to one of the early questions on this thread: at what point and in what instances do we need coordinated (or specified, if you will) mutations to get to humans (as opposed to a simple additive model of unspecified mutations along a lineal descent line)?

  93. That means, of course, that we are really looking at the mutations along a single family line, so to speak, correct?

    No. Each locus has its own “family line” as recombination scrambles them. Fixed means fixed, gone from a frequency of 1/N to 1, taken over the population or become the only allele at a given locus. Again, this is intro to pop. gen. stuff, read a good text book if you don’t think I’m playing straight.


    So that brings us back to one of the early questions on this thread: at what point and in what instances do we need coordinated (or specified, if you will) mutations to get to humans (as opposed to a simple additive model of unspecified mutations along a lineal descent line)?

    Well, yeah, that’s the question Gauger is begging.

  94. Joe,

    I’ve shown you the derivation of the math. You need to tell me what’s wrong with the math, or how the assumptions (only really finite population size) of the math don’t align with real populations. If you can’t do that, and you still deny the math, what does that make you?

  95. Human Evolution: A Facebook Dialog – By Ann Gauger – Nov. 12, 2012
    Excerpt: PM:Is it also possible that the mechanism that you refer to in your video clip is not the only/main one at play?
    Biologic: The mechanism I refer to is based on the standard Darwinian model for evolution. Published population genetics estimates for how long it would take to make *and fix* a single base change to a DNA binding site in a 1 kb segment of DNA are prohibitively long—six million years. To get a second mutation in the same DNA binding site would take in excess of 200 million years.
    Now to go from hominid to human requires many changes, most of them to gene expression patterns. It is much easier to change the DNA binding site than to change the transcription factor’s specificity. And all these mutations must work together and be beneficial to the evolving organism. The window of time available according to the fossil record and phylogenetic estimates is too short for known mechanisms to be sufficient. So do I think there are are other things at play? Yes.
    http://www.biologicinstitute.o.....ialog?og=1

  96. Haldane’s Dilemma
    Excerpt: Haldane was the first to recognize there was a cost to selection which limited what it realistically could be expected to do. He did not fully realize that his thinking would create major problems for evolutionary theory. He calculated that in man it would take 6 million years to fix just 1,000 mutations (assuming 20 years per generation).,,, Man and chimp differ by at least 150 million nucleotides representing at least 40 million hypothetical mutations (Britten, 2002). So if man evolved from a chimp-like creature, then during that process there were at least 20 million mutations fixed within the human lineage (40 million divided by 2), yet natural selection could only have selected for 1,000 of those. All the rest would have had to been fixed by random drift – creating millions of nearly-neutral deleterious mutations. This would not just have made us inferior to our chimp-like ancestors – it surely would have killed us. Since Haldane’s dilemma there have been a number of efforts to sweep the problem under the rug, but the problem is still exactly the same. ReMine (1993, 2005) has extensively reviewed the problem, and has analyzed it using an entirely different mathematical formulation – but has obtained identical results.
    John Sanford PhD. – “Genetic Entropy and The Mystery of the Genome” – pg. 159-160

    Kimura’s Quandary
    Excerpt: Kimura realized that Haldane was correct,,, He developed his neutral theory in responce to this overwhelming evolutionary problem. Paradoxically, his theory led him to believe that most mutations are unselectable, and therefore,,, most ‘evolution’ must be independent of selection! Because he was totally committed to the primary axiom (neo-Darwinism), Kimura apparently never considered his cost arguments could most rationally be used to argue against the Axiom’s (neo-Darwinism’s) very validity.
    John Sanford PhD. – “Genetic Entropy and The Mystery of the Genome” – pg. 161 – 162

    A graph featuring ‘Kimura’s Distribution’ is shown in the following video:

    Evolution Vs Genetic Entropy – Andy McIntosh – video
    http://www.metacafe.com/watch/4028086

  97. wd400:

    I’ve shown you the derivation of the math.

    You have not shown that it applies to the real world.

    You need to tell me what’s wrong with the math, or how the assumptions (only really finite population size) of the math don’t align with real populations.

    No, YOU need to demonstrate to us that the math is valid, ie applies to real populations in the real world.

    If you can’t do that, and still push the math, what does that make you?

  98. you simply have no ‘real world’ evidence that it is even possible to fixate mutations on anything like the scale postulated by neo-Darwinism for humans to have evolved from some chimp-like ancestor:

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    The preceding experiment was interesting, for they found, after 50,000 generations of e-coli which is equivalent to about 1,000,000 years of ‘supposed’ human evolution, only 5 ‘beneficial’ mutations. Moreover, these 5 ‘beneficial’ mutations were found to interfere with each other when they were combined in the ancestral population. Needless to say, this is far, far short of the functional complexity we find in life that neo-Darwinism is required to explain the origination of. Even more problematic for neo-Darwinism is when we realize that Michael Behe showed that the ‘beneficial’ mutations were actually loss or modification of function mutations not gain of function mutations.

    Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information – September 2011
    Excerpt: The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.
    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
    http://www.evolutionnews.org/2.....51051.html

    i.e. The individual ‘beneficial’ mutations were never shown to be in the process of building functional complexity at the molecular level in the first place!

    related notes:

    Response from Ralph Seelke to David Hillis Regarding Testimony on Bacterial Evolution Before Texas State Board of Education, January 21, 2009
    Excerpt: He has done excellent work showing the capabilities of evolution when it can take one step at a time. I have used a different approach to show the difficulties that evolution encounters when it must take two steps at a time. So while similar, our work has important differences, and Dr. Bull’s research has not contradicted or refuted my own.
    http://www.discovery.org/a/9951

    Epistasis between Beneficial Mutations – July 2011
    Excerpt: We found that epistatic interactions between beneficial mutations were all antagonistic—the effects of the double mutations were less than the sums of the effects of their component single mutations. We found a number of cases of decompensatory interactions, an extreme form of antagonistic epistasis in which the second mutation is actually deleterious in the presence of the first. In the vast majority of cases, recombination uniting two beneficial mutations into the same genome would not be favored by selection, as the recombinant could not outcompete its constituent single mutations.
    http://www.uncommondescent.com.....ach-other/

    As pointed out before by Dr. Gauger, the limits for multicellular creatures to fixate mutations is much worse than the strict limits found for bacteria:

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    http://www.arn.org/blogs/index.....ruit_flies

    More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012
    Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population.
    You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.
    Facing Facts
    But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes.
    http://www.uncommondescent.com.....rwin-said/

  99. wd400 @93:

    I’ve never accused you of not playing straight. There is a paradigm issue that needs to be addressed (as I’ve said and will revisit again below), and we all understand there are lots of caveats and exceptions and specific anomalies that could be discussed with the calculations, but overall I believe you’ve been sincerely explaining the calculations and I think it has been helpful.

    —–

    So it is fair to say that if we look at a current individual’s genome, in theory we can trace each locus within the genome back through its own “family line” to some progenitor. In theory any two or more loci could be traced back to the same exact progenitor, but they might just as readily have come from two different progenitors (though, ultimately, all would presumably have to trace back to the universal common ancestor, so we end up with something of a reverse-hourglass shape for the genetic lineage map — an interesting topic for another time).

    In any event, for purposes of the present discussion going back only 6M years, we could expect to have a number of progenitors at that first generation.

    So that brings us back to one of the key issues at the start of this thread: are coordinated changes needed?

    Let’s assume that our first generation progenitors 6M years ago consisted of 26 individuals A-Z. Now each of these individuals went merrily along its way, producing offspring with somewhere between 40-65 mutations/generation. Now at some point in this process an individual in lineage A received a genetic mutation that would ultimately after many generations become part of, say, a gene controlling pelvic structure, thus allowing humans to walk upright.

    How did the rest of this critical gene come about? Well, there must have been other mutations, either in line A or another line, that, when taken together with other mutations, eventually resulted in the gene in question.

    And this is key:

    Regardless of whether evolution could have taken any number of hypothetical paths, once a specific structure is in process in the actual biological realm, the remaining parts or instructions for that structure — by definition — have to have been coordinated, or the structure would not have come about.

    Stated in the simplest example with a nucleic sequence for a protein: once an organism receives that first point mutation in a nucleotide that ultimately will lead to a particular protein, all other mutations in the nucleotide sequence must be coordinated, or — again by definition — the protein will not exist. As soon as we are on the path to building any structure we are no longer in the realm of “anything goes.”

    Thus, the realization that evolution is contingent is of no help in answering the question on the table. We know certain structures exist. The salient question is: “What is the most likely explanation for the structure in question?” It is quite apparent to anyone willing to ask that question that everything had to come together just right in order for the structure to exist. So then we can get back to discussing the astronomical probabilities of mutations being accidentally coordinated and whether there might be a better explanation for the coordinated complexity we see. Stating that evolution is contingent is not an answer; it does not in any way change the awful probability calculations; it is simply a reassertion of faith in chance.

    So that brings us back to one of the early questions on this thread: at what point and in what instances do we need coordinated (or specified, if you will) mutations to get to humans (as opposed to a simple additive model of unspecified mutations along a lineal descent line)?

    Well, yeah, that’s the question Gauger is begging.

    No. That coordinated mutations are needed is a biological and engineering fact.

    Gauger is not begging the question. You are avoiding the question.

  100. wd400 wants to use math, but unfortunately for wd400 math requires proof. And even more unfortunate is the fact that population genetics is not amendable to proof.

  101. Just how long will these Darwinists continue to stretch their elastic theory just to keep it alive? Don’t they realise how the basic premises of their theory are being dealt one death blow after another. Now I often like to step away from all the noise and look at the big pattern. And the way I see it is that Darwinism has been on a state of retreat covered by a smokescreen of unproven assertions, wishful extrapolations, fossil interpretation games, ad-hoc explanations, and an endless bile of just-so stories.

    Ever since the time of Darwin who believed that variation within a gene pool was “unlimited” and so natural selection alone could account for evolution, that was shown to be false and so the basic premise of Darwinism at the time was done for. But the crafty Darwinists came together and decided to appeal so something called “mutations”, and since then we are required to believe that such rare accidents of nature could behave like a magic wand that could endow creatures with brand new novelties of functions and design. And so Darwinism survived the first death blow by administering such a crafty “CPR” and was born anew: Neo-Darwinism.

    Then came the embarrassingly huge amount of gaps in the fossil record so they said to themselves: you know what, let’s just claim that evolution sometimes works in quick bursts of rapid change that leave no traces behind and give it a fancy name “punctuated equilibrium”. How convenient!

    And now we have all this incredible research done by ID scientists demonstrating to Darwinists what should’ve been already obvious: your precious mutations DON’T WORK, they cannot create the wealth of brand new information novelties that you dream of. And even if we give them a generous benefit of the doubt and wait for mutations to get lucky enough to MAYBE start working, they would take too long to be able to account for the proposed relatively rapid human divergence, let alone the Cambrian explosion which is still crying and begging for an adequate Darwinian explanation to wipe off the tears.

    So if this is not a death blow then what is? But of course the crafty Darwinists are so determined on keeping their holy theory on life support by telling themselves: you know what, let’s just say that mutations work much faster by appealing to developmental mutations. And so we are going in circles again with Darwinists who forgot all the generations of fruit flies that did not yield any fruitful result through developmental mutations. So what’s next? Maybe in the near future we’ll hear about “super” mutations that could literally transform a species over night.

    But in the end Darwinists have no shortage of “wise guys” who would suddenly jump at you and say: there is nothing wrong with scientists correcting themselves. But the reality is that such a true statement is being used to disguise false premises that keep getting blown one by one through scientific evidence that is rejected or downplayed by those who call themselves “scientific”.

    Just what would it take to refute Darwinism in the elastic minds of Darwinists? It is ironic that such a theory that always had survival of the fittest at its core is in fact no longer fit to survive without all these patch-works and repairs that only serve to delay, not prevent, and inevitable collapse.

  102. wd400:

    6.5 million years is 450 000 15yr generations
    65 mutations * 450 000 gens * 2 lineages = 56 million fixed differences
    56 million positions in a 3.2 billion base genome is ~ 1.7% divergence (actually greater than the observed difference).

    Let’s put this into perspective: your calculation tells us that there is a 1.7% chance that a ‘neutral’ mutations has occurred at any location along the length of the genome in 6.5 million years. But the location where this ‘fixation’ takes place must be, by definition, ‘neutral.’

    This means that if a particular ‘neutral’ location had an A as a base, 6.5 million years later, there is a less than 2% chance that it will now have a T, or C, or G instead. Yet, it remains a ‘neutral’ location. So, . . . who cares if it’s a T, or C, or G, or if it’s still an A: any way you look at it, it’s a ‘neutral’ mutation; i.e., a location where ‘selection’ is not taking place.

    This paves the way for what you say next:

    Gauger is just playing the silly “over specify the target” game creationists of all ilks enjoy. It’s true that waiting for co-ordinated mutations in a very small specified region would take a long time if the first didn’t have a selective advantage. That might be a problem if you thought humanity was the goal of evolution and only very narrowly defined pathways could lead to us. But that’s not evolutionary biology’s position, so it doesn’t really matter.

    If a particular location on the genome is critical, then ‘selection’ is at work; very likely—in the vast majority of cases—by eliminating a harmful mutation, but, possibly by ‘selecting for’ a beneficial mutation.

    So, what about this particular location? Well, the probability of getting a, let us say, ‘favorable’ mutation at this particular location is 1/size of the genome, which is, approx, 3 x 10^-10/generation. (assuming a genome size of 3.5 x 10^9 nucleotides). Now the ‘effective’ population size comes into play, and then the expected time for fixation. Ignoring the time of fixation, we can use an average population size of 100,000, with a mutation rate of 100/genome/generation. Thus, per generation, there are 100 x 100,000 possibilities that a ‘particular’ location receives a SNP (or equivalent). But there is a 3 x 10^-10 chance that it will miss. The numbers show that the time for ‘hitting’ this particular location is, on average, 3 x 10^-3 chance of ‘hitting’ this location per generation. Hence, given a 20 year generation time, this means (3 x 10^3) x 20 years/generation = 6 x 10^4 years are needed to ‘hit’ this particular spot.

    And what if the mutation is the ‘wrong’ mutation? Then what?

    Well, there’s a one in three chance of it being the ‘right’ mutation, so we’ll have to multiply by 3, giving us 1,800,000 years to get our ‘beneficial’ mutation at some particular location. To get another ‘specific’ and ‘beneficial’ mutation along the length of the genome

    This is Ann Gauger’s basic argument.

    And wd400, you simply want to dismiss it out of hand.

    Your argument is that ‘any old’ mutation will do. You say: “How do we know it has to be at this exact location, and this particular base? Who says this has to be so?”

    The answer is that ‘genetics’ says it must be so. We don’t have 100,000 humans with completely random genomes. They’re constrained for the most part. And genetics (negative selection) determines these constraints.

    To hand-wave the obvious away–that is, that mutations at ‘specific’ locations are needed–is to have a rather silly attitude towards the whole enterprise here. Just because the numbers don’t work out using traditional population genetics methods, doesn’t mean you can just pretend otherwise.

    ==========================

    Now, as to the question of “substitution,” there is a great equivocation that takes place in genetics.

    Substitution is at once the ‘substitution’ of one nucleotide for another, AND, the fact that ‘neutral’ mutations are ‘substituted’ for at the same rate as the mutation rate.

    Now, the point I was making above accounts for this equivocation: i.e., it is ‘silly’ to talk about the ‘fixation’ of a ‘neutral’ mutation since it matters not one twit (by definition) what nucleotide base you happen to have at a ‘neutral’ location along the genome. So, it is better to simply call it a ‘substitution.’ (As in: “one is as good a substitute as another”)

  103. PaV,

    You’re out by an order of magnitude on your math – should be 180 000 years. But that’s per nucleotide, not the “entire length of the genome”

    Other than that, you have actually grasped the point. To think this math is relevent you have to think that environmental pressures changed that one, and only one, mutation would provide a fitness benefit and populations had to wait around for that mutation to gain the benifit. That’s question-begging on a grand scale.

  104. wd400:

    To think this math is relevent you have to think that environmental pressures changed that one, and only one, mutation would provide a fitness benefit and populations had to wait around for that mutation to gain the benifit. That’s question-begging on a grand scale.

    Can you restate this? I can’t change a word around and make sense of it.

    Unless, . . . should it read: ” . . . to think that environmental pressures, by changing that one, and only one, mutation would provide a fitness benefit, and that populations had to wait around for that mutation to gain the benefit.”

  105. The math starts with the assumption that the there is a benefit to be had if one particular mutation (right down the the nucleotide position and the actual residue it has to change to) would only arise.

    For that to be relevant to human evolution you have to think most of our evolution involved waiting for these super-specific mutations. That seems unlikely when you think about something like lactsse persistence, which has many different alleles giving the phenotype, that seems like a faulty assumption.

  106. wd400 @103:

    I’m curious. Does your view (i.e., no specific mutations required) apply only to the particular case of chimp-human transition, or do you believe it also holds generally across speciation transitions, namely that there are no specific mutations required to get from organism A to organism B?

  107. Eric, there is no specific organism B to get to from organism A. There are all these uninstantiated forms out there in Ideal space, any number of which [or none of which] could have been realized as a consequence of changes to the hypothetical common ancestor of chimps and humans and orangutans.

    Maybe humans, maybe no. Maybe chimps, maybe no. Maybe some combination of the above, or no combination of the above.

    It could just as easily have been Pooferbibbles and Grambldorps instead. We just can’t say.

    I know it sucks, but that’s science. Whatever will be will be.

  108. What mung said, basically

  109. Mung, I note your sarcasm; wd400, I note your lack of it. Pretty ironic, the two responses. :)

    I’m not talking about a hypothetical future wherever the winds of evolutionary whim might take us. I’m talking about actual organisms and systems that we know exist.

    wd400, from your response I take it, though, that it is your position that no specific mutations were required to get any of the organisms or biological systems that we see today?

    So, back to your alleles example in #105, it doesn’t really matter whether we are talking about several possible allele forms with minor point changes between them. We might as well be talking about the mammalian eye, the bacterial flagellum, the Krebs cycle, DNA itself. No specific mutations were required to produce these systems? Is that really your position?

    Please note that the following are two very different questions, and please make sure you are not conflating the two:

    (i) Did evolution have to produce this particular system?

    (ii) In order to get to this particular system (which we know exists), are specific mutations required?

  110. wd400:

    For that to be relevant to human evolution you have to think most of our evolution involved waiting for these super-specific mutations. That seems unlikely when you think about something like lactose persistence, which has many different alleles giving the phenotype, that seems like a faulty assumption.

    Aren’t you simply giving an opinion here?

    That is, ‘in your opinion’ it is unlikely that “super-specific” mutations must lead the way forward.

    I say this because the only evidence you give for this view is that there are many ‘alleles’ giving rise to lactose persistence (whatever that might be). But, given that lactose is how young mammals are fed for the most part, this might simply be some kind of pleitropic effect intended to make sure that various genetic pathways lead to what is absolutely essential for organisms to survive (they will die off if their young all die off). Of course this is a guess on my part, just as your view is a guess on your part.

    Then how does this become science?

    Having pointed out the ‘guesswork’ involved here, let me now point out that in Behe’s “Edge of Evolution” two “super-specific” mutations were required to overcome chloroquine resistance. Not just any old mutation would do.

    Well, hadn’t the malarial parasite been around for hundreds of thousands of generations? Shouldn’t there have been all kinds of ‘neutral mutations’ at the ready? So, why did it take so long for it to develop resistance? The only explanation is the need for “super-specific” mutations to arise.

    [[In your responses so far, let me note that you haven't addressed the point I've made that "substitution" is used instead of "fixation" because we're dealing with 'neutral' loci. You want to claim that 'neutral' loci become, basically, 'conserved' loci. But how? Why? And in what kind of a time-frame?]]

    Let me also point out a recent study which showed that insects feeding on the leaves of a plant that typically develops a specific kind of fungus on its leaves, developed the very same mutations for overcoming the poisoning effect of the fungus. This “super-specificity” is made clear by the fact that the very same sequence and location occurred even across the boundary of different “orders”(!) of the insects.

    I suspect that increasingly inexpensive whole genome analysis techniques will soon uncover lots and lots of these “super-specific” mutations, all of which demonstrate the need for having to “wait” for specific mutations if you want to move from functional A to functional non-A.

    So, wd400, you have your opinion, based on something that is susceptible to various interpretations, and I have an opinion that holds up to what today is being revealed by science. Why, then, ask me to let go of my view? Isn’t yours the one that is incompatible with science?

  111. Eric,

    (1) and (2) are related. But if you want to skip that and get on to (2), there aren’t many systems that only work exactly as they are now. The only one I can think of off the top of my head are a couple of residudes in ribosomal RNAs that are conserved throughout life. For everything else, even quite basic reaction like the kerb’s cycle, very divergent proteins perform the same role.

    PaV,

    It would take you 10 secs to google “lactase persistence” and realise what you’ve said about it doesn’t make any sense. It’s science because we know lactase persistence is an adaptation that has arisen several times, and every time (it seems) a different mutation gave rise to the phenotype.

    The reason I haven’t answered you’re comments about fixation and substitution is there is nothing there – if you want to try again please do, but substitution and fixation are the same thing.

    There are certainly cases in which very specific mutations are required (the Bt toxin resistance being the shining example), so that requires the same amino acid residue (which can probably arise from different DNA mutations). If you’d like to tell me what that has to do with human evolution I’d love to know.

  112. wd400:

    What mung said, basically

    Except for the Ideal and the Forms part, I bet. :)

    There are no unsubstantiated forms just waiting to be found, there is no finding going on in evolution, no searching.

    It’s just pure dumb luck that these “forms most beautiful” are there waiting to be “found.”

  113. wd400:

    (1) and (2) are related.

    But you do acknowledge that these are logically separate questions, and that answering “No” to the first one does not mean that the answer to the second one is also “No,” correct?

  114. Eric,

    Sure.

    Mung,

    Obviously. Evolution isn’t “searching” for a particular something. When the speciation process that separated us from chimps started there were many possible outcomes for the descendant populations. Selection means we only navigate between a small subset of those possible forms.

  115. With Intelligent Design evolution, evolution is searching for a particular something. And there still isn’t any evidence that any amount of mutational accumulation can account for all the physical differences between humans and chimps. The premise of common ancestry is still unscientific.

  116. wd400 @114:

    Good. So I presume you also acknowledge that someone can take an interest in, and ask, the following scientific question on its own merit, without resorting to hypothetical discussions about what evolution could have done in some other alternate universe or timeline: “Given the existence of system x, what can we infer is the most likely explanation for the origin of this system x?”

  117. Sure, but you don’t do that by plucking numbers from studies without considering their assumptions in the way Gauger has

  118. wd400:

    The reason I haven’t answered you’re comments about fixation and substitution is there is nothing there – if you want to try again please do, but substitution and fixation are the same thing.

    Not always. A fixation is always a substitution but a substitution is not always a fixation. The references have been provided that say all mutations are substitutions and we already know that not all mutations become fixed.

  119. wd400 @117:

    Doesn’t the study talk about how long it takes to get specified mutations in a particular population?

    I thought your beef with Gauger was that you don’t think specific mutations are required to get to humans.

  120. The study talks about how long it takes to get two specific mutations in the same pre-specified regulatory sequence. Gauger wants that to be a speed-limit for human evolution, but hasn’t actually argued as to why it should be.

  121. Eric:

    I thought your beef with Gauger was that you don’t think specific mutations are required to get to humans.>

    Thank God no evolutionist has ever published a paper on what specific mutations might be required to get to an eye.

    After all, just any old changes would have sufficed.

  122. No specificity required:

    ATP synthase is a molecular machine used in the production of chemical energy. It is constructed from over 40,000 atoms each in a specific place and performing a specific function.

    – David S. Goodsell, The Machinery of Life

    Any old change will do. But just try living without ATP.

  123. The study talks about how long it takes to get two specific mutations in the same pre-specified regulatory sequence. Gauger wants that to be a speed-limit for human evolution, but hasn’t actually argued as to why it should be.

    1- Because not any ole mutational accumulation will do it

    2- The changes required themselves require an ordered sequence or they do not work. The muscular-skeleton- nervous system is coordinated. You just can’t grow a leg bone without having all the supporting stuff.

  124. wd400:

    Please answer these two questions:

    1. How many functional versions of lactase enzyme exist?

    2. How many non-functional sequences of the relevant DNA string are there?

    You seem to make much of the fact that some systems can experience minor perturbations and still function, or that some systems can have a couple of alternative forms. What you still seem to be forgetting is that these functional islands represent an infinitesimally small pinpoint among the whole range of possibilities. That a couple of alternative forms of “gene x” or “enzyme y” function, does not change the fact that many very specific mutations are needed to get to the relevant functions we see today.

  125. wd400 @120:

    A speed limit?! LOL!

    She’s talking about a tiny handful of changes and asking us to actually ask some hard questions about the mutational story. If she were to include all changes she wouldn’t even be able to get through the interview without doubling over with laughter.

    It is you who takes the completely unsupportable position that no specific changes are required. And therefore, with your metaphor, there is no speed limit, because, hey, we aren’t going anywhere anyway, so we can get to nowhere in no particular time at all!

  126. Eric,

    Read a little about lactase persistence. It’s not the wildtype, it’s a new trait that has arisen almost every time humans have lived along side dairy animals (cows or horses) and, it seems, has come about due to a different mutation (at least 5 that I know about) in each case.

  127. So lactase persistence-type mutations gave us upright bipeds from knuckle-walkers/ quadrapeds?

  128. wd400:

    The reason I haven’t answered you’re comments about fixation and substitution is there is nothing there – if you want to try again please do, but substitution and fixation are the same thing.

    Please explain to me then why they use the word “substitution” instead of “fixation”?

    You haven’t answered regarding the study showing that insects ranging across different ‘orders’ developed the exact sequence, in the exact location, in developing resistance to a leaf toxin.

    As to “lactose persistence,” here’s part of what wikipedia has:

    n one study involving a Finnish population, a CT SNP at –14 kb was found in all lactase persistent individuals and absent in all hypolactasia individuals. A second SNP (G-22 kbA) was concordant with phenotype in all but a few rare individuals. Since both SNPs are located in the same gene, this has led to a genetic means of testing lactase expression in individuals. Outside of the Finnish study, a separate study also confirmed that the CT SNP at -14kb is an indicator of lactase persistence, with the exception of two individuals

    We’re dealing with TWO SNPs. This is what ‘adaptation’ looks like; and, per Behe and his EofE, this is very close to that edge (if not the edge itself).

    This is what nature tells us. And science is about “knowing” what nature wants to tell us; it’s not about our favorite theory.

  129. wd400@Eric Anderson:

    . . . and, it [lactose persistence] seems, has come about due to a different mutation (at least 5 that I know about) in each case.

    So, all this means is that the odds of ‘hitting’ an ‘exact’ location improves from 1 in 3 x 10^-9 to 5 in 1 x 10^-9. This is half an order of magnitude better than a problem that is quasi-intractable for Darwinism. Is this something to hang your hat on?

  130. @wd400:
    . . . to 5 in 3 x 10^-9. . . .

  131. PaV:

    Please explain to me then why they use the word “substitution” instead of “fixation”?

    Mostly historical, likely.

    The principle unit process in evolution is the substitution of one gene for another at the same locus.

    – J.B.S. Haldane

  132. wd400:

    So let’s make sure we have this straight. Humans have the ability already built in at birth to digest lactose. In other words, there is a system already built and functioning at the outset. The activity of the lactase enzyme is often reduced after weaning in many mammals, and naturally diminishes as the growing organism ingests less and less milk. But in some populations in which milk is regularly consumed, high levels of enzyme activity persist into adulthood. There are potentially a couple of different SNP’s (which perhaps arose by mutation) that contribute to a higher expression of the lactase gene.

    And this is the evidence you cite for the idea (the focus of this thread) that no specific mutations are required to get to humans? Holy cow! :)

  133. Holy Chocolate Cow!

  134. Eric,

    It’s one example of a recent human adaptation (you’ll have to tell me how this trait could have arisen by a method other than mutation) and it’s very clear that this trait could have arisen by at least 5 different mutations. The fact it never appears to have arisen by the same mutation suggests there are more ways for lactase persistence to arise.

    So, yes, it’s very clear case in which the the ultra-specificity of the calculations Gauger is talking about aren’t required to evolve a new adaption.

  135. wd400 @134:

    Good. So (granting just for purposes of discussion that we are dealing with an actual natural mutation, as opposed to an organism-induced trigger) we have one case in which we have, say, a half dozen possible ways to encourage the body to continue carrying out a function that it was already built to carry out.

    Did Gauger ever say that every mutation leading from the chimp ancestor to humans had to be the precise one we see? Did she ever say that there are no instances across all of human biology in which a handful of options can work? Of course not. She is saying that there are a number of specific mutations required. That is a very different matter and you are grossly misrepresenting her position.

    Further, even if we grant this particular example you are focusing on, and even if we grant a dozen more like it, there is still every reason to believe that many very specific building blocks have been required to get to humans.

    Look, you have started from what is, frankly, an absurd position, namely that no specific mutations are required to get to humans. It is clear that this assumption is not based on anything relating to the actual engineering or biology of humans, but is based on a desire to avoid dealing with the probabilities. We’re happy to grant you that not *every* DNA difference between chimps and humans is important. Now it is time for you to acknowledge that at least *some* are. It is OK to acknowledge that you were wrong, that looking at the timeframe for specific mutations in the alleged human-chimp differentiation process over 6M years is a reasonable question to consider, and that you can’t simply dismiss the whole issue with vague references to “anything goes” evolution.

  136. Mung:

    We’re not talking about genes, per se, but about mutations.

    The point I’m making is that neutral mutations are exactly that: neutral mutations. And a consequence of this is that it matters not what base shifts to what base—it’s all the same. And, hence, it makes no sense to call this “fixation” since this shifting around of bases has no effect on the organism–i.e., it’s a ‘neutral’ mutation.

    An analogy: if the color of the paint on a car changes, it affects function not one twit. But, for example, if you substituted a monkey wrench for a steering wheel, now you have a problem. IOW, there are portions of a car that are interchangeable—neutral—to function, and others that are not.

    Likewise, neutral locations are neutral locations. They’re like changing a car’s color from red to silver, and, again, it makes no sense to talk about fixation of something that has, by definition, no phenotypic effect.

  137. PaV @136:

    I hear you on the “fixation” term. But for better or worse, that is the term that has become current in the scientific discussions (noting the two uses I mentioned elsewhere).

    Regardless of what term we use to describe the accumulation of neutral mutations in DNA, the real question is whether neutral mutations can do anything for us. The whole idea of neutral mutations being wonderfully helpful for evolution is a joke. That there are some neutral mutations is true. That they would somehow sit there quietly until evolution “needs” them and then they suddenly get incorporated into a wonderful new system is absurd.

    And it also doesn’t address the probabilities (which is what neutral mutations were supposed to help with). Having a bunch of random bases sitting around in DNA is not of any help at all in getting the kind of functional complex specified information we need to build living systems. It doesn’t change the probabilities in any meaningful way at all.

  138. PaV,

    I think I see your point. Single nucleotides are not alleles and different language should be employed when speaking of the two.

    An allele can become fixed (by substitution) in a population, and yet that allele could exhibit differences at the nucleotide level in different members of the population.

    The confusion probably arises because in one case we are speaking of something physical (the nucleotides) and in the other case we are speaking of something logical (the allele).

  139. Eric Anderson:

    I hear you on the “fixation” term. But for better or worse, that is the term that has become current in the scientific discussions (noting the two uses I mentioned elsewhere).

    I don’t care if we call it “parchese”, I was trying to highlight to wd400 that different loci along the length of DNA act differently. My point was that “neutral” cites, even after “substitution”, remain “neutral” cites. What if we had ten trillion “substitutions”, what then? The organism would be just like it was before the ten trillion “substitutions” took place.

    The Darwinists want it otherwise. I think it’s required that all of this be pointed out.

  140. Mung:

    The confusion probably arises because in one case we are speaking of something physical (the nucleotides) and in the other case we are speaking of something logical (the allele).

    I quite agree. In a certain sense “alleles” only exist as a way of speaking about genetic mechanisms within population, a term that predates the discovery of DNA.

  141. wd400:

    I’ve raised some questions along the line here, and you haven’t addressed them. I don’t know quite what to make of that.

  142. Try them again PaV, I’ve mainly ignored things taht don’t make any sense…. like most of what has been written since last time I posted.

  143. wd400,

    Unguided evolution doesn’t make any sense, just like most of what you post


  144. Now it is time for you to acknowledge that at least *some* are. It is OK to acknowledge that you were wrong, that looking at the timeframe for specific mutations in the alleged human-chimp differentiation process over 6M years is a reasonable question to consider, and that you can’t simply dismiss the whole issue with vague references to “anything goes” evolution.

    Show that ultra-specified co-ordinated mutations within a single regulatory element are a requirement for adaptation and I’ll happily change my mind. Until then all this talk of “engineering” (possibly the worst possible way to think about biology… computing being the only close contender) is just waffle

  145. No, the worse way to think about biology is to think it arose and diversified via blind and undirected chemical processes. It is not only untestable but also a complete waste of time.

  146. The best way to think about biology:

    It just happened, that’s all.

  147. wd400:

    Until then all this talk of “engineering” (possibly the worst possible way to think about biology… computing being the only close contender) is just waffle

    Right. As opposed to thinking of biology as some kind of accidental assemblage of non-specified mutations that is built mostly on junk. Yeah, that’s the right way to think about biology! LOL!

    There is a reason there is a whole discipline called bioengineering and a whole discipline called bioinformatics that deals with information and codes and representations and, yes, even instructional programming protocols.

    If humans are ever successful in building a simple living cell it will be because it was carefully engineered and programmed with very specific functional elements.

    This Darwinist fantasy you are harboring about life being some kludge of anything-goes mutations in a sea of junk is such a laughable joke.

    Well, it has been a fun thread. And it is also been illuminating to see in action this absurd evolutionary fallback position with its rhetorical attempt to counteract the realities of real-world engineering and computational constraints, so we appreciate you participating.

  148. Bioengineering is about using what we know about biology to solve problems, not using what you know about engineering to understand biology. I am a bioinformaticist, and thinking biology behaves like code is a very good way to make mistakes.

  149. wd400:

    I am a bioinformaticist, and thinking biology behaves like code is a very good way to make mistakes.

    How does something “behave like a code”? How does a code behave?

    Until then all this talk of “engineering” (possibly the worst possible way to think about biology… computing being the only close contender) is just waffle

    Dennis Bray, heard of him?

    Wetware: A Computer in Every Living Cell

  150. wd400:

    I am a bioinformaticist, and thinking biology behaves like code is a very good way to make mistakes.

    What are the material requirements for the transfer of recorded information?

    Do you use RV + NS to design your information systems?

  151. Thanks for the Bray link Mung,,, along that line, you may appreciate this:

    Learning from Bacteria about Social Networking (Information Processing) – video
    Excerpt: I will show illuminating movies of swarming intelligence of live bacteria in which they solve optimization problems for collective decision making that are beyond what we, human beings, can solve with our most powerful computers.
    http://www.youtube.com/watch?v=yJpi8SnFXHs

  152. wd400 @148:

    Wow. I’m seeing lots of definitions of bioengineering along the following lines: “Bioengineers use engineering principles to analyze and solve problems in biology and medicine.” or “Bioengineering is the application of engineering design and technology to living systems.”

    Anyway, we don’t need to debate the label, because the label isn’t important. The key is that engineering principles absolutely apply to living systems. Make any machine you can think of and engineering applies. Now make a machine with biological matter, rather than non-biological matter, and now engineering principles don’t apply? LOL! What principles do then apply, pray tell; magic fantasy principles like “Stuff Happens” (Darwin be praised)?

    Also, I’m seeing some definitions along this line for bioinformatics (this one from the NIH): “Bioinformatics is a subdiscipline of biology and computer science concerned with the acquisition, storage, analysis, and dissemination of biological data, most often DNA and amino acid sequences.”

    Yeah, we wouldn’t want that computer science stuff to get us all confused now, would we? Why, we might make the mistake of thinking that biology uses data storage and retrieval mechanisms, top-down protocol heirarchies, digital code, semiotics, and the like. That would really mislead us. LOL!

  153. Eric, not too long ago there was a thread here dedicated to exploring engineering in biology.

    Check out this guy:

    http://www.amazon.com/Steven-Vogel/e/B001IQUN4S/

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