Design inference Naturalism Origin Of Life

Abiogenesis – Highlighting the Spectrum

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Recently I have been thinking a lot about one of the most interesting topics: the origin of life. Specifically, the state of research on abiogenesis, the idea that life arose through purely natural processes without any intelligent guidance or intervention. I have also been thinking about the various viewpoints I have encountered over the years regarding abiogenesis.

The various viewpoints about abiogenesis can be categorized along something of a spectrum. Although the spectrum is not necessarily symmetrical and there are probably numerous different views, I found it helpful to break them down into seven different categories in a 3-1-3 distribution, with stronger support for abiogenesis at one end of the spectrum and stronger skepticism toward abiogenesis at the other end of the spectrum. These are of course approximations and simplifications, but I believe they provide a helpful way to assess where someone is coming from in their views on the topic.

I would ask readers to let us know (i) which viewpoint most closely approximates your position, and (ii) what additional clarifications or caveats, if any, you would add to more completely reflect your position. I also offer my take below each described view.

With that in mind, here are the categories.

1. “Life arose through purely natural processes without any intelligent guidance or intervention. Furthermore, we have a pretty good understanding from a scientific standpoint of how this occurred, and at this point we are largely just filling in the details.”

Assessment. This viewpoint consists of: (i) a faith-based assertion of materialism, coupled with (ii) a misrepresentation of the scientific evidence. As a result, this is something of a minority position (given its looseness with the scientific facts). Yet it is a position we occasionally encounter, particularly when the misrepresentation serves some other propaganda need, such as Dawkins’ claim last year to a packed house in an NPR lecture series.

My Take. This is an untenable position that demonstrates a lack of intellectual and scientific integrity, and I have little patience for anyone putting forth such a deceptive claim.

2. “Life arose through purely natural processes without any intelligent guidance or intervention. Although we do not yet have a good idea from a scientific standpoint of how this occurred, in time we will uncover how it happened.”

Assessment. This viewpoint consists of: (i) a faith-based assertion of materialism, coupled with (ii) an acknowledgement of the lack of empirical evidence, but resting on hoped-for future discoveries that will confirm the materialistic position. This is a much more common position. Indeed, based on my years of experience following this issue, I would say that this is one of the most common positions, and is the position taken by most materialists as well as most scientific bodies or committees that have spoken on the issue.

My Take. This position is significantly better than the first, in that it acknowledges the current lack of viable naturalistic explanations. However, in practice it operates similarly to the first position, in that it avoids any discussion of alternate viewpoints and asserts that materialism is correct – we just need to wait for the evidence to catch up with the conclusion. As a result, it presents a veneer of intellectual integrity, but masks an underlying lack of objectivity.

3. “Life likely arose through purely natural processes without any intelligent guidance or intervention. We do not have a coherent story of how this could have occurred, and various open questions remain. Furthermore, there are some interesting arguments against a purely naturalistic scenario and in favor of intelligent guidance or design that should be considered. However, ultimately we will probably discover a plausible naturalistic scenario.”

Assessment. This is a more nuanced position that recognizes some of the weaknesses in the materialistic story and the existence of legitimate counter arguments. This position is also very common and would include individuals who are not necessarily design advocates, but who are either sympathetic to some of the design arguments or who are keenly aware of some of the limitations of purely naturalistic scenarios.

My Take. This position is more coherent and is, in my estimation, the farthest anyone could legitimately go in support of abiogenesis if they have taken an objective look at the evidence. It still relies on unspecified, hoped-for future discoveries, but allows for rational debate and discussion.

4. “Life may have arisen through purely natural processes or it might have arisen through intelligent guidance and intervention. We don’t know.”

Assessment. This is not really a position so much as a statement of a lack of position. This essentially functions as a temporary position for those who have not yet looked into the issue.

My Take. This position is rare and only temporary, but I include it for completeness and to show the centerline of the spectrum. Once people take time to look into abiogenesis, their viewpoint will inevitably shift in the direction of either #3 or #5 (in my experience, more often in the direction of #5).

5. “Life likely arose through intelligent guidance or intervention and not solely through natural processes. There are problems with essentially all naturalistic scenarios proposed to date. Furthermore, there are good reasons to think that a purely naturalistic scenario is infeasible, as well as strong arguments in favor of intelligent guidance or intervention. However, it remains possible that life arose through purely natural processes, and we should continue to search for plausible naturalistic scenarios.”

Assessment. This viewpoint is held by some intelligent design proponents, as well as many other people who do not follow ID in particular but who are skeptical of the naturalistic storyline.

My Take. This is an intellectually reasonable position that has much merit. It acknowledges the problems with naturalistic abiogenesis scenarios and the legitimacy of an alternative design explanation. However, it still reposes a (weak) hope for some future discovery that might make the untenable abiogenesis story tenable.

6. “Life almost certainly arose through intelligent guidance or intervention and not solely through natural processes. The very claim of an information-rich, functional system arising through such processes is anathema to our understanding of cause and effect in the world, has never been observed, and is not based on solid scientific footing. Furthermore, there are excellent affirmative reasons to think that life could only have arisen through intelligent guidance or intervention. Although there is no rational reason to think that a plausible naturalistic scenario will ever be discovered, there is value in continuing origin of life research, both because we will learn much about biology in the process and because we will learn more about the hurdles that a naturalistic scenario would have to overcome and the areas in which design is required.”

Assessment. This viewpoint is similar to but stronger than #5, and is perhaps the most common position among intelligent design proponents. It draws a strong, but tentative, inference based on the current state of scientific knowledge, while being open to the general value of additional research.

My Take. In my view, this position is most consonant with the current scientific evidence and, therefore, unsurprisingly, is the view that I personally favor.

7. “Life was created directly by an intelligent being without purely natural processes. To think otherwise is to deny God’s Word, which no amount of scientific undertaking can overturn. Abiogenesis research may yield some peripheral benefits, but as a scientific undertaking on its own merits it is essentially a waste of time and resources.”

Assessment. This viewpoint is occasionally found among some religious adherents. It consists of (i) a declaration of faith, based on a particular interpretation of religious text, coupled with (ii) a certain ignorance of – or perhaps disinterest in – the scientific research.

My Take. Similar to #1, this last position is essentially a faith-based declaration that has little interest in objectively evaluating the evidence. Despite having no wish to denigrate anyone’s religious views, I also have little patience for this position, both because (a) it is unhelpful in assessing the scientific research and moving our knowledge forward, and (b) it is, in my opinion, theologically unsound.

—–

Here is a simple table outlining the above views:

Summary of Views on Abiogenesis
Summary of Views on Abiogenesis

—–

As mentioned, these are broad categories, but are hopefully at least broken down enough to get the thoughts flowing.

Which position most closely resembles your viewpoint? And what additional caveats or clarifications, if any, would you include to more fully represent your position?

—–

UPDATE: Please see comments 87 and 93 for a better approach to viewpoint #7.

95 Replies to “Abiogenesis – Highlighting the Spectrum

  1. 1
    chris haynes says:

    I object to this;

    “Although there is no rational reason to think that a plausible naturalistic scenario will ever be discovered, THERE IS VALUE in continuing origin of life research, both because we will learn much about biology in the process and because we will learn more about the hurdles that a naturalistic scenario would have to overcome and the areas in which design is required.”

    They’ve been milking this scam for almost 100 years, on the public nickel. Enough is enough.

  2. 2
    Barry Arrington says:

    Eric,

    Where would Thomas Nabel fall on this spectrum? “3” is close, but you would have to substitute “natural teleology” for “intelligent guidance.”

  3. 3
    CHartsil says:

    It’s between 1 and 2, there’s been a wave of new evidence from organic chemistry and there are no ID claims worth considering.

    So I’d say 1a : Reasonable understanding, filling in details

  4. 4
    Mapou says:

    CHartsil:

    there are no ID claims worth considering.

    ID makes this claim:

    The genomes of all species are organized hierarchically.

    This is a natural consequence of intelligent design over time. Complex/newer designs are made of simpler/older designs. The result is a mostly nested tree of life, i.e., a design tree that contains a significant number of lateral branching, aka “multiple inheritance” in software design or “horizontal gene transfer” in biology. This claim has already been amply observed in nature, both at the morphological and at the genetic level.

    But it goes further. Knowing this, it should be possible, through a careful, goal-directed, comparative analysis of various genomes at the sequence level, to find this hierarchical organization. This would help in identifying the function of various genes and other sequences and give us a functional map in the shape of a 3D tree, the tree of life, if you will. This would be invaluable for medicine. The key understanding is to realize that the genome is organized hierarchically.

    PS. Darwinists should not think that they invented the “tree of life” metaphor. The book of Genesis claims prior art.

  5. 5
    gpuccio says:

    Eric:

    Can I stay with you at #6? 🙂

  6. 6
    Jim Smith says:

    I would say #6. Research is important because it supports the conclusion that life was designed. Most of the evidence supporting ID comes from mainstream science – which is a testament to the process of science and a sorry commentary on human nature – because most scientists are so biased they can’t see the meaning in their own data. I think the universe was designed to support life and that life was designed. Some would say this is a contradiction, if the universe was designed to support life then life should arise naturally – which is what Charles Darwin thought. But consider a computer. A computer is designed to run programs, but programs do not “self-assemble” a programmer is required to write them. In the same way the universe was designed and life also was designed.

  7. 7
    humbled says:

    It is safe to say option 1, 2 and 3 have been explored exhaustively and, according to the evidence or lack thereof, has been ruled out as an option grounded in reality and science. Unless new evidence comes to light these options are IMO impossible not to mention a huge waste of tax money as well as time and resources. In fact these three options are so incredible insane and at odds with reality and the observable world around us, it escapes me how any logical thinking human being could even consider them.

    Option 4 onwards are IMO the only options worth considering based on the current state of science and the complete and utter failure of materialistic science to explain anything useful. Given the 100+ years looking for answers, materialistic scientists would have discovered something by now. The fact that they haven’t is a safe indicator that further discoveries or advancements are slim. The more likely scenario would be that with each new discovery and as we advance scientifically, a purely materialistic explanation would be untenable, as we have already begun to recognise.

  8. 8
    Jim Smith says:

    The really interesting part of ID will come when we know, from scientific research, more about the constraints on design. What aspects of the design are constrained by natural law and what aspects allow the flexibility for self-expression. Those areas that are not constrained by natural law, but allow room for self-expression, will tell us something about the values and character of the designer.

  9. 9
    fifthmonarchyman says:

    Jim Smith said,

    Those areas that are not constrained by natural law, but allow room for self-expression, will tell us something about the values and character of the designer.

    I say,

    That is where my interests for the most part are as well.

    I think that a strong case has been made that materialism is insufficient to explain Abiogenesis. That puts me at about a 5 and a half.

    What I’d like to know is
    Is the life we see around us the only possible way to do it or did the designer have options in this regard?

    If he had options his particular choice would tell us something about him. I think that is where the action will be moving forward.

    Unsuccessful explanations have the benefit of narrowing the cone of choice.

    Just like Edison. We haven’t failed in our attempts to explain the origin of life we have just discovered 10,000 ways that won’t work.

    peace

  10. 10
    Cross says:

    6 and a bit.

    Life arouse: God created life; Natural process not up to the task, excellent arguments for design

    Abiogenisis Research: As per your point 6. Mostly to disprove the naturalistic, materialistic outlook that is called science these days.

    Cheers

  11. 11
    CHartsil says:

    “This is a natural consequence of intelligent design over time. Complex/newer designs are made of simpler/older designs. ”

    Funny how evolution does this with actual mechanisms while ID remains an assertion. So by what mechanism(s) were older body plans adapted into new body plans? Who did it? When? How can we falsify this?

  12. 12
    Eric Anderson says:

    Thanks, Barry @2.

    I can’t say that I am an expert on Nagel’s “natural teleology.” I think his concern about reductionism is well founded, but it is less clear to me exactly what he is proposing with natural teleology. My sense is that he is attempting to reconcile (i) the obvious problems he sees with purely naturalistic explanations of reality, with (ii) his desire to avoid recurring to anything other than purely natural causes. In a sense, therefore, I think his idea is, while interesting, potentially incoherent — perhaps like trying to have his cake and eat it too.

    To be sure, I think he has some interesting ideas about the comprehensibility of the universe and the concept that mind is not reducible to the mere physical. Probably some ideas worth pursuing. But I’m not sure he has escaped the physical, unless he allows himself to actually consider the most straight-forward explanation: that there is real teleology, apart from the nature.

    Again, I’m not well-versed in Nagel’s ideas, so I’m happy to learn if my impressions are misplaced. I guess you’re right that he would probably be closest to #3, at least in his willingness to acknowledge the problems of naturalistic scenarios and to consider alternative explanations, with his “natural teleology” being perhaps a subset of natural causes.

  13. 13
    Eric Anderson says:

    CHartsil @3:

    Thanks for your comment. In your view, what evidence from organic chemistry do you feel provides the strongest support for a purely naturalistic origins scenario?

    Also, if the broad outline of how life arose is largely understood (and we are mostly filling in the details at this point), perhaps you could point us to, or describe briefly, what that outline is?

    Thanks,

  14. 14
    Eric Anderson says:

    Mapou @4:

    ID makes this claim:

    The genomes of all species are organized hierarchically.

    Why would ID predict that species are organized hierarchically? Perhaps a particular view of one possible way in which design could be implemented would predict a hierarchical organization, but certainly not all design scenarios.

    Maybe instead we could say that ID is compatible with an organized hierarchy and, therefore, such hierarchy is not necessarily evidence for a naturalistic scenario?

    At any rate, I apologize for pursuing the OT for a moment. I really want to focus in this thread on OOL, rather than subsequent patterns in the development of life.

  15. 15
    Eric Anderson says:

    Jim Smith @6:

    Some would say this is a contradiction, if the universe was designed to support life then life should arise naturally – which is what Charles Darwin thought. But consider a computer. A computer is designed to run programs, but programs do not “self-assemble” a programmer is required to write them.

    Well said. Whether the universe was designed to support life (all the constants carefully balanced on a razor’s edge and so forth) is an entirely different question from whether life within that universe could arise from purely natural processes. It is important to keep the distinction in mind.

    Incidentally, this is one of the problems with the multiverse as an “explanation” for life. Even if we have a universe that is compatible with life, as ours no doubt is, that does not in any way explain the origin of that life.

    Indeed, the question is given the universe that we have, with its laws and constants balanced on a razor’s edge — given all that, how could life arise?

  16. 16
    Mapou says:

    CHartsil:

    “This is a natural consequence of intelligent design over time. Complex/newer designs are made of simpler/older designs. ”

    Funny how evolution does this with actual mechanisms while ID remains an assertion.

    Funny how this is a lie since Darwinian evolution has never been shown to do anything, finch beak sizes notwithstanding. No, some just so story does not count as evidence.

    So by what mechanism(s) were older body plans adapted into new body plans? Who did it? When? How can we falsify this?

    One or more intelligent alien entities did it. I’m sure they must have used advanced design tools to simulate all their prototypes to great details before releasing them into nature. It’s relatively easy to falsify the ID claim that the genome is organized hierarchically. Just do a computer analysis of about a hundred genomes. That is high enough number of samples. If the genes and sequences of each genome are not found to form a non-nested hierarchy, then the prediction is falsified.

  17. 17
    Mapou says:

    Aderson:

    Mapou @4:

    ID makes this claim:

    The genomes of all species are organized hierarchically.

    Why would ID predict that species are organized hierarchically? Perhaps a particular view of one possible way in which design could be implemented would predict a hierarchical organization, but certainly not all design scenarios.

    Maybe instead we could say that ID is compatible with an organized hierarchy and, therefore, such hierarchy is not necessarily evidence for a naturalistic scenario?

    I don’t think so. A hierarchy is a necessary result of intelligent design over time. Why? It’s because an intelligent designer wants to reuse as much of existing, tried and tested designs as possible. For example, if the designer already has the complex genetic code for echolocation working for bats, there is no point in rewriting the code in order to use the same design in a different animal, such as an echolocating whale. Just transfer the genes over to the whale, make some minor adjustments and voila. It’s the intelligent thing to do. Any other approach is stupid.

    Hierarchical design is such an important principle that it is the basis of modern software development tools. It’s called OOD or object oriented design. New complex objects are formed by inheriting the properties of simpler objects.

  18. 18
    evnfrdrcksn says:

    (long time lurker here)

    I’m sorry, but ‘objectively evaluating the evidence” means no assumptions. Every single one of the questions in the OP are chock full of assumptions. The fact is, we don’t know a lot about the origin of life, and your leading questions betray you as not serious. It almost seems like you don’t want to know.

  19. 19
    evnfrdrcksn says:

    #7 humbled said
    “It is safe to say option 1, 2 and 3 have been explored exhaustively…”

    I hardly think that’s a safe thing to say at all. Exploring is still in progress.

  20. 20
    Eric Anderson says:

    Well, this is timely:

    Purely by coincidence, my 9th grader just showed me his homework for tonight from his biology class. The kids are supposed to read the text and answer the following questions:

    1. What did the early atmosphere contain?
    2. When did the first rocks form?
    3. Name the 2 Scientists who simulated earth conditions in the lab.
    4. What are the building blocks of proteins?
    5. What did Miller’s experiment produce?
    6. Describe Microspheres.
    7. From the abiotic slew of inorganic matter, what could have evolved first?

    There are more, but these first questions caught my eye, given the current topic of discussion.

  21. 21
    CHartsil says:

    @13: It’s not really any one piece. It’s the past 60 years of organic chemistry. In naturalistic settings we’ve produced purine bases, amino acids, ribonucleotides, even self replicating micelles which can also shield bonding amino acids from natural solvents.

  22. 22
    bFast says:

    You know, just before I read this post I was searching around about the nature of ATP synthase. Interesting thing, that. A rotary motor much like the famed flagellum, but it exists in all kingdoms of life. In the evolutionary paradigm, therefore, it must have existed by the time of the universal common ancestor.

    Evolutionists look at stuff like ATP synthase, and somehow say that they have no responsibility to explain it, as that falls to the “science” of abiogenesis — not to them. This, of course, is a major cop out. The “science” of abigenesis is looking to conceive of some simple (well more likely than the UCB), evolving, replicator. The latter, of course, is vastly less complex than the simplest archae. It therefore is the unmet responsibility of the evolutionary biologist to get from simple, evolving, replicator to ATP synthase and the other 300 odd genes necessary for the simplest known life form.

    As the gap between non-life and simplest known archae is so vast, the “1” position is truly laughable.

    Positions 2 – 6 are just variations of degree of how likely it is that we have bumped into the line between God-did-it and God-arranged-it-to-be-done-via-this-mechanism. The latter view, however, is the engine that has driven science ever since we discovered that God was not a micromanager, but that he established all manner of mechanisms to get stuff done. I think it as worthy to seek out such mechanisms in the start of life as any science is worthy.

    However, any scientist that says “definitely by natural processes” is showing himself to have a commitment to philosophical naturalism, not merely methodological naturalism. Let his religious position be recognized as such.

    As for me, I am a “6”.

    The “7” position is simply dangerous in my opinion. If God made a mechanism that does it, and we pretend that he didn’t, we get hurt when that mechanism is discovered.

  23. 23
    evnfrdrcksn says:

    22-bfast
    “Evolutionists look at stuff like ATP synthase, and somehow say that they have no responsibility to explain it, as that falls to the “science” of abiogenesis”

    no. stop embarrassing yourself. “Evolutionists”?

  24. 24
    evnfrdrcksn says:

    eric @ 20

    care to explain how that’s ‘timely’?

    seems like pretty basic 9th grade biology.

  25. 25
    evnfrdrcksn says:

    also…”slew”?

  26. 26
    humbled says:

    EEvnfrdrcks you said ” #7 humbled said
    “It is safe to say option 1, 2 and 3 have been explored exhaustively…”

    “I hardly think that’s a safe thing to say at all. Exploring is still in progress.”

    You are missing the point. Scientists committed to materialistic science have had full access to funds, the latest equipment, man power etc and over the last 100+ years, and despite searching desperately, have produced nothing but a long list of failed predictions and junk science.

    If the answer was out there they would have found it by now or at least discovered or produced some measure of evidence. Having all those resources available and producing nothing but fraud and fairy tales, as well as the heavy handed way in which dissenters are/have been treated, tells me all I need to know.

  27. 27
    Eric Anderson says:

    Mapou @17:

    I think you make a good argument as to why a design process might result in a hierarchy and why it might be compatible with the same. I guess I would just back down on the idea that it is absolutely necessary. In many cases design can be disruptive, novel, previously not implemented. That is also a common feature of design. So, again, design is compatible with, but does not necessarily require, a nested hierarchy.

  28. 28
    Eric Anderson says:

    Thanks, CHartsil @21:

    I was hoping for something more than a general reference to decades of biochemistry. Many people are quite familiar with the various discoveries over the years, and have become even more skeptical that a naturalistic scenario is viable, not less.

    One specific item I am interested in, if you wouldn’t mind taking just a few moments, is the alleged self-replicating micelle. First, on what basis can we cay that it is self-replicating (as opposed to “naturally forming” which is a different matter)? Secondly, what major similarities and differences exist between a simple micelle and, say, a cellular membrane?

    Thanks,

  29. 29
    Eric Anderson says:

    evnfrdrcksn @24:

    care to explain how that’s ‘timely’?

    seems like pretty basic 9th grade biology.

    It is timely because I wrote a post in the morning, and the very same day his class is discussing this topic.

    Pretty basic 9th grade biology propaganda, perhaps. I would love to go into his classroom and talk about the Miller-Urey experiment in actual detail, getting into the assumptions, the actual results, what it might mean (or not mean) for the origin of life. Unfortunately, what the kids are getting is biology presented with the typical materialist storyline:

    What makes up proteins? Amino acids.

    What did Miller-Urey discover? Amino acids!

    Woohoo! Therefore life could have arisen through purely natural processes.

    Complete nonsense.

    —–

    Fortunately, before I even had a chance to talk to my son last night, he mentioned that as they were going through the textbook in class he noticed that there were several things presented that were just assumptions, rather than demonstrated facts. I encouraged him to keep looking for them as the reading continued, as the assumptions will be legion and the facts sparse.

  30. 30
    CHartsil says:

    Funny, I work in an adjoining field and everyone I work with is specifically convinced by the evidence. We only find more evidence of natural self replicating molecules, not less

    http://molbio.mgh.harvard.edu/.....tions.html

    They divide mechanistically, being smashed against rocks etc. A cell membrane is a single ‘sheet’ while a micelle is aggregate.

  31. 31
    Eric Anderson says:

    bFast @22:

    Evolutionists look at stuff like ATP synthase, and somehow say that they have no responsibility to explain it, as that falls to the “science” of abiogenesis — not to them. This, of course, is a major cop out.

    Quite right that this is a common cop out when abiogenesis is brought up. It rests partly on the myth that once we have a self-replicating something, then the magic of Darwinian evolution can take hold and nothing is impossible. This reproduction aspect is alleged to be central to Darwinian evolution. However, I argue it is not. Incidentally, I have a nascent post rolling around on this very issue that I haven’t yet had time to flesh out. Hopefully sometime before long.

    Positions 2 – 6 are just variations of degree of how likely it is that we have bumped into the line between God-did-it and God-arranged-it-to-be-done-via-this-mechanism.

    I understand what you’re saying, but I would describe it a bit differently (in addition to referring to a designer, rather than “God”).

    2-3 are not so much variations of degree in how likely it is that we have bumped into a designer. It is not so much an evidence-based difference between the positions. Rather, it is a difference in intellectual willingness to consider certain evidence. Indeed, at some level 1-3 are really levels of intellectual integrity, as the serious problems with abiogenesis proposals and the relevance of design arguments are quite obvious to anyone who has looked into the issue. That is why I say that #3 is as far along the naturalistic spectrum as anyone who is intellectually honest should be able to go. #2 is too definitive in its claim/assumption of materialism, and #1 is a blatant misrepresentation.

    On the other side of the spectrum, I agree with you that 4-5 might be along a continuum of how likely it is that we have bumped into the line of where a designer needs to act. #6 just ignores the line completely.

    Thanks for prompting me to think through that aspect out loud here for a moment . . .

  32. 32
    CHartsil says:

    “Evolutionists look at stuff like ATP synthase, and somehow say that they have no responsibility to explain it, as that falls to the “science” of abiogenesis — not to them. This, of course, is a major cop out.”

    Not any I’ve ever met. Creationists just have to keep in mind that us not explaining every little thing, or anything, for that matter doesn’t mean they have license to go cramming god in the gaps.

  33. 33
    Eric Anderson says:

    CHartsil, yes, I am familiar with Szostak’s work and have looked at it previously. He and his team are doing some good work. However, there are very serious issues with their approach in terms of even coming close to solving OOL.

    You keep referring to all this evidence that convinces you. Can you point to a specific discovery or a specific paper that you found particularly compelling, rather than just providing a long list of publications?

  34. 34
    Eric Anderson says:

    CHartsil, I’ll defer to bFast to respond as it was his comment, but you have perhaps not been closely involved in the debate.

    It is quite common for proponents of evolution, when abiogenesis is brought forward as a problem, to say, in effect, “Well, yes, abiogenesis is a sticky issue, but we’re not really addressing that issue. We’re just focusing on evolution.” I am glad that you would not stoop to that approach, and are willing to take abiogenesis head on, as part of the overall evolutionary storyline.

    No-one who is skeptical of abiogenesis in this discussion has proposed anything like god of the gaps. We have, however, heard several naturalism-of-the-gaps claims, without supporting evidence.

  35. 35
    CHartsil says:

    The difference being is that naturalistic models are actually making progress while ID has yet to move on from bare assertion of “Complex, therefore designed”

    http://molbio.mgh.harvard.edu/.....cience.pdf

    http://molbio.mgh.harvard.edu/.....Nature.pdf

  36. 36
    CHartsil says:

    Abiogenesis isn’t part of the evolutionary storyline or any modern evolutionary synthesis, but I’ll gladly discuss it. Abiogenesis is organic chemistry, evolution is biology. The general public may not see much of a difference but they are distinctly different fields.

  37. 37
    Joe says:

    Naturalistic models? There aren’t any. No one knows how to model unguided evolution. That is the whole problem- yours is an untestable position.

  38. 38
    Joe says:

    CHartsil-

    The issue is if living organisms were designed then we would infer they were designed to evolve and evolved by design. Evolutionary and genetic algorithms model evolution by design.

    It is only if the OoL was via blind watchmaker-type processes would we infer evolution proceeds via blind watchmaker-type processes.

  39. 39
    CHartsil says:

    “No one knows how to model unguided evolution.”

    Sure we do, organisms will replicate with variation and be subjected to differential reproductive success based on successive and cumulative changes.

  40. 40
    Joe says:

    Mother nature and father time can produce stones and rocks yet they are not capable of producing Stonehenges.

  41. 41
    CHartsil says:

    “The issue is if living organisms were designed then we would infer they were designed to evolve and evolved by design.”

    Based on what? Do you have anything besides inference? Maybe a mechanism?

    “It is only if the OoL was via blind watchmaker-type processes would we infer evolution proceeds via blind watchmaker-type processes.”

    So what other origin of life model have you got? I have yet to see any from the creationist side.

  42. 42
    CHartsil says:

    “Mother nature and father time can produce stones and rocks yet they are not capable of producing Stonehenges.”

    Do those rocks replicate with variation?

  43. 43
    Joe says:

    Chartsil:

    Sure we do, organisms will replicate with variation and be subjected to differential reproductive success based on successive and cumulative changes.

    Success is relative. Biological reproduction is irreducibly complex and differential reproduction doesn’t do anything worth talking about.

    You cannot use your “model” to show it can produce something like ATP synthase.

  44. 44
    Joe says:

    “The issue is if living organisms were designed then we would infer they were designed to evolve and evolved by design.”

    Based on what?

    Knowledge of what is being debated and the evidence. And design is a mechanism.

    So what other origin of life model have you got?

    Other than your nothing?

  45. 45
    Joe says:

    Do those rocks replicate with variation?

    Replication with variation doesn’t help you. You cannot explain biological reproduction.

  46. 46
    CHartsil says:

    “You cannot use your “model” to show it can produce something like ATP synthase.”

    1: Gap argument

    2: http://en.wikipedia.org/wiki/A.....P_synthase

  47. 47
    CHartsil says:

    “Replication with variation doesn’t help you. You cannot explain biological reproduction.”

    So you’re getting to that age huh? Well you see Joey, when a man loves a woman they share a special kiss…

  48. 48
    Joe says:

    LoL! Yeah archaeology and forensic science are gap arguments. Wikipedia doesn’t help you. There aren’t any models for unguided evolution producing ATP synthase. No testable hypothesis, no experiments, nothing.

  49. 49
    Joe says:

    So you’re getting to that age huh? Well you see Joey, when a man loves a woman they share a special kiss…

    And your position cannot explain the existence of men and women. You don’t have a mechanism capable of getting beyond populations of prokaryotes given starting populations of prokaryotes.

  50. 50
    CHartsil says:

    Archaeology works apples to apples using known mechanisms of design to explain artificial structures. It doesn’t say “Well this cell looks like this object of known design, therefore design”

    I already posted a feasible ATP Synthase model, ignoring it doesn’t make it go away.

  51. 51
    CHartsil says:

    “And your position cannot explain the existence of men and women. You don’t have a mechanism capable of getting beyond populations of prokaryotes given starting populations of prokaryotes.”

    We already know that there are hermaphroditic replicators that can replicate with other organisms. This increases genetic variability and gives us a pretty good idea of the evolution of the sexes.

  52. 52
    Joe says:

    We already know that there are hermaphroditic replicators that can replicate with other organisms. This increases genetic variability and gives us a pretty good idea of the evolution of the sexes.

    Non-sequitur

  53. 53
    Joe says:

    I already posted a feasible ATP Synthase model,

    In what way did it model unguided evolution?

  54. 54
    CHartsil says:

    “Non-sequitur”

    >You explained how there are self replicators that can also replicate sexually. This has nothing to do the original of sexual reproduction.

    Do you even think about anything you type before you post it?

    “In what way did it model unguided evolution?”

    >The F1 region also shows significant similarity to hexameric DNA helicases, and the FO region shows some similarity to H+ -powered flagellar motor complexes. The ?3?3 hexamer of the F1 region shows significant structural similarity to hexameric DNA helicases; both form a ring with 3-fold rotational symmetry with a central pore. Both have roles dependent on the relative rotation of a macromolecule within the pore; the DNA helicases use the helical shape of DNA to drive their motion along the DNA molecule and to detect supercoiling, whereas the ?3?3 hexamer uses the conformational changes through the rotation of the ? subunit to drive an enzymatic reaction

  55. 55
    RodW says:

    Eric and Mapou,

    Yes, ID is consistent with the nested hierarchy. The problem is its consistent with everything. On the other hand evolutionary change must advance in relatively small increments.
    But that statement by Mapou is just the first step in making ID a science. The next step, which is the case in all legitimate studies of design, would be to ask why the designer did it that way. What are the advantages/disadvantages of incremental vs. full-blown creation? What does it say about the strengths/weaknesses/limitations of the designer? You’d be able to ask theses questions and then answer them with data/observations and experiments. This would lead to new questions and new answers.
    IDers never do this and I think its because intuitively they know that this approach would fail spectacularly. Living things just don’t look designed.
    But lets get back to the questions: Our uniform and repeated experience with design tells us that designers use that incremental evolutionary approach because they are limited in intelligence and the algorithms can often come up with creative solutions that they wouldn’t have thought of. Also, designers have limited time, so while the algorithm solves a problem on how to design an aircraft, or what securities to buy, the designer can work on something else. Does this make sense in terms of your designer? NO. Keep in mind your designer is the same guy who is outside of space and time and created the entire universe, along with space, time and matter in 10\-32 seconds.

  56. 56
    Mapou says:

    Eric Anderson @27:

    Mapou @17:

    I think you make a good argument as to why a design process might result in a hierarchy and why it might be compatible with the same. I guess I would just back down on the idea that it is absolutely necessary. In many cases design can be disruptive, novel, previously not implemented. That is also a common feature of design. So, again, design is compatible with, but does not necessarily require, a nested hierarchy.

    IMO, the intelligent design of complex systems is necessarily hierarchical. The operative words here are ‘intelligent’ and ‘complex’. The designers may have a top level idea of what they want but the design of complex systems always proceeds bottom up. It’s simple and straightforward: First design the simple parts and then use those parts to design and build more complex parts and objects. There is no getting around this. In as far as living organisms are concerned, it is obvious that the low level components had to be simple DNA sequences. These are common to many disparate complex organisms. This is what is observed in nature.

  57. 57
    Andre says:

    CHartsil

    You are very amusing, when a biological nan tech machine is a motor with a rotor and a stator it does not look designed it is designed. Rotary motors can’t design or build them self.

  58. 58
    CHartsil says:

    Andre, nor can rotary motors replicate with variation.

    Irreducible complexity is still a gap argument

    https://www.facebook.com/groups/CreationEvolutionDebate/

    https://www.facebook.com/groups/IntelligentDesignOfficialPage/

  59. 59
    Mapou says:

    RodW:

    Eric and Mapou,

    Yes, ID is consistent with the nested hierarchy. The problem is its consistent with everything. On the other hand evolutionary change must advance in relatively small increments.
    But that statement by Mapou is just the first step in making ID a science. The next step, which is the case in all legitimate studies of design, would be to ask why the designer did it that way. What are the advantages/disadvantages of incremental vs. full-blown creation? What does it say about the strengths/weaknesses/limitations of the designer? You’d be able to ask theses questions and then answer them with data/observations and experiments. This would lead to new questions and new answers.
    IDers never do this and I think its because intuitively they know that this approach would fail spectacularly. Living things just don’t look designed.

    IDers never do this because it would contradict their religion. Most IDers are convinced that the creator and designer of the universe and life on earth is an Omnipotent and Omniscient God. This comes from religious traditions and various mental baggages that they have a hard time freeing themselves of. A hierarchically designed genome would violate the concept of God’s infinite knowledge and power that they have fallen in love with and even idolize. God’s knowledge is infinite, therefore he does not even need to design anything. The universe can be made to appear fully formed out of the mind of God. Poof. Why not, since he knows everything beforehand, right? It’s crackpot nonsense, of course. It’s pure heresy, the work of the Devil. LOL. It’s a major stumbling block in this fight. ID is thus stuck in a rut, a rut straight out of false Christian traditions from an evil era in Church history. And we had plenty of those. The truth will indeed set us free.

  60. 60
    kairosfocus says:

    CH, re 58:

    nor can rotary motors replicate with variation.

    It has already been pointed out to you that the von Neumann kinematic self replicator facility required for reproduction in the cell is full of FSCO/I, uses coded — linguistic! — algorithmic — purposeful! — information, with a complex of associated execution machines and is irreducibly complex. So, its origin is one of the first challenges to be answered.

    Where, we already know on trillions of cases of observation (with no counters) just one causally adequate source for FSCO/I. Intelligently directed configuration. As the blind needle in haystack analysis backs up.

    That’s vera causa there, justifying an inference to best explanation on only observed adequate cause.

    As for irreducible complexity in a great many cases is is a reflection of FSCO/I, with many co-adapted correctly arranged and coupled parts to achieve function. Where, per observation, knocking out any one core part kills function. Thus, it cannot be incrementally assembled and co-opting bits and pieces runs into the problems of fit and function as well as organisation. So, the logic of the situation locks out hoped for incrementalist mechanisms and makes BLIND exaptation and lucky organisation maximally implausible.

    But then, evidence and logic don’t matter if there is an a priori demand that only naturalistic blind forces are allowed to be considered.

    Ideology triumphing over evidence and logic.
    Welcome to a priori materialistic evolutionary materialist scientism.

    Please, think again.

    KF

  61. 61
    CHartsil says:

    No, the same gap argument has been asserted ad nauseum. Something being complex and us not having a time machine is still not license to cram god in any gaps and it never will be.

    ” Thus, it cannot be incrementally assembled and co-opting bits and pieces runs into the problems of fit and function as well as organisation.”

    Lenski’s E. coli did just that. Multiple, potentiating mutations drove change conferring one single novel function. We even know that if you remove any of the changes, then there’s no cit* E. coli because he saved frozen fossils of the generations.

    “Ideology triumphing over evidence and logic.
    Welcome to a priori materialistic evolutionary materialist scientism.”

    Psychological projection is a psychological defense mechanism where a person subconsciously denies his or her own attributes, thoughts, and emotions, which are then ascribed to the outside world, usually to other people. Thus, projection involves imagining or projecting the belief that others originate those feelings.

  62. 62
    bFast says:

    CHartsil, are you still going on about Lenski’s E. coli? 50,000 generations (about 1/10 the number of generations separating human and chimp) in an extreme environment has produced two whole symbiotic mutations and you are hooting and tooting about it?

  63. 63
    CHartsil says:

    bFast are you still not understanding that multiple complementary mutations in separate systems conferring a single novel function completely debunks IC?

    Not that it even required debunking in the first place seeing as how it’s just a gap argument.

  64. 64
    kairosfocus says:

    CH,

    on fair comment all you are doing at this point is insistent empty repetition of corrected errors. Perhaps, unsurprisingly.

    Next, your caricature about cramming “god” into gaps shows the underlying ideology and projection of a caricature of the design view.

    If you are to move beyond such, first try to understand that you face an inductive inference in light of observable characteristics, that there is in fact just one observed adequate source of FSCO/I (functionally specific complex organisation and/or associated information, beyond 500 – 1,000 bits) . . . indeed simply to write your objection you manifested that source; intelligently directed configuration . . . and so per the vera causa principle we are entitled to the POSITIVE inference that the FSCO/I in say DNA’s digitally coded algorithmic information traces to the same source.

    Remember, this all starts with a first cell based life in some pond or the like, including an automaton with metabolic reaction systems and machinery (think, enzymes), encapsulation, and a self replication facility, using coded algorithmic information and execution machinery, all precisely tuned to one another.

    Blind materialist faith in the magic of unobserved powers of blind chance and mechanical necessity might lead to dismissing the absence of showing adequacy of such mechanisms, but we have no obligation to kowtow to demands of a lab coat clad ideological magisterium.

    We simply point to the proved adequate cause and the implications of blind search in config spaces of the sort of scales that are implied relative to atomic and temporal resources of the observed cosmos.

    Simply not credible, absent a lot of ideological question-begging and gross exaggeration of straws clutched at. The sort of minor muts Lenski may have seen are nowhere near what is focal — incremental hill climbing at best not blindly finding new islands of function.

    But then the eye of materialist faith sees miracles in micro evo as though it suffices to answer to body plan origination including the first one.

    The alternative is patent: FSCO/I is a reliable signature of design, and inference to best empirically grounded explanation warrants the strong inference that cell based life screams: design.

    As for irreducibly complex systems the simple fact is in many cases we are plainly, directly looking at FSCO/I.

    Beyond, the process logic of interactive mechanisms such that for a core removal or deficiency of any part leads to breakdown implies that such cannot be incrementally composed as they will not work. The effect is the organism would fail.

    Blind exaptation of bits and pieces from other separately functional systems meets Menuge’s challenges C1 – 5, here using the flagellum as key example:

    For a working [bacterial] flagellum to be built by exaptation, the five following conditions would all have to be met:

    C1: Availability. Among the parts available for recruitment to form the flagellum, there would need to be ones capable of performing the highly specialized tasks of paddle, rotor, and motor, even though all of these items serve some other function or no function.

    C2: Synchronization. The availability of these parts would have to be synchronized so that at some point, either individually or in combination, they are all available at the same time.

    C3: Localization. The selected parts must all be made available at the same ‘construction site,’ perhaps not simultaneously but certainly at the time they are needed.

    C4: Coordination. The parts must be coordinated in just the right way: even if all of the parts of a flagellum are available at the right time, it is clear that the majority of ways of assembling them will be non-functional or irrelevant.

    C5: Interface compatibility. The parts must be mutually compatible, that is, ‘well-matched’ and capable of properly ‘interacting’: even if a paddle, rotor, and motor are put together in the right order, they also need to interface correctly.

    ( Agents Under Fire: Materialism and the Rationality of Science, pgs. 104-105 (Rowman & Littlefield, 2004).)

    To overthrow such, what would be needed is straightforward credible examples of FSCO/I originating in our observation by blind chance and mechanical necessity.

    The persistent absence of such cases, when the fog of rhetoric clears, simply underscores a key point: the only observed adequate cause of FSCO/I is just what the needle in haystack search challenge leads us to expect: design.

    KF

  65. 65
    Cross says:

    kairosfocus @ 64

    Great answer. Can I also add C6: must be repeatable ie assembly is just not a one off fluke.

    Cheers

  66. 66
    CHartsil says:

    Except that I’m the only one here correcting errors. You’ve done nothing but continually assert and burden shift.

    IC has already been debunked and it’s not even really necessary since, as I’ve pointed out, it’s just a gap argument.

  67. 67
    rhampton7 says:

    kf,

    This should read: To overthrow such, what would be needed is straightforward credible examples of FSCO/I originating in our observations of material causation.

    Of course, animal and/or human intelligence may be the product of completely material causes, in which case the straightforward credible examples are abundant and already known. Only if animal and/or human intelligence is at least some part supernatural can your case be made.

  68. 68
    Cross says:

    CHartsil @ 66

    “IC has already been debunked and it’s not even really necessary since, as I’ve pointed out, it’s just a gap argument.”

    And evolution isn’t? Standard answer for the hard bits to explain is “we don’t know (yet)” but the inference is always we are sure evolution did it. Evolution of the gaps.

    Cheers

  69. 69
    CHartsil says:

    No, it’s not. In case you hadn’t read my bit about Lenski, we actually watched an IC system evolve.

  70. 70
    Cross says:

    CHartsil @ 69

    A single novel function is not a fully functioning IC system like [bacterial] flagellum or the Bombardier Beetles defense system, or for that matter the complex integration nano machinery of a single cell.

    Cheers

  71. 71
    CHartsil says:

    Cross, it’s a system comprised of interdependent parts, the removal of any of which will cause the system to cease functioning. We even know the last part to be true because he froze them every X number of generations to attempt to repeat certain pathways.

    It’s IC, and it evolved.

  72. 72
    Box says:

    Cross #64,

    Arguably your C6 is covered by KF’s c4:

    C4: Coordination. The parts must be coordinated in just the right way: even if all of the parts of a flagellum are available at the right time, it is clear that the majority of ways of assembling them will be non-functional or irrelevant.

    C4 is huge! How many parts are assisting the bacterium to assemble the flagellum? One can only guess the number of the members the ‘assembly team’ … But without the miraculous simultaneous evolution of this assembly team the whole process is a non-starter.

  73. 73
    Cross says:

    Boz @ 72

    No problem with that and yes C4 is huge.

    Cheers

  74. 74
    Cross says:

    CHartsil @ 71

    “it’s a system comprised of interdependent parts”

    Could you provide a link that documents the new IC system, including some diagrams etc. of the individual parts that have appeared.

    Cheers

  75. 75
    CHartsil says:

    http://www.ncbi.nlm.nih.gov/pm.....MC2430337/

    The researchers had sequenced the entire genomes of twenty-nine clones isolated from various time points in the Ara-3 population’s history. They used these sequences to reconstruct the phylogenetic history of the population, which showed that the population had diversified into three clades by 20,000 generations. The Cit+ variants had evolved in one of these, which they called Clade 3. Clones that had been found to be potentiated in earlier research were distributed among all three clades, but were over-represented in Clade 3. This led the researchers to conclude that there had been at least two potentiating mutations involved in Cit+ evolution. The researchers also found that all Cit+ clones sequenced had in their genomes a duplication mutation of 2933 base pairs that involved the gene for the citrate transporter protein used in anaerobic growth on citrate, citT. The duplication is tandem, resulting in two copies that are head-to-tail with respect to each other. This duplication immediately conferred the Cit+ trait by creating a new regulatory module in which the normally silent citT gene is placed under the control of a promoter for an adjacent gene called rnk. The new promoter activates expression of the citrate transporter when oxygen is present, and thereby enabling aerobic growth on citrate. Movement of this new regulatory module (called the rnk-citT module) into the genome of a potentiated Cit? clone was shown to be sufficient to produce a Cit+ phenotype. However, the initial Cit+ phenotype conferred by the duplication was very weak, and only granted a ~1% fitness benefit. The researchers found that the number of copies of the rnk-citT module had to be increased to strengthen the Cit+ trait sufficiently to permit the bacteria to grow well on the citrate, and that further mutations after the Cit+ bacteria became dominant in the population continued to accumulate that refined and improved growth on citrate. The researchers conclude that the evolution of the Cit+ trait suggests that new traits evolve through three stages: potentiation, in which mutations accumulate over a lineage’s history that make a trait accessible; actualization, in which one or more mutations render a new trait manifest; and refinement, in which the trait is improved by further mutations.

  76. 76
    Cross says:

    CHartsil @ 75

    Thanks, work time in my time zone, will look into it tonight.

    Cheers

  77. 77
    Eric Anderson says:

    Cross, let me know what you think about #75. BTW, it is apparently Lenski’s 2008 article.

    So apparently, after all the claims of evidence by CHartsil, what we have are Lenski’s experiments, which have been thoroughly discussed and reviewed already. And they certainly don’t show anything approaching what is needed for major evolutionary change. And definitely not anything relating to abiogenesis, the topic of this thread.

    Color me unsurprised.

  78. 78
    CHartsil says:

    “And they certainly don’t show anything approaching what is needed for major evolutionary change.”

    It was novel function conferred from a new gene and a new transporter.

    “And definitely not anything relating to abiogenesis, the topic of this thread.”

    I didn’t bring up IC, I was just addressing it.

  79. 79
    Eric Anderson says:

    CHartsil:

    You’ve mentioned a couple of times that you actually watched an IC system come into being through an evolutionary process. I, for one, think that is a very interesting result and would like to learn more, as I’m sure many others here at UD would as well.

    Given that it is a bit off topic for this thread, I’d like to offer you the chance to do a guest post. No need to do a treatise or anything, just a half dozen paragraphs describing your research and what the results were, and we’ll elevate it to a guest post. Let me know if that is something you’d be willing to share.

    Thanks,

  80. 80
    CHartsil says:

    To be fair it’s not from my research, it’s from Lenski’s and Blount’s, but sure. Just post it here when I’m done?

  81. 81
    CHartsil says:

    Editor’s Note: The below comment was elevated to a new thread, here:

    http://www.uncommondescent.com.....is-e-coli/

    This is a pro-ID board so I doubt I need to explain irreducible complexity. When arguing against it, most will bring up Ken Miller or Nick Matzke. They have great points but theirs are indirect and theoretical pathways for systems considered IC. That’s why I’m fond of Lenski’s cit* E. coli.

    This particular strain of E. coli evolved the ability to metabolize citrate aerobically. While most E. coli can do this anaerobically, part of the definition of wild-type E. coli is actually the inablity to use citrate as a substrate aerobically. This may not have been a terribly fascinating addition of function if not for the frozen fossil records kept by Lenski et al.

    These frozen generations allowed Lenski to determine that this trait was not acquired via a single mutation as it could only be repeated after generation 20,000. Given the distinct cladistic division amongst the populations at the border generation, it was determined that there were at least two potentiating mutations prior to the cit* event.

    In this third clade a tandem duplication resulting in a novel regulatory module leading to the aerobic cit* could be repeated and verified. It has been noted since that the fitness of the population has been improving without notable upper limit, increasing based on the number of copies of the new regulatory module.

    I find this to be sufficient in warranting the dismissal of the concept irreducible complexity. In Lenski’s E. coli, we observe the rise of a new function resulting from a new gene and new gene regulation. This function is comprised of now interdependent components which demonstrably did not exist in parent generations. It is by definition irreducibly complex and it was observed to evolve.

  82. 82
    kairosfocus says:

    EA, I’m a modded 6:

    6. “[Observed, Cell-based] Life [–> per empirical evidence and associated inference to the best current explanation unbiased by a priori evolutionary materialist scientism . . . ] almost certainly arose through intelligent guidance or intervention and not solely through natural processes [–> tracing to blind chance and/or mechanical necessity without intelligent action]. The very claim of an information-rich, functional[ly specific and complex organised] system arising through such processes is anathema to our understanding of cause and effect in the world, has never been observed, and is not based on solid scientific footing. Furthermore, there are excellent affirmative reasons to think that life could only have arisen through intelligent guidance or intervention. Although there is no rational reason to think that a plausible naturalistic scenario will ever be discovered, there is value in continuing origin of life research, both because we will learn much about biology in the process and because we will learn more about the hurdles that a naturalistic scenario would have to overcome and the areas in which design is required.”

    I would add that even were cell based life to have originated by blind chance and/or mechanistic processes, it has done so in a fine tuned cosmos set up so that such cell based life is possible.

    I think you will see why I have modified 6 as indicated.

    KF

  83. 83
    Joe says:

    CHartsil is confused. All that happened with Lenski’s experiment is that the E coli could now utilize citrate in an oxygen-rich environment. They already had that ability in the an anaerobic environment.

    An IC system did NOT evolve via unguided processes.

    No new genes were formed. An existing gene was duplicated and put under the control of a different promoter, ie a promoter that was on in the presence of O2..

  84. 84
    kairosfocus says:

    F/N: On the Lenski counterexample to IC claim, I suggest a glance at CL’s remarks in Sect 5 here (and onwards) in response to Venema:

    http://www.discovery.org/a/17571

    Let me clip Sect 5, as a first example:

    ______________

    >> Section 5: Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information

    In this section, we:

    • Understand why Venema’s citation of Lenski’s “Long Term Evolution Experiments” do not demonstrate that “Complex, specified information can indeed arise through natural mechanisms”
    • Review Michael Behe’s 2010 paper in Quarterly Review of Biology which investigated Lenski’s research and found that “mutations were decreasing or eliminating the protein’s function”
    • Investigate why Lenski’s E. coli bacteria that evolved the ability to uptake citrate under oxic conditions didn’t evolve anything new and likely experienced loss-of-molecular function

    Some critics of intelligent design (ID) misunderstand ID as a denial of natural causes. For example, we have recently seen how theistic evolutionist Dennis Venema wrongly suggests that, in both a scientific and theological sense, ID denies natural causes. Venema imports this misunderstanding into his proposed methods of testing ID, suggesting that if we find natural causes doing anything, then ID is refuted.

    Venema writes: “any natural mechanism that can be shown to produce information would render [Stephen Meyer’s] argument that information only arises from intelligent sources null and void.”

    Dennis Venema’s argument collapses into this: ‘if Darwinian evolution can do anything, then ID is wrong.’ But this is not how we test ID, for ID readily allows that natural selection and random mutation can effect some changes in populations. The right question is not ‘Can natural selection do anything?’ but rather ‘Can natural selection do everything?’

    With this in mind, let’s analyze Dr. Venema’s discussion of Richard Lenski’s Long Term Evolution Experiments (“LTEE”) with E. coli.

    Where’s the Behe?

    Before discussing the LTEE, it’s important to note that from the beginning of his series for BioLogos on evolution and the origin of information, Venema didn’t just purport to critique Stephen Meyer’s arguments in Signature in the Cell. Rather he referred to rebutting the entire “Intelligent Design Movement” or what he called (following Judge Jones?) the “IDM.”

    But if Venema is going to critique the entire “IDM” using Richard Lenski’s “Long Term Evolution Experiments,” then Venema should discuss the most relevant literature of the “IDM” that discusses those experiments. He doesn’t do that.

    In Venema’s discussion of the LTEE, there is no mention of a 2010 peer-reviewed scientific paper written by the most prominent biochemist in the “IDM,” published in a prominent biology journal, extensively critiquing Lenski’s LTEE. Venema fails to note and discuss Michael Behe’s December 2010 paper in Quarterly Review of Biology (QRB), which extensively discusses and critiques Lenski’s Long Term Evolution Experiments. Instead, Venema critiques the writings of Stephen Meyer, who hasn’t commented on Lenski’s LTEE because they weren’t relevant to his arguments in Signature in the Cell about the origin of life.

    By misrepresenting Meyer’s thesis as being refuted by evidence of the power of natural selection, Venema creates a straw man. Meanwhile he ignores the substantive critiques by leading ID proponents of the very evidence he raises.

    Vague Discussions vs. Precise Discussions of Lenski’s LTEE

    As an initial salvo regarding Lenski’s LTEE, Venema writes:

    [T]here were many possible genetic states of higher fitness available to the original strain, and random mutation and natural selection had explored several paths, all leading to a higher amount of “specified information” — information that specifies increased reproduction and survival in the original environment. All this was by demonstrably natural mechanisms, with a complete history of the relevant mutations, the relative advantages they conferred, and the dynamics of how those variants spread through a population. The LTEE is at once a very simple experiment, and an incredibly detailed window into the inner workings of evolution.

    But what exactly was the “specified information” that increased? What new function was gained? Where did natural selection and random mutation produce functional, information-rich genes and proteins? Venema doesn’t say what new functions arose, what changed, or what information was gained. His claim that natural selection produced “specified information” is vague.

    By contrast, in critiquing claims that the LTEE has produced something new, Behe’s 2010 Quarterly Review of Biology paper was anything but vague:

    By examining the DNA sequence of the E. coli in the neighborhood surrounding the IS [insertion sequence] elements, the investigators saw that several genes involved in central metabolism were knocked out, as well as some cell wall synthesis genes and several others. In subsequent work, Cooper et al. (2001) discovered that twelve of twelve cell lines showed adaptive IS-mediated deletions of their rbs operon, which is involved in making the sugar ribose. Thus, the adaptive mutations that were initially tracked down all involved loss-of-FCT.

    Several years later, when the cultures had surpassed their 20,000th generation, Lenski’s group at Michigan State brought more advanced techniques to bear on the problem of identifying the molecular changes underlying the adaptation of the E. coli cultures. Using DNA expression profiles, they were able to reliably track down changes in the expression of 1300 genes of the bacterium, and determined that 59 genes had changed their expression levels from the ancestor, 47 of which were expressed at lower levels (Cooper et al. 2003). The authors stated that “The expression levels of many of these 59 genes are known to be regulated by specific effectors including guanosine tetraphosphate (ppGpp) and cAMP-cAMP receptor protein (CRP)” (Cooper et al. 2003:1074). They also noted that the cellular concentration of ppGpp is controlled by several genes including spoT. After sequencing, they discovered a nonsynonymous point mutation in the spoT gene. When the researchers examined ten other populations that had evolved under the same conditions for 20,000 generations, they found that seven others also had fixed nonsynonymous point mutations in spoT, but with different substitutions than the first one that had been identified, thus suggesting that the mutations were decreasing the protein’s activity.

    The group then decided to concentrate on candidate genes suggested by the physiological adaptations that the cells had made over 20,000 generations. One such adaptation was a change in supercoiling density; therefore, genes affecting DNA topology were investigated (Crozat et al. 2005). Two of these genes, topA and fis, had sustained point mutations. In the case of topA, the mutation coded an amino acid substitution, whereas, with fis, a transversion had occurred at the fourth nucleotide before the starting ATG codon. The topA mutation decreased the activity of the enzyme, while the fis mutation decreased the amount of fis gene product produced.

    (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).)

    If you weren’t following all the technical language, here’s what’s going on: For the first 20,000 generations of Lenski’s LTEE, very little happened. There were a few molecular adaptations observed, yet whenever we understood their molecular basis, they involved the knocking out of genes, or decreasing protein activity — in essence, a decrease in specificity. Behe summarizes:

    The fact that multiple point mutations in each gene could serve an adaptive role — and that disruption by IS insertion was beneficial — suggests that the point mutations were decreasing or eliminating the protein’s function.

    (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) (emphasis added).)

    Unlike Venema’s discussion, Behe’s is precise, giving multiple examples and detailed descriptions of the types of changes observed in Lenski’s LTEE. And Behe found that the types of changes taking place in the E. coli tended to decrease or eliminate protein function.

    Before getting into a discussion of the citrate-using strain of E. coli, Behe closes with another specific example that involved decreasing gene activity in Lenski’s LTEE:

    In an investigation of global protein profiles of the evolved E. coli, Lenski’s group discovered that the MalT protein of the maltose operon had suffered mutations in 8 out of 12 strains (Pelosi et al. 2006). Several mutations were small deletions while others were point mutations, thus suggesting that decreasing the activity of the MalT protein was adaptive in minimal glucose media.

    Looking at Table 3 of Behe’s QRB paper, not a single example of an adaptive mutation in Lenski’s LTEE entailed a gain of a new molecular function. In fact, over the course of his entire paper, Behe goes further and explains that most of our known examples of molecular adaptations in bacteria entail “loss-of-function” mutations. Somehow, Venema doesn’t discuss any of these findings.

    E coli. Could Uptake and Metabolize Citrate Before Lenski’s LTEE

    Later, when referring to a different stage of the LTEE, Venema claims that a new function did arise in Lenski’s E. coli bacteria during the experiments: the ability of E. coli to metabolize citrate. Venema claims that “One of the defining features of E. Coli is that it is unable to use citrate as a food source,” but after a series of mutations “bacteria that use citrate dominate the population.” According to Venema, these experiments show “Complex, specified information can indeed arise through natural mechanisms.”

    Yet Venema leaves out important details, creating an inaccurate impression. As we’ll discuss below, normal E. coli already have machinery to uptake and metabolize citrate, so the general fact that Lenski’s bacteria showed this ability is really quite unremarkable.

    Unfortunately, Venema’s readers on the BioLogos will never hear that. They also won’t learn that Michael Behe has written extensively about Lenski’s research, showing that the machinery for E. coli to uptake and metabolize citrate already existed in these bacteria. This isn’t an entirely new biochemical pathway. Venema fails to note that normal E. coli already have the ability to uptake and metabolize citrate. They just can’t normally uptake it under oxic conditions; Lenski’s bacteria evolved the ability to uptake it under oxic conditions used in the experiment. Then the E. coli used their normal metabolic pathways to use citrate as a food source. Behe made this point while commenting on these claims soon after they were first published in 2008:

    Now, wild E. coli already has a number of enzymes that normally use citrate and can digest it (it’s not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a “citrate permease” which can transport citrate from outside the cell through the cell’s membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, “The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions.”

    (Michael Behe, Amazon Blog, “Multiple Mutations Needed for E. Coli” (June 6, 2008).)

    Likewise, Behe’s recent 2010 paper in Quarterly Review of Biology provided an extensive critique of claims that Lenski’s LTEE showed the evolution of a new pathway that could metabolize citrate. Venema doesn’t cite or mention Behe’s QRB paper, but it too explains that E. coli already had the ability to metabolize citrate. Behe explains:

    Recently, Lenski’s group reported the isolation of a mutant E. coli that had evolved a Cit+ phenotype. That is, the strain could grow under aerobic conditions in a culture of citrate (Blount et al. 2008). Wild E. coli cannot grow under such conditions, as it lacks a citrate permease to import the metabolite under oxic conditions. (It should be noted that, once inside the cell, however, E. coli has the enzymatic capacity to metabolize citrate.) The phenotype, whose underlying molecular changes have not yet been reported, conferred an enormous growth advantage because the culture media contained excess citrate but only limited glucose, which the ancestral bacteria metabolized.

    (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).)

    Thus, Behe explains that the precise genetic mechanisms that allowed E. coli to uptake citrate under oxic conditions are not known. But Behe goes further and points out that the citrate-metabolizing E. coli strains really aren’t anything new, and that previous investigations suggest that the ability of the E. coli to uptake citrate under oxic conditions might result from molecular loss-of-function:

    As Blount et al. (2008) discussed, several other laboratories had, in the past, also identified mutant E. coli strains with such a phenotype. In one such case, the underlying mutation was not identified (Hall 1982); however, in another case, high-level constitutive expression on a multicopy plasmid of a citrate transporter gene, citT, which normally transports citrate in the absence of oxygen, was responsible for eliciting the phenotype (Pos et al. 1998). If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.

    (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).)

    Thus, previous research suggests that the adaptation which allowed these E. coli to uptake citrate under oxic conditions might be caused “by the loss of the activity of a normal genetic regulatory element.” Here’s what is likely going on here:

    Under normal conditions, E. coli can metabolize citrate; after all metabolizing citrate is an important step in the Krebs cycle, a pathway used by virtually all living organisms when creating energy.
    But under oxic conditions, E. coli lack the ability to transport citrate through the cell membrane into the cell. E. coli can do this under reducing conditions, but under oxic conditions E. coli can’t normally uptake citrate.
    If Lenski’s citrate-using E. coli are like previous E. coli which were discovered uptaking citrate under oxic conditions, then it seems likely that the bacteria underwent a mutation that knocked out the regulation mechanism of a citrate-transport gene, causing over-expression, allowing the E. coli to uptake citrate under oxic conditions.

    In other words, the machinery for both transporting and metabolizing citrate was already present in these bacteria. But a series of knockout mutations broke the regulation of pre-existing citrate transport mechanisms, causing over-expression of a citrate transport gene, allowing citrate to be transported under both oxic and anaerobic conditions. If this is the case, then clearly this example of Darwinian “evolution” entails the loss of a molecular function, not the gain of a new one. And there was no wholesale acquisition of the ability to metabolize or, as Venema put it, “use” citrate.

    In fact, as Behe notes, we don’t really yet understand the precise molecular mechanisms that caused these E. coli to be able to uptake citrate under oxic conditions. So as far as we can tell, these changes entailed the origin of no new functional genes or proteins but might have resulted from a broken regulatory mechanism. We have not seen that natural selection and random mutation can produce functional, information-rich genes and proteins, and Venema is wrong to suggest otherwise.

    Contra Venema, this example hardly shows the Darwinian evolution of a “new function,” especially since E. coli already had the ability to uptake and metabolize citrate. Venema claims that CSI has arisen, but if we don’t even know what mechanisms were involved in this change, how does he know that it is new CSI?

    What do Lenski’s LTEE Really Tell Us?

    In his QRB paper, Behe goes on to explain that to date, the known adaptations that have occurred in Lenski’s LTEE are either modification-of-function or loss-of-function changes:

    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).)

    Behe’s paper further suggests that when there are several kinds of potential adaptive mutations that might occur, loss or modification of function adaptations will be far more common than gain-of-function adaptations. He concludes:

    Even if there were several possible pathways by which to construct a gain-of-FCT mutation, or several possible kinds of adaptive gain-of-FCT features, the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.

    (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).)

    The sort of loss-of-function examples seen in the LTEE will never show that natural selection can increase high CSI. To understand why, imagine the following hypothetical situation.

    Consider an imaginary order of insects, the Evolutionoptera. Let’s say there are 1 million species of Evolutionoptera, but ecologists find that the extinction rate among Evolutionoptera is 1000 species per millennium. The speciation rate (the rate at which new species arise) during the same period is 1 new species per 1000 years. At these rates, every thousand years 1000 species of Evolutionoptera will die off, while one new species will develop–a net loss of 999 species. If these processes continue, in 1,000,001 years there will be no species of Evolutionoptera left on earth.

    If Behe is correct, then Darwinian evolution at the molecular level faces a similar problem. If, all other things being equal, a loss or modification of function adaptation is generally 100-1000 times more likely than gain of function adaptations, then eventually an evolving population might run out of molecular functions to lose or modify. Neo-Darwinian evolution cannot forever rely on examples of loss or modification-of-function mutations to explain molecular evolution. At some point, there must be a gain of function.

    Vaguely Appealing to Vast Probablistic Resources Won’t Work

    Venema closes his post on the LTEE by saying: “what the IDM claims is impossible, these ‘tiny and lowly’ organisms have simply been doing — and it only took 15 years in a single lab in Michigan. Imagine what could happen over 3,500,000,000 years over millions of square miles of the earth’s surface.”

    But vague appeals to vast eons of time and huge population sizes are unconvincing. You just have to do the math. As David Abel reminds us:

    Mere possibility is not an adequate basis for asserting scientific plausibility. A precisely defined universal bound is needed beyond which the assertion of plausibility, particularly in life-origin models, can be considered operationally falsified. But can something so seemingly relative and subjective as plausibility ever be quantified? Amazingly, the answer is, “Yes.” … One chance in 10200 is theoretically possible, but given maximum cosmic probabilistic resources, such a possibility is hardly plausible. With funding resources rapidly drying up, science needs a foundational principle by which to falsify a myriad of theoretical possibilities that are not worthy of serious scientific consideration and modeling.

    (David L. Abel, “The Universal Plausibility Metric (UPM) & Principle (UPP),” Theoretical Biology and Medical Modelling, Vol. 6:27 (Dec. 3, 2009).)

    In the case of E. coli and citrate, the bacteria already had the ability to uptake and metabolize citrate, and simply found a way to transport it under different conditions. It’s likely this occurred by overexpressing pre-existing transport mechanisms. Does this imply that anything and everything “could happen over 3,500,000,000 years over millions of square miles of the earth’s surface”? Well, ID proponents aren’t interested in making vague and ambiguous appeals to vast amounts of probabilistic resources. They want to test these questions, and follow the evidence where it leads.

    As discussed here, ID proponents have asked just how long it takes to evolve traits that require multi-mutation features. A multi-mutation feature requires multiple mutations to be present before there is any advantage given to the organism. Doug Axe’s research makes assumptions very generously favoring Darwinian evolution. He assumed the existence of a huge population of asexually reproducing bacteria that could replicate quickly — perhaps nearly 3 times per day — over the course of billions of years. Yet even here, complex adaptations requiring up to six mutations with neutral intermediates can become fixed. Beyond that, things become implausible.

    If only slightly maladaptive intermediate mutations are required for a complex adaptation, only a couple (at most two) mutations could be fixed. If highly maladaptive mutations are required, the trait will never appear. Axe discusses the implications of his work:

    [T]he most significant implication comes not from how the two cases contrast but rather how they cohere — both showing severe limitations to complex adaptation. To appreciate this, consider the tremendous number of cells needed to achieve adaptations of such limited complexity. As a basis for calculation, we have assumed a bacterial population that maintained an effective size of 109 individuals through 103 generations each year for billions of years. This amounts to well over a billion trillion opportunities (in the form of individuals whose lines were not destined to expire imminently) for evolutionary experimentation. Yet what these enormous resources are expected to have accomplished, in terms of combined base changes, can be counted on the fingers.

    (Douglas D. Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” BIO-Complexity, Vol. 2010(4):1-10.)

    If Axe is correct then we cannot always assume, as Venema seems to do, that sufficient probabilistic resources exist to produce complex features we see in life.

    Summarizing Venema’s Argument Regarding the LTEE

    In short, Venema’s argument regarding the LTEE collapses into common misconceptions about ID, which go something like this:

    (1) ID holds that Darwinian evolution cannot do anything.
    (2) If Darwinian evolution can do something then it can do anything.
    (3) Lenski’s experiments show Darwinian evolution can allow E. coli bacteria to evolve a “new function” of metabolizing citrate.
    (4) Therefore ID is wrong, and given enough time, Darwinian evolution can do anything we “imagine.”

    At each step in his argument, the facts and/or the logic is wrong:

    Regarding (1): In fact, ID does not hold that Darwinian evolution can’t do anything. Rather it claims that natural selection can do some things, but not everything. ID proponents readily acknowledge (as Behe has) that “if only one mutation is needed to confer some ability, then Darwinian evolution has little problem finding it.” The problem comes when multiple mutations are required to produce some new structure — and as Axe’s research shows, this is where Darwinian evolution typically gets stuck.
    Regarding (2): Darwin-defenders have a long history of over-extrapolating from the data. ID is scientifically cautious and concludes that no one single experiment can show that Darwinian evolution can do everything we ask of it. A single experiment showing the ability of Darwinian evolution to do X simply shows the ability of Darwinian evolution to do X; it doesn’t necessarily show Darwinian evolution can do Y, Z, and A, B, and C, etc. ID says we need to test hypotheses carefully and not over-extrapolate from observed data.
    Regarding (3): In fact Lenski’s experiments did not show the Darwinian evolution of an entirely new function. E. coli bacteria already had the ability to uptake and metabolize citrate, and the experiments simply showed they evolved the ability to uptake it under oxic conditions. This very likely required the loss of a molecular function.
    Regarding (4) ID proponents do not think it is wise or scientifically accurate to vaguely invoke vast eons of time or vast population sizes to document the alleged power of Darwinian evolution. ID cautions that Darwinian evolutionists often assume that there are sufficiently vast probabilistic resources to accomplish any task imaginable, but that assumption might not be valid. Rather than simply assuming, Doug Axe’s research finds that adaptations requiring more than six neutral mutations, or two maladaptive mutations, to provide a functional advantage would not arise in the history of the earth.

    Subsequent research by Axe and Ann Gauger suggests that it would not be uncommon for Darwinian evolution to face obstacles that exhaust the probabilistic boundaries as found by Axe’s research. In 2011, they published research in BIO-Complexity that found at least seven mutations (probably many more) would be necessary to convert one protein into a supposedly closely-related protein.

    While Darwinians may (or may not) claim that this was a real evolutionary pathway, it’s the type of pathway that is often claimed to have been traversed by natural selection over the course of life’s history. The fact that this simple conversion required more mutations to produce a new function than would be allowed under Axe’s mathematical models shows that there may be real obstacles to the Darwinian evolution of new proteins. Venema’s citation of Lenski’s LTEE certainly does not show otherwise.>>
    _____________

  85. 85
    kairosfocus says:

    F/N part 2: Let’s continue, sect 6:

    ______________

    >>Section 6: Another Bogus Claim of “Novel Function Arising Through Mutation and Selection”

    In this section, we:
    • Understand why Dennis Venema’s citation of Joseph Thornton’s steroid research does do not demonstrate a “fascinating case of a novel function arising through mutation and selection”
    • Review the multiple responses to Thornton’s research from leading ID proponents (all ignored by Venema) who found the changes were not information-rich, not necessarily produced by natural selection, entailed diminishment rather than gain of function, and well within the ‘edge of evolution’
    • See that Venema undercuts his own claims by admitting, “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors”

    In the case of Richard Lenski’s Long Term Evolution Experiments (LTEE) with E. Coli bacteria, we saw that Dennis Venema of BioLogos cited purported examples of natural selection increasing specified and complex information — but intelligent design (ID) proponents had long before critiqued these examples. For example, Lenski’s LTEE had been critiqued by Michael Behe when they first came out in 2008, and then later in Behe’s 2010 paper in Quarterly Review of Biology. Venema, however, discussed none of these critiques.

    But Venema has a second empirical example he cites to supposedly show the Darwinian evolution of what he calls “CSI on Steroids.” Citing research co-published by University of Oregon biologist Joe Thornton in 2006, Venema calls this “a second fascinating case of a novel function arising through mutation and selection.” But here too, ID proponents had extensively critiqued the experiment when it was first published. And again, Venema failed to discuss or respond to any of these prior arguments from ID proponents. It’s hard to ignore responses from the ID camp to Thornton’s research since there are so many of them. These responses were all published back in 2006 when Thornton’s research was first published:

    Michael Behe on the Theory of Irreducible Complexity
    How to Explain Irreducible Complexity — A Lab Manual
    Paul Nelson on Debating the Controversy That Doesn’t Exist
    Bruce Chapman on the Science Stories that Fizzled (and the One that Might Have Been)
    CSC Director Stephen C. Meyer Responds to Research on Irreducible Complexity
    Casey Luskin: Science Plays Politics, but Implies Behe and Snoke (2004) Supports Irreducible Complexity and ID After All

    Many of these responses will be discussed below.

    Venema claims that Thornton’s research shows “a second fascinating case of a novel function arising through mutation and selection.” As we will see, if by “novel function” Venema means “diminishment of function,” then perhaps he is correct. As a brief and cursory summary of problems with the Thornton et al. research, consider the following points:

    The Thornton et al. research cited by Venema merely found that an alleged precursor enzyme could potentially perform two functions, and then supposedly lost the ability to perform one of those functions. At worst it shows loss-of-function through two mutations. At best, this is an example of small-scale change, which the research of ID proponents like Michael Behe readily concedes is possible. Because Thornton et al.’s research only supported small-scale evolution, which ID proponents don’t question, Behe wrote in response: “This continues the venerable Darwinian tradition of making grandiose claims based on piddling results. There is nothing in the paper that an ID proponent would think was beyond random mutation and natural selection. In other words, it is a straw man.”
    Christoph Adami reviewed Thornton et al.’s research in Science, claiming it refuted ID. The research was also puffed in the New York Times as addressing intelligent design after the authors issued a press release entitled “Evolution of ‘Irreducible Complexity’ Explained,” purporting to be a direct response to “[a]dvocates of Intelligent Design.” Whether they are right or wrong, this is amusing since we see ID-critics debating over the scientific controversy that they claim does not exist.
    The authors’ press release gave a retroactive confession of ignorance, admitting that “[h]ow natural selection can drive the evolution of tightly integrated molecular systems … has been an unsolved issue in evolutionary biology.” Yet in the New York Times article, Thornton commented that “There’s no scientific controversy over whether this system evolved. The question for scientists is how it evolved.” So before this study they didn’t know how it evolved, yet somehow they knew it did evolve. It sounds like they are assuming the truth of Darwinian theory rather than testing it.
    Before the paper was published, Thornton had stated on his website that his “goal is to illustrate how a complex, tightly integrated molecular system — one which appears to be “irreducibly complex” — evolved by Darwinian processes.” After ID-theorist Paul Nelson pointed out that this implied that Thornton saw irreducible complexity as a legitimate scientific challenge, the words “irreducibly complex” magically disappeared from Thornton’s website. The episode demonstrates that ID raises legitimate scientific challenges of interest to Darwinian evolutionary biologists, even as they sometimes deny that fact for political reasons.
    In sum, this study doesn’t show how Darwinian evolution scales Mount Improbable, as Dawkins has put it. It simply shows that neo-Darwinism can get you the last 10 yards up the mountain after you’ve already spent 10 hours hiking. It’s an exercise in what Behe called “making grandiose claims based on piddling results.”

    But there’s much more to say in response to this research. Since much of the work responding to it has already been done, the best thing is simply to quote from some of these responses:

    Response 1: Michael Behe’s comments:

    The bottom line of the study is this: the authors started with a protein which already had the ability to strongly interact with three kinds of steroid hormones (aldosterone, cortisol, and “DOC” [11-deoxycorticosterone]). After introducing several simple mutations the protein interacted much more weakly with all of those steroids. In other words, a pre-existing ability was decreased.

    That’s it! The fact that this extremely modest and substantially irrelevant study is ballyhooed with press releases, a commentary in Science by Christoph Adami, and forthcoming stories in the mainstream media, demonstrates the great anxiety some folks feel about intelligent design.

    In the study the authors wished to see if two related modern proteins called the glucocorticoid (GR) receptor and mineralocorticoid receptor (MR) could be derived from a common ancestral protein. Using clever analysis the authors made a protein that they thought represented the ancestral protein. That protein binds several, structurally-similar hormones, as does modern MR. They then introduced two amino acid changes into the protein which are found in modern GR. The two changes caused the ancestral protein to bind the different kinds of hormones anywhere from ten- to a thousand-fold more weakly. That protein bound aldosterone about three-fold more weakly than cortisol. The authors note that modern GR (in tetrapods) also binds aldosterone more weakly than cortisol. So perhaps, the thinking goes, an ancestral gene that could bind both hormones duplicated in the past, one copy accumulated those two mutations to become the modern GR, and the other copy became modern MR.

    […]

    Here are number of comments in response:

    1) This continues the venerable Darwinian tradition of making grandiose claims based on piddling results. There is nothing in the paper that an ID proponent would think was beyond random mutation and natural selection. In other words, it is a straw man.

    2) The authors (including Christoph Adami in his commentary) are conveniently defining “irreducible complexity” way, way down. I certainly would not classify their system as anywhere near IC. The IC systems I discussed in Darwin’s Black Box contain multiple, active protein factors. Their “system”, on the other hand, consists of just a single protein and its ligand. Although in nature the receptor and ligand are part of a larger system that does have a biological function, the piece of that larger system they pick out does not do anything by itself. In other words, the isolated components they work on are not irreducibly complex.

    3) In the experiment just two amino acid residues were changed! No new components were added, no old components were taken away.

    4) Nothing new was produced in the experiment; rather, the pre-existing ability of the protein to bind several molecules was simply weakened. The workers begin their experiments with a protein that can strongly bind several, structurally-very-similar steroids, and they end with a protein that at best binds some of the steroids ten-fold more weakly. (Figure 4C)

    5) Such results are not different from the development of antibiotic resistance, where single amino acid changes can cause the binding of a toxin to a particular protein to decrease (for example, warfarin resistance in rats, and resistance to various AIDS drugs). Intelligent design proponents happily agree that such tiny changes can be accomplished by random mutation and natural selection.

    6) In the “least promising” intermediate (L111Q) the protein has essentially lost its ability to bind any steroid. In the “most promising” intermediate protein (the one that has just the S106P alteration) the protein has lost about 99% of its ability to bind DOC and cortisol, and lost about 99.9% of its ability to bind aldosterone. (Figure 4C)

    7) Although the authors imply (and Adami claims directly) that the mutated protein is specific for cortisol, in fact it also binds aldosterone with about half of the affinity. (Compare the red and green curves in the lower right hand graph of Figure 4C.) What’s more, there actually is a much larger difference (about thirty-fold) in binding affinity for aldosterone and cortisol with the beginning, ancestral protein than for the final, mutated protein (about two-fold). So the protein’s ability to discriminate between the two ligands has decreased by ten-fold.

    8) One would think that the hundred-fold decrease in the ability to bind a steroid would at least initially be a very detrimental change that would be weeded out by natural selection. The authors do not test for that; they simply assume it wouldn’t be a problem, or that the problem could somehow be easily overcome. Nor do they test their speculation that DOC could somehow act as an intermediate ligand. In other words, in typical Darwinian fashion the authors pass over with their imaginations what in reality would very likely be serious biological difficulties.

    9) The fact that such very modest results are ballyhooed owes more, I strongly suspect, to the antipathy that many scientists feel toward ID than to the intrinsic value of the experiment itself.

    10) In conclusion, the results (and even the imagined-but-problematic scenario) are well within what an ID proponent already would think Darwinian processes could do, so they won’t affect our evaluation of the science. But it’s nice to know that Science magazine is thinking about us!

    Behe’s point (10) is especially noteworthy since Venema writes about Thornton et al.’s research that “Over and against these lines of evidence, however, the Intelligent Design Movement claims that such novelty is inaccessible to random mutation and natural selection.” But Behe has made it clear that these kinds of modest loss-of-function changes are exactly the type of changes we might expect from Darwinian evolution. So Venema is misrepresenting the claims of the ID movement.

    In fact, Venema undercuts his own argument that this research represents significant novel CSI by admitting that: “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors.” This research does not demonstrate that natural selection and random mutation can produce functional, information-rich genes and proteins because what was produced was not information-rich. If anything, function was diminished or lost rather than gained.

    Response 2: Stephen Meyer’s Comments:

    The Bridgham et al. study published in Science is trivial. ID theorists have long known that a few mutations can slightly alter an existing protein fold. What we question is whether mutation and selection are sufficient to search the enormous combinatorial space of possibilities necessary to finding fundamentally new protein folds and structures. This study does nothing to allay our skepticism on that score.

    Contrary to what the authors assume receptor-hormone pairs do not constitute irreducibly complex systems. The receptor-hormone pair is only a small component of a signal transduction circuit that regulates other complex physiological processes. For such pairs to have any selective or functional advantage many other protein components have to be present, including the other components of a signal transduction circuit and the physiological processes that such circuits regulate. If this is the best that Michael Behe’s critics can do after ten years of trying to refute him, then neo-Darwinism is in deep trouble.

    The really interesting thing about this paper is not the science it contains–its scientific results are trivial–but the sociological dynamics surrounding the publication of these papers. The AAAS has repeatedly insisted there is no scientific controversy about intelligent design. Now Science, the AAAS flagship journal, publishes two articles taking positions on a controversy that the AAAS says doesn’t exist. Will Science now allow Michael Behe to respond or will it only publish articles about the controversy which claim that ID is wrong?

    Response 3: “How to Explain Irreducible Complexity — A Lab Manual”:

    Another response to the Thornton et al. research came from various Discovery Institute authors in a fun piece titled How to Explain Irreducible Complexity — A Lab Manual:

    What [Bridgham/Thornton et al.] do say, however, is biologically meaningless.

    A Tutorial in Evolutionary Theory

    To understand why, we need a brief primer in fundamental evolutionary theory. Natural selection preserves randomly arising variations only if those variations cause functional differences affecting reproductive output. Since Bridgham et al. tell their story by invoking natural selection (see below), the system whose origin they claim to explain must have a selectable function for it to qualify as irreducibly complex. Indeed, given that natural selection favors only functionally advantageous variations, Behe has made clear that “function” in a biological context necessarily means a selectable functional advantage, for an obvious reason: a system of well-matched parts that performs a function can’t lose that function unless it possesses one to begin with. Unfortunately, these receptor-ligand pairs do not meet Behe’s definition of irreducible complexity for an equally obvious reason: receptor-ligand pairs do not by themselves confer any selective functional advantage.

    Indeed, in Bridgham et al.’s scenario, the function undergoing natural selection is not simply MR-aldosterone binding, but electrolyte homeostasis, the complex physiological regulation of essential cellular ions such as potassium or calcium. The novel receptor MR evolved, they write, “because it allowed electrolyte homeostasis to be controlled” (p. 100).

    Natural selection is acting, therefore, not on MR-aldosterone binding alone. Indeed, it cannot, because unspecified binding confers no functional advantage.

    But that is what Bridgham et al. do not seem to understand. They think they are explaining the origin of a single receptor-ligand pair, the mineralocorticoid receptor (MR) protein and the steroid hormone aldosterone. But that is biological nonsense. It is nonsense, moreover, strictly on the grounds of evolutionary theory itself.

    Let’s suppose the newly-evolved cellular receptor, MR, interacts with a hormone ligand, aldosterone. This is a novel relationship. Now, will natural selection preserve it?

    Who knows? Without more information — that is, without more details about the cellular or organismal effect of that novel binding — the bare function “aldosterone binds to MR” is biologically vacuous.

    Compare: Pound a nail, we tell you. Where and why? you ask. Never mind that, we say, just go pound a nail. So you hammer a three-penny nail through the power supply of this blog’s server.

    In any case, the receptor-ligand pair by itself is certainly not irreducibly complex. These pairs represent only small components of complex physiological processes such as metabolism, inflammation, immunity, and electrolyte homeostasis. For such pairs to have any selective advantage as part of the regulation of larger physiological processes, many other protein components have to be present. In particular, all the other components of a complete signal transduction circuit have to be present, as well as the component parts of the physiological process that such circuits regulate. (Even the ligand aldosterone itself doesn’t exist apart from a separate enzyme that produces it, and Bridgham et al.’s gene duplication scenario does not account for the origin of this necessary component either.)

    Bridgham et al. appear to grasp the need for more details (albeit in a distressingly loose way) because both early and late in their paper they specify the functional role of MR. The receptor “is activated by aldosterone to control electrolyte homeostasis” (p. 97) they note, and evolved “because it allowed electrolyte homeostasis to be controlled” (p. 100).

    Thus, in Bridgham et al.’s scenario, the actual system undergoing natural selection is electrolyte homeostasis, not simply MR-aldosterone binding. There’s a good reason for that: as noted, the function “aldosterone-MR binding,” considered in isolation, cannot be a target for natural selection. Try it, if you think it can. You’ll quickly find that you are floating in biological limbo. Aldosterone binds to MR…MR interacts with aldosterone…MR and aldosterone…OK, enough of that. Why does MR interact with aldosterone? Hello? Can we get an organism here?

    Back to Biological Reality

    So — is the physiological system of electrolyte homeostasis, of which both MR and aldosterone are small parts, irreducibly complex? Maybe. Take a look at a physiology textbook, or even any review paper on steroid or receptor biochemistry. Bridgham et al. don’t say much about the complexity of electrolyte homeostasis, however, because they are unaware that they have completely misunderstood the relevant unit of selection in their scenario. They write (p. 98):

    It is not obvious how the tight aldosterone-MR partnership could have evolved. If the hormone is not yet present, how can selection drive the receptor’s affinity for it? Conversely, without the receptor, what selection pressure could guide the evolution of the ligand?

    By Bridgham et al. ‘s own account, however — although they don’t realize it — natural selection is not acting at this level (the MR-aldosterone relationship alone) at all. To have any selectable function, many more components need to brought into the story. Genuine irreducible complexity re-emerges, and will be quite unexplained by the Bridgham et al. scenario.

    Response 4: My Own Comments:

    [L]ook at the bottom line of what this research really found: Adami highlights that the lock and key fit of the glucocorticoid enzyme with the cortisol substrate is based upon the specificity of merely two amino acids, where the precursor molecule was also functional (lacking those 2 mutations).

    In other words, one enzyme might have evolved into another via 2 mutations. This would appear to be a fairly simple system–and, assuming it did evolve in this fashion, an unimpresive example of evolution. Two meager mutations (something which even Behe and Snoke’s (2004) simulations found could evolve under mutation and selection) is not an impressive evolutionary leap and there seems no reason to assume that many enzyme-substrate interactions might not require the simultaneous substitution of many more amino acid residues in order to function, vastly decreasing the likelihood of their evolution. (In fact, this research would not address the origin of complex molecular machines requiring many interacting parts, like the bacterial flagellum.) Even if we grant that this present system is “reducibly complex” (with regards to at least 2 meager amino acids, that is), why should we assume that all the other enzyme-substrate interactions in biology follow suit?

    The last two commentaries combine to make two important points:

    First, the fact that one precursor enzyme could potentially perform two functions, and then lost the ability to perform one of those functions, does not imply that all biologically functional enzymes can evolve in this fashion.

    Second, we must keep in mind that the research of Bridgham/Thornton et al. involved intelligently directing mutations in these enzymes. Since they did not identify specific selective advantages, intelligent agents were doing the selection in a goal-directed fashion, hoping to select for future function. This is important when we consider the research of Axe (2010), discussed in Section 3 above. Axe found that when there is no selective advantage to a given mutation, it has a much smaller chance of becoming fixed in a population.[3] Thus, while a series of intelligently directed mutations might lead back to a functional ancestor, Bridgham/ Thornton et al. have not demonstrated that this pathway is likely to have been followed under natural conditions.

    Venema stated that “If any natural mechanism can be shown to produce “functional, information-rich genes and proteins,” then intelligent design is no longer the best explanation for the origin of information we observe in DNA.” But in this example we have seen that:

    The change was not information-rich
    It’s not clear that natural selection produced this change
    Function was diminished or lost rather than gained

    In fact, Venema undercuts his own argument that this research represents significant novel CSI by admitting in a comment that: “Steroid hormones are a closely related molecules — it’s not too surprising that slightly different molecules fit into a related group of protein receptors.” ID proponents would say the same thing, which is why this research does not demonstrate that a “natural mechanism can be shown to produce ‘functional, information-rich genes and proteins.'” >>
    _______________

    In short the story is by no means the slam dunk one sided case as has been presented.

    KF

  86. 86
    harry says:

    That is a great breakdown of the various positions on abiogenesis.

    I think the discovery that even the simplest single-celled reproducing life forms consist of ultra-sophisticated, digital-information-based nanotechnology the functional complexity of which is light years beyond anything modern science knows how to build from scratch renders it irrational to conclude that life is the unintended, accidental product of mindless, purposeless natural processes. Life was no accident just as significant functional complexity (technology) is never an accident.

    The question for science is whether the fine-tuning of the Universe that made life a possibility, also, in ways we have not yet discovered, made life inevitable without another creative act by the intellect that fine-tuned and launched the Universe, or whether the first life form was a separate creative act by the intellect that fine-tuned the Universe. I think it was the latter.

    For whatever it is worth, this is the opinion of one who has spent most of his adult life working with technology, both hardware and software, but mostly software. (I was working with hardware back in the days when you could shoot trouble with an oscilloscope and actually put your finger on the particular diode or transistor that was causing the problem. Those days are long gone. ;o) When I read Signature in the Cell, which contains many convincing arguments, what was most compelling to me was the realization that cellular functionality is nothing less than ultra-sophisticated, digital-information-based nanotechnology.

    And then there is Popper’s dilemma:

    What makes the origin of life and of the genetic code a disturbing riddle is this: the genetic code is without any biological function unless it is translated; that is, unless it leads to the synthesis of the proteins whose structure is laid down by the code. But … the machinery by which the cell (at least the non-primitive cell, which is the only one we know) translates the code consists of at least fifty macromolecular components which are themselves coded in the DNA. Thus the code cannot be translated except by using certain products of its translation. This constitutes a baffling circle; a really vicious circle, it seems, for any attempt to form a model or theory of the genesis of the genetic code. Thus we may be faced with the possibility that the origin of life (like the origin of physics) becomes an impenetrable barrier to science, and a residue to all attempts to reduce biology to chemistry and physics.

    It is as though the designer of life arranged for us to realize, when we discovered the complexity of his work, that it couldn’t have come about mindlessly and accidentally.

  87. 87
    drc466 says:

    Eric,

    I think your list does an unkindness to Biblical Creationists (YECs) by excluding the majority view they hold, and including a minority view that has the ever-so-popular-but-false “creationists hate science!” implication.

    If you took a poll of most YEC organizations and individuals who spend any significant time on the CvE question, you would find a “6B” position (or 7 rewritten as a more accurate representation of Creationism) as a majority opinion:
    7. ““Life was created directly by an intelligent being without purely natural processes. To think otherwise is to deny God’s Word, which no amount of scientific undertaking can overturn. This truth finds significant support from the ID position that ‘the very claim of an information-rich, functional system arising through such processes is anathema to our understanding of cause and effect in the world, has never been observed, and is not based on solid scientific footing. Furthermore, there are excellent affirmative reasons to think that life could only have arisen through intelligent guidance or intervention.’ Although there is no rational reason to think that a plausible naturalistic scenario will ever be discovered, there is value in continuing origin of life research, both because we will learn much about biology in the process and because we will learn more about the hurdles that a naturalistic scenario would have to overcome and the areas in which design is required. Additionally, research on abiogenesis increases the growing evidence that the creation of life is a unique, unreproduceable act and that life is significantly more than just the correct assemblage of chemicals under favorable conditions, and makes the conclusions of Romans 1:20 ever more unavoidable.”

    Biblical creationist research organizations (e.g. ICR), arguably less funded than ID, spend significant time, money and effort on scientific research into such areas as radioactive decay, Carbon-14/DNA/amino acid racemization in dino fossils, etc., that they would not be doing if they in fact conformed to your overly-dismissive caricature presented in your #7 above. I would feel fairly confident that a lower percentage of YEC’s have the attitude presented in your #7, than the percentage of Evolutionists who believe the ludicrous #1 position also presented. If you can find a place in any mainstream creationist literature that actually states “we should stop doing science!” (a different proposition than “we should stop wasting taxpayer dollars on fruitless research like SETI”), I would be interested in seeing it. Just as Newton and other great scientists of his time saw the truth of God’s Creation as motivation FOR scientific research, modern Creationists also see the ongoing research done in the name of Evolution as exceedingly fruitful to their cause.
    After all, experiments such as Miller-Urey are a net win for Creationism, wouldn’t you say? 60 years later, and nobody has come up with a way to get the full array of amino acids naturalistically, or avoid the tar problem, or the racemization problem, etc. ad nauseum?

  88. 88
    Eric Anderson says:

    Note All:

    A new thread relating to Lenski’s E. Coli has been created here:

    http://www.uncommondescent.com.....is-e-coli/

    Please post further comments on that topic to the new thread.

  89. 89
    Eric Anderson says:

    Harry @86:

    Thanks for the good thoughts.

    It gets me thinking about perhaps one clarification:

    It seems there are two broad schools of thought among materialists regarding the inevitability of life arising.

    Some think life is an inevitable outcome of certain physical conditions (yet to be fully discovered and articulated, of course). They seek to eliminate the probability issue Popper brings up by claiming, in effect, that the probability is near 1 — life was inevitable. The upshot of this view is that because we see life here on Earth, then life must be ubiquitous throughout the universe. After all, if it had to happen here, then it must have happened elsewhere as well.*

    Others think that life is an incredible cosmic fluke, the luck of the draw, a wonderful coincidence. They acknowledge the terrible odds of life arising through purely natural processes, but either (a) sweep it under the rug by saying, in effect, “Well, yes it was incredibly lucky, but we are here, so obviously it happened. And by the way, improbable things happen all the time, so nothing to see here. Move on, folks.”; or (b) recur to the multiverse or some similarly hypothetical entity to help improve the odds.

    —–

    * Incidentally, I think there may indeed be other life out there, even other intelligent life, but not because it is an inevitable outcome of certain physical conditions.

  90. 90
    Cross says:

    Eric Anderson @ 77 and CHartsil

    I see the thread has moved on a bit while I had the time to read the link. There is even another thread.

    I am no biologist but it seems to me that as Joe @ 83 has said

    “Lenski’s experiment is that the E coli could now utilize citrate in an oxygen-rich environment. They already had that ability in the an anaerobic environment.”

    This occurred over 2 or three mutations in one of the strains. It is very interesting and certainly real science being done in evolution.

    For me it is showing that microevolution or adaption has occurred but I do not see the production of a new Irreducibly Complex system forming, just adaption of an existing transport system.

    This is certainly a problem for those on the extreme side of view 7 but in no way changes the way I see things.

    Certainly, some of the claims being made that this proves there is no edge to evolution and the IC systems of flagellum and the beetle defense system have been debunked are a stretch too far. Also the time frame (over 1,000,000 years) for a large creature for 2 or 3 mutations is still a big problem for evolution to achieve what is claimed.

    Cheers

  91. 91
    CHartsil says:

    “I do not see the production of a new Irreducibly Complex system forming”

    It’s a system that is comprised of multiple components that are all required to be in place to function.

  92. 92
    Cross says:

    CHartsil @ 91

    I would see it as a duplication of an existing IC system with modification. It is IC but only because it is built on an existing IC system.

    Cheers

  93. 93
    Eric Anderson says:

    drc466 @87:

    I think you make an excellent point. There are certainly those who hold to God’s word as the ultimate authority on the creation of life, but who feel that abiogenesis research should continue for reasons similar to #6. So probably what I should list is two versions of #7. In both cases their interpretation of God’s word would be the ultimate authority on the matter, but in #7a abiogenesis research would be supported, and in #7b it would be viewed as unnecessary or a poor use of resources.

    If you can find a place in any mainstream creationist literature that actually states “we should stop doing science!” (a different proposition than “we should stop wasting taxpayer dollars on fruitless research like SETI”), I would be interested in seeing it.

    Just to be clear, I never suggested anyone was against science generally, just against spending a lot of time and resources on abiogenesis-focused research, which is a situation very similar to your SETI comment. I have seen both attitudes, based either on a claim (from some scriptural interpretation) that life cannot have arisen through natural processes or that there is no other life out there, so we should stop spending resources on it. I don’t think such scriptural interpretations are sound on either account, but that is a separate matter. It is true that someone could hold to such scriptural interpretations and at the same time feel that ongoing research into either abiogenesis or SETI is warranted.

    So your larger point is well taken, namely that some who rely on their interpretation of God’s word as the authority on the matter also support a robust abiogenesis research program.

    If I get a moment, I’ll put just a quick update in the OP to point people to your comment. Thanks again for the productive discussion.

  94. 94
    harry says:

    drc466 @87

    Hello, my friend,

    Life was created directly by an intelligent being without purely natural processes. To think otherwise is to deny God’s Word, which no amount of scientific undertaking can overturn.

    It certainly looks as though the first life form must have been “created directly by an intelligent being without purely natural processes.” See my citation of renowned philosopher of science Karl Popper in post #86. There does not appear to be any natural (mindless, accidental) solution to the “disturbing riddle” with which digital-information-based life presents us. The accidental emergence of the very cellular machinery required for the utilization of the digitally-stored assembly instructions for the rest of the cellular machinery — the accidental assembly of which, without the utilization of such instructions, would be virtually impossible — was also a virtual impossibility. That is why the assembly instructions for the information-utilizing machinery must also be present in the coding regions of DNA.

    That does indeed create a riddle for materialistic, atheistic science. To believe there is a mindless, accidental solution to this riddle is similar to believing the first robot in a series of robots capable of manufacturing more robots came about accidentally. In other words, it is an irrational belief. And yet as irrational as it would be to believe that the first of such robots was a mindless accident, that isn’t nearly as dumb as believing the first life form was a mindless accident, because robotic equipment is very crude technology compared to the nanotechnology of life, and is therefore far more likely than life to come about accidentally, as unlikely as an accidental, self-replicating robot would be.

    So, I wholeheartedly agree with your first sentence. Although I don’t agree with the next. Don’t misunderstand me. I, too, believe God’s word is inerrant. It is just that, being an orthodox Catholic, I believe in the dogmatic statements of the Councils of Trent and Vatican I, which limit my interpretation of the Scriptures such that it cannot be contrary to the unanimous agreement of the Early Church Fathers regarding the Scriptures. The Fathers did not unanimously believe the creation accounts of Genesis should be taken literally. Augustine was caustic in his criticism of insisting they be taken literally.

    I am not saying Augustine was right and the others were wrong. I am just saying that Catholics are not bound to take the creation accounts of Genesis literally, although they are free to do so. The point is that if Christ kept His promise to send the Holy Spirit to the Church to be with it forever and to guide it into “all truth,” then whatever came to be unanimously believed and professed by the Early Church Fathers must have been the fulfillment of that promise, or Christ didn’t keep it. Catholics can believe what they want about many things, but to remain an orthodox Catholic one’s beliefs must not be contrary to the fruit of that work of the Holy Spirit. Now you know more than you ever wanted to know about how orthodox Catholics understand the faith. ;o)

    I remain agnostic about how to interpret the creation accounts. I believe they are historical in some sense, and are definitely not merely myths, although I do not think they were meant to be a scientific account of creation, either. Even so, I am not ready to completely side with Augustine. For example, here is how I look at the creation of Adam: To be a Christian at all, one must believe in the Resurrection of Christ and in our own bodily resurrection. To believe in that, one must believe God, at the resurrection, is going to fashion from dirt the bodies of everyone who ever lived, died and returned to the dust from which we came:

    In the sweat of thy face shalt thou eat bread, till thou return unto the ground; for out of it wast thou taken: for dust thou art, and unto dust shalt thou return.–Gen 3:19

    If God is going to fashion from dirt the bodies of everyone who ever lived and died, then what is so unbelievable about one more instance of His fashioning a body from dirt in the case of Adam? Nothing, really, at least for Christians who sincerely believe in the resurrection of the body. And Christians who don’t believe in the resurrection of the body need to ask themselves if they have really accepted the teachings of Christ.

  95. 95
    Cross says:

    Harry @ 94

    Hi Harry, great post and fully agree. I have always viewed the Genesis account as true, in a poetic way. As an example, this is part of a poem by Dorothy Mackellar that all we Aussies have to learn in primary school:

    I love a sunburnt country,
    A land of sweeping plains,
    Of ragged mountain ranges,
    Of droughts and flooding rains.
    I love her far horizons,
    I love her jewel-sea,
    Her beauty and her terror –
    The wide brown land for me!

    Anyone who has been outback in Aus knows what a great description this is, yet the ground is not really sunburnt (only skin can be), the horizon appears to go on forever but it really isn’t more so that anywhere else and last time I swam in it the sea was not full of jewels!

    As you said, the genesis accounts are not a scientific description but a poetic account of the truth underlying creation.

    Cheers

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