Common Design vs. Common Descent

I promised John Harshman for several months that I would start a discussion about common design vs. common descent, and I’d like to keep my word to him as best as possible.

Strictly the speaking common design and common descent aren’t mutually exclusive, but if one invokes the possibility of recent special creation of all life, the two being mutually exclusive would be inevitable.

If one believes in a young fossil record (YFR) and thus likely believes life is young and therefore recently created, then one is a Young Life Creationist (YLC). YEC (young earth creationists) are automatically YLCs but there are a few YLCs who believe the Earth is old. So evidence in favor of YFR is evidence in favor of common design over common descent.

One can assume for the sake of argument the mainstream geological timelines of billions of years on planet Earth. If that is the case, special creation would have to happen likely in a progressive manner. I believe Stephen Meyer and many of the original ID proponents like Walter Bradley were progressive creationists.

Since I think there is promising evidence for YFR, I don’t think too much about common design vs. common descent. If the Earth is old, but the fossil record is young, as far as I’m concerned the nested hierarchical patterns of similarity are due to common design.

That said, for the sake of this discussion I will assume the fossil record is old. But even under that assumption, I don’t see how phylogenetics solves the problem of orphan features found distributed in the nested hierarchical patterns of similarity. I should point out, there is an important distinction between taxonomic nested hierarchies and phylogenetic nested hierarchies. The nested hierarchies I refer to are taxonomic, not phylogenetic. Phylogeneticsits insist the phylogenetic trees are good explanations for the taxonomic “trees”, but it doesn’t look that way to me at all. I find it revolting to think giraffes, apes, birds and turtles are under the Sarcopterygii clade (which looks more like a coelacanth).

Phylogeny is a nice superficial explanation for the pattern of taxonomic nested hierarchy in sets of proteins, DNA, whatever so long as a feature is actually shared among the creatures. That all breaks down however when we have orphan features that are not shared by sets of creatures.

The orphan features most evident to me are those associated with Eukaryotes. Phylogeny doesn’t do a good job of accounting for those. In fact, to assume common ancestry in that case, “poof” or some unknown mechanism is indicated. If the mechanism is unknown, then why claim universal common ancestry is a fact? Wouldn’t “we don’t know for sure, but we believe” be a more accurate statement of the state of affairs rather than saying “universal common ancestry is fact.”

So whenever orphan features sort of poof into existence, that suggests to me the patterns of nested hierarchy are explained better by common design. In fact there are lots of orphan features that define major groups of creatures. Off the top of my head, eukaryotes are divided into unicellular and multicellular creatures. There are vetebrates and a variety of invertebrates. Mammals have the orphan feature of mammary glands. The list could go on and on for orphan features and the groups they define. Now I use the phrase “orphan features” because I’m not comfortable using formal terms like autapomorphy or whatever. I actually don’t know what would be a good phrase.

So whenever I see an orphan feature that isn’t readily evolvable (like say a nervous system), I presume God did it, and therefore the similarities among creatures that have different orphan features is a the result of miraculous common design not ordinary common descent.

4,651 thoughts on “Common Design vs. Common Descent

  1. Rumraket: Doesn’t that pretty much amount to the same thing in the end? It sounds really strange to me if it would group considerably more divergent sequences together in preference to grouping together those that are more similar. What am I missing?

    Consider a simple case of three species, A, B, and C. If the true relationships are ((A, B), C) but A gets a bunch of mutations while B and C get very few, then B and C will be more similar to each other than A and B, and thus you will get the incorrect tree ((A, (B, C)). And yes, this actually does happen with real data, including whole genomes, which is why we don’t cluster by similarity.

  2. John Harshman,

    I for one am not. What are they?

    This is one of the arguments in Denton’s book Evolution a theory in crisis. He argued that the difference in cytochrome c in bacteria and eukaryotic cells did not show an expected pattern based on sequence similarity. He goes on to chart several examples.

  3. Allan Miller,

    Which is not deterministic, however arch you may wish to be.

    As far as a child as an output the process becomes deterministic under the right conditions.

    Indeed, we have a mechanism for mutation too, or rather several. Again, not deterministic. I see no fundamental difference in the ‘lucky accident’ department.

    The fertilized egg is the moment where the Allan mechanism becomes mostly deterministic.

    The evolutionary process becomes mostly deterministic when?

  4. John Harshman: Consider a simple case of three species, A, B, and C. If the true relationships are ((A, B), C) but A gets a bunch of mutations while B and C get very few, then B and C will be more similar to each other than A and B, and thus you will get the incorrect tree ((A, (B, C)). And yes, this actually does happen with real data, including whole genomes, which is why we don’t cluster by similarity.

    That thing about whole genomes being affected by a higher overall mutation rate makes it make sense and seems now obvious in hindsight. -.-

    Do you know if phylogenies built from morphological data (for fossils I guess), today are also done using, for example, the maximum parsimony method? I ask because I imagine if clustering by similarity using molecular data has the
    “varying clock-problem”, that might also be a problem for morphology.

  5. colewd:
    GlenDavidson,

    Alleles are fixed in the reproductive process.Whats the difference?

    Exactly.

    Well, there’s a difference, but it’s obvious enough.

    But yes, things are up in the air, then become determined through processes. Why should evolutionary theory be different from what’s so common in life?

    Glen Davidson

  6. GlenDavidson,

    But yes, things are up in the air, then become determined through processes. Why should evolutionary theory be different from what’s so common in life?

    When we discuss reproduction it is a process we can observe and understand well. As Allan astutely pointed out there is a probabilistic element to it that does not get mostly deterministic until conception.

    The scientific method depends on deterministic elements in the process or the ability to get repeatable results. Conception……baby. Mass….curved space time. Cause….effect.

    The lack of this predictability maybe the root cause of Mung’s argument that evolution is incoherent.

  7. colewd:
    GlenDavidson,

    When we discuss reproduction it is a process we can observe and understand well.As Allan astutely pointed out there is a probabilistic element to it that does not get mostly deterministic until conception.

    The scientific method depends on deterministic elements in the process or the ability to get repeatable results.Conception……baby. Mass….curved space time. Cause….effect.

    The lack of this predictability maybe the root cause of Mung’s argument that evolution is incoherent.

    Not really an ecologist, are you? Or a historian. Those who learn from history direct the military like Hitler did (too much), as if matters are like they were in the last war.

    There are simple, predictable matters in science, and rather complex matters. The imperfect nested hierarchies are rather simple and predictable, humans evolving is not.

    “Design” has no predictability whatsoever, as it has no meaningful cause, and can’t explain life’s patterns. Try treating ID analytically once, rather than as something to be protected from all thought.

    Glen Davidson

  8. GlenDavidson,

    “Design” has no predictability whatsoever, as it has no meaningful cause, and can’t explain life’s patterns. Try treating ID analytically once, rather than as something to be protected from all thought.

    I understand the limitations of the design argument. Do you understand its strengths?If you continue to say it is not an argument it becomes clear that you have not examined it critically.

  9. colewd:
    GlenDavidson,

    I understand the limitations of the design argument.

    No you don’t, since you don’t come up with one bit of meaningful evidence for ID at all. You just bring up complexity and assume that design explains it without any observable design cause that actually does it.

    Do you understand its strengths?

    Yes, it appeals to believers.

    If you continue to say it is not an argument it becomes clear that you have not examined it critically.

    When have I said that it’s not an argument? That’s all that it is, if hardly one that convinces those committed to actual standards.

    I haven’t examined your bowl of jello very critically, as there’s nothing really there. Just your pathetic a priori belief in an unperceived “cause” that supposedly produces all of life–without you ever providing any reason to think so.

    Glen Davidson

  10. Rumraket,

    What are the strengths of the design argument, can you give an example?

    It is an argument from analogy that strongly resembles what we see in biology. Repeatable mechanisms that perform a function.
    -Transcription translation
    -DNA repair
    -the overall cell cycle
    -meiosis
    -mitosis
    -protein destruction mechanism
    -alternative splicing

    All of these appear to be the product of design. We can build all of these mechanisms with a functional cell and a 4 bit chemical code.

    Where that code came from is a mystery and is the limitation of the design argument.

    The origin of the code is also where the evolution argument hits a brick wall.

  11. colewd: It is an argument from analogy that strongly resembles what we see in biology. Repeatable mechanisms that perform a function.
    -Transcription translation
    -DNA repair
    -the overall cell cycle
    -meiosis
    -mitosis
    -protein destruction mechanism
    -alternative splicing

    All of these appear to be the product of design.

    They look like they’re the product of reproduction.

    Does it even occur to you to actually match up cause and effect in a meaningful way, or will saying “it looks designed” be as close as you get to making a case?

    Paley at least tried to argue that life appeared to be designed by an architect or artificer, since he realized what a lame and pathetic move it was to claim “it looks designed.” How does it look designed? Does it look like what known designers make? He tried to say that it is, but of course it does not. At least he tried, though, while the current crop of believers refuses to put anything on the line, since they know that it’ll be knocked down.

    The limitations of evolutionary processes are in fact what produce the best evidence for evolution, which also happens to be evidence against any known design process, save those occurring via EAs (and even there it’s just partial). The limitations of “design theory” are that it lacks any kind of explanation for anything, hence it lacks any credible evidence for design.

    Analogies (using the ordinary meaning) are not alone capable of showing anything. They may be suggestive, but they’re not going to demonstrate what happens. Furthermore, you barely have any kind of analogy at all, since basically life is very unlike what humans produce, from its lack of any evident purpose to the design-absurd constraints under which life develops.

    Glen Davidson

  12. colewd: It is an argument from analogy that strongly resembles what we see in biology.

    That isn’t even a coherent sentence.

    Repeatable mechanisms that perform a function.
    -Transcription translation
    -DNA repair
    -the overall cell cycle
    -meiosis
    -mitosis
    -protein destruction mechanism
    -alternative splicing

    All of these appear to be the product of design.

    Why do they appear that to you? They don’t to me. So explain it to me.

    We can build all of these mechanisms with a functional cell and a 4 bit chemical code.

    … and?

  13. colewd,

    As far as a child as an output the process becomes deterministic under the right conditions.

    No it doesn’t. You don’t know what ‘deterministic’ means. And, it’s no good trying to rescue yourself by placing your bets at some point after all the ‘truly’ stochastic stuff has occurred – 1.5 billion years of accidental meetings, random segregation and crossover, ‘random’ gamete choice you sweep under the carpet in favour of a split second after Allan’s immaculate (or at least noteworthy, for Allan) conception.

    Allan: Indeed, we have a mechanism for mutation too, or rather several. Again, not deterministic. I see no fundamental difference in the ‘lucky accident’ department.

    colewd: The fertilized egg is the moment where the Allan mechanism becomes mostly deterministic.

    Hogwash.

    The evolutionary process becomes mostly deterministic when?

    What’s this ‘mostly deterministic? If it’s ‘mostly deterministic’, it’s not deterministic, it’s stochastic.

  14. Rumraket: Do you know if phylogenies built from morphological data (for fossils I guess), today are also done using, for example, the maximum parsimony method? I ask because I imagine if clustering by similarity using molecular data has the
    “varying clock-problem”, that might also be a problem for morphology.

    Yes, parsimony is the most popular — nearly exclusive — method for morphological data. It doesn’t suffer from the varying rates problem because it doesn’t cluster by similarity. It can suffer from long branch attraction, though, which is a different thing.

  15. colewd:
    John Harshman,

    This is one of the arguments in Denton’s book Evolution a theory in crisis.He argued that the difference in cytochrome c in bacteria and eukaryotic cells did not show an expected pattern based on sequence similarity.He goes on to chart several examples.

    As I recall, those complaints relied on a false and naive idea of what we would expect to see. But would you care to defend them?

  16. John, to Bill:

    As I recall, those complaints relied on a false and naive idea of what we would expect to see. But would you care to defend them?

    Yes, Bill, please do.

  17. Allan Miller,

    No it doesn’t. You don’t know what ‘deterministic’ means. And, it’s no good trying to rescue yourself by placing your bets at some point after all the ‘truly’ stochastic stuff has occurred – 1.5 billion years of accidental meetings, random segregation and crossover, ‘random’ gamete choice you sweep under the carpet in favour of a split second after Allan’s immaculate (or at least noteworthy, for Allan) conception.

    I am trying to find cause and effect here. The random stuff I can do nothing about but as far as Identifying the cause of Allan I think we can nail the key event. So we have the ability to find the root cause of Allan and thus a fair use of the scientific method. Yes we are ignoring all the semi random stuff that lead up to it but thankfully there is a starting point where we can get a predictable output supporting the hypothesis.

    While the hypothesis at conception was not exactly Allan if the desired output was a child based on the combined genetics of Allan’s parents the probability of that outcome is extremely high. While I agree it is not strictly deterministic I think it is fair to say it is mostly deterministic based on the output being a child that matches Allan’s parents genetics.

    We have identified a testable cause and effect relationship.

  18. Allan Miller,

    What’s this ‘mostly deterministic? If it’s ‘mostly deterministic’, it’s not deterministic, it’s stochastic.

    You are trying to force a false equivalence by this black and white categorization. While it might help with your argument it will certainly lead to a false conclusion.

  19. colewd: While the hypothesis at conception was not exactly Allan if the desired output was a child based on the combined genetics of Allan’s parents the probability of that outcome is extremely high.

    Quoting Wikipedia
    Among women who know they are pregnant, the miscarriage rate is roughly 10% to 20% while rates among all fertilisation is around 30% to 50%.

    So the probability of that outcome would seem to be 50% to 70%. I would not call that “extremely high”.

  20. Allan: If it’s ‘mostly deterministic’, it’s not deterministic, it’s stochastic.

    colewd: You are trying to force a false equivalence by this black and white categorization.

    LOL. It is built into the meaning of “deterministic”, that it a strict limiting requirement. As Allan says, anything else should be called “stochastic” (or similar).

  21. The taxonomic hierarchies may or may not be unique. But from a common design standpoint, uniqueness isn’t required. The diagram below suggests there aren’t unique taxonomic nested hierarchies.

    Here is a diagram of shared genes. It looks very taxonomic in terms of hierarchical relationships. You can categorize groups of creatures by which genes they share.

    It doesn’t look all that friendly to an anomaly-free phylogentic hierarchy. But it fits well with the notion of common designs.

    http://www.sci-news.com/genetics/article01036.html

    According to a paper published in Nature, 70 per cent of protein-coding human genes are related to genes found in the zebrafish (Danio rerio), and 84 per cent of genes known to be associated with human disease have a zebrafish counterpart.

  22. stcordova,

    Sal, you completely misinterpret the figure. Genes are both gained and lost. You can tell which by mapping them onto a phylogeny. Bet they map pretty well and do not violate the nested hierarchy at all. And a phylogeny with more species would let you pinpoint the spots where genes were gained and lost.

    And of course what you show isn’t even a taxonomic hierarchy. Those aren’t groups within groups, they’re groups that partially overlap in all possible ways.

  23. Neil Rickert,

    LOL. It is built into the meaning of “deterministic”, that it a strict limiting requirement. As Allan says, anything else should be called “stochastic” (or similar).

    In this case as you pointed out we can take data and create a bell curve including a mean and SD. Looks like solid testable science.

    I agree. Lets change the claim for almost deterministic to a stochastic process where we can measure the output. It looks like changing the words does not change the argument.

    If we define all the possible outputs could we call it deterministic?

  24. colewd:
    John Harshman,
    https://youtu.be/hz4vYJ_0X_Y

    This short video shows cytochrome c and the genetic distance of other animals from humans.He outlines the contradictory data with common descent.

    No, that isn’t defending a claim. You can’t just send me to a video. Please state the arguments in your own words and be prepared to address criticisms yourself.

  25. John Harshman:

    Sal, you completely misinterpret the figure. Genes are both gained and lost

    That’s the usual epicyclic explanation. The problem with such explanations is the common ancestor of them all had to be chock full of genes that eventually got lost. That isn’t exactly a constructive type of evolution. What I’m saying is noted by other evolutionists in the problem of orphan genes and the method of “fixing” the problem by postulating ancestors with all the genes that eventually became orphan.

    Chickens have 48 + 105 = 153 genes that they share with humans but which humans don’t share with mice. That’s a curious pattern. And there are more of them just in that diagram alone, let alone with other creatures.

    We might try to explain the curious patterns by postulating the eukaryotic ancestor of all those creatures (like say a yeast) had all the genes in the diagram, and then the descendants lost many of the genes as they evolved. But that seems kind of an absurd postulate when contrasted to claims of evolution being constructive rather than reductive.

  26. keiths,

    Confirmation:

    Humans and chimpanzees have the exact same cytochrome c protein sequence. The “null hypothesis” given above is false. In the absence of common descent, the chance of this occurrence is conservatively less than 10-93 (1 out of 1093). Thus, the high degree of similarity in these proteins is a spectacular corroboration of the theory of common descent. Furthermore, human and chimpanzee cytochrome c proteins differ by ~10 amino acids from all other mammals. The chance of this occurring in the absence of a hereditary mechanism is less than 10-29. The yeast Candida krusei is one of the most distantly related eukaryotic organisms from humans. Candida has 51 amino acid differences from the human sequence. A conservative estimate of this probability is less than 10-25.

    This is from Theobald’s argument for common decent based on probability. The problem is this is not an argument against common design as a designer could use similar sequences for different animals. Since the designer designs the sequence there is no probability requirement. The sequence is determined by the designer. If he separately designed both humans and apes he is free to reuse the sequence.

    In order to make a probability argument you must define the probabilistic mechanism. In this case Theobald is arguing against having a similar sequence with a random process and no common descent vs a random process with common descent. He does the same thing in his 2010 paper on universal common descent.

  27. Rumraket,

    We can build all of these mechanisms with a functional cell and a 4 bit chemical code.

    … and?

    And that translates to a 20 bit code that folds into micro machines that enable life through enzymatic and other processes. This has the appearance of a 3D printing process but it uses the atoms and molecules in a much more efficient manner than 3D printers do.

  28. colewd: The problem is this is not an argument against common design as a designer could use similar sequences for different animals. Since the designer designs the sequence there is no probability requirement. The sequence is determined by the designer. If he separately designed both humans and apes he is free to reuse the sequence.

    Or, as usual, you have no expectations for design, there is no meaningful consequence for design (except it’s really complex and functional–which is properly the issue, not the conclusion), you will do nothing with design, and all you do is claim that it just is design. That’s all you want, not any messy science, not actual design expectations, not even anything different from what you’d expect of evolution.

    God can decide to make things look the same as they must had they evolved. That’s good enough for you, even though anything and everything could be said to be designed to appear as if they hadn’t been designed. It’s the ultimate excuse, the one way that design can avoid any kind of question or falsifiability challenge. It’s always confirmation for design (ooh, so complex), never a question, never any kind of expectation that one would have of human designs–like being able to think across lines of ancestry.

    Intelligent Design is fine for those who must have it. It just shouldn’t make any pretense to be anything but a sermon.

    Glen Davidson

  29. stcordova: The problem with such explanations is the common ancestor of them all had to be chock full of genes that eventually got lost.

    You forget that genes are also gained. And again, with enough of a sample we can determine where a gain happened and where a loss happened. Another thing: “loss” doesn’t necessarily mean there are no homologous sequences shared between species, just that one copy is no longer functional. While the difference between humans and chickens is enough that non-functional copies that became so soon after the split could not longer be recognized, I suspect that there would be considerable alignable sequence between humans genes and mouse pseudogenes, and vice versa. Consider the GULO pseudogene, for example.

    But that seems kind of an absurd postulate when contrasted to claims of evolution being constructive rather than reductive.

    Evolution is both. Who told you otherwise?

  30. colewd,

    Once again, why should cytochrome c be the same in some species and different in others? Can’t the designer make up his mind? And why should those differences fit into a nested hierarchy, and why should the cytochrome c nested hierarchy be so similar to the nested hierarchy of any other randomly selected gene?

  31. John Harshman,

    Once again, why should cytochrome c be the same in some species and different in others? Can’t the designer make up his mind? And why should those differences fit into a nested hierarchy, and why should the cytochrome c nested hierarchy be so similar to the nested hierarchy of any other randomly selected gene?

    Are you aware that cytochrome c in multicellular organisms preforms more functions than electron transport?

    Can you support your nested hierarchy claim for cytochrome c? I see a contradiction to this claim as a primate (bushbaby) has more differences to humans (14) then an alligator (13)?

  32. GlenDavidson,

    Or, as usual, you have no expectations for design, there is no meaningful consequence for design (except it’s really complex and functional–which is properly the issue, not the conclusion), you will do nothing with design, and all you do is claim that it just is design. That’s all you want, not any messy science, not actual design expectations, not even anything different from what you’d expect of evolution.

    The design argument is not intended for messy science. If it is correct what we are observing in nature like atoms, molecules, and living organisms were created outside space time. Science struggles outside space time. As Allan Miller says it is really strange out there 🙂

  33. colewd:
    John Harshman,

    Are you aware that cytochrome c in multicellular organisms preforms more functions than electron transport?

    No, I’m not. Is it true? And so what it it does?
    Can you support your nested hierarchy claim for cytochrome c?I see a contradiction to this claim as a primate (bushbaby) has more differences to humans (14) then an alligator (13)?

    You seem to be assuming that the nested hierarchy has something to do with a molecular clock. It doesn’t. This could simply be explained if a bushbaby has a faster evolutionary rate than an alligator. Again, nothing to do with nested hierarchy.

  34. colewd:
    John Harshman,

    How?

    Is this really something that an expert like you, at this late date, has no knowledge of? Doesn’t the NIH cover that subject? Have we not in fact discussed this with regard to nylonases?

  35. colewd,

    You are trying to force a false equivalence by this black and white categorization. While it might help with your argument it will certainly lead to a false conclusion.

    It neither helps nor hinders my argument, it’s just a poor usage of terms. And wrong. Other than that, it’s great.

    The fact remains – my existence is due to a long succession of ‘lucky accidents’, as well as some more regular processes. That’s where I came in. You haven’t dealt with that by insisting on focussing your microscope on the fresh Allan-zygote, and calling the process beyond that ‘deterministic’.

    Still, to give you something else to avoid my point with, how identical are identical twins, for example?

  36. John, to colewd:

    Is this really something that an expert like you, at this late date, has no knowledge of? Doesn’t the NIH cover that subject? Have we not in fact discussed this with regard to nylonases?

    You’re confusing colewd with Sal, John.

  37. colewd,

    This is one of the arguments in Denton’s book Evolution a theory in crisis. He argued that the difference in cytochrome c in bacteria and eukaryotic cells did not show an expected pattern based on sequence similarity. He goes on to chart several examples.

    Cytochrome c and Dayhoff diagrams. I remember that from my biochem classes in 1975. Have any other molecules been looked at since then? 🙂

    The difference between bacteria and eukaryotes should be greater than that between any 2 eukaryotes, incidentally. That’s what I’d expect. Isn’t it?

  38. Allan Miller: The difference between bacteria and eukaryotes should be greater than that between any 2 eukaryotes, incidentally.

    I honestly don’t know why that should be the case. Especially considering that eukaryotes are just a conglomeration of bacteria inside an archaeon.

    That’s what I’d expect. Isn’t it?

    You tell me. 🙂

  39. Mung:

    You want a car to go faster, you remove stuff.

    Allan:

    OK, engine out and wheels off. Now what?

    /Mungmode

    Poor Mung. Can’t even think two steps ahead.

  40. colewd,

    The morphological tree matches the molecular tree to an accuracy of better than 38 decimal places in Theobald’s figure 1. Thirty-frikkin-eight decimal places.

    Nothing you have said undermines that.

    To defend common design in the face of a number as huge as 10^38 is idiocy of the highest order. Creationism is flat-earth stupid.

Leave a Reply