Eric Holloway needs our help (new post at Panda’s Thumb)

Just a note that I have put up a new post at Panda’s Thumb in response to a post by Eric Holloway at the Discovery Institute’s new blog Mind Matters. Holloway declares that critics have totally failed to refute William Dembski’s use of Complex Specified Information to diagnose Design. At PT, I argue in detail that this is an exactly backwards reading of the outcome of the argument.

Commenters can post there, or here — I will try to keep track of both.

There has been a discussion of Holloway’s argument by Holloway and others at Uncommon Descent as well (links in the PT post). gpuccio also comments there trying to get someone to call my attention to an argument about Complex Functional Information that gpuccio made in the discussion of that earlier. I will try to post a response on that here soon, separate from this thread.

334 Replies to “Eric Holloway needs our help (new post at Panda’s Thumb)”

  1. Joe Felsenstein Joe Felsenstein
    Ignored
    says:

    Among other issues, the P in the -\log P in functional information is a cumulative P, not the probability of one outcome. Unlike the p‘s in Shannon’s formulas

  2. Corneel Corneel
    Ignored
    says:

    colewd: This is a great idea and why FI may be relevant. I think that this is very unlikely to cause uncontrolled proliferation alone without subsequent loss of FI.

    The uncontrolled proliferation is a consequence of the expression of the viral copy of Src (v-Src), which is a homolog of the gene that is native to our cells. No additional mutations in the host genome are necessary, as far as I am aware.

    Care to answer the question?

  3. colewd
    Ignored
    says:

    Corneel,

    The uncontrolled proliferation is a consequence of the expression of the viral copy of Src (v-Src), which is a homolog of the gene that is native to our cells. No additional mutations in the host genome are necessary, as far as I am aware.

    Care to answer the question?

    I think you have pointed out that information can be transferred to a genome through horizontal transfer. A legitimate point, however cancer does not usually form with a single mutation. There is initiation and then a process that follows which is something that could be measured as a reduction in FI.

  4. colewd
    Ignored
    says:

    Joe Felsenstein,

    I agree, but can you compare subtracting the number of functional bits from the total number of bits?

  5. BruceS
    Ignored
    says:

    colewd:

    How would you compare it with Shannon’s concept of mutual information?

    The answer is right there in Szostak’s first paper.

    The information content of biopolymers is usually thought of in terms of the
    amount of information required to specify a unique sequence or structure […] But different molecular structures may be functionally equivalent. A new measure of information — functional information — is required to account for all possible sequences that could potentially carry out an equivalent biochemical function, independent of the structure or mechanism used.

    That accumulation of functionally-equivalent sequences is what I understand Joe is referring to.

    I’m not sure what in that explanation is not clear to you. Perhaps it is the math? Do you suffer from Mung’s syndrome?

  6. BruceS
    Ignored
    says:

    Mung:
    Why do people allow threads like this to be derailed by talk of FI?

    What does FI have to do with the OP?

    Good thing you did not see my earlier post which brought up objective morality.

  7. Tom English Tom English
    Ignored
    says:

    colewd: Why don’t you think you can measure it [functional information]?

    What I’m saying is that it’s not inherent in nature. We may decide on a space of configurations that is real. We may define a function of the configurations in terms of some physical measurement we may make on them. But the functional information defined in terms of the configuration space and the physical measurement were not “out there,” waiting to be observed.

    The reason that functional information can be applied in many dissimilar contexts is that it’s an abstraction of ours, not some particular property of entities in nature. It’s something that is intended to aid us in explanation of physical systems. But functional information has no existence independent of the investigator who defines it.

    I’m very tired, and struggling with this. Hopefully this helps someone, if not you.

    Over and out.

  8. colewd
    Ignored
    says:

    BruceS,

    I’m not sure what in that explanation is not clear to you. Perhaps it is the math? Do you suffer from Mung’s syndrome?

    In this case I suffer from you answering a question I asked Tom English 🙂

  9. Corneel Corneel
    Ignored
    says:

    colewd: There is initiation and then a process that follows which is something that could be measured as a reduction in FI.

    The viral genome is a sequence that is associated with high functional information. Yet when it inserts into a host genome you perceive that as a reduction in FI*.

    How is that possible?

    Because the former is only functional from the point of view of the virus, not from that of the host.

    *(I’d say that the reduction occurs during integration and NOT during the process that follows)

  10. Alan Fox Alan Fox
    Ignored
    says:

    Tom English: What I’m saying is that it’s not inherent in nature. We may decide on a space of configurations that is real. We may define a function of the configurations in terms of some physical measurement we may make on them. But the functional information defined in terms of the configuration space and the physical measurement were not “out there,” waiting to be observed.

    The reason that functional information can be applied in many dissimilar contexts is that it’s an abstraction of ours, not some particular property of entities in nature. It’s something that is intended to aid us in explanation of physical systems. But functional information has no existence independent of the investigator who defines it.

    I’m very tired, and struggling with this. Hopefully this helps someone, if not you.

    Very helpful. Thanks, Tom.

  11. colewd
    Ignored
    says:

    Corneel,

    The viral genome is a sequence that is associated with high functional information. Yet when it inserts into a host genome you perceive that as a reduction in FI*.

    No, I don’t. Please re read my answer. I agree that information has been laterally transferred into the genome. To get from there to cancer requires additional genetic change which is probably a loss of FI.

  12. Alan Fox Alan Fox
    Ignored
    says:

    colewd: …probably…

    How did you estimate that probability?

  13. DNA_Jock
    Ignored
    says:

    No lateral introduction of a viral genome here:

    Rupert suffers a rearrangement that pairs BCR with ABL. Molecular biologists would refer to this as a gain-of-function mutation that causes cancer.

    Has Rupert experienced an increase or a decrease in FI?
    What process did you go through to decide?
    Follow up question will be:
    Ubj pna lbh fubj gung lbhe qrsvavgvba bs /abezny/ vf bowrpgvirL

  14. Mung Mung
    Ignored
    says:

    Tom English: Sorry if I just added to the confusion,.

    You have just added 12 bits of functional confusion.

    Tom English: But functional information has no existence independent of the investigator who defines it.

    You have just subtracted 24 bits of functional confusion.

    According to he law of conversation of functional confusion you owe us 12 bits.

  15. Entropy Entropy
    Ignored
    says:

    colewd: To get from there to cancer requires additional genetic change which is probably a loss of FI.

    If we defined function as producing cancer the cell gained functional information. Furthermore, if we specified function as producing cancer we’d have an increase in specified functional information.

  16. Corneel Corneel
    Ignored
    says:

    colewd: No, I don’t. Please re read my answer. I agree that information has been laterally transferred into the genome. To get from there to cancer requires additional genetic change which is probably a loss of FI.

    O. That is a surprise. I did not understand that you perceived the insertion of the viral genome to be an increase in FI. So according to you the oncovirus is not contributing to the subsequent development of cancer, because that requires a loss of FI? Did I understand correctly?

    If you cannot see that the virus is a pathogen working against the interests of the host, then there is nothing to gain for you from my example. I suppose it does cheer you up everytime you get influenza, right?

  17. BruceS
    Ignored
    says:

    colewd:
    BruceS,

    In this case I suffer from you answering a question I asked Tom English

    I have difficulty understanding all those emoji thingamajigs; perhaps my deficiency means I am somewhere on the internet-autism spectrum.

    I’ll take it as a good-natured request to butt-out, and so will slink off into the night. Or at least into Eric’s thread.

  18. colewd
    Ignored
    says:

    BruceS,

    I’ll take it as a good-natured request to butt-out, and so will slink off into the night. Or at least into Eric’s thread.

    The emoji was to say that what you did was usually fine but in this case I was particularly interested in Tom’s response as he has spent a lot of time on this subject.

  19. colewd
    Ignored
    says:

    Corneel,

    O. That is a surprise. I did not understand that you perceived the insertion of the viral genome to be an increase in FI. So according to you the oncovirus is not contributing to the subsequent development of cancer, because that requires a loss of FI? Did I understand correctly?

    Contribution is not the issue. The issue is the total cascade of events leading to cancer not just the initial shove or some effect in the middle of the causal chain. To get cancer you need the following.
    -Replication of cancer stem cells
    -Disabling of DNA repair
    -Disabling of apoptosis
    -Up regulation of vascular growth
    -Down regulation of immune response
    -Disabling or protein destruction

  20. Corneel Corneel
    Ignored
    says:

    colewd: The issue is the total cascade of events leading to cancer not just the initial shove or some effect in the middle of the causal chain. To get cancer you need the following.

    You are clearly not talking about nucleotide sequences any more. Where is the information encoded if not in the genome?

  21. colewd
    Ignored
    says:

    Corneel,

    You are clearly not talking about nucleotide sequences any more. Where is the information encoded if not in the genome?

    I am not sure I understand your question. Genes are clearly involved in all the process I mentioned however not exclusively.

  22. DNA_Jock
    Ignored
    says:

    colewd: To get cancer you need the following.
    -Replication of cancer stem cells
    -Disabling of DNA repair
    -Disabling of apoptosis
    -Up regulation of vascular growth
    -Down regulation of immune response
    -Disabling or protein destruction

    Well, I’m not sure what “cancer stem cells” are, but I will happily stipulate that “To get cancer, you need cancer cells replicating.” Not really news, that.
    As to the rest, you are incorrect, in some cases rather obviously so.
    By way of illustration, Rupert’s cancer does involve “disabling of apoptosis”, but it does not need “up regulation of vascular growth”, and actually has elevated DNA repair mechanisms.
    Any thoughts on Rupert’s FI?

  23. Corneel Corneel
    Ignored
    says:

    colewd: I think a better argument is that cancer is the cell not functioning properly as it degrades the overall function of the organism. Kirk Durston made a solid argument that cancer is a loss of functional information as in his example it takes less specificity of p53 for cancer then from normal cellular function including apoptosis.

    Sorry for the necromancing, but I noticed that you have consulted the oracle at UD, and that he confirmed what everybody has been telling you: cancer is associated with an increase in FI where your function is the growth rate of cancer cells (or something along those lines).

    Did this enlightening insight in any way affect your judgment of Kirk Durston’s refusal to accept that cancer involved a gain of functional information?

  24. DNA_Jock
    Ignored
    says:

    I had not seen gpuccio’s opining on FI and cancer. Thank you, Corneel, for the link.
    I guess he doesn’t realize that he just gave away the store. Bcr-Abl fits all the criteria for a massive undesigned injection of FI into the genome. It is only when you discover its provenance that the IDist will declare that it doesn’t count. This is problematic for a test that is supposed to detect provenance.
    So much for FI then.

  25. Mung Mung
    Ignored
    says:

    DNA_Jock: So much for FI then.

    That still leaves FEE, FO and FUM.

  26. colewd
    Ignored
    says:

    DNA_Jock,

    I guess he doesn’t realize that he just gave away the store. Bcr-Abl fits all the criteria for a massive undesigned injection of FI into the genome.

    If you define loss of cell regulation as function.

  27. DNA_Jock
    Ignored
    says:

    colewd: If you define loss of cell regulation as function.

    Which gpuccio does:

    I think that some in the ID fiels seem to believe that functions have to be “good”. That is not true. Functions are often “bad”. The simple functions that arise in cancer cells are certainly bad for the organisms, but they still are functions, and they arise from random events.

    That was Corneel’s point in linking to gpuccio’s comment.

  28. colewd
    Ignored
    says:

    DNA_Jock,

    The reality is the cell is using information it already has no matter how you define function. There really is no argument here but if anyone can create one out of thin air its you 🙂

  29. Corneel Corneel
    Ignored
    says:

    colewd,

    Very interesting. Thanks for replying, Bill.

    But the reality is that two people you hold in high regard produced clearly contradictory statements. Let us for a moment accept that the cell is using “pre-existing information” (which is nonsense, because completely novel arrangements are produced, such as the fusion protein that DNA_Jock alludes to). Then still gpuccio and Kirk Durston espouse two mutually exclusive viewpoints:

    – gpuccio (correctly IMO) identified carcinogenic mutations as gains in FI with function defined as contributing to the persistence and profileration of cancer cells.
    – That collides head-on with Kirk Durston’s refusal to accept that the loss of p53 protein function qualifies as an increase in FI.

    In my mind, you need to weigh the strength of both arguments and choose one side, declaring the other nonsensical. Since you seem to rely quite heavily on the pronouncements of authoritative persons, I am very interested how this psychological experiment turns out 😉

  30. colewd
    Ignored
    says:

    Corneel,

    But the reality is that two people you hold in high regard produced clearly contradictory statements.

    Taken out of context maybe but in reality they did not contradict each other. Gpuccio was making a general theoretical claim and Kirk a specific claim. If you look at specific claims and understand the cancer mechanisms they fall toward the empirical argument Kirk made based on P53 mutation and disabling apoptosis. The apoptosis mechanism already existed in the cells and mutations leading to cancer simply disabled it.

  31. colewd
    Ignored
    says:

    Corneel,

    – gpuccio (correctly IMO) identified carcinogenic mutations as gains in FI with function defined as contributing to the persistence and profileration of cancer cells.

    This is a theoretical construct as when you look at specific examples of why cell division elevates the mutations are loss of function. Could cancer theoretically create a couple of functional gain mutations, sure, but there is no evidence I am aware of it has. I was hoping Jock would pull a rabbit out of his hat 🙂

  32. DNA_Jock
    Ignored
    says:

    Bluster and ignorance is rarely a compelling argument, Bill. Here’s your rabbit.
    In this thread, I have already pointed you to [“Rupert’s”] Bcr-Abl more than once, and asking you whether you view it as an increase or decrease in FI (and asking you to justify your answer…)
    I’ll add EML4-ALK to the list. Same questions.
    EGFR variant III, OTOH, looks like a loss-of-function to me. What do you think? Why?

    In all cases, gpuccio reckons these can be viewed as increases in FI, and Kirk insists that they cannot.
    E4Rupert

  33. colewd
    Ignored
    says:

    DNA_Jock,

    In all cases, gpuccio reckons these can be viewed as increases in FI, and Kirk insists that they cannot.
    E4Rupert

    Again, Kirk is making a specific claim gpuccio is not. If you want to claim that the cancerous protein you identified is creating new FI go for it but this is a detailed argument that will take lots of research. The first basic question is how the mutation identified is initiating elevated cell division in a mature cell. I will look again and see if this question has been studied. If not you need a new rabbit 🙂

  34. DNA_Jock
    Ignored
    says:

    No, Bill.
    As I explained to you previously, any of these mutations can be viewed as an increase, or as a decrease, in FI, depending on the definition of ‘function’ that the individual choses.
    Separately (and also explained to you), claiming that these changes in FI cause any cancer is a category error.

  35. colewd
    Ignored
    says:

    DNA_Jock,

    No, Bill.
    As I explained to you previously, any of these mutations can be viewed as an increase, or as a decrease, in FI, depending on the definition of ‘function’ that the individual choses.
    Separately (and also explained to you), claiming that these changes in FI cause any cancer is a category error.

    Yes, you have made these assertions yet your arguments are not ready for prime time.

    What do you mean by a “cause of any cancer is a category error”? Who created the standard here?

    BTW what appears to be going on is the merger of the two genes you have identified are causing the cell cycle gene BCR to be caught in the on position. So how would you position this as a gain of FI given the white blood cell has lost regulation?

  36. Mung Mung
    Ignored
    says:

    Corneel: But the reality is that two people you hold in high regard produced clearly contradictory statements.

    Clearly they are not using the same definition of “function” and FI depends on how you define function. So there’s nothing contradictory about it.

    ETA:

    DNA_Jock: As I explained to you previously, any of these mutations can be viewed as an increase, or as a decrease, in FI, depending on the definition of ‘function’ that the individual choses.

    Precisely.

  37. Corneel Corneel
    Ignored
    says:

    Mung: Clearly they are not using the same definition of “function” and FI depends on how you define function. So there’s nothing contradictory about it.

    gpuccio acknowledged that the FI in cancer could be viewed as either increasing or decreasing, depending on what you decide to be the function. In the functional information thread @PS, Kirk Durston (like Bill) was incapable of seeing that the loss of p53 function could be interpreted as an increase in the FI of a cancer cell.

    Those are definitely contradictory statements, Mung.

  38. colewd
    Ignored
    says:

    Corneel,

    Kirk Durston (like Bill) was incapable of seeing that the loss of p53 function could be interpreted as an increase in the FI of a cancer cell.

    He demonstrated this based on loss off specificity of sequence which is germane to the FI definition. In the case of cancer sequence specificity was less critical then in the healthy cell for P53. Can you make argument here that challenges Kirk’s math?

    In all the cases Jock has brought we see loss of cell regulation due to receptor proteins stuck in the on position vs being regulated by ligands. How can you argue that loss of regulation is a gain of function? Even from the cancer perspective (rapid cell division is good) if the specificity is lost then FI is lost.

  39. DNA_Jock
    Ignored
    says:

    Good grief, colewd, I have already explained this to you on this thread!
    If we define function as “promotes cell division” (and Corneel and gpuccio agree with me that we can) then loss of function of p53 represents an increase in FI.
    BY DEFINITION.

    …whether any given oncogenic mutation represents an increase or decrease in Hazen’s functional information would depend on how you, the investigator, have decided to define “function”.

    and

    If you invert the ranking order (and you always can, by changing how you define “function”) then increases in FI become decreases, and vice versa, by definition.

    [Emphasis in original]

  40. DNA_Jock
    Ignored
    says:

    For completeness, here is my illustration of why you cannot claim that the cancer is due to the change in FI.

  41. colewd
    Ignored
    says:

    colewd,

    Good grief, colewd, I have already explained this to you on this thread!

    Have considered the possibility that you explanation could be wrong?

    If we define function as “promotes cell division” (and Corneel and gpuccio agree with me that we can) then loss of function of p53 represents an increase in FI.

    I agree in this strict definition this is possible. So what?

    Does it take more functional information to operate a normal cell or a cancer cell. The answer is a normal cell and that is what is critical. You can lose functional information of a normal cell and form a cancer cell starting from a normal cell.

    Corneel’s error is that Kirk was defining function not as speed of cell division but as P53 function.

  42. DNA_Jock
    Ignored
    says:

    Does it take more functional information to operate a normal cell or a cancer cell. The answer is a normal cell and that is what is critical. You can lose functional information of a normal cell and form a cancer cell starting from a normal cell.

    Lovely, Bill.

    And, as promised, here is my follow-up question:
    Ubj pna lbh fubj gung lbhe qrsvavgvba bs /abezny/ vf bowrpgvirL
    rot13 –>
    How can you show that your definition of “normal” is objective?
    🙂

  43. DNA_Jock
    Ignored
    says:

    colewd: Corneel’s error is that Kirk was defining function not as speed of cell division but as P53 function.

    No, silly. Kirk’s error was to refuse to see that Kirk’s definition of function was NOT the only one possible, as gpuccio (and now, belatedly, you) recognize.
    One man’s increase is another man’s decrease.

  44. colewd
    Ignored
    says:

    DNA_Jock,

    How can you show that your definition of “normal” is objective?

    It can go from a zygote to a mature human on its own. Kicks ass over a cancer cell 🙂

  45. colewd
    Ignored
    says:

    DNA_Jock,

    No, silly. Kirk’s error was to refuse to see that Kirk’s definition of function was NOT the only one possible, as gpuccio (and now, belatedly, you) recognize.

    Straw man alert 🙂 You have to fn kidding me if you don’t think Kirk realizes this.

  46. DNA_Jock
    Ignored
    says:

    Really? Kirk seemed pretty resistant to the idea that cancer might be associated with an increase in FI when JS and J Mercer were wiping the floor with him on Peaceful Science.

    Your definition of ‘normal’ seems rather subjective, and your estimation of what a zygote can do “on its own” seems rather optimistic.

    😮

  47. OMagain
    Ignored
    says:

    colewd: I agree in this strict definition this is possible. So what?

    Heh.

  48. Corneel Corneel
    Ignored
    says:

    colewd: You have to fn kidding me if you don’t think Kirk realizes this.

    Let’s replay that part, shall we?

    Functional information for non-functional p53 domain:

    Here, it is critical to clearly define what the function is that determines whether a sequence is functional or not. There are three perspectives we will take: a) relative to an intelligent observer, b) relative to the normal, physical p53 function c) relative to a cancerous cell. Looking at the attached data, we observe that site 180 permits only one, specific amino acid, arginine. Let us suppose that it is mutated to something else, thereby inactivating p53 so that it can no longer perform it’s function. The mutated sequence falls into the set of sequences that are non-functional relative to the normal function. Let us use the extreme lower limit of 123 bits for a functional p53 domain.

    [snip]

    c) relative to a cancerous cell: There are three possibilities relative to the physical system of a cancerous cell, setting subjective “meaning” aside.

    If p53 is still functional relative to it’s normal physical function, then the FI = 123 bits.

    If p53 is non-functional relative to it’s normal physical function, then FI is 0 bits.

    If p53 is non-functional relative to it’s normal function but has a new function to do with cancer, then we need to have some way of determining what sequences satisfy that new function, before we can estimate FI. If non-functional p53 is simply a “bystander” in a cancerous cell (i.e., doesn’t do anything), then without a function, by definition, a system has no FI. FI is contingent on a specified function. If we wish to arbitrarily say that being a “bystander” is a function, then we must realize we are no longer talking about any function required by the physical system … the system does not require “bystanders”. We are now talking about an arbitrary, subjective function that we have invented in our minds. We can still estimate FI in that context, but it no longer has anything to do with biology.

    [emphasis mine]

    I sense some perspective missing here, don’t you?
    “No, removing that wheel clamp from your car will not affect its speed, because then it doesn’t DO anything, you know”.

  49. colewd
    Ignored
    says:

    Corneel,

    I sense some perspective missing here, don’t you?
    “No, removing that wheel clamp from your car will not affect its speed, because then it doesn’t DO anything, you know”.

    From the perspective of the car it does something but not from the perspective of the wheel clamp as it goes from active to inactive. Again, Kirk’s analysis was from the perspective of P53’s function.

  50. colewd
    Ignored
    says:

    DNA_Jock,

    Your definition of ‘normal’ seems rather subjective, and your estimation of what a zygote can do “on its own” seems rather optimistic.

    It will win the race every time over a cancerous Zygote.:-) Most the world will accept an objective explanation of how a “normal” cell behaves and a cancerous cell will miss the cut.

    All kidding aside thanks for the two citations they are very valuable.

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