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

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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 thoughts on “Eric Holloway needs our help (new post at Panda’s Thumb)”

  1. colewd: 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.

    But he was asked to take the perspective of the car (the cancer cell).Yet he was incapable of seeing it like that, just like you are.

  2. colewd: Most the world will accept an objective explanation of how a “normal” cell behaves and a cancerous cell will miss the cut.

    For all you know cancer is actually the goal of the universe. Perhaps your intelligent designer wanted a cancer universe.

  3. colewd: Again, Kirk’s analysis was from the perspective of P53’s function.

    He’s not allowed to use just any old definition of the function he wants to, especially if it conflicts with how someone else defines the function.

  4. No, Mung, you have missed the point. We have covered this already.
    Kirk IS allowed to use just any old definition of function he wants to. So is Corneel, or J Mercer, or you or me.
    Kirk is refusing to countenance anybody else’s definitions of function. And the reason he is behaving in this way is because he-who-defines-the-function also gets to decide whether FI was increased or decreased, making Kirk’s arguments utterly subjective.
    Did you follow the ass-kicking that JS and JM gave Kirk at PeacefulScience?

  5. DNA_Jock: Kirk IS allowed to use just any old definition of function he wants to. So is Corneel, or J Mercer, or you or me.

    Yes, I know. I was among the first (if not the first) to point this out here at TSZ.

    DNA_Jock: Did you follow the ass-kicking that JS and JM gave Kirk at PeacefulScience?

    I’ve been following the thread.

  6. Corneel,

    But he was asked to take the perspective of the car (the cancer cell).Yet he was incapable of seeing it like that, just like you are.

    He was looking at it from the perspective of one of the most important single proteins implicated in cancer. Functional information introduced by Hazen and Szostak was put forth as a measure of the amount of functional sequences as a ratio of the total sequence space that perform a defined function. “Cancer” is not specific enough to measure it where an oncoprotein like P53 is.

  7. DNA_Jock,

    Kirk is refusing to countenance anybody else’s definitions of function.

    Jock, wake up and smell the coffee. Kirk was the only one in the discussion capable of finding a measurable protein to bring to the discussion. The opposition simple needed a counter example.

  8. Mung,

    He’s not allowed to use just any old definition of the function he wants to, especially if it conflicts with how someone else defines the function.

    JS simply needed a counter example. The counter example needs to be specific enough to measure with some empirical backup. Without measurement how do you determine gain of loss?

  9. colewd: “Cancer” is not specific enough to measure it where an oncoprotein like P53 is.

    Listen to your master’s voice, Bill

    There can be no doubt at all that the mutations in cancer cells are at the expense of the general functionality of the organism.

    But it is also true that they can be defined as “locally functional” for the cell where they arise.

    As you certainly know, my approcah to the definition of FI requires that any possible function can be accepted. If a function, any function, can be explicitly defined, we can measure the FI linked to it.

    So the cancer cell can acquire indipendence from the controls of the organism, sometimes a higher reproduction rate, and so on. When we start anticancer therapy, some cancer cells can acquire resistance, exactly as bacteria become resistant to antibiotics.

    Now, it seems rather certain that mutations in cancer cells are random events. Indeed, cancer cells, for their own nature, are mor subject to mutation than normal cells. Much more, in many cases.

    So, even if the mutation in cancer cells are always at the expense of the higher funtions of the organism, still those mutations can be said to implement local functions in the cells.

  10. Corneel,

    What does that say about FI increasing or decreasing? Maybe if cancer is decreasing function of the overall organism thats all that matters.

  11. colewd: Maybe if cancer is decreasing function of the overall organism thats all that matters.

    And there is is! Yes, I had already guessed that is what you and Kirk think.

    But whereas it may be all that matters to you, anyone involved in cancer research (like John Mercer) is bound to disagree. This is what makes Kirk’s argument utterly subjective and therefore ultimately unconvincing. See?

    ETA: It is interesting that gpuccio had no issue with assuming the perspective of the cancer cell. Perhaps that has to do with his medical training?

  12. Corneel,

    But whereas it may be all that matters to you, anyone involved in cancer research

    I am involved in cancer research and don’t see the value at this point as all the cases I have studied look like Kirks model. Over time if you can make the case that cancer FI is anything more then loss of functional FI in a non cancer cell I would be interested. I will re look at the posts and see if John brought any points that support this claim.

  13. Corneel,

    I have a mouse with a murine leukemia virus (MuLV) provirus (retroviral genome integrated into the host chromosome). That provirus has a single-base mutation that prevents it from being infectious. If that inactivating mutation is reverted, the virus activates, replicates, and starts carcinogenesis.

    This is an interesting case study John pointed to in the Kirk/Josh discussion. The question is how does carcinogenesis start? It may start from up regulation of the immune system. In this case there is a loss of function because the immune system is ligand regulated. It could also be affecting another pathway initiating cell division and cancer stem cell production. The answer is in the detail and I will take a look at this as it may support your point along with gpuccio’s.

  15. DNA_Jock,

    Research on blood levels of vitamin d and cancer. Researching biochemical pathways to determine the mechanisms. Working with the epidemiologist who discovered the correlation in 1980. I have come up with a tentative hypothesis for cancer which is up regulation of embryo pathways. You’re citing may have falsified it so it was very valuable. I was about to take leukemia out of the hypothesis until I found the mutation you identified also activated the pathway vitamin d was regulating. Cancer is a very broad subject yet researchers generally have very narrow focus. One guy I met spent his entire career on P53.

  16. Sorry, Bill, you misunderstood my question. I was not asking what your area of interest was — I was already aware of your interest in vitamin D. I was asking in what capacity are you involved in cancer research. Are you, by profession, a clinical researcher, an oncologist, a pre-clinical researcher, bioinformaticist, statistician, or some other role? What relevant post-graduate qualifications do you have? Put another way, who pays you to conduct cancer research – the NIH, NSF, Mayo, Kaiser, a pharmaceutical company, etc.? Or are you an enthusiastic amateur?

  17. DNA_Jock,

    I am a volunteer researcher specifically collaborating with a retired professor. My business is private equity investing.

  18. colewd: It may start from up regulation of the immune system. In this case there is a loss of function because the immune system is ligand regulated. It could also be affecting another pathway initiating cell division and cancer stem cell production.

    “may”, “could also be”. Sitting on that fence must be hurting by now?

    It’s funny but if the body really were designed we’d already know all the answers to these questions. That we have to pick through a nested mess of madness to determine the simplest thing about how biology works demonstrates it was not the product of conscious design.

    As you like analogies so much, here is one. Computer code designed by good programmers is structured, ordered and clean. You can learn how it works by read the tests alone or even just the code itself. You don’t need a manual, the code is the manual. Comments are not even necessary if the code is good enough.

    Computer code that we have instead evolved to solve a specific problem cannot be understood by a human once it has been generated. Of course, we can understand the smallest pieces but how it all interacts is usually a mystery. We can only hope it continues to work in the future as it did in the past if we choose to put it into use.

    When we look at biology and how it works what do you see? What of those two setups is closest to what we observe in biology?

  19. OMagain,

    It’s funny but if the body really were designed we’d already know all the answers to these questions. That we have to pick through a nested mess of madness to determine the simplest thing about how biology works demonstrates it was not the product of conscious design.

    You don’t have a human design that can self replicate, provide its own energy and has consciousness. If you understand some of the working of the cell you would realize the “design” is quite elegant for what it has to do. Have you looked at gpuccio’s article on the ubiquitin system?

    The Ubiquitin System: Functional Complexity and Semiosis joined together.

  20. OMagain: Computer code that we have instead evolved to solve a specific problem cannot be understood by a human once it has been generated. Of course, we can understand the smallest pieces but how it all interacts is usually a mystery. We can only hope it continues to work in the future as it did in the past if we choose to put it into use.

    My favorite example of evolved code is the tone discriminator circuit that only works on the particular cpu on which it evolved. Because, even though the code is digital, it depends on timing quirks in that particular piece of hardware. My own guess is that some of the circuit traces act as a tuned resonant circuit, but I haven’t seen this hypothesis published. We do know that there are necessary circuits that don’t partake in the code execution.

  21. colewd: You don’t have a human design that can self replicate, provide its own energy and has consciousness.

    You are right. That’s a knock-out punch right there. I guess we should all stop using arguments by analogy to human design, then.
    Heh.

    If you understand some of the working of the cell you would realize the “design” is quite elegant for what it has to do. Have you looked at gpuccio’s article on the ubiquitin system?

    I will concede that lambda is pretty bloody elegant. Eukaryotic cells, not so much. They absolutely reek of something that was cobbled together by a bunch of Lokis.
    There’s a famous joke about Francis Crick, the imaginal disc, and God that’s apposite here.
    P.S. thanks for the clarification re your research role. Makes sense.

  22. colewd: You don’t have a human design that can self replicate, provide its own energy and has consciousness.

    So it’s your claim that those things can only be done with extremely messy code? On what basis?

    colewd: If you understand some of the working of the cell you would realize the “design” is quite elegant for what it has to do.

    Why is “design” in quotes?

    colewd: Have you looked at gpuccio’s article on the ubiquitin system?

    Why, does it address my point that I’ve specifically asked you? Does what we see in biology look designed as we do design or evolved, as we get when we evolve code?

  24. OMagain,

    So it’s your claim that those things can only be done with extremely messy code? On what basis?

    This is not my claim.

    Why is “design” in quotes?

    Out of respecting your different opinion.

    Why, does it address my point that I’ve specifically asked you? Does what we see in biology look designed as we do design or evolved, as we get when we evolve code?

    The ubiquitin system is a quite elegant at controlling cell processes. The article is worth reading. Gpuccio’s method is a reasonable read for a very complex subject.

  25. DNA_Jock,

    You are right. That’s a knock-out punch right there. I guess we should all stop using arguments by analogy to human design, then.

    Why don’t we just take complexity of function into account.

  26. colewd: The ubiquitin system is a quite elegant at controlling cell processes.

    You are cherry picking here, you just can’t bring yourself to admit it. It’s OK, I understand.

    colewd: The article is worth reading.

    If it’s worth reading it’s worth publishing. Peer reviewed evidence for ID is thin on the ground.

    colewd: Gpuccio’s method is a reasonable read for a very complex subject.

    And a good distraction from the point you are unable to address. Biology is unlike what we’d expect a designer like the designers we are familiar with to create. It is more alike the mess we create when we evolve code.

    No doubt in evolved code there are components we could call elegant, were we to seperate them out from the morass. Yet you separate out the odd biological component from the mess and point at it and claim “design” and ignore the vast bulk left behind.

    Why?

    Actually, I already know the answer and so do you.

  27. colewd: This is not my claim.

    It is your claim. Although you never directly state it.

    colewd: You don’t have a human design that can self replicate, provide its own energy and has consciousness. If you understand some of the working of the cell you would realize the “design” is quite elegant for what it has to do.

    You will not address the point that biology is messy. You indirectly address it by seemingly admitting that it’s messy but it’s as messy as it needs to be to do it’s work. Despite the mess it’s “quite elegant” for what it has to do. That’s what you are saying here, that if I had a human design that could self replicate etc, we’d expect it to be messy too.

    colewd: Out of respecting your different opinion.

    First time for everything I suppose. Even when you are wrong you refuse to admit it without being raked over the coals (to wit, the precursor to C). That’s not respecting a different opinion. That’s winning at all costs, even at the cost of your own integrity.

  28. colewd: I am involved in cancer research and don’t see the value at this point as all the cases I have studied look like Kirks model. Over time if you can make the case that cancer FI is anything more then loss of functional FI in a non cancer cell I would be interested. I will re look at the posts and see if John brought any points that support this claim.

    Ach, now you mention it I recall you mentioning this previously. Must have slipped my mind, apologies.

    But if you don’t mind me saying so, your inability to see the constant selection pressure on cancer cells to escape the organisms control mechanisms will leave you severely handicapped in this line of work. In any patient, you may find several tumor cell lineages accumulating novel mutations that will allow them to evade the immune system or progress to malignancy. Many of those mutations are recurrent in different patients. In my view, you simply lack the framework to make sense of that.

  29. Corneel: But if you don’t mind me saying so, your inability to see the constant selection pressure on cancer cells to escape the organisms control mechanisms will leave you severely handicapped in this line of work.

    See Bill, you need to think more like a teleologist and less like an evolutionist.

  30. Corneel,

    But if you don’t mind me saying so, your inability to see the constant selection pressure on cancer cells to escape the organisms control mechanisms will leave you severely handicapped in this line of work. In any patient, you may find several tumor cell lineages accumulating novel mutations that will allow them to evade the immune system or progress to malignancy. Many of those mutations are recurrent in different patients. In my view, you simply lack the framework to make sense of that.

    A recent nobel prize was awarded for identification of the proteins responsible for down regulating the immune system in cancer. These proteins CDLA-4 and PD1 are generated when the WNT/Beta catenin pathway is up regulated. The cause of this up regulation in mature cells can be mutation to a protein in the pathway which disables the destruction mechanism of beta/catenin (part of the ubiquitin system) or low vitamin d (modified version) levels in the cell which up regulates the destruction mechanism by inhibiting WNT ligand binding. I think that arguing a gain of FI here is difficult but what I am interested in is any case where FI is being generated by cancer. Here is a short video that explains how the WNT/Beta catenin pathway works.
    https://youtu.beNGVP4J9jpgs
    I do think that the adaptive immune system is capable of generating FI but limited amounts.

  31. Mung: See Bill, you need to think more like a teleologist and less like an evolutionist.

    That might actually work, but what Designer would want to create a really efficient cancer?

  33. Corneel: That might actually work, but what Designer would want to create a really efficient cancer?

    The kind that wants to avoid arguments of the sort that go like this:

    Just look at how inefficient and poorly designed that cancer is. What sort of incompetent designer would design a cancer like that?

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