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Topic: Jonathan Wells: Using Intelligent Design Theory to Guide Scientific Research
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posted 13. May 2004 21:04
Using Intelligent Design Theory to Guide Scientific Research
by Jonathan Wells
Abstract: Intelligent Design theory (ID) can contribute to science on at least two levels. On one level, ID is concerned with inferring from the evidence whether a given feature of the world is designed. This is the level on which William Dembski's explanatory filter and Michael Behe's concept of irreducible complexity operate. It is also the level that has received the most attention in recent years, largely because the existence of even one intelligently designed feature in living things (at least prior to human beings) would overturn the Darwinian theory of evolution that currently dominates Western biology.
On another level, ID could function as a "metatheory," providing a conceptual framework for scientific research. By suggesting testable hypotheses about features of the world that have been systematically neglected by older metatheories (such as Darwin's), and by leading to the discovery of new features, ID could indirectly demonstrate its scientific fruitfulness.
To read the entire paper, click here.
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charlie d.
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posted 17. May 2004 14:23
I may have some comments, but first I would need to ask a few questions. Is Jonathan Wells going to be around to answer? I've never seen him around here, that I remember.
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andyg
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posted 17. May 2004 18:48
quote:
Take, for example, research on the vast regions of vertebrate genomes that do not code for proteins. From a neo-Darwinian perspective, DNA mutations can provide the raw materials for evolution because DNA encodes proteins that determine the essential features of organisms. Since non-coding regions do not produce proteins, Darwinian biologists have been dismissing them for decades as random evolutionary noise or "junk DNA." From an ID perspective, however,
it is extremely unlikely that an organism would expend its resources on preserving and transmitting so much "junk." It is much more likely that noncoding regions have functions that we simply haven't discovered yet. Recent research shows that "junk DNA" does, indeed, have previously unsuspected functions. Although that research was done in a Darwinian framework, its results came as a complete surprise to people trying to ask Darwinian research questions. The fact that "junk DNA" is not junk has emerged not because of evolutionary theory but in spite of it. On the other hand, people asking research questions in an ID framework would presumably have been looking for the functions of non-coding regions of DNA all along, and we might now know considerably more about them.
I would like to propose a moratorium on criticism of the concept of "Junk DNA", as it is misused in discussions almost as frequently as criticisms of terms like "gill slits" and "survival of the fittest". Whoever came up with the term should have been locked in a metal box with duct tape over their mouth.
It was known even before the term was coined that many regions of non-coding DNA are functional, the most obvious examples being promoter and enhancer sequences. It is also clear that much non-coding DNA has the appearance of former coding regions that have been duplicated and inactivated by retroviral insertion and recombination, and whose composition fits that which would be predicted by genetic drift. Howard Hershey recently wrote a nice short article on this.
Howard Hershey Article
In a related article, Stephen Schaffner reported from the recent genomics meeting at Cold Spring Harbor that deletion of "gene deserts" in mice - some of which contain over a thousand regions of non-coding DNA conserved across vertebrates - has no apparent effect. If these regions did have function, it is clearly redundant.
In summary, it is clear that some regions of non-coding DNA does have function (and this has been known for a long time), that other regions of non-coding DNA appear dispensable, and finally, that to label something as non-functional is necessarily provisional and therefore hopelessly presumptuous. Attacking the term "junk DNA" in a critique of evolutionary biology is dangerously close to a straw man argument.
Andy
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posted 19. May 2004 18:43
Jonathan Wells has agreed to engage in occasional (what I told him would be) sincere, civil
critics of his article.
This will not be the standard "post and run" fare that has plagued Brainstorms in the past. So, charlie d., you are free to post your critique and can expect to receive a response from Wells.
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charlie d.
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posted 19. May 2004 20:16
Thanks. I'll try to play nice. ![[Wink]](wink.gif)
My comments have not much to do with the "centriolar turbine" hypothesis, since I am no biophysicist. Most of my questions have to do with Wells' statement about cancer, which is the ultimately the key question Wells thinks his TOPS approach and the "turbine hypothesis" can shed light onto.
Wells says that one of the ID implications that are assumed as true by TOPS is quote:
... that cancer originates in higher structural features of the cell rather than in its DNA...
However, when discussing the implications of his hypothesis to cancer, Wells says quote:
If centrioles generate a polar ejection force, the presence of too many centriole pairs at either pole could result in an excessive polar ejection force that subjects chromosomes to unusual stresses that cause breaks and translocations.
This is indeed, AFAIK, the assumption most scientists who study the role of centrosome defects and cancer are working under. However, the idea there is that DNA breaks and translocations are then the direct, immediate cause of cancer (in the sense of deregulation of the cell cycle and survival genetic programs) through several well-known mechanisms of oncogene activation (deregulation, activating point mutations, amplification etc), or tumor suppressor gene inactivation (mostly crippling mutations and deletion). If TOPS assumes that these DNA defects do not in fact play a causative role in cancer, what other pathogenetic mechanisms does Wells propose for chromosome breaks and translocations? I just can't imagine any that are not DNA mutation-related.
The second question deals with the causes of the centrosome defects themselves. Assuming that centrosome defects are the primary cause of cancer, as proposed by Wells, the hypothesis still does not address what the ultimate cause is. We know gene mutations occur all the time, spontaneously, so no new mechanisms have to be postulated in that case. Indeed, as far as I understand it, most scientists working of the centrosome-cancer link envision that these defects originate back in mutations of genes involved in centrosome biogenesis and regulation (basically, that the primary cause would still be mutations, but then centrosome defects would generate genetic instability and accelerate the process). How does Wells envision centrosome defects arise, if not genetically?
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Rex Kerr
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posted 21. May 2004 03:33
I am also not a biophysicist, but I am close. Since Wells' hypothesis is a biophysical one, I wonder whether he has done at least order-of-magnitude calculations to see if the mechanism is feasible? A diagram of the wobble would be nice to see, also. I can't quite envision how it would work mechanically--what exactly is moving and what is fixed? What are the forces involved?
There are a number of considerations that Wells' may wish to treat in greater detail (or maybe he already has). For example, how do you keep a nanobubble from dissolving into the surrounding fluid? Even with nanobubbles, there will be significant friction because of the viscosity of the fluid--how much is this? What is the energy cost of maintaining 10kHz revolutions? Is a force five times stronger than gravity enough to move anything significant inside a cell or do any damage?
In any case, my main comment is that I would like to see a more thorough treatment of the biophysics. If a clear diagram is provided, I can even provide a few of the calculations one might want to make.
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Jonathan Wells
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posted 22. May 2004 08:41
Concerning my hypothesis that centrioles generate the polar ejection force (PEF) and that an excessive PEF causes chromosomal instability, Charlie D. writes:
quote:
This is indeed, AFAIK, the assumption most scientists who study the role of centrosome defects and cancer are working under.
I am not aware that anyone has previously proposed a link between (a) centrioles and PEF, or (b) excessive PEF and cancer. Although the correlations between abnormal centrosomes and chromosomal instability (CIN) and between CIN and carcinogenesis are well established, I haven't seen any suggestions in the literature that these correlations are due to abnormal centrioles and excessive PEF.
Charlie D. also writes:
quote:
DNA breaks and translocations are then the direct, immediate cause of cancer (in the sense of deregulation of the cell cycle and survival genetic programs) through several well-known mechanisms of oncogene activation (deregulation, activating point mutations, amplification etc), or tumor suppressor gene inactivation (mostly crippling mutations and deletion). If TOPS assumes that these DNA defects do not in fact play a causative role in cancer, what other pathogenetic mechanisms does Wells propose for chromosome breaks and translocations?
I agree that CIN leads to various DNA defects that play a role in carcinogenesis. Other investigators have noted that there is no consistent pattern in such DNA defects (i.e., they vary from one type of cancer to another, and sometimes from one tumor to another of the same type in a different individual). Those investigators did not conclude that DNA defects are irrelevant, but only that CIN is the common denominator in carcinogenesis. I agree. Cancer is a complex disease, and there are surely many factors at work at various stages of the disease. My hypothesis is not about the downstream DNA defects, which everyone agrees are involved in disease progression, but only about how centrosomes might cause the CIN that apparently underlies those defects.
Finally, Charlie D. writes:
quote:
The second question deals with the causes of the centrosome defects themselves. Assuming that centrosome defects are the primary cause of cancer, as proposed by Wells, the hypothesis still does not address what the ultimate cause is.
That's correct. In fact, many causes might contribute to centrosome defects. One of those might be DNA mutations, as Charlie D. suggests; but there might also be other causes that are independent of DNA. For example, centrosomes are known to be sensitive to all kinds of intra- and extracellular stimuli; some of those might be known carcinogens such as smoke and asbestos. TOPS does not preclude a role for DNA mutations, but I would argue that by rejecting a neo-Darwinism-inspired overemphasis on DNA TOPS encourages scientists to see mutations as just one factor in the larger context of the cell and organism.
I might add that I am merely proposing a hypothesis. I am not arguing that I have disproved neo-Darwinism or shown that DNA-centered cancer research has no value. Even if the hypothesis turns out to be true, it will merely demonstrate the value of taking a different approach to solving a biomedical problem.
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charlie d.
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posted 23. May 2004 11:36
quote:
I am not aware that anyone has previously proposed a link between (a) centrioles and PEF, or (b) excessive PEF and cancer. Although the correlations between abnormal centrosomes and chromosomal instability (CIN) and between CIN and carcinogenesis are well established, I haven't seen any suggestions in the literature that these correlations are due to abnormal centrioles and excessive PEF.
Yes, I am not aware of anyone proposing PEF as a source of mutations either. I was referring more generally to the link between aneuploidy/chomosomal instability and genetic mutations leading to neoplastic transformation. quote:
I agree that CIN leads to various DNA defects that play a role in carcinogenesis. Other investigators have noted that there is no consistent pattern in such DNA defects (i.e., they vary from one type of cancer to another, and sometimes from one tumor to another of the same type in a different individual). Those investigators did not conclude that DNA defects are irrelevant, but only that CIN is the common denominator in carcinogenesis. I agree. Cancer is a complex disease, and there are surely many factors at work at various stages of the disease. My hypothesis is not about the downstream DNA defects, which everyone agrees are involved in disease progression, but only about how centrosomes might cause the CIN that apparently underlies those defects.
Sure, but nothing requires that any specific genetic defect be found in all cancers, or all cells in the same cancer. There are so many genes and genetic programs involved in cell proliferation control, it would be surprising to find otherwise. The fact that there is no consistent pattern of gene mutation in cancer is about as significant as the fact that that there is no consistent pattern of aneuploidy in cancer either - cancer is a progressive disease, which develops over time from the accumulation of multiple defects in a population of cells arising from a single original clone. Heterogeneity should be the norm in these instances - we know it is.
Personally, while I think it is entirely conceivable based on current knowledge, to propose neoplastic transformation without aneuploidy (indeed, there certainly is some evidence for this possibility), I can think of no model in which aneuploidy alone can cause transformation without first inducing gene mutations (amplification, overexpression, activating/inactivating mutations, gene fusions, etc). Thus, the proximate cause of neoplastic transformation is the alteration of genetic programs involved in cell cycle control. Whether the more distal causes inducing the necessary gene alterations are centriolar defects, aneuploidy, cosmic radiation, cigarette smoke or radon in the basement is important, but does not impinge on the basic theoretical model of cancer as a disease of somatic cell genetics.
I think even Peter Duesberg and his associates (the "investigators" you seem to be talking about - but why not give them public credit?) who are the staunchest proponents of this hypothesis, would agree with this. quote:
TOPS does not preclude a role for DNA mutations, but I would argue that by rejecting a neo-Darwinism-inspired overemphasis on DNA TOPS encourages scientists to see mutations as just one factor in the larger context of the cell and organism.
I might add that I am merely proposing a hypothesis. I am not arguing that I have disproved neo-Darwinism or shown that DNA-centered cancer research has no value. Even if the hypothesis turns out to be true, it will merely demonstrate the value of taking a different approach to solving a biomedical problem.
I appreciate you are just proposing a hypothesis, and I can only wish ID advocates would turn to this kind of activity much more often. I also agree that any scientist can find inspiration for their work wherever they please. Many great scientific ideas are the direct product of chemical intoxication, after all!
I also understand that you are not saying your hypothesis disproves neo-darwinism. However, you do specifically say that one of the implications of ID is that cancer originates somewhere else than DNA, that there is evidence that this is indeed the case, and that your hypothesis fits in this kind of new paradigm that has been disregarded by "darwinian" mainstream science (or something to that effect).
My argument here is that these claims are wrong. As I said, mutations are already known to originate from many different sources, radiation, chemical mutagens, chromosomal instability, etc; perhaps, as you propose, PEF may be one of these sources. Ultimately, however, it is DNA mutations (in their various forms) that cause cancer. Mainstream science has not disregarded these more distal causes either - carcinogenesis is an entire field of study dedicated to understanding precisely how mutations come about, from whatever source. Centrosome studies originated fully within the current paradigm.
Your hypothesis about how PEF is originated by centrioles could be entirely valid, again I am not equipped to judge it, but I am sure the reviewers of your actual paper will be. I just disagree with loading your legitimate hypothesis with over-interpretations. I am sure you did not do that in your mainstream manuscript, so why do it here? As is, much of the paper reads like a piece of advocacy, and the science in it almost as an afterthought. I don't think neither PCID nor your own hypothesis gain from this kind of approach.
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Evan
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posted 23. May 2004 15:03
I am not qualified at all to discuss the biological details of Dr. Wells’ hypothesis, and of course I support any ideas that might help us better understand the causes of cancer.
But I am interested in Wells’ discussion of the role that Intelligent Design Theory (IDT) played in producing this hypothesis. One of my continuing interests is understanding exactly what claims IDT makes, and understanding the extent to which it is metaphysics (and beyond scientific investigation) as opposed to being potentially an aspect of science itself. In his paper, Wells offers some thoughts on IDT as a “metatheory” that I would like to discuss.
Wells begins by distinguishing two aspects of ID. The first is the one that truly intersects with empirical science: “On one level, ID is concerned with inferring from the evidence whether a given feature of the world is designed.”
The second is the idea that adopting the view that the world is designed (without regard to whether the above inference has been empirically validated) can lead to useful and novel hypotheses that people working from other metatheories might not see.
quote:
On another level, ID could function as a "metatheory," providing a conceptual framework for scientific research. By suggesting testable hypotheses about features of the world that have been systematically neglected by older metatheories (such as Darwin's), and by leading to the discovery of new features, ID could indirectly demonstrate its scientific fruitfulness.
The question that immediately arises is this: does the “fruitfulness” of a metatheory actually bear, even indirectly, on the scientific validity of the theory implied by the metatheory? This is, does this second aspect of ID as a metatheory have anything at all with establishing the validity of the first aspect? This is the question I wish to address.
The assumptions of TOPS
Wells proposes a Theory of Organismal Problem-Solving (TOPS), which contains a number of provisional assumptions based on IDT;
quote:
(1) Darwinian evolution (the theory that new features of living things originate through natural selection acting on random variations) is false, and
(2) ID (the theory that many features of living things could only have originated through intelligent agency) is true.
While these are the two main premises of ID, I don’t see how this paper bears on them at all. However, I think we can understand a bit more why Wells thinks they are connected to this paper by looking at what Wells offers next:
quote:
TOPS then explicitly rejects several implications of Darwinian evolution. These include:
(1a) The implication that living things are best understood from the bottom up, in terms of their molecular constituents.
(1b) The implications that DNA mutations are the raw materials of macroevolution, that embryo development is controlled by a genetic program, that cancer is a genetic disease, etc.
(1c) The implication that many features of living things are useless vestiges of random processes, so it is a waste of time to inquire into their functions.
[Sidenote: I am not sure why Wells lumps all these statement under the category of “Darwinian” evolution. The phrase “Darwinian” evolution is such a loaded phrase that I would prefer to just refer to “the theory of evolution.”]
Let’s look at these three statements,
(1a) The theory of evolution implies that “living things are best understood from the bottom up, in terms of their molecular constituents.”
This is a general statement about all of science, not just biology and not just evolution. Furthermore, this is false. Sometimes scientists take a reductionist view and try to explain things form the bottom up: how do quarks make protons; how do protons, neutrons and electrons make atoms; how to molecules make cells, etc. But other times scientists work from the top down: how does the rain cycle work, how does an ecological system restore equilibrium, how do the parts of the body function as a more-or-less integrated whole.
Understanding how integrated system functions is a very important part of science. Science generally understands that things can be studied at many levels, and that properties emerge at higher levels that are certainly not obvious if one looks merely at the most basic constituent parts. For instance, in respect to human beings, many different holistic (or semi-holistic) lines of research are going on that look at the ways the body functions as an organized whole.
It is just not true that the theory of evolution, or biology in general, believes that “living things are best understood from the bottom up, in terms of their molecular constituents.”
I also understand that ID believes that this holistic functioning could not have arisen through natural evolutionary processes. But that is not the issue being addressed in Wells’ paper, and it is not reasonable to just take this as an implicit background assumption. Modern science does look at the integrated functioning of systems, and modern scientists do believe these systems evolved.
(1b) The theory of evolution implies that “that DNA mutations are the raw materials of macroevolution, that embryo development is controlled by a genetic program, that cancer is a genetic disease, etc.”
I am not qualified to discuss the details of genetics, but I do believe that our understanding of the complexities of how genes work and how they interact with their immediate environment is growing all the time, and Charlie has offered references to this. When Darwin first offered his theory, genes were unknown. When genes and DNA were first discovered, the first ideas were relatively simple ones about “one gene, one trait,” point mutations, and so on. Our understanding has grown since then.
And by whom has that work been done? Mainstream scientists. The details of macro-evolution, embryological development, and cancer are being studied by scientists who are willing to question our current understanding in light of new evidence. Irrespective of what “metatheory” they are inspired by, the work is done in terms of empirical investigation - how does this work? what happens in the world? A theory of “Darwinian” evolution does not hinder this. No one believes we understand it all right now, and therefore science progresses.
(1c) The theory of evolution implies that ”many features of living things are useless vestiges of random processes, so it is a waste of time to inquire into their functions.”
Similar considerations as in (1b)apply to this point. The theory of evolution does predict that there will be vestiges of the past in the present, and that some of them will no longer be functional. This does not mean that we might not learn that some things we thought were such non-functioning vestiges are in fact functioning in ways we didn’t understand. Hurray for science - that’s how it works. But it is not a compelling argument to claim that since scientists knew less in the past than they know now, their fundamental paradigm is wrong.
The point of these comments is to try to show that Wells has offered a false connection between the hypothesis which is the scientific heart of his paper and his belief that ID as a theory (as a opposed to a metatheory) is supported by his hypothesis. In my opinion, his misrepresentation of what he sees as elements of “Darwinian” evolution excessively color what he sees as the relevance to ID of the paper.
Chinese medicine
In order to make this point another way, I would like to give a different example.
Chinese medicine has an ancient metatheory about the body and health involving such ideas as energy channels, meridians, chakras, and so on; and they have had various practices based on these concepts, including acupuncture, massage, eating yin and yang foods, and so on.
In the past decades certain aspects of Chinese medicine have been shown to be effective even though they didn’t match the Western medicine paradigm, and certain concepts have been shown to correlate with hitherto unknown or at least under-appreciated parts of human physiology.
Here’s a specific example. Chinese medicine (as well as some psychiatric theories and Western alternative health practices) holds that memories are stored all over the body, and that repressed or painful memories are then shielded from expression by a type of tension or “body armor” that can be released, with beneficial consequences, by acupuncture and massage.
Now recently Scientific American had an article (April 2004) on research done with the glial cells that surround neurons. Glial cells were previously thought to be involved almost exclusively with cell maintenance functions. However the research showed that the relationship between glial cells and neurons was much more complicated and bi-directional. Among other things, the article points out that glial cells increase in proportion to neurons in more intelligent animals, and the article concludes by wondering whether memory and learning might be associated with and stored in the glial cells throughout the body.
This hypothesis is consistent with the concepts of Chinese medicine. Scientists working from a tradition of Chinese medicine would find this research compelling and could easily generate further hypotheses that might be more fruitful than those generated from a traditional Western brain- and neuron-based approach.
Does all this support the inference that Chinese metatheory is “true” in the sense that we “really” have energy channels and chakras and auras? Or is it “just” that the Chinese medicine paradigm is a fruitful metaphor that has enabled the Chinese to think about things without the detailed physiological knowledge that is now arising via science?
Of course there will be many who say that the Chinese paradigm is true - that we have an intangible and immaterial presence that coexists with the physical body, and so on. But as far as science is concerned, that is extra. One need not embrace that meta-theoretical paradigm in order to accept the science.
And how does this apply to ID?
I believe that the same considerations apply to ID as a metatheory (or for that matter, to many other metatheories including those posited by the world’s major religions.)
Approaching science as if things were designed (either in the overall laws present since the beginning of the universe or as emergent properties at various times since then) may be a fruitful paradigm by which to generate hypothesis for study, and it may be a personally satisfying metatheory for one to incorporate into one’s overall belief system. But that does not mean that the metatheory itself is affirmed just because it is consistent with (or even inspires) scientifically available evidence.
To be more specific: in this case, the fact that Wells believes his theory was inspired by an ID-oriented metatheory as opposed to his understanding of a “Darwinian” perspective does not add any scientific validity to his first aspect of ID: “On one level, ID is concerned with inferring from the evidence whether a given feature of the world is designed,” nor with his statements that "(1) Darwinian evolution (the theory that new features of living things originate through natural selection acting on random variations) is false, and (2) ID (the theory that many features of living things could only have originated through intelligent agency) is true.
His hypothesis, irrespective of whether it turns out to fruitful or not, does not bear on these statements about ID as a scientific theory.
[ 23. May 2004, 17:50: Message edited by: Evan ]
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Jonathan Wells
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posted 24. May 2004 13:08
Rex Kerr wrote:
quote:
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Since Wells' hypothesis is a biophysical one, I wonder whether he has done at least order-of-magnitude calculations to see if the mechanism is feasible? A diagram of the wobble would be nice to see, also. I can't quite envision how it would work mechanically -- what exactly is moving and what is fixed?
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The diagram and order-of-magnitude calculations are in the paper posted on May 13 at the beginning of this discussion. (A link to the PDF is provided in the initial posting.)
Rex Kerr also wrote:
quote:
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Is a force five times stronger than gravity enough to move anything significant inside a cell or do any damage?
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Good question. The PEF may work in conjunction with microtubule-associated motor proteins ("chromokinesins"), with the PEF acting primarily to bias movement away from the poles. If the hypothesis is true, then in cells about to undergo malignant transformation the PEF will increase after the onset of anaphase (since the centriolar turbines will fail to shut down), and the force will increase to much more than 5g.
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Charlie d. wrote:
quote:
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The proximate cause of neoplastic transformation is the alteration of genetic programs involved in cell cycle control. Whether the more distal causes inducing the necessary gene alterations are centriolar defects, aneuploidy, cosmic radiation, cigarette smoke or radon in the basement is important, but does not impinge on the basic theoretical model of cancer as a disease of somatic cell genetics. I think even Peter Duesberg and his associates (the "investigators" you seem to be talking about - but why not give them public credit?) who are the staunchest proponents of this hypothesis, would agree with this… Centrosome studies originated fully within the current paradigm.
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I'm familiar with Duesberg's work (indeed, I know Peter personally), but the work on which I rely (and which I cite in my paper) deals with chromosomal instability in general and translocations in particular, not with aneuploidy.
Actually, centrosome studies originated before the rise of the current molecular paradigm, but it is true that they continue to be conducted within this paradigm. My point is that "the basic theoretical model of cancer as a disease of somatic cell genetics" has not lived up to its promise -- namely, to illuminate the cause of cancer in a clinically fruitful way. It seems to me that a new approach is warranted. Charlie is betting on the eventual success of the genetic approach; I'm betting on a different approach. Only time and further research will show which (if either) is successful.
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Finally, Evan wrote:
quote:
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The fact that Wells believes his theory was inspired by an ID-oriented metatheory as opposed to his understanding of a "Darwinian" perspective does not add any scientific validity to his first aspect of ID: "On one level, ID is concerned with inferring from the evidence whether a given feature of the world is designed," nor with his statements that "(1) Darwinian evolution (the theory that new features of living things originate through natural selection acting on random variations) is false, and (2) ID (the theory that many features of living things could only have originated through intelligent agency) is true."
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The scientific validity of ID depends on empirical findings and the logic of the design inference. In my opinion, there is already enough evidence to warrant the conclusions that (a) some features of the world are designed, and (b) Darwinian evolution is false. The truth of ID does not depend on its scientific fruitfulness, and nowhere do I claim that my hypothesis bears on the truth of ID or the falsity of Darwinism. All I maintain is that my hypothesis (and others currently being generated within an ID framework) may help to demonstrate the fruitfulness of ID in guiding scientific research.
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charlie d.
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posted 24. May 2004 21:00
quote:
I'm familiar with Duesberg's work (indeed, I know Peter personally), but the work on which I rely (and which I cite in my paper) deals with chromosomal instability in general and translocations in particular, not with aneuploidy.
Perhaps, but the most prominent and vocal scientist among the small group of biologists who insist that DNA mutations are not central to neoplastic transformation is Duesberg. Vogelstein, which you cite, is certainly big on genetic isntability, but of a kind in which DNA mutations still play a crucial role. For instance, the 1998 review that you reference makes very clear a) that "cancer results from the accumulation of mutations in the genes that directly control cell birth or cell death" and b) that genetic instability, while indirectly responsible for the DNA mutations that cause transformation, is often itself genetically determined.
If Vogelstein is your standard, than the "ID implication" that cancer does not originate in DNA mutations has already been proven false. At least, it seems to me Duesberg is somewhat closer to the ideas you are trying to propose here. Anyway, who to cite and where is a personal choice, so that's all I'm going to say on the topic. quote:
Actually, centrosome studies originated before the rise of the current molecular paradigm, but it is true that they continue to be conducted within this paradigm. My point is that "the basic theoretical model of cancer as a disease of somatic cell genetics" has not lived up to its promise -- namely, to illuminate the cause of cancer in a clinically fruitful way. It seems to me that a new approach is warranted. Charlie is betting on the eventual success of the genetic approach; I'm betting on a different approach. Only time and further research will show which (if either) is successful.
Well, I would also be more cautious about stating what has or has not lived up to any clinical promise. Cancer genetics has been certainly very fruitful in the clinical field. From molecular diagnosis, to risk assessment of carriers of common cancer-causing mutations (most notably for breast and colon cancer), to gene-expression based diagnosis and prognosis of malignancies such as lymphomas, to therapies targeted to the products of specific oncogenes (e.g. tyrosine kinase inhibitors), it seems to me that "gene-centered" cancer biology has already quite a few notches on its belt. On the other hand, cancer genetics explicitly predicts that most cancers are going to be heterogenous, hard to treat, and prone to develop resistance to therapies, which is indeed what is observed.
Speaking more broadly, if I'm allowed, I would also add that because cancer is such a critical subject, directly affecting millions of people's lives, I think prudence is advisable when publicly making generalizations which may end up influencing patients' choices. Duesberg and HIV should serve as an example in this regard.
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Rex Kerr
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posted 25. May 2004 00:07
I thank Johnathan Wells for his response, but I see that I wasn't specific enough with my comments. I am familiar with the diagram and angular momentum calculations.
What I was hoping for was a more detailed diagram showing the geometry and forces on each component of interest--for example, how is the polar ejection force, at 20um from the spindle pole, transduced?
The reason I am interested in a diagram is that inertia is typically a very weak force at cellular scales. For example, at constant pressure, fluid flow through a pipe scales as the fourth power of the diameter ("Poiseuille's law") due to viscosity. Thus, at very small scales, viscosity is typically overwhelming. Diffusion, rather than inertia, is dominant.
With the information given so far, I cannot be confident enough of any diagram I draw to be able to estimate viscosity-based drag. My intuition is that inertia lasts for milliseconds at best on that scale (picoseconds for water molecules!), and that therefore gradual angular acceleration over twenty minutes is very unlikely at a molecular scale.
I hope that the paper that has been submitted includes calculations demonstrating that my intuition is flawed. But if not, I remain skeptical about the biophysical plausibility of the wobble model.
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Evan
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posted 25. May 2004 22:33
I appreciate Wells’ response, but I am still unclear as to what relationship he sees between his hypothesis and ID.
First, it is clear that Wells is not claiming that his hypothesis is connected to the scientific validity of ID, for he says
quote:
The scientific validity of ID depends on empirical findings and the logic of the design inference. In my opinion, there is already enough evidence to warrant the conclusions that (a) some features of the world are designed, and (b) Darwinian evolution is false. ...
nowhere do I claim that my hypothesis bears on the truth of ID or the falsity of Darwinism.
On the other hand, he does claim that his hypotheses is an example of “using Intelligent Design Theory to guide scientific research,’ stating that
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ID could function as a "metatheory," providing a conceptual framework for scientific research. By suggesting testable hypotheses about features of the world that have been systematically neglected by older metatheories (such as Darwin's), and by leading to the discovery of new features, ID could indirectly demonstrate its scientific fruitfulness
But what is not clear is what is it about ID, even as a “metatheory,” that has suggested the hypothesis Wells offers? It is true that it is an unorthodox hypothesis, and, as Wells clearly understands, may or may not turn out to be true, but it seems to me that it is a testable hypothesis totally within the province of mainstream “non-ID” science.
As I pointed out in my earlier post, Wells’s justification for considering his hypothesis as “guided by ID” is based on his mischaracterization of various aspects of science as being part of an “older” metatheory, and his identifying ID theory with statements that, for the most part, are actually incorporated in various mainstream scientific perspectives.
So as far as I can tell, there is no ID there - neither theory nor metatheory.
The other subject I brought up in my previous post, which Wells does not address, is whether the fruitfulness of a metatheory has anything to do with the scientific validity of any theory that might be associated with it (the metatheory.) For instance, one can (and many do) subscribe to the metatheory (and its associated theology) that God has created a world fully endowed to both create, as a derived creator, the intelligible world we experience and our human ability to comprehend it as such. This metatheory has inspired countless scientists to explore the detailed workings of nature, with great success.
However, other metatheories, some entirely different, have inspired other people to believe in and search for the same regularities as the theist, and both groups have found the same details - science provides a common ground upon which metatheories can rest.
Many metatheories can be fruitful, but that fruitfulness itself does not provide evidence that the metatheory is “correct.” Only if the metatheory puts testable hypotheses about itself on the table can it move from metatheory to theory, and in this case Wells says clearly that he has not done that here.
Therefore it is not useful nor relevant, really, to claim that his hypothesis is “guided by ID” because he clearly claims to not mean that it actually bears on any scientific hypothesis about ID. His hypothesis rests on a belief that science has neglected seeing things as holistic systems and that development is a more complicated affair that a simple gene-driven paradigm would suggest, but lots of people working from lots of metatheories (and scientific theories) also believe this. However, without any connection to any specific testable hypothesis about design itself, it is, I think, misleading to claim that this lends any support to ID, even in the very vague way of “indirectly” demonstrated ID’s “fruitfulness.”
[ 25. May 2004, 22:41: Message edited by: Evan ]
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Jonathan Wells
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posted 26. May 2004 18:48
Rex Kerr questions whether the angular acceleration described in my hypothesis can overcome viscosity effects that dominate events at the subcellular scale. This question is quite reasonable, but I think it may be based on a misunderstanding of what I'm proposing.
My hypothesis proposes two forms of angular acceleration. The first involves the acceleration of the centriole pair inside the centrosome. When the Archimedes' screws first start rotating at the beginning of prometaphase the angular velocity of the centriole pair is zero. With the turbines generating a constant torque, the pair's revolutions would accelerate at a rate of approximately 10 Hz/sec, so that after twenty minutes their angular velocity would be of the order of 10 kHz. Viscosity effects would cause the fluid inside the centrosome to revolve with the pair (assuming the absence of friction due to nanobubbles on the inner walls).
The second form of angular acceleration would occur in the spindle, which would wobble due to the eccentricity of the revolutions of the centriole pair. This angular acceleration -- the centrifugal-like polar ejection force -- would be immediately transmitted to all objects in the spindle by microtubules.
The vortexer analogy might help here. Some vortexers have a variable speed control, so one can start from zero and slowly increase the speed of the wobble; this is the first form of angular acceleration. The contents of a test tube inserted into the cup of the vortexer experience an angular acceleration (i.e., a centrifugal-like force) that forces the contents to climb up the inside of the tube; this is the second form of angular acceleration.
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Evan
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posted 26. May 2004 21:33
I won't post on this further unless Wells chooses to return and discuss it, but he has not responding to either of my points: what does ID have to do with his hypothesis, even as a "metatheory?", and in what ways, if any, does the "fruitfulness" of a metatheory bear on any aspect of an hypothesis’s scientific validity?
And if the answer to both these two questions is “it doesn’t,” then why preface the hypothesis with the discussion of ID?
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