Meyer claims that specified complex information can only arise from an intelligent source, justifying that claim by citing a series of examples. One of those examples is computer code. In my previous post, I suggested that this was not an adequate example because of fundamental differences between computer code and DNA information. An obvious question is whether there is an example of specified complex information that is not derived from an intelligent source but solely from physical or chemical functionality. In this post I would like to offer just such an example.
The magnificent example of antibodies was presented by Dr. Craig Story in the December 2009 issue of Perspectives on Science and Christian Faith, Vol. 61, No. 4, p.221. (if you aren’t a member or don’t have a subscription, copies are available from the ASA office for $10 plus shipping and handling; contact asa@asa3.org.) In his article, Craig explains how the immune system works, focusing on the importance of the inherent randomness in the process. In this post, I would like to offer a physicist’s interpretation of his paper, with a focus on the information content. Craig has graciously reviewed these comments and corrected my errors in biology.
Stem cells in our bone marrow continuously produce a population of pre-B cells, so called because they are precursors to B cells, which manufacture antibodies when mature. These pre-B cells are all identical and have the same antibody gene DNA. This population therefore has a relatively low information content. All the complexity is within the cell and there is no diversity in the population of cells. As the pre-B cell population prepares to moves into the body, the cells undergo a transition into B cells. In the process, key segments of DNA in each cell are rearranged randomly to form a unique and novel DNA sequence. The process is described in detail in Craig’s paper. It is a constrained process so that the resulting antibody protein is always a particular folded configuration that may have affinity to an antigen, but the gene segments are randomly rearranged and joined to alter the magnitude of the affinity. The result is a population of B cells, each one of which is different in terms of its antibody DNA. This means that we have a transformation of a low information population of pre-B cells to a high information population of B cells, with reference to their antigen-binding abilities. The complexity has increased dramatically but we do not yet have specificity.
As a B cell moves through the body, it may or may not encounter an antigen with which it has affinity. If it does not, the B cell dies and that particular configuration no longer exists in the body. However, if an antigen appears with which a B cell has some degree of affinity, the B cell will attach to the antigen. In this case, that B cell will reproduce through cell division to create clones of itself. This process occurs throughout the population of B cells with the result that only B cells with some affinity to the environment of antigens survive. This is a basic level of specificity.
There is another level of specificity that Craig describes. A first-responder B cell usually will have a relatively small degree of affinity to an antigen. As this cell reproduces itself, an enzyme enhances the mutation rate of only the portion of the antibody genes that determines the affinity. In some cases, mutation rates can reach as much as one nucleotide per cell division. This means that the subpopulation of this particular B cell grows with a dynamic diversity of various degrees of affinity to that antigen. The cells with the strongest degree of affinity will preferentially attach to the antigens, leaving those with weaker affinity without antigens and therefore a death sentence. Over time, this subpopulation will be predominantly one with strong affinity to this particular antigen. This, in a nutshell, is why vaccines work.
In the bigger picture, this example shows how a homogeneous population of pre-B cells is transformed to a dynamically diverse population of B cells, with a tremendous increase in information content. This complex information then becomes highly specified by fine-tuning to match the antigens to which they are presented. The result is a high degree of specificity and complexity with no involvement of an intelligent designer as an immediate cause. This does not, of course, preclude the sustaining involvement of an Intelligent Designer at a metaphysical level.
Craig points out the critical role of randomness as a key characteristic of the cellular processes involved in the immune system. The random process of gene rearrangement is necessary to ensure a sufficiently broad range of binding specificities, such that some of them are almost sure to bind to one part of each pathogen. His example also illustrates clearly how highly complex and highly specified information is derived directly from a population of relatively low-information cells. Hence, the argument that Meyer makes that all complex specified information comes from an intelligent source does not withstand scrutiny.
The antibody example is a beautiful illustration of the basic processes of evolution. It begins with the common ancestry of the stem cells that produce an ancestral population of pre-B cells that are essentially identical. Descent with random variability occurs in the generation of the B cells, which are all unique with respect to their antibody gene DNA. Natural selection describes the way in which B cells that do not bind to an antigen will die while those that do bind to an antigen proceed to reproduce clones. The random variability of the dynamically diverse population of antibodies ensures the formation, within a short period of time, of antibodies with affinity to virtually any antigen. The subsequent way in which those B cells acquire stronger affinity to that antigen is a type of adaptation. Darwin suggested that these basic processes, operating over a long period of time, could account for the origin of species. Little did he suspect that these very processes are active continuously in our bodies on a relatively short time scale to provide a vital line of immunological defense.
Ide,
You’re asking a slightly different question, which is also interesting. The previous question was, when do we see the first increment of CSI to produce something “similar to what we now recognize in RNA and DNA”? This time you said, “The first step need not immediately lead to anything as complex as RNA or DNA.” Maybe you’re not changing the target of the question, but it seems a bit like it.
My first response is that this isn’t separate from origin of life (OOL) research, but rather a part of it. My second thought is that perhaps this has already been demonstrated. This isn’t my field of expertise, certainly, so someone will have to correct if I’m wrong.
I’ll ask first, does a string or organized structure of molecules contain more complexity than a set of disconnected atoms or molecules? It seems to me that if the atoms join together to form organized structures, that there is more complexity expressed. If so, this is exactly the result that the Miller-Ulrey experiment proved could happen — spontaneous assembly of things resembling amino acids, etc.
The next question would be whether that complexity could be considered *specified* complexity. Here is at least one area where definitions might get into trouble. Using the distinction of specificity as either functional or abstraction, were these amino acid structures specified complexity? As I understand it, they weren’t exactly functional in the same way as amino acids in living things are functional, but how can we say for sure that they weren’t functional? And who is to say there is not abstraction involved? If we see a structure that looks very much like an amino acid, we might have to consider it specified at an abstract level, because of its similarity to other recognized building blocks of living organisms.
So does this self-assembly of complex structures from simpler structures represent enough of a “first step” toward introducing CSI through natural processes? I don’t know, but I’ll throw it out for discussion. If not, why not? If so, then obviously there are still many signicant hurdles to explain the progression from there to living organisms.
Jon
Jon,
Helpful questions and insights. I hope you share my feeling that we are making some progress. I‘ll try to address your points in order
1) “Maybe you’re not changing the target of the question, but it seems a bit like it.” What I intended to do was identify a simpler target but one that has to be hit before the next target can be reached if the process follows an evolutionary, step by step mechanism.
2) The question could be different from origin of life research if the question were directed to something other than organic chemistry as in computational evolutionary algorithms.
3) “Does a string or organized structure of molecules contain more complexity than a set of disconnected atoms or molecules?“ I believe this is a two-step question. First, linking molecules in a structure or letters in a word clearly reduces degrees of freedom, reduces entropy and therefore increases Shannon information. Second, whether or not there is CSI depends on whether or not function can be demonstrated. For example, one could envision an exhaustive set of experiments related to the work of Axe looking for appearance of protein functionality in sequence space. Or, find an evolutionary algorithm that produces more CSI than was originally embedded in it.
4) I must strongly disagree that “this is exactly the result that the Miller-Ulrey experiment proved could happen — spontaneous assembly of things resembling amino acids, etc.” Miller-Urey is just chemistry doing what chemistry does when the laws of chemistry are followed. As far as I know we think those laws were all embedded in our universe from the first nanosecond.
5) The function/abstraction differentiation is something I need some help from you and Randy in understanding. To my way of thinking something either “functions” or it doesn’t. Proteins can demonstrate functionality. Words can demonstrate readability, etc.
6) As to “If we see a structure that looks very much like an amino acid, we might have to consider it specified at an abstract level, because of its similarity to other recognized building blocks of living organisms,” my light hearted response would be, “If it walks like a duck and quacks like a duck and is similar to a duck but isn’t a duck then it ain’t a duck.” Why not? Because it lacks duck function. You can see I need more help on abstraction vs. function.
I’ll conclude by saying “Amen” to “obviously there are still many significant hurdles to explain the progression from there to living organisms.”
Ide
To anyone,
Let’s not let this helpful discussion die. It seems to me that the title of this thread “Complex Specified Information Without an Intelligent Source,” indicates the intention to grapple with a truly fundamental issue.
In response to Jon’s question as to whether or not this is really just the issue of the origin of life I’d like to lay out my understanding of the many hurdles to be crossed that are governed by the laws of chemistry before the issue of CSI enters the picture.
1) Origination: All the nucleotides required must be formed. Jon referred to Miller-Urey that made the first leap forward on this. Despite over a half century of active investigation it is not clear to me that we’ve really made much progress. Even the starting environment still seems to be up for grabs.
2) Deracimization: So far we have no concept of a natural process that can lead to a segregated isolate of pure levo-rotary monomeric precursors.
3) Polymerization: A probable natural process for the production of a polymer of sufficient degree of polymerization to be of biologically interesting length, say a shorter protein, hasn’t been found even for a racemic polymer. Poisoning of potential polymerization pathways remains a daunting problem in a natural environment.
4) Information: Only after steps 1) through 3) are resolved do we confront the issue of how a step-by-step polymerization process can produce the CSI code required for functionality.
With that positioning can we again return to “Complex Specified Information Without an Intelligent Source?”
Ide
I had not checked this thread for a couple of months. I appreciate the detailed and thoughtful conversation between Ide, Randy, and Jon – and I also appreciate Terry Gray’s contribution.
Given the central role antibody generation plays in this discussion, I just wanted to alert readers to the letters by Craig Story, Larry Parsons, and Mihretu Guta in the last pages of the June 2010 issue of Perspectives in Science and Christian Faith. The PSCF blog (http://www.asa3online.org/PSCF) has threads on the main articles from that issue of PSCF, but this thread here is probably the most relevant for discussion of those letters by Story, Parsons, and Guta.
Chuck Austerberry
To All,
With my thanks to Chuck for interesting input and help in keeping this discussion going. It seems to me that the title of this thread “Complex Specified Information Without an Intelligent Source,” indicates the intention to grapple with a truly fundamental issue. I’d hate to see it diverted or die.
In response to Jon’s question as to whether or not this is really just the issue of the origin of life I thought it might help for me to lay out my understanding of the hurdles to be crossed that are governed by the laws of chemistry before the issue of CSI enters the origin of life picture.
1) Origination: All the nucleotides required must be formed. Jon referred to Miller-Urey that made the first leap forward on this. Despite over a half century of active investigation it is not clear to me that we’ve really made much progress. Even the starting environment still seems to be up for grabs.
2) Deracimization: So far we have no very promising leads for a natural process that can lead to a segregated isolate of pure levo-rotary monomeric precursors.
3) Polymerization: A probable natural path for the production of a polymer of sufficient degree of polymerization to be of biological interest, say a shorter protein, hasn’t been found even for a racemic polymer. Poisoning of potential polymerization pathways remains a daunting problem in a natural environment.
4) Information: Only after steps 1) through 3) are resolved do we confront the source of CSI question. That is, how can a totally natural step-by-step polymerization process produce the CSI code required for functionality.
With that positioning can we again return to “Complex Specified Information Without an Intelligent Source?”
Ide
Ide,
I greatly appreciate that you mentioned several times that we should return to “CSI without an intelligent source.” I am still waiting for your reponse on that topic. Perhaps you missed my comment from several days ago, since you never referred to it.
If you recall, I have asked you repeatedly about the increase of CSI without an intelligent agent in the antibody example. You first offered a detour into cosmology which turned out to reveal a very different idea of what CSI actually was. Now you are asking us to solve the riddle of the origin of life before discussing information, which seems to be another detour. We all agree that the origin of life has not been solved. Your first three points merely point to the spectrum of research to be done. As an argument from incredulity, it may play well in Peoria but not in this crowd. The only reason that information, and CSI in particular, comes into play is that Meyer (and hence the majority of the ID community) claims that the information argument indicates that only an intelligent agent can answer those first three points. My point is that his argument is falsified and that the search for the origin of life must continue elsewhere.
That is why we must discuss information here. As I said in the other note, any definition of information that includes living cells leads to an observation that such information changes (increases or decreases) during the course of the development of an organism and from generation to generation. The antibody example is one small subset of that grand process which is amenable to study step by step. Yes, let’s keep our focus on it.
Randy
I see two perspectives concerning the example of antibody production.
One perspective focuses on the DNA rearrangements that result in antibody-encoding genes. Much like DNA transposition events, and with its mechanism likely evolved from a certain class of transposase enzymes encoded by certain transposons, this perspective makes the simple point that randomness is functional and can generate information. This perspective also uses examples of randomness functionally employed by human agents to show that random processes can be functional and productive.
Another perspective focuses on events upstream, or downstream, of those DNA rearrangements. This second perspective focuses on anything or everything that must precede the DNA rearrangements themselves, including the origins of DNA itself. It also focuses on the positive and negative selection which winnows the outcomes of the random DNA rearrangements and preserves only those which encode antibodies that 1) have the potential to bind foreign antigens but 2) do not bind self antigens very tightly. This perspective emphasizes that the random DNA rearrangements themselves would not even occur, let alone be productive and beneficial, without the special molecular, cellular, and organismal contexts in which they occur. This perspective also uses examples of randomness functionally employed by human agents to show that an intelligent agent is involved in making those random processes functional and productive.
Both perspectives are correct, of course.
How does this apply to divine creation of living beings with immune systems? I see two options, in theory, for the Christian:
1) The fruitfulness of random mutations winnowed by natural selection suggests, as Craig Story puts it in his recent letter in PSCF, that “God does not micromanage the minute details.” God is still sovereign and involved, just not in a way that is observable or testable by science.
2) God does micromanage the details in the sense of somehow causing (and not merely foreknowing) the particular outcomes of the processes which are unpredictable and thus random from our perspective.
ID theory suggests that, at least in some cases, scientific evidence favors only option #2, and contradicts option #1. I do not agree.
In my opinion, it’s impossible to adjudicate between #1 and #2 using science. I also think #1 and #2 are theologically equivalent in their orthodoxy; I do not think much is at stake doctrinally in the choice between #1 and #2.
The choice between #1 and #2 can often seems so important to us, but I suggest that’s mostly due to other concepts that often get linked (unnecessarily, in my opinion) to either one or the other of the two options.
Chuck
Chuck, good points. How would one be able to detect option #2? What is the trademark for God to micromanage the details? Aren’t the laws of nature just our shorthand of the description of how God micromanages the details? Or would micromanagement require an inability to generate such a description? Does the lack of a description have any implications other than our incomplete knowledge?
Well, I guess this digresses from our main point somewhat, but the key relevance is the antibody example and what Craig points out is the inherent randomness in the process. We know that this type of randomness is a vital part of biological processes and we know God sustains it. But we really don’t know how. But then, no other theory from ID or creation science, or whatever does either.
Randy
Randy,
As to “You first offered a detour into cosmology which turned out to reveal a very different idea of what CSI actually was.” I had hoped I had responded to your satisfaction since I didn’t recall hearing from you on it. Then Jon raised a very similar issue suggesting I had changed the target of the question. I’ll repeat my response to him from May 11.
“I‘ll try to address your points in order
1) “Maybe you’re not changing the target of the question, but it seems a bit like it.” What I intended to do was identify a simpler target but one that has to be hit before the next target can be reached if the process follows an evolutionary, step by step mechanism.””
Jon also suggested I was really changing the issue to origin of life which led to my second response to him.
“2) The question could be different from origin of life research if the question were directed to something other than organic chemistry as in computational evolutionary algorithms.”
So let me repeat “What I intended to do was identify a simpler target but one that has to be hit before the next target can be reached if the process follows an evolutionary, step by step mechanism.”” I then posted on May 20 my view as to where origin of CSI stands in the causal chain after the “creative” powers vested in the laws of physics and chemistry, as they are now understood, have been exhausted. Randy, forgive me but why didn’t that post respond to your challenge “Now you are asking us to solve the riddle of the origin of life before discussing information,” even before you posted it?
Meanwhile I thank Chuck for directing our attention to Larry Parson’s letter in the June PSCF. His distinction of randomness as a cause as distinct from randomness within a CSI rich system better makes the point I was attacking. It seems intuitively helpful to me to step back from the complexities of potential generation of additional, completely novel CSI within organized CSI rich environments and seek to find a natural mechanism for the initial production of CSI beyond any embedded in the first 10^-35th nanosecond of creation. I don’t see how creation of novel CSI can be rigorously differentiated from cooption of preexisting CSI in CSI rich systems. To do so would seem to require a complete inventory of all the previously existing CSI.
It seems to me that the issue of where and how God intervened in the causal flow of nature might be irrelevant. If it can be established that CSI can be produced within the confines of the laws of physics and chemistry, as we currently understand them, doesn’t that question go away?
If no one wants to address this simpler question with regard to “Complex Specified Information Without an Intelligent Source,” or if this is not the proper forum for the simpler discussion I’ll be happy to take it up anywhere you may suggest.
Ide
Craig Story responds (in part) to Larry Parsons by saying: :This [randomness as a cause] is a curious near-personification of the term, as if randomness becomes the creator rather than God, and I can see how this view would be unsettling.” Story does not view randomness as a cause, apparently.
That said, I understand the perspective you and Parsons are taking, Ide. To you, the important question is whether CSI can emerge naturally, de novo, in a context originally lacking in any CSI. Randy, Craig Story, and I feel more comfortable drawing general conclusions from the specific case of antibody generation, notwithstanding that the example certainly starts long after the ultimate beginning!
Must those of us willing to generalize the lesson (that random processes in the right context can generate CSI) defend our willingness to generalize, or must those of you unwilling to do so defend your unwillingness to generalize? Who knows? I think we both benefit from both perspectives being in play. As Randy and others have noted, there are practical problems with trying to start “from scratch” given our relative ignorance about the earliest stages of evolutionary creation. So from our perspective, insisting on answering all those chemical evolution questions and questions about earliest lifeforms, before taking any lessons from antibody production, would be to neglect applying what little we do know at this point.
Craig Story writes: “I do not see why, in principle, the very same processes of variation and selection would not operate on whole organisms whose genomes are known to have mixed and mingled in complex ways over planetary time scales.” I might change his “would” to “could.” None of us can say for sure whether the generalization holds.
Meyer and other ID proponents haven’t been able to convince me that the generalization fails. But, Craig Story and Randy and I probably can’t demonstrate that the generalization must hold either. I think Randy’s point is, the amount of CSI can change via natural processes. You might be impressed only upon seeing a change from zero to some positive amount of CSI. But I wonder, when has there ever been absolutely no CSI? Or, how could one ever set up an experiment in which there is an isolated system with no CSI? Wouldn’t the isolation itself be introducing contextual CSI?
Finally, I note your statement: “It seems to me that the issue of where and how God intervened in the causal flow of nature might be irrelevant. If it can be established that CSI can be produced within the confines of the laws of physics and chemistry, as we currently understand them, doesn’t that question go away?”
No, to me the question does not at all go away. I would probably phrase the question a bit differently, and perhaps avoid the word “intervened,” but trying to imagine divine action still seems a worthwhile exercise, even if we cannot show scientifically that some kind of action by an intelligent agent is necessary. For apologetic and other purposes, it might seem appealing to be able to say to the skeptics that natural processes are insufficient, so there must be an intelligent designer of some sort. I just don’t think science will ever be able to do that for a completely unidentified, unconstrained, potentially omnipotent designer. We can certainly counter the skeptics when they claim that science disproves the existence of a God who acts. But I don’t think the way to do so will be by claiming that science proves the existence of an intelligent designer.
Cheers!
Chuck
Interesting post, Chuck, and lots to chew on. Where to start? Perhaps with “Must those of us willing to generalize the lesson (that random processes in the right context can generate CSI) defend our willingness to generalize.” I have less of a problem with generalizing than in accepting the implied “lesson.” I’m not sure what definition of generalize you intend but for the sake of discussion it seems to be, “To draw inferences or a general conclusion from an established principle.” Your implied principle seems to be “that random processes in the right context can generate CSI.” Forgive me, but has that principle been established? If not, how can it be taught? Why am I not justified in seeing it as an unproven assertion? Randy rejected my argument back on May 4 that there has to be a demonstration of creation of new CSI that is different from any preexistent CSI rather than just duplicating and or rearranging preexistent CSI. Otherwise how can there be a “lesson” to generalize? (I won’t repeat my duplicating and rearranging an encyclopedia illustration of the problem.) Neither side seems able to marshal arguments convincing to the other. Doesn’t this suggest that we need a less complex context to explore?
I think that all will agree that in nature effects have causes. If in nature we find CSI it must have been caused. Since we are here, creation is a brute fact to be accepted. Chuck asked a relevant question. “But I wonder, when has there ever been absolutely no CSI?” My previously stated position on this was “According to the current understanding of the origin of the universe, given six numbers, see Reese, and four forces, quantum behavior described by quantum mechanics and gravitational interactions that seem to conform to general relativity all possible material outcomes can be developed.” The laws of physics must have been a part of the original CSI set and the laws of chemistry can in principle be developed from quantum mechanics. So we agree. After the creation there was this minimum set of CSI.
Now there is more CSI and much, much more complex unspecified information. Exactly “What?” and “How come?” are the fundamental questions. Let’s consider an illustration helping to clarify the difference between increasing CSI and merely accumulating more complex information. Consider the Cosmic Microwave Background Radiation. It is the earliest observable outgrowth of the natural processing of the universe’s initial CSI. All of us have probably seen the fascinating maps of CMBR produced by NASA’s Wilkinson Microwave Anisotropy Probe (WMAP). This clearly shows an immense amount of complex information. But it contains no more CSI than the original set just as complex fractal patterns contain no more CSI than the algorithm that produced them.
Does it have a natural cause? Seems so. Calculations based on quantum fluctuation in the initial primordial particle soup have been shown to account for the temperature distributions we observe. The current universe of stars, galaxies, solar systems and planets represent further development of complex information but neither requires nor produces more specification. The original CSI set and 13.7 billion years are sufficient to account for all the inanimate aspects of the universe today. The grand scale appears to have been confirmed by sophisticated cosmological calculations. The nitty gritty of minor rocky planets like ours, possibly including the organic polymers closest to those of life forms, are just the overlay of chemistry.
So let’s return to Chuck’s perception that “Story does not view randomness as a cause, apparently.” If that is Story’s view I would have to disagree. If you allow the generally agreed cosmological story as outlined above, randomness has clearly been shown to be a cause. More specifically, randomness has been shown to be the cause of complex information. It just hasn’t been shown to be the cause of complex SPECIFIED information.
So the basic question to be addressed is how did the CSI of life arise and find it’s way into the life forms we see? To argue that appearance of additional CSI out of a sea of available CSI gets around that problem, even if that can be demonstrated and I haven’t seen it yet, is to beg the fundamental question.
I hope this helps clarify my position.
Ide
Thanks. Yes, it does clarify.
I had overlooked your rejection of Randy’s argument that antibody gene rearrangements, in the context in which they occur, generate new CSI.
I was jumping to the issue of whether a “lesson” , namely that new functional CSI arises via some natural processes, could be generalized. I see now that we don’t agree on whether there even is a “lesson” to generalize.
I must admit that I don’t understand how you can say that no new net CSI is generated in the B cells. If I understand correctly, you think the same quantity of CSI is already there, and just gets reshuffled.
I guess I don’t see a way to move on given our divergent understandings. But if you think of something to suggest, I plan to keep reading and replying when I can.
Best wishes.
Chuck
Ide, I would agree with Chuck. Your definition of CSI seems so different and changes with almost every paragraph that it is hard to maintain a dialog. I think I have responded to each one of your points in one comment or another but apparently you haven’t understood it that way.
Maybe we should reset the conversation and just focus on the specific antibody example and stick solely to Meyer’s definition of CSI. I think there can be no doubt that the population of antibodies is a set of information that is both complex in its scope and specified in the sense of matching the environmental antigens. That information is not contained in the initial set of pre-B cells and it was not “brought in” from any external source. Nor did it come into being from the action of any intelligent agent of any kind (yes, yes, God did it, but we’re talking immediate causes). It was generated through processes that have a random characteristic (no, randomness isn’t a cause, it is a characteristic of a cause). At what point would you disagree with the above?
Randy
P.S. No, your encyclopedia example was not relevant or accurate. Rearranging or adding or changing words most definitely increases the amount of information, changes the complexity, or modifies the specificity.
OK. No one wants to address the source of the first additional increments of CSI. Can’t say I blame you. I haven’t been able to find anyone willing to take it on although I had a Nobel Laureate say that his friends tell him it’s no problem. But he never put me in touch with his friends.
Now Randy has given us something really simple to chew on. In the analogy of an encyclopedia Randy feels “Rearranging or adding or changing words most definitely increases the amount of information, changes the complexity, or modifies the specificity.” May I ask how the random modification of initial specificity in an encyclopedia can produce anything other than degradation? What increase in CSI might I hope for? Perhaps the inclusion of some scientific discovery made after publication?
Cheers,
Ide
Ide, I did reply to that point of yours. Perhaps you missed that comment. Essentially I said the concept is erroneous and the question isn’t valid. There never were “first additional increments of CSI.” This is part of a false view of CSI. CSI has developed continuously over time.
May I ask you to consider the CSI from a state point of view and not a process point of view first, just to clarify the situation. Let’s put all “processes” in a black box. Now consider the following series of text:
1. TAHT
2. TAHT TAHT TAHT
3. NIEM THAT KEAM
4. MINE THAT MAKE
5. MAKE THAT MINE
Again, we know nothing of the processes that might lead from one step to another. Analyzing just those five different steps, what do we learn? From 1 to 2 there is an increase in total information from a physical complexity point of view but not much in significance. There is also an increase in information (at least from a Kolmogorov perspective) in going from 2 to 3. Going from 3 to 4 is an increase in specificity since now the collection of letters conforms to some in a dictionary. And going from 3 to 4 is another increase in specificity since it corresponds to some meaning and signficance. Of course all of this specificity requires a reference to an external information source such as a dictionary and a knowledge of the English language. But, however it happened, there is an increase in CSI, correct?
By exactly the same analysis, going from pre-B cells to antibodies is an increase in CSI. Can we agree on that?
In this case we can open the black box and see what’s inside and, voila, there is no intelligent agent in the black box.
Randy