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Mike Behe makes a useful distinction

Recently, an item in Nature News promised big things for the evolution of bacteria:

Beneficial mutations in the bacterium Escherichia coli occur 1,000 times more frequently than previously predicted, according to research from a group in Portugal.

In a study of E. coli populations of various different sizes, Isabel Gordo and her collaborators at the Gulbenkian Science Institute in Oeiras, Portugal, found that thousands of mutations that could lead to modest increases in fitness were going unseen because good mutations were outperformed by better ones

The authors say that the work could explain why bacteria are so quick to develop resistance to antibiotics.

“It’s changed the way I think about things,” says Frederick Cohan, a biology professor at Wesleyan University in Middletown, Connecticut. He adds that although the principles involved were understood, no one expected to find such a high rate of adaptive mutation.

So have the found the answer to evolution? Well, no.

Mike Behe, author of Edge of Evolution comments,

It’s critical to distinguish between “beneficial” mutations and “constructive” mutations. It can be “beneficial” to an organism in some circumstances to render a gene nonfunctional by degrading it. If that is the case, then any of a very large number of change to its amino acid sequence will do the job, and so the rate of “beneficial” mutations will be very high. I discuss this in The Edge of Evolution. For example, it is beneficial in malaria-ridden territory for humans to degrade the functioning of an enzyme abbreviated G6PD. A very large number of separate mutations to that gene have been isolated, all of which are “helpful” because they all mess up the protein’s activity. In his long term evolution experiment with E. coli Richard Lenski has identified about a half dozen “beneficial” mutations — they *all* appear to be degradative mutations. It seems very likely that the report below is just identifying beneficial-but-degradative mutations. That’s interesting, but degradative mutations tell us nothing about how molecular systems can be constructed.

So, no.

Also, at the Post-Darwinist:

Everybody is anti-science now.

How I got interested in the intelligent design controversy (podcast)

Is science stalled? Many more scientists but no significant increase in new discoveries? Former editor of New Scientist comments.

And at Mindful Hack:

Roger Scruton weighs in on the anti-God crusade.

Another human vegetable wired for thought? What is going on?

Middle Ages tech support

Why Darwinists should throw away any family planning/limitation aids they may own.

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23 Responses to Mike Behe makes a useful distinction

  1. At some point the Darwinists are just going to have to step away from the crack pipe. Maybe we need a twelve step program to help them recover. The first step would be to admit that a random walk is powerless to create specified complexity.

  2. I don’t understand why it is so hard for evolutionists to understand that adaptations come at a cost to preexisting molecular abilities and Genetic information. I mean the guy who did the study was working on the molecular level wasn’t he?

    Excerpt from Sanford’s book Genetic Entropy: Bergman (2004) has studied the topic of beneficial mutations. Among other things, he did a simple literature search via Biological Abstracts and Medline. He found 453,732 “mutation” hits, but among these only 186 mentioned the word “beneficial” (about 4 in 10,000). When those 186 references were reviewed, almost all the presumed “beneficial mutations” were only beneficial in a very narrow sense- but EACH mutation consistently involved loss of function changes-hence loss of information.(That’s a 100% loss of function find out of 1/2 a million searched!!!) While it is almost universally accepted that beneficial (information creating) mutations must occur, this belief seems to be based upon uncritical acceptance of RM/NS, rather than upon any actual evidence. I do not doubt there are beneficial mutations as evidenced by rapid adaptation yet I contest the fact that they build meaningful information in the genome instead of degrade preexisting information in the genome.

  3. [...] Evolutionists like to cite “beneficial” mutations as the source of the creative power of evolution. There’s just one problem: all the so-called “beneficial” mutations that have been observed involve a degradation of information. Biochemist Michael Behe recently pointed this out, and I can’t do any better than the post at Uncommon Descent at describing the evolutionary spin machine. These icons link to social bookmarking sites where readers can share and discover new web pages. [...]

  4. He adds that although the principles involved were understood, no one expected to find such a high rate of adaptive mutation.

    I’d suggest caution in the way we characterize this development. There are mutations which are adapative and suggest front-loaded capabilities.

    In an almost forgotten article at ARN, Behe talks about designed mutations. I have thought some forms of antibiotic resistance could be designed mutations. Such mutations will not cause macro-evolution, but highly optimize the process of micro-evolution.

    We have an echo of that in how the human immune system methodically mutates DNA in B-cell maturation.

    The bottom line is there could be more subtleties to this.

    To see that Adaptive Mutations are not the same as Random Darwinian Mutations see:

    A True Acid Test: Response to Ken Miller

    and

    The Unsuitability of B-Cell Maturation as an Analogy for Neo-Darwinian Theory.

    An adaptive mutation has an anticipatory quality toward certain environmental stresses.

    Truman describes the situation with the human immune system, and it could well describe e-coli’s adaptive strategy as well:

    Proposed evolutionary processes which supposedly produced first bacteria and eventually humans are assumed to not have been driven by intelligent guidance. We must clearly distinguish between true randomness and a purposeful algorithm to cover a search space to converge on an intended goal.

    (A) Where fired shotgun pellets actually impact is only in an incomplete sense “random”. The gun barrel, triggering mechanism, explosive mixture, size and number of pellets, etc. are organized to solve a class of problem. Although the specific target need not be known in advance, the topology of desired outcome (in time and space) is part of the shotgun design. The design covers a constrained range of possibilities: it cannot kill bacteria nor whales (area), nor destroy satellites (distance) and needs a triggering mechanism (time). This permits a non-random outcome, such as killing a bird at a specific time and place with a high probability, with little risk of collateral damage.
    The designer of the apparatus need not specify the exact picometer each pellet will end up at. It suffices to ensure within a high probability that when used in the correct context and manner, the “random” behavior of the ensemble of pellets is within the intended tolerance.

  5. scordova,
    I find the immune system response very interesting. It shows a plasticity in lifeforms that you would expect in organisms if the NDE theory were actually true. Yet the principle of “Genetic Entropy” remains intact for the immune system response is proven not to be a “permanent change” to the genome of the species. i.e. the species becomes susceptible to reinfection after varying periods of time! Plus newborns quickly lose immunity to the infection that the parent-s had!
    I think that genetic entropy will also be found to be obeyed on another level too for the imune system. I believe that the immune system is “reset” to its original state because the original state is optimal for fighting off infections,,,i.e. the immune system as a whole is degraded from optimal condition for fighting off new infections when it has “old temporary information” stored in its “ram” memory which is “slowing down” a response to a infection in the quickest time possible.
    I believe someone on this blog may be able to back up my assertion with empirical evidence.
    Anyone?

  6. Hall’s results and similar results from other laboratories led to research in the area dubbed “adaptive mutations.” (Cairns 1998; Foster 1999; Hall 1998; McFadden and Al Khalili 1999; Shapiro 1997) As Hall later wrote,

    Adaptive mutations are mutations that occur in nondividing or slowly dividing cells during prolonged nonlethal selection, and that appear to be specific to the challenge of the selection in the sense that the only mutations that arise are those that provide a growth advantage to the cell. The issue of the specificity has been controversial because it violates our most basic assumptions about the randomness of mutations with respect to their effect on the cell. (Hall 1997)

    Michael Behe quoting and commenting on Barry Hall

    Darwinian evolution argues that the mutations are “random with respect to fitness”.

    To understand what “random with respect to fitness” means, consider the opposite, namely, “non-random with respect to fitness”.

    To illustrate, consider a person, say an athelete, who deliberately works to change himself. The change is deliberate, pre-meditated, and teleological.

    An adaptive mutation is similar. It is a mutation that occurs as strategy to evolve it self to an anticipated environment. That means, areas of its genome which were not mutating earlier, get energized and start making changes, almost as if the population realized it better start trying to prepare itself for continued adversity or else die.

    Adaptive mutations are in contrast to random mutations. Random mutations aren’t anticipatory toward any change, adaptive mutation are.

    It should be emphasized, adpative mutations are limited to a repertoire of highly specialized changes. They wouldn’t be expected to lead to macro-evolution, unless of course macro-evolution were front loaded.

  7. I think I found some preliminary evidence that immune system responses increase the “genetic entropy” of the immune system when looked at as a whole!

    A Patient Conference on Non-Hodgkin’s Lymphoma

    January 8, 2004

    Ian Flinn, M.D., Ph.D. & Louis F. Diehl, M.D.

    The third principal is Law of Diminishing Returns. When looking at the time to recurrence of this disease, every time the disease is treated, the patient’s response rate is a little less and the duration of response is a little greater. This phenomenon is shown in two ways below. In the first table, the data indicate that the first time chemotherapy is used, 88% of the patients respond and the response lasts for 31 months. With each succeeding treatment the response goes down to 78%, 76% and 68%. The duration of response change is even more dramatic going from 31 months with the first treatment to 13, 13 and 6 months. Although we now have multiple new therapies, the fact remains, that with each subsequent therapy, the ability to control the disease is a little less.

    What do you think scordova?

  8. What do you think scordova?

    I can’t quite affirm that citation as sufficient. However, as you know, I was the first big advocate of Genetic Entropy at UD, and I still am. In fact, the blogsphere and wikipedia hardly knew of Sanford’s book until johnnyb told me of the book and I started heavily advertising it.

    For sure the human body suffers genetic entropy in somatic cells (that’s why we die), and Sanford extends that to reproductive cells.

    The parts I would be cautious about Sanford’s work is although a mountain may generally go down hill from it’s peak, it doesn’t mean the descent never has a pause…..

    Like the human brain, the immune system arguably acquires and stores information. It might not be correct to suggest there is NEVER a gain of information, but rather a general tendency to lose information. A human brain will succumb to genetic entropy when it dies, but it does not mean that the brain doesn’t gain information somewhere along the way. Same is true for the immune system, and possibly populations of creatures. Genetic entropy is correct (at the cellular, organismal, and population level), but it does not mean there cannot be short term gains of information…

    In like manner, one of Behe’s biggest supporters, James Shapiro, points out bacteria occasionally acquire novel information through non-Darwinian means. See: Who are the (multiple) designers? James Shapiro offers some compelling answers

    ABSTRACT: 40 years experience as a bacterial geneticist have taught me that bacteria possess many cognitive, computational and evolutionary capabilities unimaginable in the first six decades of the 20th Century. Analysis of cellular processes such as metabolism, regulation of protein synthesis, and DNA repair established that bacteria continually monitor their external and internal environments and compute functional outputs based on information provided by their sensory apparatus. Studies of genetic recombination, lysogeny, antibiotic resistance and my own work on transposable elements revealed multiple widespread bacterial systems for mobilizing and engineering DNA molecules. Examination of colony development and organization led me to appreciate how extensive multicellular collaboration is among the majority of bacterial species. Contemporary research in many laboratories on cell-cell signaling, symbiosis and pathogenesis show that bacteria utilize sophisticated mechanisms for intercellular communication and even have the ability to commandeer the basic cell biology of “higher” plants and animals to meet their own needs. This remarkable series of observations requires us to revise basic ideas about biological information processing and recognize that even the smallest cells are sentient beings.

    So yes, there is an Edge of Evolution, but Behe’s book (written for the popular audienciences) necessarily touches upon the first layer of subtleties.

    He points out RANDOM DARWINIAN mutation cannot create novel proteins, but Shapiro suggests that ADAPTIVE computationally-directed mutation might. Though Shapiro won’t concede the point, ADAPTIVE computationally direct mutation is suggestive of design.

    I think it’s a bit hasty to say “no” new beneficial mutation arises. That may be true of humans, malaria, and HIV, and unstressed E. coli (like in Lenski’s lab) undergoing mild amounts of mutation, but what about the critters Shapiro studies?

    What also of Spetner’s environmentally induced adaptive mutation (Spetner is advocate of ID-NREH, I forgot what NREH stand for)? It could be environmental stress will trigger certain kinds of adaptive mutation which are non-random. We have seen E. Coli under stress begin to mutate differently when not under stress. Lenski presumably had unstressed bacteria in a random walk, and as Behe was delighted to point out, Lenski’s bugs didn’t change much.

  9. And one more interesting site on this subject:

    How Vaccines Compromise the Immune System

    http://en.epochtimes.com/news/6-2-11/38052.html

    I take this site’s evidence over the immune overload naysayers because “There are as many as a 100 million unique antibodies circulating through our bodies at any given time, but just three or four of these might be effective against any particular disease,” said Michael Deem, the John W. Cox Professor in Biochemical and Genetic Engineering and professor of physics and astronomy. “When we get sick, the immune system identifies the particular antibodies that are effective, as it rapidly creates and mass produces mutant white cells called B cells that make only these antibodies.”

    So the evidence for actual immune overload will be very hard to discern (hence the naysayers). Yet the site I linked too does a broad enough statistical analysis in order to discern the compromised immune system from to many diseases introduced by vaccination!

    Thus the principle of “Genetic Entropy” appears to be valid for the immune system also.

    The linked to paper also clearly shows why it is very important to have B-cells that are not too “hyperactive”, since they can quickly turn on ones own body if too “hyperactive”

  10. I agree with you about genetic entropy being violated in a very narrow sense temporarily, scordova, yet just like the entropy of the universe these are minor variations from the law.

    As a sidelight I wanted to ask you what do you think the final foundational law of biology will look like? Will it look more like Dembski’s conservation of information postulation or do you think it will take on a more entropic nature? as compared to the first and second laws of thermodynamics?

  11. I think the lactase persistence mutation is a good example of a adaptive mutation which defied tremendous mathematical odds yet still obeyed Genetic entropy since the mutation “lost” a instruction to turn the lactase enzyme off.
    So even in frontloaded conditions under stress i think the principle of Genetic Entropy may still be strictly adhered to in the genome when taking into account overall functional information.

  12. bornagain77,

    Before I respond, let me at least go back to the original post by Denyse.

    There could be indeed thousands more beneficial mutations than thought, and we should really think of the immune system B-Cells as already being an example of that.

    In the immune system, the human body deliberately makes slight variations in every B-cell. From Wiki:

    The human body makes millions of different types of B cells each day that circulate in the blood and lymph performing the role of immune surveillence.

    I would argue in comparable manner, bacterial populations are designed to be highly variable so as to assist them in fending off threats to the population. This variablity does not necessarily lead to large scale emergence of novel complexity. Rather it enables it to quickly create antibody resistance.

    I think it is hasty to point to every form of variability or mutation as an example of “genetic entropy”. Even creationists (including probably Sanford) view the immune system variability as a methodical designed process, not inherently and accidental mutation “genetic entropy” of DNA that just happens to save us from being killed.

    I think 1000 more beneficial mutations being found in bacteria doesn’t negate Behe’s thesis, Behe merely points out, that evidentially, even all these 1000 more beneficial mutations don’t lead to large scale innovation any more than the millions of “beneficial” mutations in B-cells, don’t radically transform the cells in living human being.

    All those millions of B-cell mutations don’t cause us to acquire magical powers in our lifetime, yet their is no question we have millions of “beneficial” mutations every day in the sense we have all these little B-cells strategicially positioned in a surveillence mode.

    By way of comparison, these 1000 mutations in bacterial could be the counter part to the immune systems “surveilence mode”. I have forseen this for years, actually. Those bugs were intelligently designed, and so were those mutations. If we accept design for the mutations in human B-cells, we can accept it for these 1,000 more mutations in bacteria.

  13. Spetner is advocate of ID-NREH, I forgot what NREH stand for)

    Non-Random Evolutionary Hypothesis

  14. Optimal median position for the genome may be a key phrase when discerning “Genetic Entropy”.
    As you allude to scordova, there is an apparent optimal median position that the organism will adhere to in the long term as demonstrated by numerous experiments on e-coli, i.e. if we drift to far from this optimal median position the bacteria or organism will quickly lose “survivability”.

  15. esteemed French scientist Pierre P. Grasse has stated “What is the use of their unceasing mutations, if they do not change? In sum, the mutations of bacteria and viruses are merely hereditary fluctuations around a median position; a swing to the right, a swing to the left, but no final evolutionary effect.”

  16. if we drift to far from this optimal median position the bacteria or organism will quickly lose “survivability”.

    CORRECT! And designed mutation can help restore some of the necessary variation back into the population if it gets too specialized — unless of course the specialization results in a serious loss of information (like cave fish or moles losing their ability to see).

    The human immune system is constantly dumping variable B-cells into the system. If the B-cells were too specialized we would die!

    Again, we have to be careful to distinguish :

    1. mutation that is the result of real genetic entropy

    2. mutation that is the result of design

    We tend to think mutation is always accident, but that is not necessarily so as Royal Truman pointed out.

  17. I think this is a good place to throw this in. I posted an analogy on youtube demonstrating the straw man nature of Ken Miller’s argument. I also explained why ID is science.

    Whether this is posted as a comment or not, I hope the mod will check out the videos:

    http://www.youtube.com/watch?v=zZuPMp-60jg

    and

    http://www.youtube.com/watch?v=FxdSB8Ky8FI

  18. Just a comment about the B (and T) cell system, because I feel that there is some confusion about that.
    In the development of the immune system, there are two different stages where the organism pusposefully utilizes mutation to achieve a definite goal. In both instances, mutation is efficiently caused (or favoured) by the organism itself, and in that sense it is not “spontaneous”, but “designed”. It can, as far as we know, be random, in the sense that it is not aimed at a specific result. So we can say that it is a case of designed random mutation, aimed at a specific target (Ig genes), but not at a specific result.

    The purpose of the mutation, however, is very different at the two different levels where it happens.

    The first level is the “ontogenic” maturation of the immune cells, and the purpose of the mutation is to create a wide repertoire of basic antibodies, which can cover with some laxity the space of possible antigens (more correctly, epitopes), so that the organism is endowed with a basic repertoire to react, usually at low affinity, with (almost) any possible epitope in nature. We should notice that, at this first level, nothing is known to the organism of any specific antigen, so the process is just the very intelligent utilization of a randomly created diversity to cover a potential space of information. No selection takes place at this level, except for the very important, and very designed, removal of the clones reacting with the “self”.

    The second level, instead, takes places when there is a specific primary immune response to an antigen. The first antibodies produced versus a new antigen are the compatible “basic” ones from the general repertoire. Typically, the specifity of these immediate antibody response is low (in other words, the antibodies have a low avidity for the antigen). But, in a few months, the response becomes refined, and the avidity of the antibodies becomes high. How does that happen?

    Although the process has been discovered quite recently, and not everything is understood, it seems that the organism again uses a process of designed random mutation, aimed at the existing immune cells producing the first, low affinity, antibody. But this time the process is very different. A very specific and intelligent selection determines the output. Though the mutations themselves are probably random, they:
    a) are directed at an existing conformation (the first antibody) which alredy corresponds roughly to the target (the antigen, or rather the epitope).
    b) are specifically selected according to a known information (the epitope itself).

    In other words, the organism already possesses all the necessary information aout the “mirror” target (the epitope of the antigen). We have to remember that, at the start of the immune response, epitopes are processed by the immune system, in particular by the antigen presenting cells. That information is obviously stored someway, and is used again by the immune system to “select” the clones with mutations which have yielded an antibody with higher affinity to the antigen, and to block all the others.
    So, in this case, we have a very efficient, designed selection according to a pre-existing information (the antigen itself) which has been acquired by the immune system from the outside world. No significant new information is randomly created. The system uses an existing information (the antigen) to mold a specular information (the high affinity antibody), starting with an existing approximate information (the low affinity antibody) selected from a generic repertoire by means of the antigen itself. Random mutation is used only as a “molding” technique, followed by specific intelligent selection, because the system, though knowing the information about the antigen, has no idea about how to model the corresponding antibody. So, a trial and check algorithm is used through the means of designed random mutation in a strictly controlled context.

    Doesn’t all that sound so very very much as intelligent design?

    And, just to avoid misinterpretations, all these mutations happen exclusively in a very definit subset of somatic cells (the pertinent immune cells). In that sense, they are completely non random. And none of them is transmitted genetically. The basic repertoire is built again each time by each new organism, but through the same method. And the high affinity antibodies against a specific antigen are present only in those individuals who have had an immune response to that antigen, at least a few months before. Nothing of that is transmissable. Only the processes are genetically transmitted.

    By the way, the T cell system undergoes the same process (first level) to build the necessary repertoire of T cell receptors (cell immunity). The process is the same, but the interested genes and cells are completely different. I am not aware, anyway, of any knowledge about a “maturation” of the affinity after the first immune response (second level), but I have not really checked.

  19. they are completely non random. And none of them is transmitted genetically.

    Thank you for your informative and detailed explanation, gpuccio.

    In the human immune system the mutations are not transmitted genetically. But by way of slight extension, if the mutations in the immune system were designed, it would stand to reason at least some genetically inherited mutations are designed to evolve populations as well.

    Again, it is clear some mutations in the human body are clearly at variance with the teleological goals of the system, wherease some mutation (like in the immune system) are not.

    It is entirely possible there is an anologous situation with the mutations found in bacteria or HIV. Some of the mutation could be classified as designed optimized toward a goal, and some can be classified in terms of a degrading entropy. But in either case, the mutations seem to be limited in the transformations which they can effect, and thus the Edge of Evolution still holds.

  20. Yet Scordova,
    I still hold that Genetic Entropy holds for the organisms immune system since it must vary from its optimal median position. An optimal median position that it is eventually reset to. i.e though information of specific antigens are being gathered it comes at a cost of overall original effectivity of the immune system hence a loss for the functionality of the information in the original organism and thus this site’s reference to back my tentative claim.

    How Vaccines Compromise the Immune System

    http://en.epochtimes.com/news/6-2-11/38052.html

    Plus I wanted to ask you scordova or one of you other guys this question;

    I wanted to ask you what do you think the final foundational law of biology will look like? Will it look more like Dembski’s conservation of information principle or do you think the final law of biology will take on a more entropic nature? as this subject compares and relates to the first and second laws of thermodynamics?

  21. I wanted to ask you what do you think the final foundational law of biology will look like? Will it look more like Dembski’s conservation of information principle or do you think the final law of biology will take on a more entropic nature? as this subject compares and relates to the first and second laws of thermodynamics?

    The notion of specified complexity (CSI) is more primitive than entropy (as in decay of CSI) since the notion of such an entropy has no defintion appart from the definition of CSI.

    It might be a worthy project to express Genetic Entropy as the decay of CSI and thereby unify the two notions under one concept.

    That was one of the minor criticism of Sanford’s book in that Sanford relied more on Werner Gitt’s notions of biological information rather than Bill Dembski’s. But that is a minor point.

    Also, using the notion of CSI, it might be possible to distinguish designed mutations from those that would be considered random, undesirable noise.

    I want to get away from the notion that ALL mutation necessarily implies genetic entropy. The varieties of diversity we see in biology strike me as a designed feature, not a defect.

    That a llama an camel can descend from one ancestor, or a wolf, dog, jackal, and fox can descend from a common ancestor, or that cabbage, broccoli, cauliflower descended from wild mustard strikes me as designed mutation, not genetic entropy. These were front-loaded, designed mutations in the highest sense. Spetner’s NREH and Baraminology and probably Behe’s front-loading strongly argue for these notions.

  22. scordova,
    So it is very possible that the “final” law of biology will actually encompass characteristics of both the first law as in Dembski’s work and the second law as tentatively set forth by Spenter And Sanford?
    I like that scordova, that makes sense to me at first glance. The “law” will take into account both the qualities of the transcendent information and the qualities of the “entropic” material upon which the information is inlaid.

    I agree that some mutations in speciation are “designed” and frontloaded in to the parent species, Yet the overall functional information of the original parent species is decreased since the variability of the sub-species is now more limited than the variability of the parent species. Wouldn’t you agree that overall genetic entropy is being strictly adhered to even in speciation?

  23. The “law” will take into account both the qualities of the transcendent information and the qualities of the “entropic” material upon which the information is inlaid.

    There is no information without the capacity for entropy of some sort. Shannon’s famous paper defining information defined it in relation to some notion of entropy. The two notions can’t be separted.

    But there are piles of subtleties that haven’t been quite worked out.

    As he developed these ideas, Shannon needed a name for the incompressible stuff of messages. Nyquist had used intelligence, and Hartley had used information. In his earliest writings, Shannon favored Nyquist’s term [intelligence]…..
    John von Neumann…advised Shannon to use the word entropy….Use “entropy” and you can never lose a debate, von Neumann told Shannon–because no one really knows what “entropy” means….Shannon accepted von Neumann’s suggestion. He used both the word “entropy” and its usual alebraic symbol,H. Shannon later christened his Massachusetts home “Entropy House” — a name whose apporopirateness was apparent to all who set eys on its interior.

    “I didn’t like the therm ‘information theory’” Robert Fano said, “Claude didn’t like it either.” But the familiar word “information” proved too appealing….

    William Poundstone
    Fortune’s Forumula

    Further:

    The introduction of information theory and its application to thermodynamics has led to the conclusion that entropy, a basic concept of that science, is a measure of the observer’s ignorance of the atomic details of the system. When we measure the pressure, volume, and temperature of an object, we have a residual lack of knowledge of the exact position and velocity of the component atoms and molecules. The numerical value of the amount of information we are missing is proportional to the entropy. In earlier thermodynamics, entorpy had represented, in an engineering sense, the energy of the system unavailable to perform external work. In the modern view, the human mind enters once again, and entropy relates not just to the state of the system but to our knowledge of that state.

    Harold Morowitz
    Emergence of Everything

    At issue with the debate over mutation. When is a mutation informative and when is it entropy? I’m very hesitant to class ALL mutations soley as “entropy”. The issues are much more subtle than most people suppose.

    Measuring things in terms of selection (as in beneificial or detrimental) is a too crude a way to characterize biology. To see why read: Airplane magnetos, contingency designs, and reasons ID will prevail. Lewontin and Andreas Wagner came to the same conclusions independently.

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