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Random Degradation and Natural Deselection

Truth in advertising would have random mutation and natural selection renamed to reflect what’s really happening.

Orthodox evolutionists tell us that mutations are random when plotted against fitness but this is not the case. Mutations are random when plotted against position in the genome. An error can occur anywhere and it’s pretty much an unpredictable location at this point. But the effect of errors are certainly not random. These errors in duplication are occuring in highly optimized systems and as anyone with common sense and a bit of insight into the behavior of complex machines knows, random failures seldom if ever result in improved performance. Random mutations are in fact random degradations. I have yet to see compelling evidence that any so-called random mutation resulted in improved performance except perhaps a few trivial and arguable examples of an organism escaping the effect of a toxin by minor change in an enzyme which may very well be a directed change. The vast majority of random mutations, if not all random mutations, are neutral at best and immediately fatal at worst.

Since natural selection must by definition act on changes in fitness (differential reproduction), and those changes in fitness caused by random mutation are always or almost always detrimental, natural selection is really natural deselection as it works in almost all cases to deselect organisms whose genome has wandered from its optimized incarnation through random degradation.

Orthodox evolution theory’s weakness isn’t survival of the fittest. That’s readily explainable by the theory of random degradation and natural deselection. The weakness is arrival of the fittest. If there were a law requiring truth in advertising for orthodox evolution theory the problem of arrival of the fittest would be more easily understood.

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36 Responses to Random Degradation and Natural Deselection

  1. Orthodox evolutionists tell us that mutations are random when plotted against fitness but this is not the case.

    Are you suggesting that because 1/3 of all mutations are not beneficial, 1/3 are not neutral, and 1/3 are not bad that therefore the effect of mutations are not “random”?

    Also aren’t these two statements:
    Mutations are random when plotted against position in the genome.

    and

    minor change in an enzyme which may very well be a directed change.
    Contradictory?

  2. Just curious,

    I’m fairly interested in the idea of no mutation being an actual net gain in functional genetic information. So far, the idea is good. However, someone pointed me to the true acid test recently, and after looking at it, it seems that a new function was added, new genes were sequenced, and no other function was destroyed (other than the initial removal of one of the genes involved in the multipart structure of lactose digestion).

    It seems that none of the “new” genes were the same as the old genes that were removed.

    Does this not constitute an addition in functional genetic information without the removal or degradation of another?

    Nathan
    http://www.nathanrice.org

  3. One of the (many) miracles of living systems is that they have survived and made viable copies of themselves for so long, in spite of random errors. Human engineers have produced nothing anywhere close to this kind of self-replicating and self-correcting design.

  4. [...] Dave Scott has a good article over at Uncommon Descent arguing that mutations, the driving generative force behind the theory of evolution, should be more accurately called degradations. [...]

  5. We might add that the prevailing theory that serves as an adjunct to Darwinism, is that of a gradualistic (Lyelllian) geology. There’s a lot of evidence suggesting that catastrophism better explains much of the fossil record. Seen this way, the fossil record becomes simply a record of the catstrophe survivors, which only serves then to underline the incredible “stasis” of species. (As you’ve pointed out before, “things suddenly appear, and then suddenly disappear”, and they remain fairly the same in the interim.) So how did those “arrivers” arrive?

  6. Dave,

    It truly is a good way to shine light on the subject. Similar to what Jehu mentioned.

    It is degeneration, loss of information, not gain, loss of function, not increased ability. We see it all across the spectrum.

    For example, just look at the many breeds of dogs. Some are so specialized that they now have severe problems associated with their breeding. This indicates strain on the DNA system, not gain.

    This is a very demonstrable fact in genetics as well as known disease in breeds.

    This happens in nature as well. Polar bears loose their pigment. This is a loss of information, not gain. Specialized survival thru selective breeding of natural environments. But if we toss polar bears into the lower 48 states, what will happen?

    External variances happen from informations already available to the genome. What we observe is a straining of that information thru environmental sieves.

    Its beautiful to see, but it does not explain the origination of information, only loss of such.

  7. Michaels7
    This happens in nature as well. Polar bears loose their pigment. This is a loss of information, not gain.

    They also have partially webbed feet. Is this also a loss of information? What would count as an addition of information?

  8. Are you suggesting that because 1/3 of all mutations are not beneficial, 1/3 are not neutral, and 1/3 are not bad that therefore the effect of mutations are not “random”?

    Correct. A random fitness distribution would not be biased to favor or exclude any given fitness values. Mutations that are random in respect to where they land in the genome are not at all random in the effect they have. They very predictably confer no benefit. If you can predict the outcome of something with a high level of confidence it isn’t a random outcome.

    Also aren’t these two statements:
    Mutations are random when plotted against position in the genome.

    and

    minor change in an enzyme which may very well be a directed change.
    Contradictory?

    Yes it is contradictory which means it’s not a random mutation but a directed mutation. Recent research is indicating that when bacteria acquire resistance to antibiotics it isn’t a random mutation that’s responsible. The bacteria react to stress and start rapidly trying to find a cure much the same way humans look for new drugs. See here:

    http://www.uncommondescent.com/archives/85

    as well as elsewhere on this blog

    http://www.google.com/search?s.....cent%2ecom

  9. Nathan

    Bacteria (fungi too) appear to be equipped with mechanisms that allow them to adapt their digestive enzymes to the substrate. It isn’t random mutation serendipitously stumbling on new digestive enzymes but rather a purposeful result obtained by rapid construction and test of enzymatic trial balloons.

    One of the many failed predictions of orthodox evolution is that mutations happen at the same rate everywhere in the genome. In fact they don’t. Mutation rate varies across the genome and in the case of e.coli was found to be harnessed and governed according to need.

    To Stop Evolution: New Way Of Fighting Antibiotic Resistance Demonstrated By Scripps Scientists

  10. Correct. A random fitness distribution would not be biased to favor or exclude any given fitness values.

    I think you are using the word “random” to mean “uniform probability density function”, when evolutionary biologists are using it to mean “stochastic”, or un-deterministic.

    It is true that random fitness distribution that happens to be a uniform PDF would not be biased towards good, bad, or neutral mutations, but the vast majority of real random distribution functions are highly biased. When evolutionary biologists say that random mutations are “random with respect to fitness” they mean that the outcome is modelled as a stochastic process, not that all outcomes are equally likely. See: http://www.genetics.org/cgi/co.....163/4/1519 for example. If know of no evolutionary biologist who claims that the distribution function of mutations against fitness is uniform.

    If you can predict the outcome of something with a high level of confidence it isn’t a random outcome.
    Again, I think you are using the word “random” to mean a high-entropy (or close to uniform) distribution over sample space. I do not believe this is what evolutionary biologists mean when they use the term.

    The bacteria react to stress and start rapidly trying to find a cure much the same way humans look for new drugs.
    I know of no evolutionary biologist who has claimed that mutation rates are not effected by the environment – clearly changes to an environment (radiation, temperature extremes, and other problems) will effect the number of mutations in a cell. I believed that what’s at question here is whether the distribution of the mutations over fitness space changes as a result of the changes in environment.

  11. evolutionary biologists are using it to mean “stochastic”, or un-deterministic

    But they’re not undeterministic in relation to fitness. They’re never or almost never positive fitness changes.

    I know of no evolutionary biologist who has claimed that mutation rates are not effected by the environment – clearly changes to an environment (radiation, temperature extremes, and other problems)

    That wasn’t what I claimed. What I claimed was that orthodox evolution predicts that environmental factors such as these will produce a random distribution of mutations by location in the genome. In fact what has been found to happen is that environmental stresses such as these are not randomly distributed but occur at at a higher rate in genes where change is needed.

    The Scripps paper suggests that a way to fight antibiotic resistance is by disabling the mechanism that seletively increases mutation rates during times of stress which they call “stopping evolution”. In this case evolution isn’t driven by random mutations but is rather driven by directed mutations. They suggest disabling the direction mechanism.

  12. Franky172,

    Do you have evidence that the ancestor of the polar bear did not already have the genetic information for such adaptation to the environment?

  13. franky172,

    Did you ever get around to designing a program that could generate an english word with 500 or more informational bits using Darwinian mechanisms? If I remember correctly it was having problems with 80 bits or so.

  14. [...] Just read an excellent point by DaveScot over at Uncommon Descent, and it basically goes like this: [...]

  15. Grizzly-Polar bear hybrids, unusual in the wild, but it happens…
    http://en.wikipedia.org/wiki/G.....ear_hybrid

  16. Michaels7
    Do you have evidence that the ancestor of the polar bear did not already have the genetic information for such adaptation to the environment?

    Are you claiming that the ancestor to the polar bear had the information for building webbed feet in their genome? What evidence do you have for this claim? As far as I know there is no evidence to suggest that early mammals had that information in there genome, or that polar bear webbing is genetically similar to that of other webbed animals.

    patrick
    Did you ever get around to designing a program that could generate an english word with 500 or more informational bits using Darwinian mechanisms?

    No – I never ran the program again, but there’s no reason to think that the proram will stop at 10-letter words. However there is relatively good reason to think that no 50-letter word will ever be found – because there are no possible 25-letter parent words. I believe there are other reasons a GA is ill-suited to the problem for the reasons outlined on the web-page – http://www.duke.edu/~pat7/publ.....rdPt2.html

    Do we agree that the results indicate a 10^6 fold performance increase for blind darwininian search over exhaustive searches?

  17. Franky

    Are you claiming that the ancestor to the polar bear had the information for building webbed feet in their genome?

    Your desperation is showing. Polar bears are descended from animals with fins aren’t they? Ever seen fins without webbing?

    This is your last comment in this thread. You’re just cluttering it up with nonsense and pedantry.

  18. franky,

    As far as I know there is no evidence to suggest that early mammals had that information in there genome, or that polar bear webbing is genetically similar to that of other webbed animals.

    Your not aware of any evidence either way are you? As for early mammals, you are obviously not aware that mammals from the Jurassic era have been found with webbed feet. Of course, I don’t believe that has anything to do with the partially webbed feet on the polar bear. My guess is that the partial webbing on the polar bear is the result in the disruption of a gene that causes cleaving between the digits during fetal development. This would be an example of an information loss mutation. This mutation occurs in humans sometimes causing partially webbed hands and/or feet.

  19. DaveScot: “The vast majority of random mutations, if not all random mutations, are neutral at best and immediately fatal at worst.”

    It’s interesting that a lot of beneficial mutations do appear when humans start selecting. From an ID standpoint we just call this variation already present in the genome, but evolution has a problem here.

    For example why can we breed so many different dogs in a relatively short time, while the wolf(ancestor of the dog) doesn’t evolve much at all? Possible answers:

    1. natural selection doesn’t work at all,
    2. or the wolf is located on a peek in the fitness landscape. But doesn’t that mean that a breed of dogs less fit then wolfs would show some fast evolving when put back in nature? This based on the rate evolution is going when humans are selecting.

  20. “Random mutations are in fact random degradations. I have yet to see compelling evidence that any so-called random mutation resulted in improved performance except perhaps a few trivial and arguable examples of an organism escaping the effect of a toxin by minor change in an enzyme which may very well be a directed change.”

    Check out Hemoglobin S, a mutation of a single amino acid in the beta-globin protein. Under so-called normal conditions, this mutation reduces the fitness of the homozygously affected individual (sickle-cell disease) and thus appears to support the first sentence of the quoted statement. Surprisingly, under other conditions (exposure to infection with plasmodium, a malarial parasite), this mutation confers increased fitness to the heterozygously affected (“sickle-cell trait”) by protecting the individual against plasmodial infections. So here is what one could view as a random mutation that degrades the human genome. However, it does both, being detrimental under some and yet salvaging under other conditions. http://sickle.bwh.harvard.edu/malaria_sickle.html.

    I don’t see how that would qualify as a “directed change”, as supposed for the “trivial” exceptions. Another exception?

  21. I don’t know if my last post when through, think I lost it uploading…

    Anyway, regarding the hemoglobin s. It is important to note here that selective advantage does not indicate informational significance – by selecting for the mutant allele natural selection would, as Dave says, actually be “deselecting” from the initial allele.

    Darwinists seem to continue promoting the idea that selective advantage = functional complexity, yet every example that is used is little more than confirmation of exactly what the quantitative analysis suggested (that the opposite of Darwinism is occurring).

  22. ds: “Orthodox evolution theory’s weakness isn’t survival of the fittest. That’s readily explainable by the theory of random degradation and natural deselection. The weakness is arrival of the fittest.”

    E.D. Cope, the American paleontologist (famous for his competition with O.C. Marsh to discover the most Dinosaur fossils) agreed, ds:

    It is well understood that in [the struggle for existence] the individuals best provided with means of self-preservation necessarily survive, while the weak in resources must disappear from the scene. Hence those which survive must display some especial fitness for existence under the circumstances of their environment, whatever they may be. So the “survival of the fittest” is believed to be a law of evolution, and the process by which it is brought about has been termed “natural selection.” The works of Darwin and others have satisfied biologists that this is a vera causa.

    Before the excellence of a machine can be tested, it must exist, and before man or nature selects the best, there must be at least two to choose from as alternatives. Furthermore, it is exceedingly improbable that the nicely adapted machinery of animals should have come into existence without the operation of causes leading directly to that end. The doctrines of “selection” and “survival” plainly do not reach the kernel of evolution, which is, as I have long since pointed out, the question of “the origin of the fittest.” The omission of this problem from the discussion of evolution, is to leave Hamlet out of the play to which he has given the name. The law by which structures originate is one thing; those by which they are restricted, directed, or destroyed, is another thing.

    — E.D. Cope, The Origin of the Fittest (1887), p. 225.

  23. Matthew D: ”Darwinists seem to continue promoting the idea that selective advantage = functional complexity”.

    Your reply does not address my post. I made no claim of a change in genomic complexity. To pre-empt any such an argument, I chose the well-defined case of hemoglobin S as opposed to other, slightly more complex mutations that also protect against malaria.

    Rather, my post addressed the initial, somewhat dismissive, statement that “natural selection is really a natural deselection” of the mutant phenotype, and nothing else. Reality is more complex than that, since here is a case where the expected selection against the mutant genotype turned into a selection for it, because of a new circumstance (exposure to plasmodium infection).

  24. Davescot so what are you saying that natural selection doesn’t occur at any level? It’s my understanding that ID does in fact say that natural selection occurs just the extent of change available to natural selection can’t produce new species. On another tread you were happy to lump a Tassie tiger in with wolves, one of them is a mammal and one is a marsupial. There is a fair whack of generic change there so what would you see as the mechanics of that.

  25. Nathan,

    Regarding the “true acid test”, Miller makes his usually slimey argument. What Hall’s experiment suggests is organism have been programmed with adaptive foresight which is definitely non-Darwinian evolution. See Behe’s A True Acid Test:
    Response to Ken Miller
    .

    Salvador

  26. No – I never ran the program again, but there’s no reason to think that the proram will stop at 10-letter words. However there is relatively good reason to think that no 50-letter word will ever be found – because there are no possible 25-letter parent words.

    As in, there are no intermediates? If so, thanks for making my point for me.

    EDIT: If it’s not immediately obvious what my point was:

    Here we have a situation where intermediates are well below 500 informational bits and thus there is nothing to select for that will help much in reaching the goal. Thus this canyon must be bridged in one giant leap, making it difficult for Darwinian mechanisms.

  27. Patrick
    As in, there are no intermediates? If so, thanks for making my point for me.

    Yes. This is what I’ve stated elsewhere re: the sparsity of the english language as a the number of letters in a word gets large. What exactly do you believe that this shows?

    I’ll repeat my previous question: Do we agree that the results indicate a 10^6 fold performance increase for blind darwininian search over exhaustive searches as long as the seach space is sufficiently dense?

  28. Blind? Your program may use Darwinian mechanisms but the performance of the search is largely dependent on the implementation. If the selection filter is too broad in relation to the target area the performance could be worse. Or if it’s significantly narrowed like the “methinks it is like a weasel” program then the search performance will be very fast indeed.

    Don’t tell me you put no thought into designing the best approach for using Darwinian mechanisms? There’s certainly more than one way to implement them, and if used carefully under certain conditions they produce results.

  29. Patrick
    If the selection filter is too broad in relation to the target area the performance could be worse. Or if it’s significantly narrowed like the “methinks it is like a weasel” program then the search performance will be very fast indeed.
    The selection filter was the one spelled out in the original question – set the fitness of a word to the length of the word in letters if it is a valid word, 0 elsewise. I’m not sure what other selection filter you would want to consider.

    Don’t tell me you put no thought into designing the best approach for using Darwinian mechanisms?
    I chose the simplest methods of mutation and cross-over that I could think of so as to avoid any claims that I was inputting information into the process. The code is freely available, if anyone has suggestions for more generic techniques for mutation and crossover, or has ideas as to where my design artificially aids the search, I would be interested to hear them.

  30. “The vast majority of random mutations, if not all random mutations, are neutral at best and immediately fatal at worst.”–DS

    Some genetic mutations in my cafeteria
    Caused tangible, testable real-life hysteria.
    Flagella cut loose
    When the meat went chartreuse,
    Both brewing AND battling bacteria!

  31. I’m not sure what other selection filter you would want to consider.

    I’ll quickly list several implementations I can think of:

    1. “methinks like a weasel” approach
    2. Your approach.
    3. Fitness of the word is determined by length and whether any letter out of 10 matches ANY word. (Example: “nxxcxxxxxsx” is selected for matching “narcissism”). Letters selected as matching a word can still be randomized in the next iteration, so a match can be made with a different word.
    4. It’s been a while since I looked at your program but I’m assuming you’re using ASCII? Fitness of the word is determined by length and the absence of any non-alphabetical characters. As in, fitness is 0 if the generated string contains any character outside of the 52 English alphabet characters (26*2 considering upper and lower case).

    As a filter, they’re listed from “narrow” to “broad”. I’m sure I could think of more. Point is, 1 and 2 are more likely to produce results. 3 and 4 still use Darwinian mechanisms but aren’t designed as well as the top two.

    Now if you could think of a approach that could hit upon 500 informational bits then you’d have a challenge to ID. Especially if that approach is relevant to biology since generating 500 informational bits with no major DIRECT intermediates is the issue at hand.

  32. 3. Fitness of the word is determined by length and whether any letter out of 10 matches ANY word. (Example: “nxxcxxxxxsx” is selected for matching “narcissism”). Letters selected as matching a word can still be randomized in the next iteration.

    This is certainly do-able; I imagine it will result in longer strings being found, since there are significantly more “livable” strings under this condition.

    4. It’s been a while since I looked at your program but I’m assuming you’re using ASCII?
    The code as written actually does not modify the binary representation of characters, but only the characters themselves; so any letter can mutate to any other letter. This means that instead of 2^8 bits of information, each character only contains 26 (~2^5) bits of information. This is represented accurately in the analysis I posted (the brute search is over the same space).

    I’ll let you know if I do the analysis of #3.

    Now if you could think of a approach that could hit upon 500 informational bits then you’d have a challenge to ID.
    Other researchers have developed GA’s that can find long strings of multiple words forming sentences. Would these fit your description?

  33. Oops. I just realized I wrote that one letter is 26 bits of information – of course, 26 ~ 2^5 is 5 bits of information (4.7 to be technical). I meant to say it is equivalent to searching over base-26 representations.

  34. Other researchers have developed GA’s that can find long strings of multiple words forming sentences. Would these fit your description?

    I repeat:

    Especially if that approach is relevant to biology since generating 500 informational bits with no major DIRECT intermediates is the issue at hand.

    Depending on how fitness is defined/designed in an indirect pathway I think it could be done (as in, I highly doubt a direct pathway will work). But to put that into perspective:

    In the “The Evolutionary Origin of Complex Features,” published in Nature in 2003 by Lenski, the selective forces that have 100% probability affixed are those for various simple binary arithmetic functions, which are ultimately used to build the “equals” (EQU) function, and for the EQU function itself. What’s more, the more complex the function, the greater the reward given to the digital organisms for it. There is no analogy for such selective forces in nature. Nature doesn’t care whether something is more or less functionally complex; it only cares whether it can survive in a particular environment. And what happens when no step-by-step rewards are given for functional complexity? An article on AVIDA in Discover magazine last year (Feb. 2005) stated, “When the researchers took away rewards for simpler operations, the organisms never evolved an equals program.” By building rewards into the system — i.e. providing/designing a highly constrained fitness function — the programmers gave the system a purpose. Hence its creative power:

    dynamics.org/Altenberg/FILES/LeeEEGP.pdf

    “Both the regression and the search bias terms require the transmission function to have ‘knowledge’ about the fitness function. Under random search, the expected value of both these terms would be zero. Some knowledge of the fitness function must be incorporated in the transmission function for the expected value of these terms to be positive. It is this knowledge — whether incorporated explicitly or implicitly — that is the source of power in genetic algorithms.”

    So essentially the design of the program would (1) need to produce a positive result and (2) incorporate modern Darwinism (feel free to incorporate other proposed mechanisms besides RM+NS) and (3) need to be relevant to biological reality. #3 has proven to be the tough one.

  35. (3) need to be relevant to biological reality. #3 has proven to be the tough one.

    I agree 100% that the simulation is not an accurate model of biological reality. I only meant the analysis to show that the underlying idea of random mutation combined with a selection critera generates interesting forms faster than blind search.

    If I ever write a GA to model biological reality, I’ll let you know :)

  36. I only meant the analysis to show that the underlying idea of random mutation combined with a selection criteria generates interesting forms faster than blind search.

    Sometimes people think that because I’m an ID proponent that I believe Darwinian mechanisms are completely useless. That’s not so. In the right hands I believe GA’s to be a powerful tool if designed correctly around the intended goal.

    I’m also something of an ID heretic since I consider it may be possible for “emergent complexity” to occur under certain rare cases in an already complex system that’s designed in certain ways. This hasn’t been observed yet but ID may have to be modified to incorporate such scenarios just like Darwinism has been modified so much over the years.

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