Darwinism Information Intelligent Design

Ann Gauger on why Darwinism = information loss

Spread the love

Not gain.

Darwinism, as taught in school, is the claim that natural selection acting on random mutation generates huge levels of information, not noise. Here is what really happens:

Ann Gauger of the Biologic Institute here:

Microbiologist Ralph Seelke and I published a paper in 2010 where we demonstrated that cells always, or nearly always, take the easiest road to success. Given a choice between a simple two-step path leading to repair of two genes needed to make tryptophan, versus a one-step path that eliminated expression of the those genes, only one out of a trillion cells went down the path toward making tryptophan, even though that path would ultimately be much more beneficial. Why did this happen?

The genes to be repaired were overexpressed — too much of their products were made. Because one of the genes was broken in two places, no tryptophan could be made. Thus both genes were expensive to keep around. It was easier for the cell to break the useless genes than to repair them — one step instead of two — and the cells, having no foresight, took that path. Some of those cells deleted the genes, thus losing the information needed to make tryptophan for good.

In fact, that is what we observed. Nearly all the cells inactivated the genes (only one out of a trillion didn’t). Some of the cells even deleted the genes, thus losing the capacity to make tryptophan for good. Darwinian evolution travels by the shortest road, without regard for where it’s headed. And if the shortest road is to break an existing function — to lose information — that’s the path it chooses. More.

That clearly has implications for understanding cancer. The cancer cell is defective as a useful cell, but highly fit when lethal, due to dumped information:

Cancers develop when one or more normal functions in a cell are disrupted or broken. The ironic thing is that for the cancer cells, this breaking increases their fitness, their rate of growth and cell division, and thus is beneficial — to them. Normal constraints have been removed, allowing uncontrolled growth.

In that sense, cancer is a form of devolution. We looked at devolution here: Devolution: Getting back to the simple life:

Most of the time, when we think of evolution, we mean mechanisms for the growth of complex new information. After all, entropy (the tendency for disorder to increase over time) can satisfactorily explain loss of information. Yet, in the history of life, some forms survive while — or even by — losing information (devolution).

Which may not be good news for other parts of the life form or ecosystem.

See Talk to the fossils: Let’s see what they say back for more ways evolution can actually happen.

Here’s the abstract:

New functions requiring multiple mutations are thought to be evolutionarily feasible if they can be achieved by means of adaptive paths-successions of simple adaptations each involving a single mutation. The presence or absence of these adaptive paths to new function therefore constrains what can evolve. But since emerging functions may require costly over-expression to improve fitness, it is also possible for reductive (i.e., cost-cutting) mutations that eliminate over-expression to be adaptive. Consequently, the relative abundance of these kinds of adaptive paths–constructive paths leading to new function versus reductive paths that increase metabolic efficiency–is an important evolutionary constraint. To study the impact of this constraint, we observed the paths actually taken during long-term laboratory evolution of an Escherichia coli strain carrying a doubly mutated trpA gene. The presence of these two mutations prevents tryptophan biosynthesis. One of the mutations is partially inactivating, while the other is fully inactivating, thus permitting a two-step adaptive path to full tryptophan biosynthesis. Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken. This finding has particular significance for models of gene recruitment, since weak new functions are likely to require costly over-expression in order to improve fitness. If reductive, cost-cutting mutations are more abundant than mutations that convert or improve function, recruitment may be unlikely even in cases where a short adaptive path to a new function exists. (Public access) Pdf

Follow UD News at Twitter!

50 Replies to “Ann Gauger on why Darwinism = information loss

  1. 1
    Learned Hand says:

    Darwinian evolution travels by the shortest road, without regard for where it’s headed. And if the shortest road is to break an existing function — to lose information — that’s the path it chooses.

    She acknowledges early on that one in a trillion cells don’t take the short road. Darwinian evolution is what happens to populations, not individuals, right? When the population is way over a trillion cells, then you can’t just ignore the fact that some replicators take a slower but ultimately more successful strategy. As long as the minority eventually reaches a better solution, it’ll be favored by natural selection. I don’t think she’d disagree with this.

    What’s the Biologic Institute up to these days? Their research page doesn’t show anything published in 2015 at all; BIO-Complexity doesn’t seem to have published anything either. Are they going concerns?

  2. 2
    PaV says:

    What if the effective population size is 10,000, or, a 100,000? Then what do you get?

  3. 3
    Learned Hand says:

    Probably not fixation of the slower strategy, I’d guess.

  4. 4
    Virgil Cain says:

    Learned Hand:

    Darwinian evolution is what happens to populations, not individuals, right?

    Natural selection, ie Darwinian evolution, pertains to individuals.

  5. 5
    bFast says:

    Learned Hand, “When the population is way over a trillion cells, then you can’t just ignore the fact that some replicators take a slower but ultimately more successful strategy.”

    Wow, that solves the question of human evolution, doesn’t it. We are at the most populous point in human history, and have a population of about 7 billion. For most of (pre)human history, we’ve been down at a few million.

    Learned hand — population solves it. Nope.

  6. 6
    Learned Hand says:

    Was anything I said inaccurate, or misleading in context? Do you think Gauger would actually disagree with what I wrote?

  7. 7
    asauber says:

    “Darwinian evolution is what happens to populations, not individuals, right?”

    Evolutionists: Trotting Out The Same Tired Evasions Since Apes Became Men.

    Andrew

  8. 8
    Learned Hand says:

    I feel like I triggered a reflex here. bFast is upset that Gauger’s bacterial example assumes population sizes that aren’t relevant to humans–but doesn’t seem to think the underlying point is wrong. Asauber thinks evolution applying to populations rather than individuals is an evasion of… something, I can’t tell what. Not much has been communicated here, guys.

  9. 9
    SteRusJon says:

    Learned Hand,

    Ann Gauger is giving you a “best case scenario” where in a strongly selectable improvement is only two changes away. She notes, honestly, that there is a one in a trillion chance that the two change fix will be found. You clutch the one in a trillion chance to your bosom and completely ignore the larger point that since the “best case scenario” is so remote that the “worser case scenarios” of 3, 4, 5, 6… changes away from improvement are so far out of reach, especially where small populations are concerned, that any rational human being should conclude the must be a different answer.

    Stephen

  10. 10
    Learned Hand says:

    I think a rational being should conclude that the answer would depend on the inputs. The inputs she’s talking about don’t seem all that problematic to me. Others would be. Perhaps her next paper will expand the scope of her inquiry and explore the boundary.

    (ETA, which I should have said from the beginning, I think the title of the post is very misleading. Gauger doesn’t seem to be saying that “Darwinism=information loss.” I don’t think she’d disagree with what I wrote in my first comment, despite the hostility it’s drawn from the other commenters.)

  11. 11
    ppolish says:

    Some of us are old enough to remember when “Made in Jspan” meant low quality. That is, until Dr W.Edwards Deming taught them the concept of “Continuous Improvement” (CI).

    CI is a guided process steeped in statistics. Soon enough, Japanese Manufacturing experienced a “Cambrian Explosion” of better and better designs. Crappy steel wind-up toy cars became Honda and Lexus. Dr Deming became a hero in Japan:)

    Continuous Improvement is the foundation of Nature. Evo Bio guys/gals need to take some business classes. Understand the real world a lot better. Guided and purposeful is Nature.

    In a nutshell, CI says ignore the random defects. They’re random for crying out loud. Concentrate on the defects that are not random. Defects with a cause. Attack the non random if you want to improve. Its how Nature improves.

  12. 12
    Andre says:

    Ppolish

    I remember those days anything out of Japan was known as japcrap…. I am 100% certain that in 2015 it’s no longer a political correct term and I’m in all likelihood going to be labelled a racist, bigot and hater for saying the word. So before anybody loses a brain, please slowdown to a panic and realize I’m only lamenting on the old days.

  13. 13
    Sebestyen says:

    @Learned Hand: https://www.youtube.com/watch?v=KX5jNnDMfxA

    Sounds familiar?

    Sebestyen

  14. 14
    Axel says:

    Deming also prompted cooperation between the workers, instead of competition, but knew it would not be acceptable in the US. However, I believe times have changed!

    He gave them self-belief, the fuel, I suppose, of the Nipponese-Cambrian Explosion. Must have been a remarkable man.

    Also, the money saved and presumably made available for R and D, as a result of MacArthur’s imposition on the CEO’s of an income ratio that was a very low multiple (by our depraved standards, at least) of the entry-level worker, must have been helpful.

  15. 15
    Splatter says:

    I think your assessment is correct Leonard. I don’t see how information loss is relevant here. Her article is, in essence, about improbability. The fact that a desirable mutation is highly unlikely needs to be weighed against the population size. Is there some other aspect I’m missing? The fact she observed the mutation in a lab on a short time scale surely indicates it could be found in nature on a geologic time scale?

  16. 16
    Splatter says:

    Thinking a little further, I guess the improbability of two stage adaptive mutations (1:trillions) helps to hit home how improbable a multistage adaptation would be–astronomically so. So the argument is an extrapolation from empirical evidence, and real measurements, which is refreshing. It basically implies the whole history of life has to rest on adaptive/beneficial mutations that are within the reach of mutations that occur jointly at a couple of sites only. Such a path to every form of life has to exist from the origin of life to the present day.

  17. 17
    Learned Hand says:

    I think your assessment is correct Leonard.

    Oh, I wish I’d thought of “Leonard Hand” when I first registered. Not many people would get it, but it’s a lot cleverer than just using some guy’s name.

  18. 18
    REC says:

    The spin on this paper is getting even more unbelievable. Due to failures in the experimental system, the only question the paper asks is which of two mutually exclusive adaptations happens first: reversion of two specific bases in one gene (without intermediates that are more fit), or any one of a number of changes that inactivate the same pathway.

    The gross over-expression of the proteins in the experimental system imposes a huge fitness cost on the bacteria. Think viral infection-the cells have been hijacked and are spending energy churning out DNA and proteins they don’t want and that are likely toxic.

    Gauger’s own paper shows a variety of single mutations or insertions that spare the bacteria from this cost rapidly sweep her cultures. So before they can find the two steps to evolve tryptophan synthesis, they have punted the pathway, surviving instead by chugging along on the small amount of tryptophan she provides for survival.

    In the 4 years since the paper came out, has she fixed the failed experimental system? The lacZ reversion assay is done on an episome (single copy, little to no cost to bacteria). Why not do the RIGHT experiment, and then tell us the results?

  19. 19
    ppolish says:

    Continuous Improvement, robot style.
    http://newsdaily.com/2015/09/r.....-children/
    Natural Selection the guided way. Purposeful.

  20. 20
    tjguy says:

    One of the mutations is partially inactivating, while the other is fully inactivating, thus permitting a two-step adaptive path to full tryptophan biosynthesis. Despite the theoretical existence of this short adaptive path to high fitness, multiple independent lines grown in tryptophan-limiting liquid culture failed to take it. Instead, cells consistently acquired mutations that reduced expression of the double-mutant trpA gene. Our results show that competition between reductive and constructive paths may significantly decrease the likelihood that a particular constructive path will be taken.

    OK, so evolutionists are people who believe that things with a one in a trillion chance of happening happened over and over again, almost like clockwork, so that the first cell could grow into everything we see all around us.

    And this one in a trillion odds that was listed was only for a two step process. What if more steps are required? Reminds me of Behe’s Edge of Evolution research. It quickly turns into ridiculous odds, as if one in a trillion were not bad enough!

    One in a trillion! Would that ever happen even once? But evolutionists need it to happen over and over and over again! Too incredulous for my little brain.

  21. 21
    Learned Hand says:

    One in a trillion! Would that ever happen even once?

    The odds are the odds. Whether it would happen even once depends on how many times the dice are rolled. What specific odds are you talking about, and what are the numbers?

  22. 22
    Virgil Cain says:

    REC- What experiment could be conducted to show that natural selection and/ or drift can produce a new functioning multi-protein machine?

    What experiments are evolutionists conducting to support their claims?

  23. 23
    bloodymurderlive says:

    Learned Hand I had the same question in mind as I read the article, and you are exactly right to ask it. I’m disappointed that you’ve been largely dismissed, but I will try my best as a layman… The idea of Darwinism is that, while beneficial permutations are outnumbered by deleterious ones, it only has to happen once (within the breeding population) for the change to become fixed. Now, that is the idea; I’m not sure how true that is from a population genetics point of view, but nevertheless… I can understand the confusion about the article because it doesn’t explain what happens when that 1-in-a-trillion event does occur, it just says it’s rare then leaps to the conclusion that Darwinism = information loss overall. So what I think the article meant, and that it did not explain well, is to ask this question: What happens to those rare adaptive gains through generations? Well, since they are so vastly outnumbered by adaptive loses, they are near-certain to be eliminated anyway by the proclivity of cells to favor the simplest adaptation (information loss). It’s crucial to keep in mind that nature does not select for creativity, it selects for fitness. And it turns out that “fitness” usually means information loss. So even if you have information gain, it simply cannot compete with nature’s bias for information loss.

    I hope I explained that in a way that makes sense.

    I think you might appreciate the paper by Behe (linked in “leaky faucet”), published in the same year, but articulated differently: http://goo.gl/hw14Jq

  24. 24
    Starbuck says:

    I wonder if creationists ever google or do they justmake stuff up as they go along, i see dozens of hits some, of which are pretty impressive ancestral ressurrection experiments, which elucidate how multi protein machines evolve

  25. 25
    Virgil Cain says:

    Starbuck- No one knows how multi-protein machinery arose. No one knows how to test the claim that natural selection and/ or drift can produce such a thing.

    So please, spare us your spewage.

  26. 26
    REC says:

    And again, no one even tries to defend the paper.

    Whatever big big numbers IDers tell you come from this paper are the result of a experimental system that imposes a fitness cost on the bacteria. Deactivation of the system through mutation allows the bacteria grow faster. These mutations sweep the population rapidly.

    So you’re looking for two mutations not in a fair system, but one rigged to fail.

  27. 27
    bloodymurderlive says:

    I don’t enough to defend the paper, but Behe’s analysis of long-term bacteria experiments seemed to independently corroborate the phenomenon of adaptive information loss.

  28. 28
    Carpathian says:

    Virgil Cain:

    What experiments are evolutionists conducting to support their claims?

    What experiments are IDists conducting to support their claims?

  29. 29
    Virgil Cain says:

    Carpathian, We already know that you are a scientifically illiterate coward. We don’t need you to keep proving it.

    We have been over the experiments IDists conduct to support our claims. Your willful ignorance is not an argument.

  30. 30
    Virgil Cain says:

    REC- AGAIN, what do you have? Lenski doesn’t help you.

  31. 31
    Starbuck says:

    No response fron creationists regarding the myriad of ancestral ressurrection experriments which elucidate how multi protein machines evolve, pathetic

  32. 32
    Dr JDD says:

    Care to provide this creationist with some references supporting your claim Starbuck?

  33. 33
    Virgil Cain says:

    No response from evos regarding the evolution of multi-protein machines via natural selection and/ or drift- or any other materialistic process.

  34. 34
    Virgil Cain says:

    Defending Ann- Random mutations are noise and noise always causes a loss of information.

  35. 35
    SteRusJon says:

    Dr JDD,

    Starbuck has invoked the “literature bluff” Unless he can produce a specific paper or two that supports whatever point he is attempting to make, there is no need to pay any attention to him. It is not our responsibility to hunt down his rabbits for him.

    However, out of curiosity, I went to Google and did a search. I found one hit that seemed to hold promise that I would find his point. It was a reference to a study in progress titled “Experimental Evolution and Genomic Analysis of an E. Coli Containing a Resurrected Ancestral Gene”. The gene in the research produces the Elongation Factor (EF) protein.

    Some of what I read brought a smile to my face. In one place they ask the question “Will the ancient protein evolve exactly into its modern descendant, or in what other ways the bacteria and the ancient gene will co-adapt?” Later they state, “Null alleles (in genes infB and nusA) are detected in one evolved lineage for the EF protein-protein interaction network. These mutations result in a loss of function in Initiation Factor (IF2) protein (an essential protein involved in the ribosomal machinery) and a nusA protein (a transcription regulatory protein), and are known to interact with EF…” (emphasis mine)

    If Starbuck’s point was that it is easier to break something that create a new, better mousetrap, he succeeded.

    There you are Starbuck. Did you make your point with me or not?

    Stephen

  36. 36
    Alicia Cartelli says:

    Perhaps these were some of the papers that Starbuck was referring to?

    Resurrecting the Ancestral Steroid Receptor: Ancient Origin of Estrogen Signaling. Thornton et al.

    Evolution of Minimal Specificity and Promiscuity in Steroid Hormone Receptors. Eick et al.

    Biophysical mechanisms for large-effect mutations in the evolution of steroid hormone receptors. Harms et al.

    Evolution of increased complexity in a molecular machine. Finnigan et al.

    Molecular analysis of the evolutionary significance of ultraviolet vision in vertebrates. Shi & Yokoyama

    Reconstruction of Ancestral Metabolic Enzymes Reveals Molecular Mechanisms Underlying Evolutionary Innovation through Gene Duplication. Voordeckers et al.

    Hyperstability and Substrate Promiscuity in Laboratory Resurrections of Precambrian ?-Lactamases. Risso et al.

    An epistatic ratchet constrains the direction of glucocorticoid receptor evolution. Bridgham et al.

  37. 37
    Virgil Cain says:

    Alicia:

    Perhaps these were some of the papers that Starbuck was referring to?

    Which paper(s) support natural selection and/drift producing multi-protein machinery? Please be specific

  38. 38
    Alicia Cartelli says:

    They all provide evidence for the evolution of molecular machinery, Virg.

  39. 39
    Virgil Cain says:

    Alicia Cartelli is an equivocating imbecile. MULTI-PROTEIN machinery you ignorant arse. Grow up.

  40. 40
    Alicia Cartelli says:

    Virtually all cellular machinery is multi-protein, Virg. They probably don’t mention that in your biology pop-up book though.
    Toodaloo!

  41. 41
    Virgil Cain says:

    Alicia, Your position cannot account for any proteins. And the Thornton paper was about one enzyme. One is not multi.

    I bet they didn’t mention that in your kindergarten class.

  42. 42
    Alicia Cartelli says:

    Wrong again, Virg.
    The Thornton paper is about the estrogen receptor, which not only dimerizes (that’s two proteins) but also binds co-activators, forming a multi-protein complex.
    I will not be responding to you again, it’s just too unfair.

  43. 43
    Virgil Cain says:

    Alicia- buy a vowel:

    The Thornton paper is about the estrogen receptor, which not only dimerizes (that’s two proteins) but also binds co-activators, forming a multi-protein complex.

    The estrogen receptor is NOT multi-protein machinery. What is wrong with you? And yours can’t explain the co-activators.

    I will not be responding to you again

    All you do is misrepresent what I post. It’s as if you have the pathological arse gene.

  44. 44
    Virgil Cain says:

    Alicia has failed, miserably, to answer this question:

    Which paper(s) support natural selection and/drift producing multi-protein machinery? Please be specific

    ID is not anti-evolution so saying the papers are about evolution is cowardly equivocating. I asked for evidence for natural selection and/ or drift producing it. Unfortunately no one can model such a thing.

  45. 45
    Mung says:

    Virgil, there is a massive amount of evidence of natural selection and/drift producing multi-protein machinery published in millions of papers. You can either go read them all and find out for yourself, or you can just believe it is true, like Alicia.

  46. 46
    Virgil Cain says:

    Mung, I have looked and haven’t found any papers that show “evidence of natural selection and/drift producing multi-protein machinery”.

  47. 47
    bloodymurderlive says:

    So… Nobody responded to my first comment directed at LearnedHand… Since I am a layman, this can only mean one of two things: 1) I’m so wrong that nobody wants to even bother correcting me, or 2) I’m right, but nobody really thinks it’s an important point.

    All I want to know is: Am I right or am I wrong? Did I correctly interpret the point that Ann is trying to make? Help a layman out…

  48. 48
    Upright BiPed says:

    Bloody,

    I won’t attempt an answer to your question because I haven’t been following along. But I will welcome you to UD. Hope you stay a while…

  49. 49
    bloodymurderlive says:

    Thanks Upright BiPed. My main comment is at 23, followed by a very quick, separate point at 27. Any feedback, however brief, would be much appreciated.

  50. 50
    EugeneS says:

    Bloodymurderalive #23,

    The same occurred to me as I was reading the OP. As I am also a layman in biology, I think that you are right )

    In terms of information gain/loss, evolution can lead to information gain but its magnitude is statistically insignificant. It is noise in comparison to the amount of information there needs to be for evolutionary oscillations to even start.

    Imagine you get a verbal message from you friend who asked you to pass this message on to an addressee by email. When you heard the message say over the phone, you misheard a bit (e.g. that the meeting is to start at 10am) and interpreted it wrong (say that the meeting is to start at 11am). However, when you typed it, you accidentally corrected it and typed ’10am’. Obviously, when you incorrectly received it, there was an accidental information loss on your part. However when you relayed it, this loss was accidentally compensated for. It is important to realize that the whole exercise started off with an initial meaningful message (which is long enough).

    A similar sort of thing is the case with evolution (there you have selection which makes it special though). We need to bear in mind that evolution does not select for a future function. Instead, it selects from among existing functions. Functions must somehow appear first. The evolutionist treatment of this is unacceptable. Functions can only have intelligent origin (via decision making and planning). All this evolutionist gubbins about co-optation and gene duplication is bluff because it assumes the existence of sophisticated machinery that makes decisions about when and how to switch from one function to another. Co-optation is the major argument from people like Ken Miller. I am nobody compared to him in biology really but people of his caliber are expected to take such things into consideration (either he does not know these things, which I find hard to believe, or he must be taking them for granted, which he should not be).

    ID is not anti-evolution in principle though. The question of the actual limits of evolution is non-trivial and different from the main ID claims.

    The main ID claim is that intelligence is irreducible to naturalistic causation (chance and law-like necessity). In particular, in relation to biology this translates to the claim that the best explanation of the existence of organisms being decision making systems is intelligence via decision making.

Leave a Reply