The Panda's Thumb Legacy Archive — pandasthumb.net

Haldane's non-dilemma

Posted 1 July 2007 by Ian Musgrave

Quick, before I start the post proper, guess how many beneficial mutations separate us from the last common ancestor of humans and chimpanzees. Write your guess on a bit of paper, then read on. Over at Uncommon Descent, Dave Scott opines
"Coyne and his chance worshipping peers are stuck between a rock and a hard place. The rock is gradualism and the hard place is Haldane's Dilemma (http://en.wikipedia.org/wiki/Haldane's_dilemma) . As gradualism gets more gradual Haldane's Dilemma gets more difficult to overcome -- there's a limit to the number of mutations that can become fixed. As gradualism gets less gradual then the improbability of simultaneous beneficial mutations becomes more difficult to overcome. A truly classic example of being stuck between a rock and a hard place!"
The "simultaneous beneficial mutations" argument is a relatively new (or at least rejigged) argument that is dealt with elsewhere (see also here). However, Haldane's dilemma has been a favoured argument in anti-evolution circles for a long time. Unfortunately for the anti-evolutionists, Haldane's dilemma has never been a barrier to evolution, despite their misrepresentations. Recent work from the Human, Chimpanzee and Macaque genome projects underlines the fact that Haldane's dilemma does not prevent evolution, and it is worthwhile revisiting one of the core anti-evolution arguments relating to it in the light of these results. Firstly, some background to the issue. In 1957, the evolutionary biologist JSB Haldane published a paper that calculated, based on a series of assumptions, that on average it took about 300 generations for a beneficial allele to go from initial appearance to being present in all members of a population (the allele is "fixed" in the population). This figure was pretty well constant over a range of selection intensities [1]. Anti-evolutionist Walter ReMine has latched onto this paper, claiming that it presents severe problems for evolution. His key claim is that Haldane's dilemma makes it impossible to fix more than 1,667 beneficial mutations since the last common ancestor of humans and chimps (ReMine, "The Biotic Message", page 217). ReMine claims that 1,667 beneficial mutations are too few to make a poet-philosopher from an ape, therefore Haldane's dilemma shows evolution cannot account for humans. The recent genome results directly address this argument, but before I tackle this, I'd like to cover a few misrepresentations. The misrepresentation starts in ReMines presentation of Haldanes paper.
"In the 1950's the evolutionary geneticist JBS Haldane, calculated the maximum rate of genetic change due to differential survival. He reluctantly concluded that there is a serious problem here, now known as Haldane's Dilemma." ReMine, pg 208, first para. Emphasis added.
Contrast this with what Haldane actually wrote (this is the entire summary from the paper).
"Unless selection is very intense the number of deaths needed to secure the substitution by natural selection, of one gene for another at a locus, is independent of the intensity of selection. It is often about 30 times the number of organisms in a generation. It is suggested that in horoletic evolution, the mean time taken for each gene substitution is about 300 generations. This accords with the observed slowness of evolution" (page 524 Haldane JBS. (1957). The cost of natural selection. J Genet, 55, 511-524) Emphasis added.
Haldane several times points out his calculations accord with observed rates of evolution. In the entire paper (nor in his later 1961 paper), there is NO mention of any serious problem. ReMine further misrepresents Haldane and the significance of his work:
"His calculations show that many higher vertebrate species could not plausibly evolve in the available time" (ReMine op cit).
In fact, Haldane gives two examples where the evolutionary rates accord with his calculations (average rate of speciation in the carnivora, and mammalia on page 522, his conclusion: "the agreement with the theory developed here is satisfactory"). Haldane also gave examples where evolution could fix substitutions faster than under his assumptions (see page 523, where he discusses radiation of species into environments with few or no competitors, and the introduction, where he discusses intense selection). Haldane also explicitly acknowledged that these were preliminary approaches to developing a mathematical treatment of selection. In 1961 produced a paper where he revised his approach, and found at least one more circumstance where evolution could proceed faster than with his original assumptions. What the real problem is: One of the consequences of Haldane's calculation is that it sets an upper limit to the amount of allelic variation (heterozygosity) in the genome. Under Haldanes's assumptions, if different alleles of genes represent deleterious variants being selected against, too much variation means that the organisms fitness fall below survivable levels. When the variation in the genomes of several organisms was measured, it was way above the limits that would be survivable if Haldane's assumptions held. The problem is not that evolution is too slow; the problem is that it is much faster than Haldane's limit. Lets restate that, the amount of measured variation in the genome meant that if Haldane's assumptions were right, all vertebrates would be dead. So we know that Haldane was wrong. Exactly where he was wrong occupied many pages of journal articles in the 60's and 70's. Kimura (Kimura, 1968) used the heterozygosity problem to advance the neutral theory. In neutral theory, most mutations are neutral with respect to fitness, and neutral alleles are fixed by drift. Since the alleles have no effect on fitness, a very large number of allelic variants can be in the population and not reduce its fitness, thus solving the heterozygosity problem. Several others proposed selectionist explanations using different assumptions to Haldane's that could drive more substitutions. The technical details need not concern us here, suffice it to say there were a number of models which could exceed Haldane's "speed limit" (soft selection, truncation selection and gene hitchhiking for example. All of which have some experimental and observation evidence, see Ewens, 1969, Grant and Flake 1974, Smith, 1968 and many others in the reference list). The discussions over Haldane's dilemma rapidly got subsumed into the larger neutralist vs adaptionist debate. In the end, the evidence came down on the side of the neutralists, and it is accepted that the majority of variation in genomes is due to neutral mutations [2]. How many benefical mutations? While the majority of variation is neutral, the question remains exactly how much variation is due to selection, and does it break Haldane's "speed limit". Recent comparisons of Human and Chimp genomes, using the Macaque as an out group, have given us a good idea of how many genes have been fixed since the last common ancestor of chimps and humans (Bakewell, 2007). 154 Actually, that's 154 of 13,888 genes. Given that we have around 22,000 genes [3] in our genome (http://www.ensembl.org/Homo_sapiens/index.html), then if the same percentage of beneficial mutations holds for the rest of the genome, no more than 238 fixed beneficial mutations is what separates us from the last common ancestor of chimps and humans. You are probably sitting there astonished that we are around 240 genes away from our last common ancestor with the chimp and saying "this can't be right"[4] (how much did the guess you wrote down differ from the real thing?). However, this result agrees with previous estimates of the number of positively selected genes (Arbiza, 2006, Yu 2006). You can argue until the cows come home about whether you can get around Haldane's assumptions using truncation selection, soft selection or whatever, the plain fact is that humans and the last common ancestor of humans and chimps are separated by far fewer fixed beneficial mutations than even Haldane's limit allows. Now, it's likely that the above values is an underestimate, and the some weakly selected genes have been missed, but it is in accord with previous studies using smaller gene sets (Arbiza, 2006, Yu 2006). Even if you say we missed half of the genes that underwent selection (very unlikely), the number of beneficial genes fixed by natural selection would be around 480, and the real number is certainly less (Arbiza, 2006). The above study only covered protein coding genes, not regulatory sequences, and most biologists expect that changes in regulatory sequences played an important role in evolution. Getting at the number of beneficial mutations in regulatory genes that have been fixed by natural selection is a lot harder, but it seems like around 100 regulatory genes may have been selected (Donaldson & Gottgens 2006, Kehrer-Sawatzki & Cooper 2007). Again, even if we set the number of regulatory genes that have been selected as the same number as the most wildly optimistic estimate of protein coding genes fixed by natural selection, then we end up with 960 fixed beneficial mutations, below ReMine's calculation of Haldane's limit [5]. This means Haldane's dilemma is irrelevant to human evolution. Conclusion: Haldane's dilemma has never been a problem for evolution, but the technical nature of the arguments involved made it difficult to clearly demonstrate anti-evolutionists misuse of the "dilemma". Also, the difficulty in getting the original papers meant that the distortion of Haldane's work by anti-evolutionists was not obvious. Now Walter ReMine's claim that 1667 beneficial mutations is too few to generate a philosopher poet from the common ancestor of chimps and humans is shown to be trivially false from comparison of the human and chimp gemone. As this claim was the keystone of ReMine's argument, Haldane's dilemma should disappear as an anti-evolutionist claim. Notes: [1] The actual "dilemma" of Haldane's Dilemma, is that, under a number of limiting assumptions at modest selection intensities, you cannot speed up the rate of substitutions by simultaneously selecting multiple beneficial mutations. If you increase the number of mutations you select, you have to decrease selection intensity to stop the population going extinct. Haldane himself never used the term "Dilemma", and it isn't used all that often in the technical literature. For a fuller discussion of Haldane's calculations see Robert William's explanation. [2] Well, technically, the Nearly Neutral model won. Also, biology being what it is, in some organisms (like the fruit fly Drosophilia) there is a slight excess of benefical vs neutral mutations. But generally, neutral or nearly neutral mutations rule. [3] In the light of the human genome project, it is amusing to consider this paragraph from Remine, in his 1993 book (page 249). "The evolutionary scenario, as presently told, requires that the expressed portion of the genome must be less than one part in 164. That is only 0.6%, since the typical gene is 1000 nucleotides, that could encode about 22,000 genes. That is not enough to encode all the things that make humans." Current evidence is that around 1.2% of the genome codes for protein, about the same amount for structural RNA and another 5% for regulatory sequences. [4] While we are around 240 genes away from the LCA, we are around 594 genes way from the chimp, they have fixed about 50% more genes since the LCA than we have. Most of the genes substituted are for immune and reproductive system genes, and only a handful seem to have anything to do directly with brain function. [5] ReMine calculated his substitution number with a chimp human split of 10 Million years, if we used the currently accepted 6 million years for the split, the figure is 1,000, still above the optimistic estimate for gene differences. For a good (mostly) non-technical discussion of Haldane's dilemma, from a slightly different perspective to the one I present here, see Robert William's Haldane pages. For a more technical paper with simulations showing that selection can exceed Haldane's limit see Nunney 2003. References relevant to Haldane's dilemma, see particularly Flake and Grant.
  • Arbiza L, Dopazo J, Dopazo H. (2006) Positive selection, relaxation, and acceleration in the evolution of the human and chimp genome. PLoS Comput Biol. Apr;2(4):e38.
  • Bakewell MA, Shi P, Zhang J. More genes underwent positive selection in chimpanzee evolution than in human evolution. (2007) Proc Natl Acad Sci U S A. May 1;104(18):7489-94.
  • Christiansen FB. (1990 Feb). Simplified models for viability selection at multiple loci. Theor Popul Biol , 37, 39-54.
  • Donaldson IJ, Gottgens B. (2006) Evolution of candidate transcriptional regulatory motifs since the human-chimpanzee divergence. Genome Biol. 2006;7(6):R52.
  • Ewens WJ. (1969 Mar 15). Mean fitness increases when fitnesses are additive. Nature, 221, 1076.
  • Felsenstein J, (1971) On the biological significance of the cost of gene substitution. The American Naturalist 105, 1-11.
  • Flake RH, and Grant V. (1974 Sep). An analysis of the cost-of-selection concept. Proc Natl Acad Sci U S A , 71, 3716-20.
  • Grant V, and Flake RH. (1974 Oct). Solutions to the cost-of-selection dilemma. Proc Natl Acad Sci U S A , 71, 3863-5.
  • Haldane JBS. (1957). The cost of natural selection. J Genet, 55, 511-524
  • Kehrer-Sawatzki H, Cooper DN (2007). Understanding the recent evolution of the human genome: insights from human-chimpanzee genome comparisons. Hum Mutat. Feb;28(2):99-130.
  • Kimura M. (1968 Feb 17). Evolutionary rate at the molecular level. Nature, 217, 624-626.
  • Mukai T, Schaffer HE, and Cockerham CC. (1972 Dec). Genetic consequences of truncation selection at the phenotypic level in Drosophila melanogaster. Genetics , 72, 763-9.
  • Nunney, L (2003) "The cost of natural selection revisited", Ann. Zool. Fennici. 40:185-194.
  • O'Donald P. (1969 Mar 1). "Haldane's dilemma" and the rate of natural selection. Nature , 221, 815-7.
  • ReMine WJ, (1993) The Biotic Message, St Paul Science.
  • Smith JM. (1968 Sep 14). "Haldane's dilemma" and the rate of evolution. Nature , 219, 1114-6.
  • Sved JA, Reed TE, and Bodmer WF. (1967 Mar). The number of balanced polymorphisms that can be maintained in a natural population. Genetics, 55, 469-81.
  • Taddei F, Radman M, Maynard-Smith J, Toupance B, Gouyon PH, and Godelle B. (1997 Jun 12). Role of mutator alleles in adaptive evolution. Nature , 387, 700-2.
  • Yu XJ, Zheng HK, Wang J, Wang W, Su B.( 2006) Detecting lineage-specific adaptive evolution of brain-expressed genes in human using rhesus macaque as outgroup. Genomics. 88(6):745-51.

    • 66 Comments

    TheBlackCat · 1 July 2007

    Very nice explanation. I would be interested to see a more in-depth explanation of "lethal" heterozygosity levels and the various ways later researchers were able to account for them. It sounds like an interesting topic and useful for stopping any creationist who tries to bring Haldane up as an argument.

    I guessed 300.

    caligula (Esko Heimonen) · 1 July 2007

    I want to once more point out something. As I claim in the "Discussion" section of the Wikipedia "Haldane's dilemma" article, Haldane(1957) entirely omits intraspecific competition. I give the most obvious example of this concept in the form of intraspecific competition over territory. Without evolving one bit against external selection pressures imposed by the environment, a subpopulation can evolve to become better at intraspecific territorial contests. By inhabiting territories most suitable for reproducive success, the subpopulation, a new genotype, "steals" fitness from others in the species. This kind of development doesn't change the average fitness of the population as a whole one bit, because it is just a case of re-distribution of a finite resource in the ecological niche between genotypes -- it's literally a transfer of fitness benefits from the native genotype to the new optimal genotype.

    Such evolution does not involve new environmental selection pressures and, hence, does not reduce the average fitness. Yet it is just as capable of driving allele substitutions as is adaptation to environmental challenges. This is because intraspecific competition creates a genetic load between the native genotype and the optimal genotype. The tendency of the optimal genotype to hog resources from the old genotype grants the optimal genotype a better-than-average fitness. When the frequency of the optimal genotype is still tiny, this doesn't hurt the native genotype all that much. But as the optimal genotype increases its frequency, it starts to really harm the fitness of the native genotype, whose fitness falls below average. At the same time, the fitness of the optimal genotype itself also suffers, because it is harder to compete against your peers than against the old genotype. By the time the old genotype has gone extinct, the fitness of the optimal genotype has again returned to the original mean fitness: there are only peers left, and it is just as hard to conquer a territory from them as it was for the old genotype to conquer a territory from its peers.

    I believe similar thinking applies to many other kinds of resources, including social status (especially the alpha male status in a harem species).

    David Stanton · 1 July 2007

    "Now Walter ReMine's claim that 1667 beneficial mutations is too few to generate a philosopher poet from the common ancestor of chimps and humans is shown to be trivially false from comparison of the human and chimp gemone. As this claim was the keystone of ReMine's argument, Haldane's dilemma should disappear as an anti-evolutionist claim."

    You are an optomistic individual. Facts did not stand in the way of the Second Law of Thermodynamics argument, or any other creationist talking point for that matter. I predict that every creationist claim ever made will made forever by someone, no matter how many times they are proven do be dead wrong. And this will be especially true for claims of a technical nature where apeal to authority will be more effective and the truth harder to grasp.

    Still, an excellent synopsis of the topic. None of the above should take away from importance of new evidence interpreted in the light of old theories.

    I guessed 500.

    argystokes · 1 July 2007

    Recent comparisons of Human and Chimp genomes, using the Macaque as an out group, have given us a good idea of how many genes have been fixed since the last common ancestor of chimps and humans

    — Ian
    Presumeably this should read "mutations," rather then "genes" where I've highlighted?

    Apeman · 1 July 2007

    I think everyone should take the numbers with a grain of salt.

    1. Number of positively selected genes != Number of positively selected alleles.

    2. Statistical tests for positive selection in the human or chimpanzee lineages are vastly underpowered. True positives in these tests are likely to be biased towards genes that have undergone sustained selection over the last 5 million years.

    3. Tests for positive selection in recent human history (last 10,000 years or so) have found more candidates for selection as the human-chimp comparisons (which cover the last 5 million years or so) have. This is almost certainly because population variation data provides much more power.

    Still, the overall point is right. Even if the post is off by an order of magnitude or two, the number of selection events involved in shaping the human species is strikingly small. There are something like 40 million genetic differences between humans and chimps. The vast majority of these were clearly neutral.

    Don Smith, FCD · 1 July 2007

    You are probably sitting there astonished that we are around 240 genes away from our last common ancestor with the chimp and saying "this can't be right"

    — Ian
    I think you are confusing us with religious fundamentalists who can't tolerate being closely related to a "dumb animal". :) I also guessed 300.

    Joe · 1 July 2007

    Sorry to be dense, but in note 4, you state "Most of the genes substituted", are those for human, or chimp genes?

    caligula · 1 July 2007

    My "guess" was borrowed from Sean Carroll's "Endless Forms Most Beautiful": a few thousand adaptations, including genes and genetic switches.

    Torbjörn Larsson, OM · 1 July 2007

    Thank you, I have thought that this subject would be worth a thorough analysis with the new available data. Yet it turned out more decisive than I expected. I guessed 300 (no kidding).
    Most of the genes substituted are for immune and reproductive system genes
    I am growing quite tired of the constant discussion on chimps frivolous social behavior and large balls. ;-) But perhaps you incorporate human genes as well, in which case it may be a sign of the cramped conditions that human reproduction takes place in. :-(

    William E Emba · 1 July 2007

    You are probably sitting there astonished that we are around 240 genes away from our last common ancestor with the chimp and saying "this can't be right".

    — Ian Musgrave
    What's probably more remarkable is that about half of the differences are the human loss of olfactory ability. Smells are directly linked to emotions, whereas sight and sound have to go through internal cascades and channels. The result, apparently, is that we can engage the world in a much more rational manner than chimpanzees, who are forever distracted by hot-button distractions. (I think Robert Sapolsky Monkeyluv discusses this, but I'm not certain.)

    Torbjörn Larsson, OM · 1 July 2007

    the cramped conditions that human reproduction takes place in
    Better make that the later part of reproduction, no specific complaints about the beginning of the process. ;-)

    jeannot · 1 July 2007

    Excellent article.
    However, I have one question:
    Is the detection of positive selection acting on a gene (Ka/Ks) more likely if many positive mutations occurred in that gene?

    Anyway, it seems to me that a number of PSGs should not be considered as a number of mutations. Particularly, one could argue that, during adaptation, several successive beneficial mutations may happen in a given gene.

    Am I missing something?

    jeannot · 1 July 2007

    Ok, Apeman raised the same objections, only with better formulation.

    Bond, James Bond · 1 July 2007

    The fact is that nearly all mutations are slightly harmful. (I'll leave the handful of questionable beneficial mutations alone for right now) Thus your problem is how does natural selection get rid of harmful mutations that are below its radar screen before they spred throughout the entire population. Genetic meltdown is sure to occur and indeed such a scenario would fit in well with the majority of extinctions in the fossil record that are not caused by natural catastrophies

    caligula · 1 July 2007

    even if we set the number of regulatory genes that have been selected as the same number as the most wildly optimistic estimate of protein coding genes fixed by natural selection, then we end up with 960 fixed beneficial mutations

    — Ian Musgrave
    I assume that a "regulatory gene" means a binding site in DNA for a Hox gene, or a "genetic switch". I'm a bit puzzled about Ian's wording even if. It's as if he found it unlikely that these regulatory DNA sequences have experienced as many adaptations, relatively, as protein coding genes. But I find it likely that there have been an order or even many orders of magnitude more adaptations, relatively, in regulatory regions. Isn't the basic message of "evo-devo" that, after the Cambrian, evolution has been mostly about regulatory changes, rather than about new cell types or proteins? If this thinking applies, then it simply may not be valid to estimate the number regulatory adaptations based on the number of new proteins.

    Ian Musgrave · 1 July 2007

    Presumeably this should read "mutations," rather then "genes" where I've highlighted?

    — argystokes
    You're substituting mutant alleles (ie one version of a gene for another version of a gene), rather than mutations per se, but that could have been worded better.

    Gary Hurd · 1 July 2007

    I was way far off. I guessed around 1000 split between chimps and human. I thought about 25,000 genes, 2% difference going each way.

    Oops! I must read all those Science and Nature magazines that got stuffed under the bed! I will read the science literature more than the freaking creationist's crap from now on.

    Thanks for a good read, Ian.

    Ian Musgrave · 1 July 2007

    Tests for positive selection in recent human history (last 10,000 years or so) have found more candidates for selection as the human-chimp comparisons (which cover the last 5 million years or so) have. This is almost certainly because population variation data provides much more power.

    — Apeman
    And these tests are far more subject to false positives. Remember microcephalin? And microcephalin was a strong candidate. Many of these candidates will be found to be false positives. Still, the point is that the number of selected genes from either sets of estimates is explainable by natural selection. ReMine wanted a way to substitute a hundred thousand genes, which is completely irellevant.

    Sir_Toejam · 1 July 2007

    Haldane's dilemma has been a favoured argument in anti-evolution circles for a long time.

    The misrepresentation starts in ReMines presentation of Haldanes paper.

    ReMine Re-Mine the guy couldn't be named more appropriately. It's like someone with a last name of Bird, who researches birds. It makes me think it must be a pseudonym, it just fits so perfectly.

    Sir_Toejam · 1 July 2007

    Thus your problem is how does natural selection get rid of harmful mutations that are below its radar screen before they spred throughout the entire population.

    *shakes head ala Lewis Black* this is so full of contradiction i can't even make fun of it. >:(

    Apeman · 1 July 2007

    And these tests are far more subject to false positives. Remember microcephalin? And microcephalin was a strong candidate.

    Not outside of Chicago. There's more solid work out there, which I think will hold up, but we'll see...

    Still, the point is that the number of selected genes from either sets of estimates is explainable by natural selection. ReMine wanted a way to substitute a hundred thousand genes, which is completely irellevant.

    Agreed!

    Chip Poirot · 1 July 2007

    Since my own knowledge of genetics is pretty limited, I wasn't even able to hazard a guess. Even so, 240 strikes me as an interesting number. There's enough information 240 genes to make a difference. But how much of a difference?

    The more I learn about actual chimp and bonobo behavior in the wild and the more I compare chimp/bonobo physiology and behavior with human, the more I am struck by how small the differences sometimes are.

    When you think about it, the distance from a chimp to Lucy is not that far at all-and then to go from Lucy to the genus homo is not very far at all. Then its just a hop, skip and jump till you get something that looks modern and acts almost modern. And then, it's just minute changes to go from antecessor to something fully, completely modern.

    If I think about it this way, 240 genes makes sense. No wonder creationsts can't tell ape skulls from human ancestor skulls-in a very real way, they are the same. They just are not the same of course in the way creationists think they are.

    Henry J · 1 July 2007

    Re "As this claim was the keystone of ReMine's argument, Haldane's dilemma should disappear as an anti-evolutionist claim."

    Is that like the way the 2nd law of TD argument disappeared once it was refuted in more than a dozen different ways? ;)

    Re "The result, apparently, is that we can engage the world in a much more rational manner than chimpanzees, who are forever distracted by hot-button distractions."

    Now that's interesting - a strong sense of smell interferes with thinking? Who'd have thought it!

    Henry

    Bond, James Bond · 1 July 2007

    This still doesn't solve your problem at the level of SNP to the genome. To prove evolution you would have to demonstrate that the genome has more than a slight flexiblity to random mutations.

    Evolution's most flaw, to being scientifically validated, is the absolute inability of any natural methods to account for the generation of meaningful information in the DNA.
    Naturalists always try to establish scientific validity for evolution by pointing to suggestive similarities while ignoring the foundational principle of science (genetic entropy) that contradicts their preconceived philosophical bias. For example, naturalists say that evolution is proven true when we look at the 98.8% similarity between certain segments of the DNA in a Chimpanzee and compare them with the same segments of DNA of a Human. Yet that similarity is not nearly good enough to be considered "conclusive" scientific proof. For starters, preliminary comparisons of the complete genome of chimps and the complete genome of man yield a similarity of only 85 to 90% (Ross; Creation as Science). Secondarily, at the protein level only 29% of genes code for the exact same amino acid sequences in chimps and humans (Nature, 2005). As well, our DNA is found to be 92% similar to mice as well as 92% similar to zebrafish (Simmons PhD., Billions of Missing Links). So does that make us 92% mouse or are we 92% zebrafish? Our DNA is 44% similar to a fruit fly; So are we therefore 44% fruit fly? Our DNA is 18% similar to the weed thale cress; So does that make us 18% thale cress? No, of course not!! This type of reasoning is simple minded in its approach and clearly flawed in establishing a solid scientific foundation on which to draw valid inferences from! Clearly, we must find if the DNA is flexible enough to accommodate any type of mutations happening to it in the first place. This one point of evidence, (The actual flexibility of DNA to any random mutations), must be firmly established, first and foremost, before we can draw any meaningful inferences from the genetic data we gather from organisms!! Fortunately we, through the miracle of science, can now establish this crucial point of DNA flexibility. The primary thing that is crushing to the evolutionary theory is this fact. Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or to the life-form having the mutation (Gerrish and Lenski, 1998)! Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Yet at the same time, the evidence for the detrimental nature of mutations is overwhelming for doctors have cited over 3500 mutational disorders (Dr. Gary Parker).

    "It is entirely in line with the al nature of naturally occurring mutations that extensive tests have agreed in showing the vast majority of them to be detrimental to the organisms in its job of surviving and reproducing, just as changes ally introduced into any artificial mechanism are predominantly harmful to its useful operation" H.J. Muller (Received a Nobel Prize for his work on mutations to DNA)
    "But there is no evidence that DNA mutations can provide the sorts of variation needed for evolution... There is no evidence for beneficial mutations at the level of macroevolution, but there is also no evidence at the level of what is commonly regarded as microevolution." Jonathan Wells (PhD. Molecular Biology)

    Man has over 3 billion base pairs of DNA code. Even if there were just a 1% difference of DNA between monkeys and humans, that would still be 30 million base pairs of DNA difference. It is easily shown, mathematically, for it to be fantastically impossible for evolution to ever occur between monkeys and man, or monkeys and anything else for that matter. Since, it is an established fact that at least 999,999 in 1,000,000 of any mutations to DNA will be harmful and/or , then it is also an established fact that there is at least a 999,999^30,000,000 to one chance that the monkey will fail to reach man by evolutionary processes. The monkey will hit a end of harmful/fatal mutations that will kill him or severely mutilate him before him. The poor monkey barely even gets out of the evolutionary starting gate before he is crushed by blind chance. This would still be true even if the entire universe were populated with nothing but monkeys to begin with! This number (999,999^30,000,000), is fantastically impossible for any hypothetical beneficial mutation to ever overcome! Worse yet for the naturalists, mathematician William Dembski PhD. has worked out the foundational math that shows the mutation/natural selection scenario to be impossible EVEN IF the harmful/fatal rate for mutation to the DNA were only 50%. The naturalist stamps his feet again and says that symbiotic gene transfer, cross-breeding (yes they, desperately, suggested cross-breeding as a solution), gene duplication and multiplication of chromosomes, alternative splicing etc .. etc .. are the reasons for the changes in DNA between humans and apes. They say these things with utmost confidence without even batting an eye. Incredibly, this is done in spite of solid evidences testifying to the contrary. Indeed, even if a hypothetical beneficial mutation to the DNA ever did occur, it would be of absolutely no use for it would be swallowed in a vast ocean of slightly detrimental mutations that would be below the culling power of natural selection!
    "We see the apparent inability of mutations to truly contribute to the origin of new structures. The theory of gene duplication in its present form is unable to account for the origin of new genetic information" Ray Bohlin, (PhD. in molecular and cell biology)

    caligula · 1 July 2007

    Hate to repeat myself, but...

    I find in an invalid extrapolation to estimate the number of adaptations in regulatory sequences based on the number of adaptations in protein coding sequences. The message of evo-devo is not just that "changes in regulatory sequences played an important role in evolution". The message of evo-devo is that changes in regulatory sequences played the most important role in evolution of macro-organisms since the Cambrian explosion. The interesting differences between human and chimp are not really based on differences in proteins or cell types. Our differencs are anatomical, and thus, according to evo-devo, are based on differences in regulatory sequences. I think one should wait until someone does a similar study on regulatory sequences before making declarations.

    Ian Musgrave · 1 July 2007

    I find in an invalid extrapolation to estimate the number of adaptations in regulatory sequences based on the number of adaptations in protein coding sequences.

    — caligula
    But that's not what's happening. We only have evidence for around 100 regulatory mutations, less than the half number of protein mutations. So if we assume that we have undercounted the regulatory mutations (a good assumption), and set the number of regulatory mutations to be the same as an overestimate of the number of protein mutations to be safe, we are still within ReMine's limits. There is no assumption that the regulatory gene mutations must be the same number as protein gene mutations, just using overestimates for both to be safe. As well, there is no need for there to be more regulatory site mutations. Regulatory site mutations are considered to be more important than protein-coding gene mutations in most vertebrate and human evolution, as I said in the article. However, regulatory gene mutations give you more bang for your buck, so to speak. A single regulatory gene mutation making Australopithecines more neotenous would have an enormous effect, in terms of human evolution. So the assumption there must be more regulatory mutations than protein coding mutations is erroneous. I wouldn't be surprised if there were more, but just because they are (very) important, doesn't mean there must be more of them (or at least huge amounts that exceed ReMine's version of Haldane's speed limit).

    PvM · 1 July 2007

    We see the apparent inability of mutations to truly contribute to the origin of new structures. The theory of gene duplication in its present form is unable to account for the origin of new genetic information

    Totally incorrect. We in fact have quite a few good theories of evolution of complexity and information. See for instance Schneider or Adami. Simple as that, evolutionary theory can very well account for the evolution of complexity and information

    PvM · 1 July 2007

    Of the random mutations that do occur, and have manifested traits in organisms that can be measured, at least 999,999 out of 1,000,000 (99.9999%) of these mutations to the DNA have been found to produce traits in organisms that are harmful and/or to the life-form having the mutation (Gerrish and Lenski, 1998)

    Are you just making up these quotes?

    David Stanton · 1 July 2007

    "There is no evidence for beneficial mutations at the level of macroevolution, but there is also no evidence at the level of what is commonly regarded as microevolution." Jonathan Wells (PhD. Molecular Biology)"

    If you think about it or just a minute, this is obviously total nonsense. If mutations are random with respect to the needs of the organism, then it is inevitable that some of them would be beneficial, at least in certain environments. In fact, there is no known mechanism to prevent this. And of course we have lots of examples of beneficial mutations:

    Antibiotic Resistance in Bacteria
    Genetics 160:823-832 (2002)

    HIV Resistance in Humans
    Am. J. Hum. Gen. 62:1507-15 (1998)

    Mutations in Immunology
    EMBO Journal 12:4955-4963 (1993)

    Lactose Metabolism in Bacteria
    Nature 335:142-145 (1988)

    Nylonase in bacteria
    Ap. Envir. Micro. 61:2020-2 (1995)

    PvM · 1 July 2007

    Seems that Bond is bornagain77 from Uncommon Descent. Welcome... You may actually learn something from those who do not quote mine science.

    PvM · 1 July 2007

    How does it feel to be deceived by Ray Bohlin?

    "We see the apparent inability of mutations to truly contribute to the origin of new structures. The theory of gene duplication in its present form is unable to account for the origin of new genetic information" Ray Bohlin

    Creationist and 'scientist' who presented his article here. I do understand why BornAgain77 does not give actual references. Let us know if you care to be educated in these matters? As a Born Again, Ex-Yec'er, I am always willing to help out a confused fellow Christian

    theMilkMan · 1 July 2007

    Professional evolutionary biologists are hard-pressed to cite even one clear-cut example of evolution through a beneficial mutation to DNA that would violate the principle of genetic entropy. Yet at the same time, the evidence for the detrimental nature of mutations is overwhelming for doctors have cited over 3500 mutational disorders (Dr. Gary Parker).

    Fun-fact for the evolutionarily challenged: Lactose intolerance is genetic. Does this mean that those suffering from this condition have aquired a detrimental mutation? Nope. Virtually all adult mammals are lactose intolerant, and so were our common ancestors. But, about 10,000 years ago or so, a mutation arose that allowed farmers to drink tasty, nourishing milk. This happened not just once, but independently in multiple locations were humanity had just learned how to keep cows. What are the chances of that? (Answer: pretty good)

    Apeman · 1 July 2007

    Oh, oh, this is my favorite...!

    Even if there were just a 1% difference of DNA between monkeys and humans, that would still be 30 million base pairs of DNA difference. It is easily shown, mathematically, for it to be fantastically impossible for evolution to ever occur between monkeys and man, or monkeys and anything else for that matter. Since, it is an established fact that at least 999,999 in 1,000,000 of any mutations to DNA will be harmful and/or , then it is also an established fact that there is at least a 999,999^30,000,000 to one chance that the monkey will fail to reach man by evolutionary processes. ...

    If you had actually read the (Nature, 2005) paper you cite earlier in your post, you would know that most of the 30,000,000 DNA differences between apes(*) and humans are demonstrably neutral, meaning they were neither detrimental, nor particularly advantageous, when they occurred. There is therefore nothing "fantastically impossible" about this number. If you had actually read the original post, you would now also know that the number of likely beneficial differences we do see between human and ape DNA are well within reasonable theoretical limits. (* apes are not monkeys, thank you very much)

    David Stanton · 1 July 2007

    James Bond wrote:

    "The theory of gene duplication in its present form is unable to account for the origin of new genetic information" Ray Bohlin, (PhD. in molecular and cell biology)"

    Well, I don't know what the "theory of gene duplication" is, but I do know that the idea that new genes and new function can arise through gene duplication is well supported by good genetic evidence. For example, this publication:

    Kapfer et al. (2005) Metabolic functions of duplicated genes in Saccharomyces cerevisiae. Genome Research 15:1421-30.

    documents four different pathways by which duplicated genes can acquire new functions. Of course there is also very good evidence that many gene families were produced by these processes as well.

    Science Avenger · 1 July 2007

    James Bond said: Evolution's most flaw, to being scientifically validated, is the absolute inability of any natural methods to account for the generation of meaningful information in the DNA. Naturalists always try to establish scientific validity for evolution by pointing to suggestive similarities while ignoring the foundational principle of science (genetic entropy) that contradicts their preconceived philosophical bias.
    When you talk like this it only serves to alert us that you aren't being scientific. You are using the language of the con man, not the scientist.

    raven · 1 July 2007

    Yet at the same time, the evidence for the detrimental nature of mutations is overwhelming for doctors have cited over 3500 mutational disorders (Dr. Gary Parker).
    Bit of selection bias here. Lets assume there are also 3500 mutations that are beneficial. Do you think those people would go to the doctor and say, "Gee Doc, I'm unusually healthy, unusually intelligent, unusually physically fit, emotionally stable, etc.., so what is wrong with me? Obviously they would not. In point of fact, there are dozens of examples of beneficial mutations. Even Behe's mangled example of chloroquine resistance in malaria is highly beneficial to the parasite. In humans sickle cell anemia is a survival trait in malarial areas, adult lactose metabolism is a recent human trait found in those populations that drink milk, i.e euros and africans, there are some cardiovascular traits involving lipid metabolism that are known to be anti-artherosclerotic (this is now the main killer in industrial age countries), human skin pigment differs from the tropics to the poles and is clearly adaptive, a mutation ccrdelta32 confers resistance to several viruses including HIV and on and on. If goddidit and the earth is 5,768 years old, one could ask why there are any mutations, deleterious or otherwise. Is this the jehovah version of roulette? Ball drops, too bad, you have Tays-Sachs or hemophilia. Every time you look at the Intelligent Designer, he looks more like a fumble fingered idiot. Or just maybe his name is chance and necessity.

    raven · 1 July 2007

    Here is an example of a beneficial mutation in humans. Apo A1 Milano was discovered because these people have low levels of CV disease. Giving this variant to "normals" can actually regress arthersclerotic plaques, one of the few treatments shown to do so and the holy grail of CV medicine. It is now in a phase 11 trial. Stakes are high here. Artherosclerosis contributes to heart attacks and strokes. These CV problems combined will kill 2/3 of the US population.
    Curr Atheroscler Rep. 2006 Mar;8(2):163-7.Links Recombinant apolipoprotein A-IMilano for the treatment of cardiovascular diseases.Calabresi L, Sirtori CR, Paoletti R, Franceschini G. Center E. Grossi Paoletti, Department of Pharmacological Sciences, University of Milano, 20133 Milano, Italy. Apolipoprotein A-I(Milano) (apoA-I(M)) is a natural variant of apoA-I characterized by a cysteine for arginine substitution at position 173 of the primary sequence. ApoA-I(M) carriers have much less atherosclerosis than expected from their very low plasma high-density lipoprotein (HDL) cholesterol levels, suggesting that the variant might be protective. Synthetic HDL (sHDL) made with a recombinant form of the dimeric A-I(M) (A-I(M)/A-I(M)) and phospholipids given in single or multiple injections is effective in inducing the regression of atherosclerotic plaques, preventing arterial restenosis, and limiting cardiac dysfunction after ischemia/reperfusion injury. In a phase II trial in patients with acute coronary syndromes, a short-term treatment with A-I(M)/A-I(M) sHDL caused a remarkable reduction of atheroma burden. Although at early stages of drug development, A-I(M)/A-I(M) sHDL holds vast promise for the treatment of a variety of cardiovascular diseases in humans.

    Ian Musgrave · 1 July 2007

    lots of stuff, including.. Naturalists always try to establish scientific validity for evolution by pointing to suggestive similarities while ignoring the foundational principle of science (genetic entropy) that contradicts their preconceived philosophical bias. For example, naturalists say that evolution is proven true when we look at the 98.8% similarity between certain segments of the DNA in a Chimpanzee and compare them with the same segments of DNA of a Human. Yet that similarity is not nearly good enough to be considered "conclusive" scientific proof. For starters, preliminary comparisons of the complete genome of chimps and the complete genome of man yield a similarity of only 85 to 90% (Ross; Creation as Science).

    — Bond, James Bond
    One of the main points of my essay was the Walter ReMine seriously mislead people over Haldane's dilemma, attributing to Haldane a position Haldane did not in fact take. ReMine is a leading light of the anti-evolutionist movement, but he got something really simple incredibly, badly wrong. Now, what leads you to believe Ross is not misleading you as well? In fact, the above paragraph reveals a woeful misunderstanding of evolutionary biology, as well as a caviller disregard for the actual facts (for example, there is no such thing as "genetic entropy"). The comments section is not a good place to go into all the details, but Ross's figures are wrong, and they don't mean what he thinks they mean. See this post for an extended discussion of what human chimp genome similarity is and what it means. If you continue on, you will see that not only ReMine and Ross, but also Wells and Bohlin, are misleading you. All you have to do is look at the actual research sources to see that they are misunderstanding and misrepresenting the research. Do some independent research on actual research papers, then report back here.

    caligula · 2 July 2007

    We only have evidence for around 100 regulatory mutations, less than the half number of protein mutations.

    — Ian Musgrave
    Thanks for the response. But have regulatory mutations been studied anywhere nearly as extensively as protein coding genes? I still think that that is an important question here.

    There is no assumption that the regulatory gene mutations must be the same number as protein gene mutations, just using overestimates for both to be safe.

    That is precisely why I keep on insisting that regulatory sequences should have a separate study; to be safe. Now, if we already have good empirical reasons for expecting that regulatory substitutions have been quite rare, too, then I have no objection...(cont)

    So the assumption there must be more regulatory mutations than protein coding mutations is erroneous. I wouldn't be surprised if there were more, but just because they are (very) important, doesn't mean there must be more of them (or at least huge amounts that exceed ReMine's version of Haldane's speed limit).

    (cont)... but so far I remain unconvinced that we have. In any case, I find the number of adaptations in protein coding genes fairly irrelevant. We are not smart because our brain cells radically differed from other brain cells. We use the same "old" hardware, but just even more massively parallel fashion than our closest cousins. Likewise, walking upright, hand dexterity, speech, etc. aren't due to dramatic differences in our cells. They are all anatomic differences. What if your question up there at the beginning of the article had been something like: "by how many cell types do we differ from chimps" or "how many differences do we have to chimps on cellular level"? Who would have been surprised by the small number? Who would have even cared? It is the anatomical differences we're interested in here, and the number you gave tells us little about those differences. I'm not trying to be annoying, but I remain unconvinced by this article alone -- I honestly think that regulatory regions need to be studied rigorously, too.

    caligula · 2 July 2007

    Oh, and Ian. Yes, I agree (as a layman) that regulatory mutations seem to be very powerful at least sometimes. I recall that a mouse embryo grew "bat's fingers" after the expression region of a single growth accelerating gene was extended manually in the lab. But I still want to be safe rather than sorry.

    caligula · 2 July 2007

    Since, it is an established fact that at least 999,999 in 1,000,000 of any mutations to DNA will be harmful and/or , then it is also an established fact that there is at least a 999,999^30,000,000 to one chance that the monkey will fail to reach man by evolutionary processes. The monkey will hit a end of harmful/fatal mutations that will kill him or severely mutilate him before him.

    — Jamed Bond
    I assume you are speaking about DNA under constraint here? Otherwise you could not call it an "established fact" that by far most mutations are "harmful". You assume that the bigger the portion of harmful mutations is, the more probable it is for a harmful mutation to become fixed in the population. Such an assumption is utter nonsense. The frequency of harmful mutations is decided by the mutation rate, not by the beneficial/harmful ratio. As is quite demonstrable by standard population genetics, purifying selection prevents harmful mutations from becoming fixed at any reasonable or even somewhat unreasonable mutation rate. The rate of harmful mutations does affect the average fitness of the population, that much is true. But whether harmful mutations create a problem for survival remains unclear. For example, Nachman(2000) uses U-value 3 which is based on the assumption that we have 70,000 genes. Such a U-value creates what creationists seem to call the "Nachman's U-Paradox", although Crow and others have quite a bit to say even about that. However, with the U-value 1, based on the current gene count of about 23,000 genes, the effect of harmful mutations is a small fraction of the effect estimated by Nachman(2000). If, on the other hand, one claims that the effects of harmful mutations on exons or DNA binding sites is only slightly harmful, i.e. nearly neutral... well, that would be interesting. Not only would that amount to saying that there is indeed a way to break down complex biological structure gradually, protein by protein, without immediate loss of function. It would amount to saying that even the functionality of individual proteins can be destroyed gradually, without immediate loss of function. Such extreme faith in the evolvability of IC systems from scratch is not present among evolutionists, so far as I know. But is evolution too slow if, indeed, mutations are beneficial only at probability 10^(-6)? Let's see. Assume 10,000 loci each with a mutation rate 10^(-5), and a population size 100,000. Now, we have beneficial mutation occurring at total frequency 10^(-11). On the other hand, each generation we have 10^9 mutating loci. Hence, we have a beneficial mutation occurring every 100th generation. Assume that 2/3 of these beneficial mutations are killed early by drift, to reach the rate of beneficial mutations which succeed in building up enough critical mass for selection to prevail over drift: one adaptation every 300th generation. This is, of course, just a rough order of magnitude.

    Popper's Ghost · 2 July 2007

    You are probably sitting there astonished that we are around 240 genes away from our last common ancestor with the chimp and saying "this can't be right"

    No, I'm sitting here astonished that you would confuse differences with beneficial differences, when that's the whole point.

    EoRaptor · 2 July 2007

    I think one should wait until someone does a similar study on regulatory sequences before making declarations.

    — caligula
    Does this story in the NY Times (free registration) describe the type of study you are talking about? The article talks about studies showing both the importance of regulatory sequences in evolution and development, and about a sort of multi-layer functionality for any given sequence. What I take away from the article is the sense that there's a LOT more going on in the genome than IDiots are capable of dealing with.

    Popper's Ghost · 2 July 2007

    Walter ReMine seriously mislead people

    The English language seems to have recently suffered a detrimental mutation that substituted "lead" (pronounced "leed") for "led" (pronounced "lehd").

    caligula · 2 July 2007

    Does this story in the NY Times (free registration) describe the type of study you are talking about?

    No. I'm talking about a peer-reviewed study on the number of changes in our regulatory sequences since the divergence. Nothing more, nothing less.

    Steviepinhead · 2 July 2007

    Ah, c'mon PG. Just 'cause Ian's a little "cavillier" with his spelling, doesn't mean you should overlook his good points!

    Though, I must admit, "mislead" for the past tense does tend to yank my chain as well.

    You kin led a horse to water, but you can't make 'im drunk.

    Torbjörn Larsson, OM · 2 July 2007

    "how many differences do we have to chimps on cellular level"
    Um, but since the majority of evolution has been centered around the immune system (for obvious reasons), couldn't that result in changes on a basic level? Receptors, surfaces, et cetera. IIRC the Loom had a post detailing some such differences. Bond:
    ignoring the foundational principle of science (genetic entropy)
    Pounding on the same point so eloquently treated by Ian, but damn... First, the article was treating Haldane's dilemma (and the piggyback of the latest creationist strawman of evolution proper, "simultaneous beneficial mutations") and its resolution in the perspective of the latest data. Throwing up other strawmen isn't an answer. Except perhaps to implicitly concede the result. Second, there is no 'genetic entropy' principle in science, which is obvious if you try to find it. A methodological principle, such as the mediocrity principle, may be consistent with scientific practice, but in the end of the day it must be consistent with evidence. For example, the perfect cosmological principle may be consistent with a cosmology of multiverses, but it is now know to be inconsistent with our particular universe. This is why scientists prefer to rely on laws, which are directly derived from tested theories and observations, instead of relying on principles that are abstracted from theories and may or may not be useful for forming new ones. It is unclear what you mean exactly, but if you mean that "generation of meaningful information" is not happening by evolutionary mechanisms, it is directly contradicted by evidence. For example, in your example of gene duplication. But also in genetic algorithms.

    Torbjörn Larsson, OM · 2 July 2007

    "how many differences do we have to chimps on cellular level"
    Um, but since the majority of evolution has been centered around the immune system (for obvious reasons), couldn't that result in changes on a basic level? Receptors, surfaces, et cetera. IIRC the Loom had a post detailing some such differences. Bond:
    ignoring the foundational principle of science (genetic entropy)
    Pounding on the same point so eloquently treated by Ian, but damn... First, the article was treating Haldane's dilemma (and the piggyback of the latest creationist strawman of evolution proper, "simultaneous beneficial mutations") and its resolution in the perspective of the latest data. Throwing up other strawmen isn't an answer. Except perhaps to concede the result. Second, there is no 'genetic entropy' principle in science, which is obvious if you try to find it. A methodological principle, such as the mediocrity principle, may be consistent with scientific practice, but in the end of the day it must be consistent with evidence. For example, the perfect cosmological principle may be consistent with a cosmology of multiverses, but it is now known to be inconsistent with our particular universe. This is why scientists prefer to rely on laws, which are directly derived from tested theories and observations, instead of relying on principles that are abstracted from theories and may or may not be useful for forming new ones. It is unclear what you mean exactly, but if you mean that "generation of meaningful information" is not happening by evolutionary mechanisms, it is directly contradicted by evidence. For example, in your example of gene duplication. But also in genetic algorithms.

    Torbjörn Larsson, OM · 2 July 2007

    The English language seems to have recently suffered a detrimental mutation that substituted "lead" (pronounced "leed") for "led" (pronounced "lehd").
    What, never heard of "lead poisoning"? It is correlated with detrimental effects on the brain, I hear.

    Patricia Princehouse · 2 July 2007

    I guessed 100 as the minimum number I figured would be necessary. I wouldn't be surprised if some of those 54 extras were to fall by the wayside eventually...

    -Patricia

    Mark Studdock, FCD · 2 July 2007

    I hate to jump in the middle of this delightful conversation but I have a question about mutations that I cannot even begin to understand how one would go about finding any sort of "scientific" answer to. But perhaps someone can point me somewhere...or people can get back to guessing a number.

    Here is the question: If all biological life has come about by selective forces acting upon randomly generated genetic mis-information (mutational errors in nucleic acid sequences), about how many information building mutations (leaving aside the category of beneficial mutations which we have a few examples in sickle cell, lactose tolerance, and the few mentioned above etc) have occurred? What would be a rough reasonable number to posit here? I realize this is probably beyond calculation, but just think about it. If mutations figure heavily into the gradual or even not so gradual transformation of for example an early mammalian organism into modern day pandas, social wolves, echo-locating bats, echo-locating whales, philosophical people, so on and on and on.... how many mutations are we thinking to be necessary here. Add this mammalian figure to figures explaining each of the other classes, and then add in the mutational divisions among the various phyla... well it boggles the mind?

    But lets just say it had to have happened this way and that our current scientific understanding is not tentative but absolutely right on. What kind of a number are we looking at here?

    I really am curious about this? Is there a scientific opinion?

    MS

    Popper's Ghost · 3 July 2007

    Ah, c'mon PG. Just 'cause Ian's a little "cavillier" with his spelling, doesn't mean you should overlook his good points!

    How does mentioning one error imply anything about what I have or haven't overlooked?

    What, never heard of "lead poisoning"?

    What's with you guys and your fallacious inferences? Of course I have, and of course that's irrelevant here.

    Science Avenger · 3 July 2007

    Who is "you" Frank? You do understand that many of the people that comment on this site are not atheists, right?

    raven · 3 July 2007

    kansas troll again: Frank on July 3, 2007 6:58 AM (e) And therefore their is no God? Isn't that the conclusion you really want the public to draw?
    To answer your question for the X000th time. Science is about the truth and making the world a better place. It has been very successful at both. kansas troll, do you think being a troll makes people convert to christianity? Do you think confusing there for their makes people convert to christianity.? You have an uphill battle anyway. 82% of the US population self identifies as christian. Many of the rest are jewish, muslim, etc..Even the trolls have converted if you are a typical example. Who is left?

    raven · 3 July 2007

    If mutations figure heavily into the gradual or even not so gradual transformation of for example an early mammalian organism into modern day pandas, social wolves, echo-locating bats, echo-locating whales, philosophical people, so on and on and on.... how many mutations are we thinking to be necessary here.
    Your point is a little too vague and large (IMO) to answer. To answer it as any more than a guess would also take days. Assuming you are not trolling, break it down. What would be the number of mutations between the earliest bilateralian and human? The ealiest bilateral would most likely be something like a flatworm. The nematode C. Elegans has 20,000 genes by sequencing and could be taken as best proxy for an early metazoan. Oddly enough, fast forwarding 1/2 billion years or so, and humans have about the same number, 20,000-30,000. Compare C. elegans or primordial bilateralian with humans and make an estimate of the number of mutations involved. It is sort of moot anyway. The earth is 4.5 billion years old, life is 3.6 billion years old, and a lot can and has happened. FWIW, my impression is that what is rate limiting for evolution is not mutations at all but selection pressure. When new ecospaces open up, the first organisms to arrive often undergo rapid adaptive radiations to grab as much territory as possible.

    harold · 3 July 2007

    Frank -
    And therefore their is no God? Isn't that the conclusion you really want the public to draw?
    NO, nobody said anything about that, and plenty of the pro-science posters here are religious. By the way, watch out for "their" and "there". It's a common mistake, but if you're already saying something stupid, it can make you look even stupider.

    Torbjörn Larsson, OM · 3 July 2007

    Mark:
    about how many information building mutations (leaving aside the category of beneficial mutations which we have a few examples in sickle cell, lactose tolerance, and the few mentioned above etc) have occurred? [...] how many mutations are we thinking to be necessary here.
    I'm not a biologist, but I could stick out my neck here. I believe the above can be answered. But first we must separate out the meaningful questions, that are tangled together above. First, since speciation doesn't concern information but function, there is no specific answer how many mutations or other types of variations that are necessary for a speciation. For the biological species conception a difficulty to crossbreed defines the species (a functional requirement, btw), and AFAIK it could be due to a single variation. Which in turn could be due to a single mutation. Second, as for complexity there is no single measure of information that can cover all characteristics of a system. So if we want to know which mutations build information we have to pick one measure that we know, if we find the question interesting. (As you can see of the above, biology couldn't care less.) One easy measure, or perhaps groups of measures, of information with some relevance here is used in bayesian inference. Since you are asking which mutations contribute we don't need to define the specific measure, but can look at how information is created. In bayesian inference a set of hypotheses is build, which are given a priori weight of probabilities to be correct. Each time an observation is made, a posteriori probabilities is made by updating which hypotheses were correct. This is among other things popular in machine learning, where bayesian methods are common. Now, the bayesian inference equation is also used for modeling asexual populations in population genetics. Here the a priori probabilities are allele frequencies, and selection or drift updates the frequencies for each generation. Now we can answer your question. If we consider a population (with a population of alleles) that survives as having learned about their environment, all variation counts in building information. The information describes the problem to find a subset of alleles that are sufficient to build a population in an environment. If we consider a population that survives selection as having learned (the hard way) about some specific constraints of their situation, the beneficial mutations discussed by Ian are those who counts as building information. The information describes the problem to find a subset of alleles that are necessary to build a population in an environment. While I was writing this, raven has given her answer. It seems to correspond with the above - your question needs to be broken down into meaningful parts, and anyway it comes down to how much you (or your studied population! :-) is interested in variation (the first answer above) or selection (the second answer above). As you can see from above or elsewhere the question of information is too contingent and totally removed from the mechanisms of evolution theory. It may one day be a complement to other types of data that is observed in biology, but it is of no value today AFAIK.

    Torbjörn Larsson, OM · 3 July 2007

    What, never heard of "lead poisoning"?
    What's with you guys and your fallacious inferences?
    Aw, you killed my joke! No with panache either, but by deadpanning it. ;-)
    Of course I have, and of course that's irrelevant here.
    Ah, c'mon PG. You can't get a reaction out of kicking a dead joke. :-P

    Flint · 3 July 2007

    Who is "you" Frank? You do understand that many of the people that comment on this site are not atheists, right?

    But atheists do not conclude that there is no god. Atheists *presume* that anything for which there is no evidence, does not exist until such evidence is found. This is a policy position, not a conclusion. It is not possible to conclude that there are no gods. It is (currently) not possible to conclude on the basis of evidence that there ARE any gods either. Logically, belief in gods rests on "you can't prove I'm wrong", and lack of belief rests on lack of evidence.

    Steviepinhead · 3 July 2007

    Sigh. I guess I'll have to mourn my poor joke as well.

    It wasn't much but, hey, at least Popper's Ghost took the time to kick it while it was down.

    p-ter · 3 July 2007

    apeman alluded to this, but it's important to note that tests of the sort used in Bakewell et al. are not going to detect genes where only a few adaptive changes have taken place. They're likely only going to detect genes involved in constant fairly powerful selection-- things like arms races with pathogens, etc. The real "meat", so to speak, of our divergence with chimps likely goes undetected with tests like that.

    Torbjörn Larsson, OM · 3 July 2007

    it may be a sign of the cramped conditions that human reproduction takes place in.
    A comment on another thread make me realize that evolution around reproduction is also and mostly "the war of the sexes", literally. (Females and males competing against each other for the most offspring.) Duh!

    Mark Studdock, FCD · 3 July 2007

    Thank you for the responses to my query given above? But minus the information increasing component, what are we looking at, as far as numbers of selected and then fixed (err..relative to later changes?) mutations.

    And as per raven's suspicion that the real "rate limit[er] for evolution is not mutations at all but selection pressure",... Can we quantify that and then somehow add the two?

    MS

    raven · 3 July 2007

    Actually, that's 154 of 13,888 genes. Given that we have around 22,000 genes [3] in our genome (http://www.ensembl.org/Homo_sapiens/index.html), then if the same percentage of beneficial mutations holds for the rest of the genome, no more than 238 fixed beneficial mutations is what separates us from the last common ancestor of chimps and humans.
    Thank you for the responses to my query given above? But minus the information increasing component, what are we looking at, as far as numbers of selected and then fixed (err..relative to later changes?) mutations. And as per raven's suspicion that the real "rate limit[er] for evolution is not mutations at all but selection pressure",... Can we quantify that and then somehow add the two?
    You are not getting answers because no one knows. The best data we have is macaque-chimp-human, all sequenced. Per this thread, it is estimated that 238 beneficial mutations separate us from them. The primordial bilateran probably lived about 600 million years ago but it could be even a billion. Our phylum, the chordates shows up in the cambrian, 450 million years ago and already looks pretty complicated. The average species is estimated to live 5 million years. Say there are 200 species between primordial and us and 238 mutations per species. That would imply that in the last billion years, 50,000 mutations have become fixed sequentially, flatworm to human. This estimate and $1.50 will get you a cup of coffee at Starbucks. Not an expert on evolutionary thought by any means. But I believe my conjecture about the rate limiting step being selection pressure is correct. Consider the mammals. Our lineage is ancient, going back to the tertiary, hundreds of millions of years old. Mammals were small and obscure for most of this history. Then one day an asteroid slammed into Yucatan and the dinosaurs went away. Shortly afterwards there was a recovery and the large megafaunal space was dominated by....mammals. A lot of ecospace became available and the animals with hair and teats grabbed it. One of my minor gripes about the creo myth is it is static, unreasonable, and most of all boring. The real world is a far more complicated, mysterious, and intricate place.

    khzcqixeg mzeyxwglb · 14 July 2007

    liayo nymtl aglcmq obzyaslm dnvbe jdys pcan http://www.drnpcu.jgnbtzcyd.com

    DavidB · 18 July 2007

    I commented on Haldane's Dilemma a while ago here:

    http://www.gnxp.com/blog/2006/04/haldanes-dilemma-should-we-worry.php

    Briefly, in my view there are several ways out of the Dilemma, but it should be taken more seriously than has been fashionable since the 1970s. John Maynard Smith always took it seriously (despite back in 1968 having shown one of the 'ways out'), and George C. Williams also argues against some of the popular 'solutions'. These are not names to be trifled with.