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What? Only an “extremely occasional” mutation is beneficial? But Darwinism… ?

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From Jessica Hamzelou at New Scientist on a study in Iceland that shows that old fathers pass on more mutations than old mothers:

“If a sequence is not present in the parents but is present in the child, then it’s new,” says Stefánsson. They discovered that 80 per cent of new mutations come from the father, and that the number of mutations increases in line with the age of the parents.

…

These mutations won’t all be harmful. We’re all born with at least 70 new mutations, and most of these don’t affect the way our bodies and brains work. “The vast majority of mutations don’t matter, says Leo Schalkyk at the University of Essex. “There might be the occasional mutation that is deleterious, or the extremely occasional mutation that is beneficial.” More.

But Darwinism is natural selection acting on random mutations, creating the thousands of apparently irreducibly complex structures we see in life forms. Enforced in the academy and legislated for the schools. And probability is one of those subjects that, if you dare address it, marks you out as a doubtful person for even wondering.

Darwinism increasingly resembles a totalitarian political philosophy in that the official communications are rigidly controlled but then someone inadvertently gives the game away: But better watch your back if you ever think of trying to do the math.

See also: “To what can science appeal if not evidence?” Rob Sheldon responds

Comments
gpuccio, "it remains vastly unclear why different cells undergo different epigenetic destinies. It seems to be a huge sum of cascades of events, controlled in some way by some basic information in the cell, but I am afraid that we really don’t understand anything of how the whole process is really controlled (and i suppose you will agree with me!)." Yes, I agree, but I wouldn't say that we don't understand anything, because I think we understand a little more than we did before. :) Besides, we know that the Darwinists understand it almost completely. And that's encouraging. :) Thanks for the explanation. Here's an old paper on alleged DNA differences within the same individual: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2992694/pdf/humu0031-1174.pdfDionisio
October 2, 2017
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Dionisio: 1) Different cell types in the human body have the same DNA (genomic sequence), as a rule. There are, however, important exceptions: a) Gametes b) Immune cells, which undergo specific DNA rearrangements in a very limited portion of their DNA. Moreover, recent attention has been given to "intraindividual somatic variations"m that is differences in DNA in cells from the same individual, even if the meaning and extent of those variations are still not well understood. 2) However, even if the DNA sequence is roughly the same, the DNA state is certainly very different in different cell types, due to constant epigenetic influences that determine the type and state of each cell. 3) In principle, epigenetic events should be determined by information in the genome, too. Or by epigenetic information pre-existent in the cell (for example, in the original gametes). Therefore, it remains vastly unclear why different cells undergo different epigenetic destinies. It seems to be a huge sum of cascades of events, controlled in some way by some basic information in the cell, but I am afraid that we really don't understand anything of how the whole process is really controlled (and i suppose you will agree with me! :) ). 4) In principle, epigenetic markers that are in the genome sequence are the same in all cells. But, again, the state of those markers can be very different in different cells. Moreover, all other epigenetic events which are not connected to the genome sequence, or only to it, like DNA methilation, or hystone post-translational modifications, are certainly different in different cells. But, in some way, those modifications must "know" to which DNA sequences they must be applied, and that should depend on the DNA sequence itself, or on its state.gpuccio
October 2, 2017
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EugeneS, Very interesting issues you've brought up @20 & @24. I'm glad gpuccio got involved in this mini discussion. It feels strange to be in the middle of a friendly discussion between two doctors (one academic, another medical). I'm sure you both are gracious enough to not require a doctoral degree at least for this time. :)Dionisio
October 2, 2017
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gpuccio, Thank you for the insightful comment @23. Could the following questions somehow relate -at least slightly- to your comment @23 in response to the comment @20 by EugeneS? Do different cell types within the human body have the same DNA (both coding and non-coding)? I they do, then why are they different? Is it because the epigenetic switches? Do different cell types have different epigenetic markers/ switches - different by position and/or type? Or do they all have the same epigenetic markers/switches (by position and type) but they get turned on/off differently? Thanks.Dionisio
October 2, 2017
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GP Thank you very much indeed. Here is what I have on the issue: http://academic.brooklyn.cuny.edu/biology/franz/biology38/_files/1836.pdf https://www.scientificamerican.com/article/tiny-genetic-differences-between-humans-and-other-primates-pervade-the-genome/ http://sciencerefutesevolution.blogspot.co.uk/2017/07/monkeys-are-not-our-relatives.html The second link has a nice picture (which does say it portrays only protein-coding differences). However, it does not say that these are the only differences. The third one is very interesting in that it mentions epigenetic differences. Unfortunately it does not cite any academic sources. In Dembski's and Well's popular book on design it is pointed out that even 1% difference when it refers to code could be crucial. DNA is not a novel. In the case of two printed copies of a novel that are 1% different we could say they are practically identical, because we as readers can very easily identify those differences as typos. But in the case of DNA, we cannot say that. Using a computer analogy, a single typo in a bootloader file, for example, can be really fatal.EugeneS
October 2, 2017
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EugeneS: Well, that is a serious issue indeed. I have not really delved deeply in it, but according to this paper: http://genome.cshlp.org/content/15/12/1746.long The difference between the two genomes, whole genomes, at least as measured in 2005, should be: About 1% difference in SNPs (single nucleotide mutations) About 3% for indels That is, about 4% total difference in raw nucleotide sequence. I think the difference is extremely low for the exome. Human and chimp proteins are really almost identical, in most cases. What does that mean? First of all, there are differences, especially in non coding DNA, and they could be important, probably are in many cases. But it is really difficult, at present, to understand their meaning. Even some of the small differences in proteins could have a functional role, but we must also allow for some neutral variation between the two genomes. The really amazing thing, IMO, is that the genomic differences seem really low if compared to the huge functional differences between us and chimps. Now, neo-darwinists seem to interpret that fact in the sense that there are really no big differences between us and chimps, or that small genomic differences can, by magic, generate huge differences in nervous system organization, and so on. Of course, they are free to believe these things, but I certainly beg to differ. For me, the striking similarity between the genomes is evidence of the simple fact that the differences cannot be really explained in terms of genomics only, or of genomics as we understand it today. IOWs, I believe that there is a huge functional difference between us and chimps, and therefore a huge informational difference. But, by far, we don't understand where the information is recorded. But we will, I am certain of that. In time we will. For the moment, we could derive some inspiration from the opposite fact that, for example, C. elegans and C. briggsae present striking genomic differences, but are very much similar species under many aspects.gpuccio
October 2, 2017
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EugeneS @20: Ochen interyestnye vaprosy. Spasibo!Dionisio
October 1, 2017
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@13 error correction: gpuccio @11Dionisio
October 1, 2017
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Gpuccio I am sorry to be off-topic. But I have a question for you. Could you provide some context into the hype of 98% homology between chimp and human. I read somewhere that the 2% difference only accounts for protein coding regions. Is that the case? If this is correct, then the difference is underestimated. As far as I know, this figure is only about substitutions and not about insertions or deletions. So it does not account for a lot of new function in humans. But that is a slightly different matter. My main interest is whether the original comparison was done for protein coding DNA only. With this figure of "just a few percent" difference in that context there is a lot that is conveniently untold. It is an underestimate in many respects. Many Thanks.EugeneS
October 1, 2017
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Extremely rare and occasionally beneficial doesn't produce the dramatic change across higher taxa that must happen if Neo-Darwinism is real. Lenskis bacteria have managed nothing in 60,000 generations of extreme selective pressure that wasn't already present in the genome ( citrate consumption) and the inability of NS to meet the claims of Darwism has been acknowledged by honest evolutionists. That's why this statement appears on the front page of The Third Way of Evoultion: "Moreover, some Neo-Darwinists have elevated Natural Selection into a unique creative force that solves all the difficult evolutionary problems without a real empirical basis." Without an empirical basis indeed. Neo-Darwinism has been falsified and even evolutionists are admitting as much.Florabama
September 30, 2017
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Gordon Davisson, Why is this supposed to be a problem for “Darwinism”? A low rate of beneficial mutations just means that adaptive evolution will be slow. Which it is. Yep! Fits beautifully into the evolutionary process of a few pound land walking rat into140 ton whale...Can't argue with that! -;)J-Mac
September 30, 2017
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Dionisio: "Note that my questions were very easy compared to yours." Yes, I am a very bad guy! :)gpuccio
September 30, 2017
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gpuccio:
Moreover, as the process seems not to leave any trace of itself in the proteomes we can observe today, because those functionally intermediate forms simply do not exist...
I love this convenient feature of evolution. The absence of evidence is evidence!Mung
September 30, 2017
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Furthermore, those who no longer consider themselves “Darwinists”, for obvious reasons, such as Larry Moran, PZ. Myers insist on Neural Theory with the emphasis on random genetic drift.
I always wondered what was wrong with PZ Myers and now I finally know. It's his Neural Theory. :)Mung
September 30, 2017
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A low rate of beneficial mutations just means that adaptive evolution will be slow. Which it is.
Except when it isn't. You left that out. Improbable DestiniesMung
September 30, 2017
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gpuccio @10, Please, don't ask difficult questions or present difficult problems. Be nicer to your interlocutors. Don't get so serious. This is just about biology. :) Remember that two years ago a Canadian biochemistry professor stopped discussing with me because I didn't ask honest questions. I subtly used the 'tricky' word 'exactly' that was not highlighted in bold characters. Mea culpa. :) My mistake granted my interlocutor the right to quit the incipient discussion. Note that my questions were very easy compared to yours. :)Dionisio
September 30, 2017
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What is "extremely rare"? If it's 1 in a billion with today's population we should get 7 every generation. Even if 6 of those are lost we are left with 1 per generation.aarceng
September 30, 2017
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Gordon Davisson: You say: "And not as slow as it might appear, since the limiting rate is the rate of beneficial mutations over the entire population, not per individual." Yes, but any "beneficial" mutation that appears in one individual will have to expand to great part of the population, if NS has to have any role in lowering the probabilistic barriers. That means that: 1) The "beneficial" mutation must not only be "beneficial" in a general sense, but it must already, as it is, confer a reproductive advantage to the individual clone where it was generated. And the reproductive advantage must be strong enough to significantly engage NS (against the non-mutated form, IOWs all the rest of the population), and so escape genetic drift. That is something! Can you really think of a pathway to some complex new protein, let's say dynein, a pathway which can "find" hundreds of specific, highly conserved aminoacids in a proteins thousands of aminoacid long, whose function is absolutely linked to a very complex and global structure, a pathway where each single new mutation which changes one aminoacid at a time confers a reproductive advantage to the individual, by gradually increasing, one step at a time, the function of a protein which still does not exist? If you can, I really admire your imagination. 2) Each of those "beneficial mutations" (non existing, IMO, but let's suppose they can exist) has anyway to escape drift and be selected and expanded by NS, so that it is present in most, or all the population. That's how the following mutation can have some vague probability to be added. That must happen for each single step. While that is simply impossible, because those "stepwise" mutations simply do not exist and never will exist, even if we imagine that they exist the process requires certainly a lot of time. Moreover, as the process seems not to leave any trace of itself in the proteomes we can observe today, because those functionally intermediate forms simply do not exist, we must believe that each time the expansion of the new trait, with its "precious" single aminoacid mutation, must be complete, because it seems that it can erase all tracks of the process itself. So, simple imagination is not enough here: you really need blind faith in the impossible. Credo quia absurdum, or something like that. Then you say: "Although many beneficial mutations are wiped out by genetic drift before they have a chance to spread through the population, so that decreases the effective rate a bit." Absolutely! And it's not a bit, it's a lot. If you look at the classic paper about rugged landscape: http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0000096 you will see that the authors conclude that a starting library of 10^70 mutations would be necessary to find the wild-type form of the protein they studied by RM + NS. Just think about the implications of that simple fact. You say: "Beneficial mutations don’t have to happen “in a row”, they can happen entirely independently of each other, and spread independently via selection." Yes, but only if each individual mutation confers a strong enough reproductive advantage. That must be true for each single specific aminoacid position of each single new functional protein that appears in natural history. Do you really believe that? Do you really believe that each complex functional stricture can be deconstructed into simple steps, each conferring reproductive advantage? Do you believe that we can pass from "word" source code to "excel" source code by single byte variations (yes, I am generous here, because a single aminoacid has at most about 4 bits of information, not 8), each of them giving a better software which can be sold better than the previous version? Maybe not even "credo quia absurdum" will suffice here. There are limits to the absurd that can be believed, after all! You say: "You may be thinking of the argument from irreducible complexity, but that’s an argument that evolution depends on mutations that are only beneficial in combination, which is a different matter." No, the argument of IC, as stated by Behe, is about functions which require the cooperation of many individual complex proteins. That is very common in biology. The argument of functional complexity, instead, is about the necessity of having, in each single protein, all the functional information which is minimally necessary to give the function of the protein itself. How many AAs would that be, for example, for dynein? Or for the classic ATP synthase? Here, the single functional element is so complex that it requires hundreds of specific aminoacids to be of any utility. If that single functional element also requires to work with other complex single elements to give the desired function (which is also the rule in biology), then the FC of the system is multiplied. That is the argument of IC, as stated by Behe. The argument for FC in a single functional structure is similar, but it is directly derived form the concept of CSI as stated by Dembski (and others before and after him). And finally you say: "And FYI evolutionists dispute how much of a problem this actually is. But again, that’s another matter." It's not another matter. It's simply a wrong matter. Both FC and IC are huge problems for any attempt to defend the neo-darwinian theory. I am not surprised at all that "evolutionists" dispute that, however. See Tertullian's quote above! :)gpuccio
September 30, 2017
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What roles do the beneficial mutations play in the evo-devo movie? Dev(d) = Dev(a) + Delta(a,d) Are they nominated for the (peer-reviewed) academic award? In the auto industry, in order to change a car model, one must change the process required to produce it. And cars are nothing compared to the simplest biological systems. Does the penny drop now? Ok, then y'all may continue your discussion. :)Dionisio
September 29, 2017
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Gordon Davisson- You don't build a vison system by mutating areas that have nothing to do with vision systems. The "mutations in a row" is in response to Dawkins' "cumulative selection" pipe-dream which requires the "right" mutations to accumulate within the genetic system responsible for the adaptation under construction. Vision systems are built by the "right" mutations accumulating in the genetic system responsible for constructing them. But first that system had to be constructed from the accumulations of the "right" mutations. A developmental organization system just happened evolved from a system that was doing just fine without one. But hey, on a planet that just happened to pumped out living organisms it didn't want nor need, that shouldn't sound so surprising or counter-intuitive.ET
September 29, 2017
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In Darwinian Wonderland you can get banana cupcakes from stones if you "give evolution enough time"kurx78
September 29, 2017
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ET@3 I was going to write the same thing... Furthermore, those who no longer consider themselves "Darwinists", for obvious reasons, such as Larry Moran, PZ. Myers insist on Neural Theory with the emphasis on random genetic drift. This is how they put it: "First thing you have to know: the revolution is over. Neutral and nearly neutral theory won. The neutral theory states that most of the variation found in evolutionary lineages is a product of random genetic drift. Nearly neutral theory is an expansion of that idea that basically says that even slightly advantageous or deleterious mutations will escape selection — they’ll be overwhelmed by effects dependent on population size. This does not in any way imply that selection is unimportant, but only that most molecular differences will not be a product of adaptive, selective changes."J-Mac
September 29, 2017
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I'm new at this and not as knowledgeable as others who comment. Gordon Davisson's comment is not clear to me. Isn't it true that even if the step-wise mutations happened over the entire population, the mutations would have to happen relatively at the same time within the entities that the mutations will combine? And don't the mutations, let just say just a two step-wise mutations, have to occur, one in the male and one in the female? And won't these two individuals have to produce an offspring for these two step-wise mutations to come together? If the population size is very small, I could see where this may be feasible. But assuming a population size of a million, equally divided by male and female, isn't it just a one in 250,000,000,000 chance (500,000 x 500,000) chance the two would be partners? Factoring in the time element and the probability of being in the same location vicinity, isn't just a 2 step-wise mutation virtually impossible? As I say, I'm new to this and not as knowledgeable as others. Please help me better understand the mathematics. Thank you!Mark from CO
September 29, 2017
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Why is this supposed to be a problem for "Darwinism"? A low rate of beneficial mutations just means that adaptive evolution will be slow. Which it is. And not as slow as it might appear, since the limiting rate is the rate of beneficial mutations over the entire population, not per individual. Although many beneficial mutations are wiped out by genetic drift before they have a chance to spread through the population, so that decreases the effective rate a bit. If I've accounted for everything the overall rate of fixation of beneficial mutations per generation should be: (fraction of mutations that're beneficial) * (fraction of beneficial mutations that aren't wiped out by genetic drift) * (# of mutations per individual) * (population). Florabama's description is exactly wrong. Beneficial mutations don't have to happen "in a row", they can happen entirely independently of each other, and spread independently via selection. You may be thinking of the argument from irreducible complexity, but that's an argument that evolution depends on mutations that are only beneficial in combination, which is a different matter. (And FYI evolutionists dispute how much of a problem this actually is. But again, that's another matter.)Gordon Davisson
September 29, 2017
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The fact there is only the "extremely occasional" mutation that is beneficial absolutely falsifies Darwinism, but even one doesn't accept this clear reality, extremely occasional does nothing for evolution. Darwinism needs thousands perhaps millions of "extremely occasional" beneficial mutations to happen a row across thousands of generations to build a new organ system. Like flipping a million heads in a row, Darwinism is fantasy.Florabama
September 29, 2017
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Not to mention the fact that "beneficial" is a relative commodity and includes a loss of function, eg those who don't need better eyes.ET
September 29, 2017
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MUNG - LOL!!!Tom Robbins
September 29, 2017
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The hidden secrets of Darwinism. You have to be at least level six in the Darwin Cult in order to be taught the mysteries of how an extremely occasional beneficial mutation happens at just the right time in just the right place in just the right organism who just happens to need a better eye. No doubt beneficial mutations were much more common in the far distant past.Mung
September 29, 2017
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