The Central Paradox of Evolution

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Discussion by: godzillatemple

I'll preface this as usual by stating that I am an atheist with a strong acceptance of the scientific method, and this is in no way an attempt to "disprove" the theory of evolution.  I am also a layman in the field, however, and am hoping somebody with a little more knowledge can provide me with some elightenment.

It has been said repeatedly that the two fundamental concepts of evolutionary theory are random mutation and natural selection.  As I understand the concepts, this means that (1) random genetic mutations periodically occur in some (if not all) organisms and (2) if a mutation is beneficial to an organism's survival (or somehow makes it more attractive to the opposite sex, if you're talking about higher order organisms), that organism will be more likely to reproduce and pass its genes on to the next generation.  Thus, small changes accumulate over time and eventually lead to new species.

Hopefully I have stated that correctly.

Here comes the apparent paradox, however.  When asked why it's impossible to view evolution as it occurs, the answer is inevitably that it occurs on a very long time scale and that the individual mutations are too small to notice until they have had time to accumulate through many generations.  If the individual mutations are so small, however, how can any of them actually contribute to the survivability or selection of the organism?  I mean, it's easy to think about a gross mutation like an extra finger or new skin coloration affecting my chances of mating and passing along my genes, but how would a mutation too subtle to be detected affect whether I am able to find a mate or not?

Please help me understand what I am missing here.

223 COMMENTS

  1. Please help me understand why you expect others to read Darwin’s “Origin” and “Descent”, and all of Dawkins’ books, then distil three billion years’ worth of evolution into a couple of sentences?

    This will not answer your question, nevertheless, according to Google those who accept that humans evolved from lower species are: Icelanders 85%, French 80%, Italians 72%, Turks 26%, then Brazilians 59% and Australians 71%. So it seems that the closer people are to the equator, the harder Richard Dawkins has to work to convince them.

  2. Hi Godzillatemple,

    Just to clarify your wording: Random genetic mutations occur in all organisms, for several reasons. Random genetic mutations can be deleterious, neutral or beneficial in their effects on the gene vehicle, which is the organism.

    If a genetic mutation benefits an organism at least until it has reproduced – and in some cases assists the offspring until it is self-sufficient – then that mutation, if it is passed on during sexual genetic shuffling, can be selected by increasing its frequency in the gene pool of that species, which can take many generations to have noticeable effects within species.

    Very small improvements don’t just affect whether you find a mate, but aid your survival until you have the ability or opportunity to mate. Any minute benefit can help you improve your chances of avoiding or fighting disease and injury, starvation, finding or catching the right varieties of food – or avoiding becoming food….

    Speciation can only take place if there are divisions within species – usually geographical separations – so that the two groups do not interact for long enough that the genetic differences accumulate enough that interbreeding is no longer attempted or isn’t viable – which can take millions of years – so the 2 groups have become separate species.

    There are many good books that will help you understand in depth how evolution by natural selection works – it’s a very complex and wonderful subject that emerges from simple basics – that modern science has expanded upon greatly in the last 60 years.

    All of Professor Dawkins books are complimentary in this area, and I enjoy re-reading them all multiple times. Since you have a young son, learning all about ‘The Magic Of Reality’ will be the best thing you can do for both of you. I’m a well-read non-scientist of 63 who has learned much in my 50 years of non-religious exploration of Life, The Universe, and Everything…. Mac.

  3. I think you have fallen into a common trap – creationists can’t avoid it, it seems – in that you seem to be arguing from before the fact, even though we are all after the fact. If an organism has survived at all, then any small changes have been either (1) beneficial or (2) neutral – whatever they consisted of. And they didn’t come about evenly within the population.

    While small changes occurred, the environment was almost certainly changing, too, so that evolutionary pressures themselves changed over time. Neutral mutations became beneficial as well as new beneficial mutations arose. With that sort of flux, it is impossible to say precisely how useful any mutation was at a given time. All we can say is that (1) it wasn’t harmful (because the organism survived), and (2) it must have been beneficial at some stage (else it would have disappeared by natural ‘dilution’.

    As Richard Dawkins has pointed out, eyesight of 2% efficacy is better than that of 1% efficacy (assuming the environment remains the same).

    In any case, it is not a paradox, let alone a ‘central’ one of evolution.

  4. I think there is a point here. Prof Suskind stated there are more random permutations than protons on the universe. I often see talks where people dismiss DNA as just mutating ‘randomly’ but that doesn’t seem to give it the credit it deserves. I posted a discussion on nano-cellular communications and the quantum spaghetti monster but no sign of it yet. Don’t get me wrong. I am an athiest to my core. But I think when you see these favourable genetic drifts e.g gluteus muscle in humans evolving in response to running, it almost seems like DNA had the ability to respond to physiological pressure. Just like we dismiss the DNA intercodon repeats as junk DNA I wonder if it will come back to be the key to our understanding the cell when are able to enter the nano world much better. Think cosmological constant. Cosmic microwave background (not just interference as initially thought)

    • In reply to #6 by Subatomicmantra:

      But I think when you see these favourable genetic drifts e.g gluteus muscle in humans evolving in response to running, it almost seems like DNA had the ability to respond to physiological pressure.

      This misses a huge part of the random mutations concept: that, for every genetic mutation that is beneficial, there are a lot more that aren’t. You can’t look at the former and think it’s too incredible that it’s come about by chance, because that ignores the denominator it had to work with; that’s like saying someone who took random shots at a target and then concealed the shots that missed target is a sharpshooter. It’s survivorship bias.

      As for the OP, what’s the problem? “Undetectable by human eyes” doesn’t mean “Too small to be selected”. If it’s advantageous for a population of birds to grow longer beaks, then a millimetre can be the difference between getting enough to eat and going hungry. A longer beak is more likely to obtain more food simply because it has more options available to it when faced with a natural variety of hole sizes, even if the difference between gaining food and not gaining it in some scenarios is so small that it looks negligible to humans who aren’t involved.

    • In reply to #6 by Subatomicmantra:

      I think there is a point here. Prof Suskind stated there are more random permutations than protons on the universe. I often see talks where people dismiss DNA as just mutating ‘randomly’ but that doesn’t seem to give it the credit it deserves. I posted a discussion on nano-cellular communications an…

      ‘Gluteus muscle evolving in response to running’

      Are you suggesting that this muscle improves with generations as a consequence of running? Or are you saying that the human with a well developed gluteus muscle is better able to run?

      • Firstly may I say what a relief it is to be able to discuss these things with people who obviously do a lot of thinking, reading etc. I am new to the board and as a scientist look forward to changing my views and opinions based on new info that comes forth. In response to above I think I mean both. Yes the gluteus is selected. But isn’t it interesting why it develops. My real thought block is wether it develops BECAUSE sussecive generations are running . So here’s the thought experiment (not made but by me but at a science lecture) .. If I lift weights all day and so do my 10000 generations . Will my 10001 be born with big muscles.? If so that is DNA responding to physiology. Yes there will be selection but that surely can’t explain the drift can it? Zebras don’t seems to sprout wings and fly away from lions. This keeps bugging me. And the issue of lost or failed mutations may not equate to the numbers. Again not my view but with the number of DNA base pairs the possible combinations are more than protons in the universe. I just feel a bit sorry for DNA when we say its all random. Maybe the molecule is ‘cleverer’ than we think? No quantum spaghetti monster attacks please I’m talking about physiological nanocellular responses – something we on the bio world are only beginning to understand. Don’t forget out of the billions if years it took us to evolve most of that was on the cell itself. Many thanks again for your thoughts In reply to #11 by Nitya:

        In reply to #6 by Subatomicmantra:

        I think there is a point here. Prof Suskind stated there are more random permutations than protons on the universe. I often see talks where people dismiss DNA as just mutating ‘randomly’ but that doesn’t seem to give it the credit it deserves. I posted a discussio…

        • In reply to #13 by Subatomicmantra:

          Firstly may I say what a relief it is to be able to discuss these things with people who obviously do a lot of thinking, reading etc. I am new to the board and as a scientist look forward to changing my views and opinions based on new info that comes forth. In response to above I think I mean both….

          I’m interested: what kind of science do you do?

          There are two suggestions to account for your experiment. The first is some kind of Lamarkism in a genetic context: that the body changes in response to its environment, and that change feeds back into the DNA molecules which are inherited by the next generation. The second is called the Baldwin Effect: that the body doesn’t change and then edit the DNA itself, but that the DNA mutates normally and those descendants whose mutations enable them to deal with the repeated body change better (for instance, making your descendants slightly better at handling weights) get passed on and accumulate. Both ideas predict that your distant descendants could be born ready to lift heavy weights.

          I won’t go into too much detail here, but Lamarkism is the least likely of the two. With the possible exception of white cells in the immune system (though I confess this isn’t something I’ve looked into), there’s no known mechanism for getting body modifications back into the genes. DNA works via proteins, which go on to build the rest of the body in ways we don’t fully understand, but which involve a lot of folding and cell division before the child is born. But proteins can’t change, and then go back and edit the corresponding bit of genetic code, and other environmental causes of mutation are just that – causes of mutation, with no systematic connection to the host body as would be required for Lamarkism. Dawkins talks about more objections in The Blind Watchmaker, but the gist is that Lamarkism is not as easy to prove as it’s simple logic would suggest.

          However, I think you’d be on firmer ground if you posited the Baldwin Effect. That too, needs some conditions, though. How well you lift weights must have some impact either on your ability to survive or your ability to reproduce. For instance, if we performed your experiment and artificially bred for a race of humans who were unusually strong, we would have to tally the weights lifted by all the people in one generation, and then select those who lifted the heaviest weights to breed, excluding the others. That’s a restriction on reproduction. At first, selection would single out not necessarily people who were strong to begin with, but people who find it easier or are better at becoming strongest through training. If we continued the experiment for long enough, eventually we could end up with people who became more and more able to train themselves towards big muscles and who would be stronger to begin with too, until the babies are probably born with the muscles (give or take, say, the fact that the babies need to be born and to grow up, and other engineering limitations to the human design).

          I find this fascinating because the Baldwin Effect can reconcile learning and instinct as well, and it explains why adaptions can often look Lamarkian. For instance, animal species might switch back and forth between being able to do something and having it built-in like an instinct depending upon how much their livelihood depended upon it in their environment.

          • In reply to #17 by Zeuglodon:

            there’s no known mechanism for getting body modifications back into the genes

            That may be right but have you heard of epigenetics? Im no expert at that but it is a potential mechanism that could explain Lamarckism. It involves changes that are heritable without altering the DNA sequences, perhaps you are interested.

            http://en.wikipedia.org/wiki/Epigenetics

          • In reply to #35 by tangyit:

            In reply to #17 by Zeuglodon:

            there’s no known mechanism for getting body modifications back into the genes

            That may be right but have you heard of epigenetics? Im no expert at that but it is a potential mechanism that could explain Lamarckism.

            Epigenetics usually involves switching on or off existing genes.

            It has been discussed before on this site:-

            http://old.richarddawkins.net/articles/642737-is-epigenetics-a-revolution-in-evolution

            http://old.richarddawkins.net/articles/642295-epigenetic-memory-key-to-nature-versus-nurture

          • In reply to #17 by Zeuglodon:

            there’s no known mechanism for getting body modifications back into the genes

            That may be right but have you heard of epigenetics? Im no expert at that but it is a potential mechanism that could explain Lamarckism. It involves changes that are heritable without altering the DNA sequences, perhaps you are interested.

            http://en.wikipedia.org/wiki/Epigenetics

            Alan4Discussion has already pointed this out But I’d like to expand a little on what he has said. Epigenetics has not been shown to stay in a population permanently, up to about 3 generations in rats (I believe). So for this reason it is not something that will survive long term in evolution. In addition to this as Alan4Discussion pointed out it acts by turning genes on and off. So it clearly is important as a multiplier of complexity in an individual organism and its direct off-spring BUT it acts on turning on and off genes that are already there. This means those genes it turns on and off needed first to be selected for before they can be expressed or not. Selection can therefore only act on genes that exist and have been introduced into the gene pool by random mutations and selected for by natural selection. Lamarck I believe cut off generations and rats tails never succeeding in having a baby rat born with a shorter tail until someone pointed out that the Jews had been carrying out a very similar experiment for a couple of thousand years without any discernible effect.

            In reply to Godzillatemple:

            Are those the sorts of “random mutations” that are actually likely to occur within a single generation, however? Or are still the sort of changes that would take many, many generations to appear?

            They are the sorts of random mutations that exist within a population all the time. There will be probably hundreds of mutations in you and me that we have no idea are there right now. Sexual reproduction increases the mix also maximising variety so any population while having largely the same genes none of us (excepting identical twins) look much alike or have all the same attributes. So Natural Selection cuts out the weakest at that time (those genes it removes may in different circumstances be those that may have in different situations been of advantage).

            To get species separating generally a population needs to be isolated in conditions, geography or time or the mix of genes can shuffle the cards back to little change overall. So noticeable change in say beak size can be observed within a couple of decades or even years in say finches, were as birds loosing their wings as is happening to Galapagos Cormorants would likely take much, longer.

            Cain Toads released in Australia (stupidly) have devastated local wildlife due to their poisonous skins and eggs. But as a child I noticed dead ones on their backs in my back yard with their guts open and their tongues ripped out. Recently I heard this was local crows that have learnt to turn them over and peck out their guts and tongues which are not poisonous (behavioural adaptation, crows who pecked out the wrong bits are dead crows and don’t breed), some snakes and goannas are starting to tolerate the toxins, cain toads are becoming prey. As they migrate to the Northern Territory the toads in the lead have longer legs. Why would natural selection favour them, well they can jump faster and therefore exploit new territories before their shorter legged brothers and sisters, this also means any other toads they breed with are likely to share genes for longer legs (there may be many different genes that make legs longer- these guys and ensuring their off-spring have them, toads aren’t fussy they will breed with shoes or even drying up squashed toads on the side of the road). If an earth quake or volcano separated a population (not going to happen Australia is geologically fairly inactive) then there may end up being a population of long legged toads (as the population at this time all share long legged genes). What will probably happen in time as the shorter legged toads catch up is that they may have advantages that allow for selection against long legged toads or compete on a more even basis and the leg length over decades will reduce again.

          • In reply to #42 by Reckless Monkey:

            In reply to #17 by Zeuglodon:
            Recently I heard this was local crows that have learnt to turn them over and peck out their guts and tongues which are not poisonous (behavioural adaptation, crows who pecked out the wrong bits are dead crows and don’t breed).

            Crows learn to do all sorts of things. Before smoking was made illegal in public places crows were seen picking up smoldering cigarette stubs and holding them under their wings to smoke out parasites.

            I’ve also seen crows sliding down snowy rooftops. For fun. Not terribly scientific, but cool.

          • That’s great.. I totally get it now seriously I do thanks a lot for the info on Lamarkism vs Baldwin effect it does completely make sense. By the way in response to above I am an eye surgeon so have a medical degree and postgrad oin ophthalmology. Hope that makes me a scientist! (uk nhs) My initial concept came from staring into the living eye everyday through a microscope and seeing how the cells behave down a microscopic scale in vivo. The way cells show cellular memory particularly in wound healing is stunning to watch hence my DNA question. Sorry about the zebra wings analogy but now I get concept of minor drifts. I saw the Alice Roberts programme. Great. Got some reading to do!In reply to #17 by Zeuglodon:

            In reply to #13 by Subatomicmantra:

            Firstly may I say what a relief it is to be able to discuss these things with people who obviously do a lot of thinking, reading etc. I am new to the board and as a scientist look forward to changing my views and opinions based on new info that comes forth. In re…

        • In reply to #13 by Subatomicmantra:

          Firstly may I say what a relief it is to be able to discuss these things with people who obviously do a lot of thinking, reading etc. I am new to the board and as a scientist look forward to changing my views and opinions based on new info that comes forth. In response to above I think I mean both….

          I was going to suggest that you appear to favour some sort of Lamarkian process at work, but I notice Zeuglodon #17 has already put that in the mix. I also suspect the possibly that you may slip in the hand of god at this point.

          An interesting tv program hosted by Dr Alice Roberts featured on this site a week or so ago. I think you’d find it very interesting because she actually mentions the gluteus muscle and the advantage it conferred in our ability to run on the plains. It gave us a huge advantage by being able to outrun our quarry.

        • In reply to #13 by Subatomicmantra:

          Firstly may I say what a relief it is to be able to discuss these things with people who obviously do a lot of thinking, reading etc. I am new to the board and as a scientist look forward to changing my views and opinions based on new info that comes forth.

          Others have dealt competently with several issues , so I will just pick out this section: -

          If I lift weights all day and so do my 10000 generations . Will my 10001 be born with big muscles.?

          No. Not unless the capacity to grow big muscles is an individual genetic trend, and is beneficial to your survival, to a greater extent than the negative effect the extra time and demand on your resources places on you by doing so. This could disadvantage you and your offspring, in competition with other humans. (eg. Some competitor uses small muscles to grow more food and raise more children while you are exercising, also requiring less food to do so.)

          If so that is DNA responding to physiology.

          No! Natural selection picks out advantaged individuals from existing DNA who are better adapted to survive and reproduce, than the general population.

          It has more to do with eliminating the uncompetitive to make space for the offspring of the more competitive.

          Yes there will be selection but that surely can’t explain the drift can it?

          Drift is a separate process from selection.

          Definition – http://www.biology-online.org/dictionary/Genetic-drift

          Zebras don’t seems to sprout wings and fly away from lions. This keeps bugging me.

          Zebras can’t sprout wings because evolution only makes tiny drift changes, and beneficial changes, one small step at a time, modifying existing structures.

          Flying fish could gradually grow larger fins, bats’ fingers could grow longer to gradually evolve into wings, and small feathered dinosaurs’ arms could gradually change into wings, but large heavy horses don’t get to fly. They are evolved to run and kick.

        • …If I lift weights all day and so do my 10000 generations . Will my 10001 be born with big muscles.? If so that is DNA responding to physiology. Yes there will be selection but that surely can’t explain the drift can it? Zebras don’t seems to sprout wings and fly away from lions. This keeps bugging me. And the issue of lost or failed mutations may not equate to the numbers. Again not my view but with the number of DNA base pairs the possible combinations are more than protons in the universe.

          There are two things here that are dealt with much better than I can at the end of Unweaving the Rainbow. But here goes:

          1. Acquired traits are not inherited – DNA does not respond to external stimuli like that (a heavy dose of radiation might be different, but it will hardly result in many beneficial mutations). Your question belongs to the world of Lamarckism – a pre-Darwinian attempt to explain evolution that was superseded by natural selection. Our DNA at our death is unchanged from that at our birth, except for any copying errors, or for any traumatic events like radiation damage. You can train as rigorously as you like, but the results will not be passed on. (The impulse to train, though, might be a genetic trait you were born with, and it might be passed on.)

          2. There is nothing much on a zebra that might become wings. All winged vertebrates have wings that are adapted from limbs (usually the front limbs). But the front limbs of a zebra have already been adapted very well for running and it is questionable whether natural selection would have much to work on now, especially given that all the digits (toes) except one have disappeared. Natural selection can’t go in reverse (with a few very limited exceptions) so the missing digits would be unlikely to be reconstituted. What does not happen is that wings (or anything else) sprout from nothing.

          Then there is the question of what the evolutionary pressure might be for zebras to fly. They avoid lions very well as it is (there is no shortage of zebras) so why would they adapt to a different way of avoiding lions? Zebras are large animals – far bigger and heavier than anything that does fly, so that it would probably not be a success anyway.

          Having written all this, I see that Alan4discussion has answered it already, and better than me. Ah well!

      • In reply to #11 by Nitya:

        In reply to #6 by Subatomicmantra:

        ‘Gluteus muscle evolving in response to running’

        Are you suggesting that this muscle improves with generations as a consequence of running?

        I was wondering the same thing… sounds almost Lamarkian to me.

        Steve

        • In reply to #129 by Agrajag:

          In reply to #11 by Nitya:

          In reply to #6 by Subatomicmantra:

          ‘Gluteus muscle evolving in response to running’

          Are you suggesting that this muscle improves with generations as a consequence of running?

          I was wondering the same thing… sounds almost Lamarkian to me.

          It’s funny, when I first read the comment, I wondered why no one had picked up on it. I thought perhaps I was missing some vital point. That’s why I asked for clarification.

  5. Complex adaptations evolve through many small, only slightly beneficial mutations. That’s what we mean when we describe big changes as “too slow to see”. What that means isn’t that the mutations are invisible, but that you don’t have time to see many of them. We see such mutations all the time in both experiments and field work. If you look at the fossil record, you can see gradualism in many adaptations (the rest only look less gradual than they were because the fossil record is incomplete), and you can also radiometrically realise they took flipping ages. Just look at the adaptation of the bones of the inner ear in the amphibian-to-reptile-to-mammal transition. You wouldn’t even see one step of the process complete in a lifetime, since completion means a new gene goes from being rare to being near universal. That example is also good for another point: just because an adaptation is useful, it doesn’t mean you can see it outside the body with the naked eye. Maybe you need to X-ray, or take tissue samples, or use a microscope, or analyse the changing biochemistry or the immune system or whatever, or statistically study behavioural patterns, or look at how spermatozoa are treated in a female body.

  6. You are making a few errors here, 1) survival may be a close thing. 2) evolution may not always be visible to be happening. 3) sexual selection is limited to your choices.

    1)There will often be situations in which survival is a close thing. Think about a heard of Zebra running from a pack of lions. All sorts of factors in split seconds can make the difference between Zebra A or Zebra B being eaten. It may be just luck but often little things can have an impact, slightly better stamina, slightly better speed or manoeuvrability, slightly wider or narrower stripes might be slightly more confusing to a running lion. You don’t have to outrun the lion, just the Zebra nearby you.

    Now in different conditions these may change, circumstance may favour speed over manoeuvrability or recent rain may have made the ground muddier so absolute speed may not be selected against so the factors in a herd will get evened out to some extent. But, if there is a long drought or similar event a particular set of attributes may become far more common, say more efficient use of water. Now you will see genes shift in a particular direction. These may be at the level of genes and have no outward signs. Only after populations are separated for some time do these small differences build into a new species. Tigers and Lions are very similar Inside Natures Giants dissected both after their skins came off there was very little to see between them.

    3) We pick up on very minor differences when choosing a mate. Smell, a little more sheen on the feathers, in humans subtle clues like how white the eyes are etc. are all indicators of health. a change in a gene might have a very big impact on say how much testosterone is produced which could have a large impact on physical appearance. I could go on but if you are choosing from a group of animals around you that look almost identical you will go for the small changes.

  7. Reckless Monkey at #8 makes some good points which I want to elaborate on. I studied economics, but I am pretty sure there is an economic principle at work in evolution (and many other things) – that is the multiplier/accelerator principle, which says, in short that little changes can have big effects.

    Outside economic ideas, consider the 100m sprinter who is 0.001sec faster than his closest rival. You might not think that very much, but if he sprints at his best every time he races, though he only has a tiny advantage over the rest of the field, he will win 100% of the time.

    The other idea of being drought resistant, means that in very severe drought, perhaps the individuals with the mutation are the only ones to survive and hence in one generation, you have a massive change.

    Incidentally, I’m more in the school which thinks that whilst random mutation may happen randomly, the effects on species happen quickly when they happen – if that makes sense.

    A famous example is the peppered moth.

  8. Here comes the apparent paradox, however. When asked why it’s impossible to view evolution as it occurs, the answer is inevitably that it occurs on a very long time scale and that the individual mutations are too small to notice until they have had time to accumulate through many generations. If the individual mutations are so small, however, how can any of them actually contribute to the survivability or selection of the organism? I mean, it’s easy to think about a gross mutation like an extra finger or new skin coloration affecting my chances of mating and passing along my genes, but how would a mutation too subtle to be detected affect whether I am able to find a mate or not?

    A lot of really good explanations have been offered for this but let’s take this from the reverse view: If the mutations were large and easily viewable over the generations, then we would see a far wider disparity in the generations and the process of evolution would occur at a far more accelerated pace. Meaning all species would evolve so widely over the generations that survival would be far less likely (the chances of the far larger mutations all being beneficial and all being adaptable would decrease by a large degree) and the result would be far different than what we see now.

    A really good and often overlooked example of this are virus strains. The strains that survive are the ones capable of adapting to the antiviruses we introduce or are able to bypass the immunities we develop over time. we can actually track the virus mutations over the long course and see the changes that have taken place and show hoe the process of evolution works and why the time frames in which they occur are so vital to how things appear as they currently do.

  9. It’s about populations, not about the individual. If it happens that the mutation survives countless reproductions and is then shared among a population, whether it is a benefit or a hindrance, or neutral, it will get passed on down the generations. A mutation beneficial to the individual or the group has a higher chance of being transmitted, because, well, it’s beneficial. In small groups, mutations would have a bigger, less subtle impact, and will become significant as the population starts to grow again.

    That’s my layman view anyway.

  10. Zebras don’t seems to sprout wings and fly away from lions.

    I assume this is an oversimplification but the evolution of any given species, as well as the points where species diverge don’t generally cause mutations as random as that. If zebras have managed to survive as they with their ability to run as well as other means (where they are in a crowd of zebras in relation to a predator, how much faster one zebra is than another) flight is neither the most useful nor the most reasonable evolutionary trait one would evolve in its given environment. Such a mutation would truly be random, and any such mutation would not automatically ensure the zebra’s survival. Consider that most winged creatures are usually smaller than humans with far less mass and are generally evolved for adapting to all the rigors of flight.

    But as I said, I assume this was an oversimplification being used in your example.

  11. Please help me understand what I am missing here.

    your manners

    it has been 37 years since publication of The Selfish Gene and you come to the authors website to complain that you haven’t read it

  12. Thanks for all the responses so far!

    To clarify a bit, I have no problem whatsoever accepting that small changes can (and do) accumulate over long periods of time. My question was solely about the “natural selection” part of the equation. If it takes thousands (or millions) of years for the “very small improvements” to accumulate to the point where they are actually noticeable, then how can they affect whether an individual lives long enough to pass on his or her genes? And by “noticeable,” I mean significant enough to provide some advantage, either in attracting a mate or surviving within the current environment.

    Reckless Monkey pointed out some examples of how “very small” changes could, in fact, have an impact on survival or sexual selection. If what he says is true, that pretty much answers my question right there. Are those the sorts of “random mutations” that are actually likely to occur within a single generation, however? Or are still the sort of changes that would take many, many generations to appear?

    CdnMacAtheist said:

    If a genetic mutation benefits an organism at least until it has reproduced – and in some cases assists the offspring until it is self-sufficient – then that mutation, if it is passed on during sexual genetic shuffling, can be selected by increasing its frequency in the gene pool of that species, which can take many generations to have noticeable effects within species.

    Very small improvements don’t just affect whether you find a mate, but aid your survival until you have the ability or opportunity to mate. Any minute benefit can help you improve your chances of avoiding or fighting disease and injury, starvation, finding or catching the right varieties of food – or avoiding becoming food….

    I guess this is basically what I was looking for, and I suppose it also explains why some species end up being evolutionary “dead ends,” as it were. Random mutations get passed along and accumulate until the change has either a positive or a negative effect on the species’ survivability. If positive, then the lineage continues. If negative, then the species dies out.

    On a related note, I’m curious if we know why certain species seemingly have not evolved at all in hundreds of millions of years (so-called “living fossils”)? I understand that they may be perfectly suited to their environment, but wouldn’t there still be random mutations occurring all the time that cause some survival neutral changes to accumulate over time? Or are we assuming that species is so perfectly fine-tuned to its (presumably stable) environment that any change whatsoever would in effect be negative and therefore selected against? Or do we simply not know the answer (which is a perfectly valid answer in and of itself)?

    • My own view on this is that early evolution to the point where we get to the basic vertebrate structure , is certainly the most interesting. Once the vertebrae structure was arrived at I think evolution by natural selection does account for the animals we see today. What is interesting though is how did the complex organs develop? I’d say that there was an accumulation of random traits and when by chance they became useful they were then naturally selected for. It seems silly to me that every single intermediary step in the development of complex organ was beneficial to the organism.

      In reply to #18 by godzillatemple:

      Thanks for all the responses so far!

      To clarify a bit, I have no problem whatsoever accepting that small changes can (and do) accumulate over long periods of time. My question was solely about the “natural selection” part of the equation. If it takes thousands (or millions) of years for the “very…

      • In reply to #20 by Pauly01:

        It seems silly to me that every single intermediary step in the development of complex organ was beneficial to the organism.

        Huh? Let’s say a slow zebra appears. He is going to be lion chow because lions look for slow zebras. He is going to be shunned by the cute female zebras because they are attracted to the jocks. Even if his genes by fluke made it to the next generation, they would be a hindrance from then on until they were eliminated.

        In a very small population, I supposed it is possible a worse trait could displace a better one by a statistical fluke, but normally there would be so much competition, a weak trait would stand little chance of taking over the entire species. I suppose the other way it could happen if a trait had a tiny advantage in one niche and an alternate trait had a tiny advantage in another niche. Both could persist.

        • Rodey
          Your talking about attributes such as quality. Quality of vision, speed,aesthetic value.etc. I’m talking about evolution to explain organs of animals , the endocrine system etc. in building these systems , early evolution, I think it’s reasonable to say traits were inherited but not naturally selected for. I think a culmination of these unselected traits struck it lucky and were then useful and selected. I can’t see how it could have happened any other way. As I said once the basic vertebrate body was established then natural selection took over.

          In reply to #71 by Roedy:

          In reply to #20 by Pauly01:

          It seems silly to me that every single intermediary step in the development of complex organ was beneficial to the organism.

          Huh? Let’s say a slow zebra appears. He is going to be lion chow because lions look for slow zebras. He is going to be shunned by the cute fem…

          • In reply to #73 by Pauly01:

            Rodey
            As I said once the basic vertebrate body was established then natural selection took over.

            How did the vertebrate body become established if not by natural selection?

          • Yeah ,

            What I’ m saying is that every stage in the development of an organ was not beneficial to the organism. Isn’t it possible that traits were simply inherited and embellished without conferring a better chance of survival or reproductive success. After enough random embellishment of a trait , it then became useful and was selected for , thus flooding the gene pool with the trait. It does not make sense to me that every single step of change had to be beneficial to the organism.

            Isn’t it possible that a trait can be neutral in terms of survivability and reproductive success , but it can still be randomly embellished by the laws of genetics and inheritance. Of course there will come a tipping point where it suddenly become useful and is further adapted by the environment.

            In reply to #83 by bob_e_s:

            In reply to #73 by Pauly01:

            Rodey
            As I said once the basic vertebrate body was established then natural selection took over.

            How did the vertebrate body become established if not by natural selection?

          • In reply to #84 by Pauly01:

            Yeah ,

            What I’ m saying is that every stage in the development of an organ was not beneficial to the organism. Isn’t it possible that traits were simply inherited and embellished without conferring a better chance of survival or reproductive success. After enough random embellishment of a trait , i…

            Understood. I guess it depends how you analyse it. On the level of the individual, and a succession of individuals there will be forwards and backwards steps as random changes occur. You’d have thought that for a change to be incorporated on a species level and become part of its phenotype the change would have to confer a positive effect otherwise how would it spread through the whole population?

            So as fish converted their swim bladders to lungs, for example, some members of the population would have the ability to extract oxygen from the air better than others, by minute degrees, without it conferring a selective advantage. Once the ability to extract oxygen began to confer a survival advantage, that’s when it would have spread through the population by natural selection.

            So looking like this on the level of the individual you are right, there would be inheritance of traits which initially did not give that step up of evolution. But on a species level the change only occurred once it was beneficial.

            I think that makes sense.

      • In reply to #20 by Pauly01:

        My own view on this is that early evolution to the point where we get to the basic vertebrate structure , is certainly the most interesting. Once the vertebrae structure was arrived at I think evolution by natural selection does account for the animals we see today. What is interesting though is how…”It seems silly to me that every single intermediary step in the development of complex organ was beneficial to the organism.”

        isn’t the evolution of the eye explained in this way? ie, each intermediary step being beneficial in that it created an ever-so-slightly more useful ‘eye’ (from a single light sensitive cell, to a little cup, to a lense being added, to the pinhole camera eye of the nautilus, to our own camera eye)?

  13. Yes that’s interesting. I think your talking about macro evolution like the evolution of the kidney. What good is half a kidney? I’d like to add to your questioning on evolution by asking

    If one kidney has evolved , how can another kidney evolve , Why 2? I buy 1 liver , 1 pancreas , 1 heart , 1 brain but why 2 kidneys?

  14. I am reading “The selfish gene” by Richard Dawkins. I am less than half way thru it but it seems to answer your question. I would recommend it.

    Thank you. I only just recently heard of this book, but haven’t yet read it and wasn’t aware it addressed my specific question. I will definitely add it (and “Climbing Mount Improbable”) to my list of books to buy. Then, all I have to do is actually find time to read them (and hopefully understand them as well).

  15. godzillatemple

    On a related note, I’m curious if we know why certain species seemingly have not evolved at all in hundreds of millions of years (so-called “living fossils”)? I understand that they may be perfectly suited to their environment, but wouldn’t there still be random mutations occurring all the time that cause some survival neutral changes to accumulate over time?

    Only a random mutation that confers a slight advantage will accumulate. A random mutation that doesn’t shows no selective advantage and thus there is no real driver for it to proliferate or even remain in the genome. Some neutral ones can and do build up over time but there is no requirement for them to do so and they do not alter the phenotype – hence the organism doesn’t change, only the accumulation of neutral mutations. Harmful ones will disappear with the organism. But never underestimate the fact that the power of selective pressure only comes into play when needed. Evolution doesn’t strive to make things better – it’s more like a stroppy teen it’s happy with just good enough.

  16. Hi godzillatemple,

    As I understand the concepts, this means that:

    1) random genetic mutations periodically occur in some (if not all) organisms and …

    Random genetic mutations happen all the time. The mutation rate of an organism probably changes in response to environmental stress – I understand that this is currently an area of research with no clear results. It might be that mutation rates vary for a whole series of reasons, this is what the fossil record appears to demonstrate.

    In theory, like a Marvel Comic character, a mutation might also lead to a new advantageous result – but I know of no studies looking for such events. Obviously super-powers would not result, but a tiny additional advantage, like getting suddenly a little bit more sensitive to some sounds, is theoretically possible.

    Part of the problem is that what would count as an advantageous mutation? As we will see (below), a mutation could be initially negative or simply of no immediate consequence – it might only be obviously advantageous much later – long after today’s Observer has passed away.

    Another thing is that negative effects are far easier to observe. For example UV light damages DNA, which may result in error prone attempts by the cell to perform DNA repair – cancer, for example, can then result.

    However, it is not the mutation itself that is important – it is:

    a. The mutation of DNA in cells that will directly affect offspring.

    b. The heritability of alleles that result from mutations in DNA.

    2) If a mutation is beneficial to an organism’s survival or somehow makes it more attractive to the opposite sex … that organism will be more likely to reproduce and pass its genes on to the next generation.

    With my edit, your understanding is correct. Wherever sexual reproduction occurs we can say that sexual selection may be an additional factor.

    Thus, small changes accumulate over time and eventually lead to new species.

    Hopefully I have stated that correctly.

    I’m no expert, but it looks bang on to me.

    Here comes the apparent paradox … When asked why it’s impossible to view evolution as it occurs, the answer is inevitably that it occurs on a very long time scale …

    Check out Drosophila melanogaster and Escherichia coli, we’ve been directly observing evolution – in some suitable species – for over a century. As a rule of thumb, the bigger the organism the more difficult it is to see evolution in action. But, the universality of scientific principles teaches us that evolution must be happening constantly.

    Of course, DNA science has begun to reveal ways in which we can observe evolution in every species. Even before that studies of our own case have observed the effects of our use of antibotics on the evolution of bacteria that are harmful to humans.

    Then there is Charles Darwin’s favourite – and still fully valid – example: Domestication and breeding. By using our own skill to manipulate the environment, and opportunities to mate, we can show how alleles change generation-by-generation, even without knowledge of DNA and mutations.

    So, in summary, evolution is highly visible, and in many different ways.

    … and individual mutations are too small to notice until they have had time to accumulate through many generations.

    It is important to note that each cell in an organism contains DNA sequences (sticking to large animal examples), and that the sequences in each individual cell can mutate. However, every cell is not involved in reproduction. Thus, if I stay out in the Sun too long, expose too many of my cells to mutation potential via UV exposure, and get cancer, I will be able to reproduce without automatically giving rise to offspring that have cancer. Also if I, and the next hundred generations of my offspring after me, pump iron every day – the 101st generation will not be born with big muscles.

    This is the difference between individual lives and alleles. If my great-great-grandchildren have exactly the same shade of brown hair as me there is a higher probability that this physical trait (allele) came from me. If my great-great-great-grandchildren (and every generation between) are all weightlifters it doesn’t equate to an allele that demonstrates that my branch of the human family have DNA that produces big muscles. But, it might be evidence of a genetic sequence that produces the behaviour pattern (allele) of going to the Gym five times a week and exercising, principally, our arms.

    When we speak of mutations and genetics we are usually talking about mutations that occur during the reproductive process itself. As I understand it, the full picture is more nuanced than that, but let’s understand the basics – let’s learn to walk before we try any running.

    Biologists talk about alleles. What they mean by allele is a trait; a physical trait that we can see – like longer arms, or a population trait – such as resistance to a disease or parasite revealed by population statistics, or a behaviour – like a species of monkey who’s younger generations are suddenly spending more time on the ground than in the trees. Some alleles can only be revealed if we have historical data on a species (all those busy 17th to 20th Century Zoologists have left us a fabulously useful legacy).

    Today, we can also, of course, see far more alleles through our microscopes – so an outwardly invisible change such as an internal organ’s size or function can be observed. Add to that our latest instruments, ultrasound to regularly check examples of physical alleles normally hidden, cameras to record behaviour alleles, and DNA sequencing to help link mutations to alleles.

    If the individual mutations are so small … how can any of them actually contribute to the survivability or selection of the organism?

    As we can see from the Biologists’ use of the term allele, linking DNA sequences to how it’s organism is and behaves takes painstaking work on the organism and it’s environment and history. A DNA sequence is kind of like the rudder on a boat. It’s only a small component, but it can have a dramatic effect on the overall body (in terms of the body’s development and functional direction rather than simply its angle of travel). Unlike rudders and boats, DNA and alleles are not a simple cause-to-effect relationship. This has been shown very clearly in the case of the domestication of the Silver Fox. From this example we see that a change in allele frequency in a population cannot simply be selected in isolation. As I understand it this is not only the result of genetic sequences having more than one effect each – but also the interactions between sequences.

    I mean, it’s easy to think about a … mutation like an extra finger or new skin coloration affecting my chances of mating and passing along my genes, but how would a mutation too subtle to be detected affect whether I am able to find a mate or not?

    This is where Charles Darwin comes into his own. To get the full – and most clearly written – effect I suggest you read On the Origin of Species, but here’s a précis. The first, most effective and most crude, reason is death. If an invisible mutation leaves you open to a disease that most of the your Tribe is immune to you could simply die before finding a suitable mate. A more subtle version of this is a mutation that is invisible but makes you infertile – now even if you find a mate you fail to reproduce. Even more subtle would be a mutation that makes you more able to withstand a long period without water. No-one would suspect. Indeed you pass on this trait to your grandchildren (via your children, obviously) and still no-one suspects. Then your Grandson gets spectacularly lucky; a prolonged drought kills most of his competition and he ends up living polygamously and having a hundred children. That’s lucky in the genetic sense, obviously, and not in a family relations and house-maintenance way.

    It’s not just that mutations can be positive, and negative. It’s also that mutations must lead to increased offspring that survive to adulthood. Any such mutation will only really be detectable in the later version of your species if the mutation is passed to your offspring.

    Thus, a genetic mutation could occur – be invisible for generations – and suddenly come into its own due to a change outside the individuals, even outside the Tribe. An obvious example that, the evidence suggests, drove our own ancestors’ evolution is climate change.

    I am not a Biologist so if anyone out there can see a mistake in my description I will be very happy to read a correction – I’m always ready to learn.

    I hope that helps, godzillatemple?

    Peace.

  17. I hope that helps, godzillatemple?

    Immensely (assuming, of course, that what you wrote is accurate). Thanks for taking the time to answer my questions so thoroughly.

    Growing up, I always had a fascination with physics and astronomy, but never really had much experience with biology other than a high school biology class where we focused mainly on anatomical structures and dissecting various creatures. In fact, I don’t recall evolution ever being mentioned at all. So, obviously, I have a lot of catching up to do…

    • In reply to #24 by godzillatemple:

      Hi godzi,

      Immensely [helpful] (assuming, of course, that what you wrote is accurate).

      Your most welcome. I like answering this kind of question because, as Christopher Hitchens’ observed, with science we’re free – encouraged even – to go back and say to ourselves; How do I know that, how do I know it’s true?

      As with any explanation on the basics of a rich and nuanced subject, there will be people who don’t like the way I put it. That said, I’m confident that I’m at least 90% right.

      Growing up, I always had a fascination with physics and astronomy, but never really had much experience with biology …

      Me too. I was a Space Age kid (I was just old enough to see the first Moon landing live on TV) and at school I preferred Physics and Chemistry.

      I think you’re going about it the right way. Once you understand evolution the rest of biology just makes so much sense. I wish they’d done it that way at school – I would have had far better grasp of the subject.

      Peace.

  18. And in other news, my copy of “The Greatest Show on Earth” just arrived in today’s mail. I’m not sure when I will have time to read it, but I am looking forward to the experience. I don’t know if any of my questions are addressed in this particular book, however, as it appears to primarily be about showing the evidence for evolution and not really about explaining how evolution actually works. I suspect that, for that, I will have to get a copy of “The Selfish Gene” as others have suggested.

    So much to learn, so little time…

    • In reply to #26 by godzillatemple:

      And in other news, my copy of “The Greatest Show on Earth” just arrived in today’s mail. I’m not sure when I will have time to read it, but I am looking forward to the experience. I don’t know if any of my questions are addressed in this particular book, however, as it appears to primarily be abou…

      You should love this book if you appreciate good literature, as well. It was a pleasure to read.

  19. You should love this book if you appreciate good literature, as well. It was a pleasure to read.

    Yes, that was the main reason I decided to buy it. It’s easy enough to tell somebody with questions to just “read a book,” but not all of us have the patience or background to slog through a long, dry science textbook. The reviews on “The Greatest Show On Earth” were pretty unanimous in their praise of Dawkin’s writing style and accessibility, however. I don’t really need to be convinced as to the “evidence of evolution”, but I’m sure it will be informative nonetheless.

  20. To add a few points to those made –
    I think it was Darwin who wrote of species often arising at marginal areas, in a wide sense. Thus, individuals experiencing climate change can be placed in a situation where small differences really do count and lead to marked selection pressure to change. This may happen through staying put while an area dries out (I think that happened in Australia over thousands, not millions for years. Another way, of course, is for the animal to move to another climatic zone. A good example would be humans, where over the tens of thousands of years that the journey out of Africa into the north, it is clear that white skin was better in gloomier climes (less easy to make vitamin D, which if lacking deforms the pelvis or the legs, amongst other bones, through rickets. Mutations towards albinism would thus give advantage to reproduction, as (with the large head of Homo aspens, and the tilt of the pelvis from bipedalism, means that even very small advantages in the birth canal could be literally life and death for mother and infant. However, albinism in the tropics would increase the risk of fatal skin cancers, while offering no vitamin D / anti-rickets advantage was warm climates have more sun, and more change to expose the skin. Another Homo mutation was probably sickle cell anaemia where the red blood cells can be in ‘sickle’ form – in this case an advantage in malarial areas, as the half (heterozygote) form gives some malarial resistance, while the homozygous (both genes) does lead to higher risk of ‘sickling’, which makes the blood cells more likely to jam in small blood vessels & can be fatal. Thus, like albinism, a mutation favours selection for a trait in some areas and against it in others – with counterbalancing risks. Thus, as humans moved north over a period of a few thousands of years, small mutations could have major impact on survival.

    Of course, Darwin’s observations of species evolving (apart from ancestors) in different environments was classically in islands – real ones, such as the Galapagos (different amounts of rain, different tortoises & finches), or virtual ones, in respect to mountains. Regarding giant pandas, (I think) a long time ago, some bears found themselves on mountains with not a lot else apart from bamboo plants. Those that evolved enough to digest it a bit could stay. But over time, they came to only eat bamboo (it was all there was), despite their ancestral short carnivorous gut not really being ideal for low nutrition vegetation. Arguably, giant pandas are a good example of how evolution does not always work, ie does not all fits in, is not miraculous or amazing. Even without humans pandas would be very precarious – every now and again all the bamboo in one species dies back after flowering, and the smallest change in climate in their mountain islands affecting the bamboo could wipe the out bamboo-reliant pandas.

    Another area which could lead to faster change, though one I know rather less of, is DNA effect multiplication, ie DNA does not code for genes in a straightforward way, 1 gene = one phenotype. There can be replications of genes, so mutations in the sense of of increases (or decreases) in replications can increase the expression of that gene, without a mutation in the gene itself. Another factor is control over gene expression (which is another kind of multiplier apart from replication)- it seems the genes controlling the expression of other genes are important. As I said, I do not have details, but it is a way to get a big effect quickly (in terms of an organism, I think gene control is involved in metamorphosis, eg caterpillars to butterflies. But others may know more.

    Finally, of course some mutations are quite drastic – albinism being one. In species living in the arctic, albinism would be a very quick winning camouflage, for prey and predator.

  21. If the mutation is benign, it will continue to be passed on. Ultimately it may sophisticate into a potent gene.

    Let’s say a mutation made the human liver a slightly different color. No one would see it. They would pass that mutation on to their children. The ability to fold one’s tongue is not a survival trait, but there it is. Eventually that trait could become problematic or highly beneficial to survival or breeding strategies. That’s a benign mutation that we can at least observe, but I believe the same occurs at the GATC level.

    There’s a largely dismissed concept of Orthogenesis, which I believe was an early attempt at answering your question. Though no one takes it seriously, looking it up may be helpful. The basic premise is that mutations follow a trajectory, that there is an internal mechanism that guides in a blind but intentional manner, thus the benign mutations are just waiting to fully express.

    • In reply to #33 by This Is Not A Meme:

      If the mutation is benign, it will continue to be passed on. Ultimately it may sophisticate into a potent gene.

      Let’s say a mutation made the human liver a slightly different color. No one would see it. They would pass that mutation on to their children. The ability to fold one’s tongue is not a su…

      do harmful mutations sometimes survive? and if so, do they sometimes survive for long periods?

      • In reply to #222 by doubting thomas:

        do harmful mutations sometimes survive? and if so, do they sometimes survive for long periods?

        You have to take each one on a case by case basis in context. A mutation might shorten the average life span of an individual, but also make that individual more sexually attractive so as to increase mating opportunities. Something might be harmful for organisms living in small groups but get propagated if it increases cooperation that helps enough in large groups. The point is that for evolutionary purposes, you should not be looking at a mutation in terms of being helpful or harmful to an individual, but rather, helpful or harmful to the propagation of that gene in a given breeding population.

  22. “If the individual mutations are so small, however, how can any of them actually contribute to the survivability or selection of the organism?” (OP)

    That is a perfectly good question (you’re not the first to raise it) about signal-to-noise ratio which is a potential problem for a purely genetic account of evolution. It requires a quantitative answer. No one here has offered such an answer, and I can’t recall a quantitative treatment in “The Selfish Gene” or “Climbing Mount Improbable”.

    • In reply to #39 by logicophilosophicus:

      That is a perfectly good question (you’re not the first to raise it) about signal-to-noise ratio which is a potential problem for a purely genetic account of evolution. It requires a quantitative answer. No one here has offered such an answer, and I can’t recall a quantitative treatment in “The Selfish Gene” or “Climbing Mount Improbable”.

      Oh dear. This argument is a good example of trying to predict the progress of something when we can only see it in hindsight. We do not know the precise evolutionary steps that organisms went through to get where they are, but we can assume that each step was an advancement (or at the very least was neutral) since the organisms have survived successfully. It is only a problem for “a purely genetic account of evolution” if we assume that the pace of evolution was constant, with every generation having (for instance) slightly longer legs.

      You are right, I think, that this does not appear in the two books you name, but I’m sure it does in Climbing Mount Improbable.

      • In reply to #40 by Pabmusic:

        In reply to #39 by logicophilosophicus:

        Oh dear indeed. The point is that without a quantitative justification, it it unclear how evolution happened. The key words (in addition to quatitative) were purely genetic. There may be (there may need to be) other factors at work. And no genome ever made a cell, for example.

        I believe you are mistaken in thinking CMI addresses this.

        • In reply to #46 by logicophilosophicus:

          In reply to #40 by Pabmusic:

          In reply to #39 by logicophilosophicus:

          Oh dear indeed. The point is that without a quantitative justification, it it unclear how evolution happened. The key words (in addition to quatitative) were purely genetic. There may be (there may need to be) other factors at work…

          I’m unclear as to what might be meant by a ‘purely genetic [account of evolution]. This may be a gap in my knowledge – and of course inheritance is taken to be genetic – I think via nuclear and mitochondrial DNA in eukaryotic organisms. But while neo-Darwinistic evolution starts with genetic mutation it really happens through natural and sexual selection, ie genes and genetic mutation alone would not account for adaptive evolution. The results of selection are transmitted genetically, but genes are so to speak the medium not the message. I don’t know how that might be quantified – others may. I think that relatedness can be quantified genetically through DNA comparisons and phenotypal resemblances (expressed characteristics) analysed in cladistics – ‘family trees’ of species: and that such genotypal ‘family trees’ usually matches the phenotypal ones well.

        • In reply to #46 by logicophilosophicus:

          And no genome ever made a cell, for example. ??????

          Look up asexual and sexual reproduction. Cells containing genomes, are copied and reproduced all the time.

        • In reply to #46 by logicophilosophicus:

          In reply to #40 by Pabmusic:

          In reply to #39 by logicophilosophicus:

          Oh dear indeed. The point is that without a quantitative justification, it it unclear how evolution happened. The key words (in addition to quatitative) were purely genetic. There may be (there may need to be) other factors at work. And no genome ever made a cell, for example.

          I believe you are mistaken in thinking CMI addresses this.

          Hi Logicophilosophicus, If you are still following this thread could you expand on this I’m uncertain what you are trying to say here. Are you talking about the origin of DNA or are you suggesting DNA does not now code for proteins which make cells?

        • In reply to #46 by logicophilosophicus:

          In reply to #40 by Pabmusic:

          In reply to #39 by logicophilosophicus:

          …I believe you are mistaken in thinking CMI addresses this.

          You are right (it was late when I wrote this). I meant The Blind Watchmaker, in particular the chapter ‘Puncturing Punctuationism’, which addresses issues about the rate at which selection occurs.

  23. To add a few points to those made – I think it was Darwin who wrote of species often arising at marginal areas, in a wide sense. Thus, individuals experiencing climate change can be placed in a situation where small differences really do count and lead to marked selection pressure to change.

    Some excellent points there, Steve. I’ve been thinking about how minutely small changes could possibly have an effect on an organism’s survival in what is basically a stable environment, but perhaps I’ve been looking at the problem backwards. If we assume that small mutations are occurring all the time and eventually causing significant changes over time in a given species, then any sudden change in the environment could certainly have a massive effect on survivability. Again, not because any small mutation made an individual organism more or less suitable for its environment, but because the species as a whole had changed to a point where it was better or worse suited to a changed environment.

    Of course, that still makes me wonder about the so-called “living fossils.” If natural selection works because species are constantly changing until an environmental change causes them to die out, then how come some species don’t seem to change much at all over millions of years? PG mentioned that “Only a random mutation that confers a slight advantage will accumulate,” but I don’t understand why that would be the case. Why do dogs have dewclaws, for example? Are we assuming there must have been some advantage to having one toe on each foot slowly become non-functional over time, or is it enough that a non-functional toe didn’t have any negative effect and was therefore passed down?

    • In reply to #41 by godzillatemple:

      Of course, that still makes me wonder about the so-called “living fossils.” If natural selection works because species are constantly changing until an environmental change causes them to die out, then how come some species don’t seem to change much at all over millions of years?

      You’ve said it yourself; ‘species don’t SEEM to change’. However, their DNA is mutating and evolving all the same. It may be that the way a particular organism evolves is not visible to us; we tend to judge books by their covers. Or, think about the way natural selection works- changes which confer a survival advantage OR enable an organism to reproduce more effectively are selected. If an organism stays in the same environment for long periods the change may be to continually optimise the organism for that environment.

      For example; the shark. Sharks appear very similar to sharks we find in the fossil record, but the body shape is optimal for the shark’s environment, and you’d assume that many of the sharks physical and behavioural adaptions are so well adapted for their environment that any significant changes will not increase their chances of reproducing. So evolution will maintain the status quo despite changes to the DNA.

      PG mentioned that “Only a random mutation that confers a slight advantage will accumulate,” but I don’t understand why that would be the case. Why do dogs have dewclaws, for example? Are we assuming there must have been some advantage to having one toe on each foot slowly become non-functional over time, or is it enough that a non-functional toe didn’t have any negative effect and was therefore passed down?

      I don’t know much about dogs but I’m assuming a dewclaw is a non-functional physical component. Why would this have hung around if it’s not needed? But think about it – dogs are bred; artificially selected by us. There is no pressure from natural selection for the dog to be optimised, and I’m assuming there is no pressure from artificial selection for dogs without dewclaws. So why would that part of the dog’s anatomy change?

      I’m sure there are better examples of seemingly useless physical characteristics from the natural world, but evolution does not have foresight, so anything which has evolved will have conferred an advantage some time in the past, but unless the lack of the characteristic does the same it cannot ‘un-evolve’.

    • In reply to #41 by godzillatemple:

      Of course, that still makes me wonder about the so-called “living fossils.” If natural selection works because species are constantly changing until an environmental change causes them to die out, then how come some species don’t seem to change much at all over millions of years?

      While living “fossils” have a similar body plan to their related ancestors they are genetically different species. They may have only changed slowly or not a lot in their body form, but they have changed.
      http://news.nationalgeographic.co.uk/news/2013/13/130418-coelacanth-genome-evolution-oceans-animals-science/

  24. To get species separating generally a population needs to be isolated in conditions, geography or time or the mix of genes can shuffle the cards back to little change overall.

    An excellent point, and one I hadn’t considered. That probably explains the whole “living fossil” conundrum as well. Thank you.

  25. While living “fossils” have a similar body plan to their related ancestors they are genetically different species. They may have only changed slowly or not a lot in their body form, but they have changed.

    Fantastic article, thanks! I had no idea science had progressed to the point where we could determine how fast an organism had evolved by looking at its DNA. Exciting times, eh?

    I wonder, btw, whether the Coelacanth’s deep sea environment has anything to do with the slower than normal rate of evolution. Perhaps they are not exposed to whatever typically causes random mutations to the same degree as other organisms (Cosmic rays? Solar radiation? Radioactive isotopes?) Just a thought…

    • In reply to #49 by godzillatemple:

      While living “fossils” have a similar body plan to their related ancestors they are genetically different species. They may have only changed slowly or not a lot in their body form, but they have changed.

      wonder, btw, whether the Coelacanth’s deep sea environment has anything to do with the slower than normal rate of evolution. Perhaps they are not exposed to whatever typically causes random mutations to the same degree as other organisms (Cosmic rays? Solar radiation? Radioactive isotopes?)

      Protection from mutating radiation might be a factor – had not thought of that. But I wonder if coelocanths and other ‘living fossils’ are such because their niche hasn’t changed or has been replicated and they long ago got to a fairly optimal solution, given their ancestral form. So, the deep sea has not changed a lot for aeons, likewise -and even more remarkably – the stromatolites that can thrive in some shallow inlets go back around 2 billion years, ie one of the earliest forms of life is still around! Of course, such organisms continue to be subject to selection pressure: for the stratoliths, only inlets with too high a salinity for ‘grazing’ animals are tenable – the stratoliths having started well before any multicellular animals evolved.

  26. “When asked why it’s impossible to view evolution as it occurs, the answer is inevitably that it occurs on a very long time scale and that the individual mutations are too small to notice until they have had time to accumulate through many generations.”

    Too small to notice by whom? I can now see why the first chapter in Origin was “Variation Under Domestication”; Chuck must have anticipated that your “paradox” would have been foremost in the minds of his skeptical readers. We can easily see how different domestic breeds that we have today were selected based on the natural variation already existing in the ancestral population. Although the individual differences between members in that ancestral population of say, cows, was “slight”, it was noticiable enough to human breeders looking for certain characteristics. Continue this process for many generations, and anyone can see how this would give rise to new varieties.

    Not even the dullest creationist would argue that all the different varieties of domestic animals and plants that we have now existed in the wild in the past.

    Now, couldn’t a similar process happen in nature, with human selection being substituted by the natural environmental conditions? In fact it must be so, as not all phenotypes stand an equal chance of survival in a given environment, and some of the difference b/t the different phenotypes is heritable.

    The reason that you can’t see this happening now is the significant length of time between generations or rounds of reproduction for most organisms. If you had just 10,000 years, you could observe enough generations to see the changes in some of these populations with your own eyes. However, with sufficiently short-lived and rapidly reproducing organisms, you can see it. Antibiotic resistance is one well-known example of “real-time” evolution.

    Finally, we can also see why the variations that lead to evolutionary change are almost always slight, particularly if we consider modern organisms. As they are already well adapted to their current environments (a reasonable assumption), any large scale change would have a much greater chance of being deleterious than being advantageous. R.A. Fisher’s famous microscope analogy explains this concept nicely.

    Hope this helps.

  27. It is not impossible to observe evolution. We see it in many controlled breeding experiments (artificial selection). What you need to understand is that ‘species’ is a somewhat arbitrary term (a label of convenience) when looking at the fossil record. We can define it more precisely as when two members of a species have differentiated enough that they can no longer reproduce and have fertile offspring (see horses, mules and donkeys). The problem with this definition is that it tends to exclude species like bacteria (that have extremely high reproductive rates) because they don’t need sexual partners to reproduce. For them we have to go back to the blunt ‘fossil’ definition of a species where we make an arbitrary decision about whether or not a species has differentiated enough to LABEL them as two separate species.

  28. Let’s say you have a mutation that lets you run at 30.1 km/hr vs 30.0 km/hr. In most of the chases in your life, that advantage has no effect. However, if you get chased by a predator that can run at 30.0km/hr but not 30.1, it really matters. You live rather than die.

    Also consider that the advantage need not acquire to you, but to some of your ancestors carrying the mutation. In theory, it need not even have effect until a second mutation bumps your speed to 30.2.

    Read The Selfish Gene. It is all about the ability of genes to spread. Individuals are secondary.

    • In reply to #54 by Roedy:

      Let’s say you have a mutation that lets you run at 30.1 km/hr vs 30.0 km/hr. In most of the chases in your life, that advantage has no effect. However, if you get chased by a predator that can run at 30.0km/hr but not 30.1, it really matters. You live rather than die.

      Yes, and also you don’t even have to run faster than 30.0 km/hour in all herd animals you only need to run at say 25.1km/h 0.1km/h faster than your mate next to you who can only run at 25km/h.

      I was watching one of my Attenbourgh collection a couple of weeks ago and they were looking at some African herd animals (cannot remember the name) and they pointed out that lions don’t do well against them most of the year because the gang up together against the lions, but in breeding season when the male are all exhausted by fighting and barely able to stand the Lions pick them off with comparative ease. Now here you can see a really powerful selection going on not only have the fittest been more likely to breed with the females who are able to run at full pelt away from the lions, but the weaker males too exhausted to get eaten before the breeding next season. Except of course the sneaky F^&kers who don’t fight much but use the opportunity to inseminate the doe’s while the big guys are belting each other up. They like the doe’s can run like hell.

  29. You may want to look up the story of people that are immune to HIV. This is a random mutation. It can’t be seen and isn’t obvious but it will undoubtedly help these people survive and reproduce. Think about how more greatly beneficial it would be in a pre-condom world.

  30. imagine a shed made of a thousand bricks . gradually add more bricks ( reusing the original bricks).
    each time you can build better and better and more elaborate sheds eventually passing through bungalows , mansions , hotels , palaces.
    if you are only allowed to add a couple of bricks every 10 years although you can always build some kind of viable building, change is so slow that noone sees anything much happening in a life time . a million years later a few snapshots of a bungalow , a mansion ,a hotel and a palace are found (fossils) . people viewing these snapshots find it hard to believe that the palace evolved from the shed.
    at each stage the type of building is only minutely influenced by the current housing needs (environment).
    sorry this analogy is rather lumbering but I hope you might see my point.
    (its really a version of the climbing mount improbable argument)

  31. Ok I am going to throw a spanner in the works here. From my last post yesterday morning I had a brain light bulb eureka moment when it all made sense. I spent the day staring into space and people asking me what was wrong. I said I was tired (not that I was thinking about quantum biology) ok here goes- this is relavent to the question and the posts in the sense that I still have issue with the word random meaning completely random. I thought if a lot of things last night so will start in no particular order.

    DNA mutations are sometimes effected by the environment. If you are older you are more likely to have offspring with trisomy 21. Similarly other genetic conditions or mutations are more common than some meaning that DNA has the tendency to break / fault/ mutate in a particular way. Perhaps due to structural properties. Some of these give you the extra finger the initial question mentioned – polydactyly. Ok. Also on the cell membrane there are lots of channels e.g. Sodium/ potassium transport channels. This suggests that the cell habits the world near quantum mechanics. Now when you talk about randomness and quantum you see wierd stuff. I am sure you are all aware if the photon experiment – two slit exp I think – cant explain it well but it goes that when a photon goes through the slits instead of it ending up randomly on the plate you get these two lines. Totally not random and suggestive that one photon knows where the other photon went and ends up on the other slit. Apologies to physics profs for that terrible explanation but I have read the experiment about 10 times and as a biologist never explain it right.

    Ok quatum stuff and DNA already not behaving
    randomly. Let me go further. There was a programme in bbc radio 4 last week called beyond belief. The researcher did scientific analysis into the near death experience. Amazing. In short people who had the near death exerperience were able to accurately describe their resuscitation compared to a control group who also were resusitated and were asked to guess what happened (as they said they did not float above the bed and look down) it sounded very scientific in the methodology and the researcher concluded that consciousness is something that is external rather than internally created and perhaps all life may access it. Ok where am I going with this – well when we atheists say its all random it makes us look very nihilistic (if that is the right word) the fact that strange things happen in quantum land for example and all the amazing stuff that happens in the cell should give us an appetite for wonder (book) – the fact that religious nutters have stolen it and claimed that the man with the beard built it all in seven days puts us in the camp that we believe in nothing and its all random.

    Last point in summary – actually two- the 300 million year old fish (great article above thanks) that suggest that random mutations took place but they must all have been negative right? Surely in 300 million years DNA could have done a bit better? Ok a bit harsh on DNA but this my point about external environmental forces acting on DNA it didn’t change over 300 million years as the environment didn’t change but we have to accept in light of the random argument that it did but couldn’t come up with anything? Also when I attended prof dawkins lecture last month someone asked him why homosexuality had not been selected out. He said that in terms of human evolution they may have stayed back at camp while hunter gatherers went out and as they were often bi sexual they could pass their genes on. Now in light if what I am saying above that DNA mutates in tendency I propose that such traits can’t be selected out or even be passed down as the molecule will vary any way e.g myopia. What I am saying is that if you had parents that were neither short sighted or gay some of their descendants will be as the molecule splices in a particular pattern e.g trisomy 21 (downs ) rather that it all being totally random. Sorry if that sounded like a rant but it was so great to get it finally out

    • In reply to #63 by Subatomicmantra:

      I still have issue with the word random meaning completely random. I thought if a lot of things last night so will start in no particular order.

      When talking about random mutations in evolution, we are looking at factors like background radiation causing changes in genes, and copying errors in the replication process – such as sections of DNA joining up in a new position, or duplicate copies of genes or whole chromosomes being made. These are processes well understood. Many organisms have increased chromosome numbers as a result of polyploidy. (http://en.wikipedia.org/wiki/Paleopolyploidy)

      http://en.wikipedia.org/wiki/File:PaleopolyploidyTree.jpg

      While approximately random, the processes are not totally random, as some sections of DNA are more vulnerable to damage than others. Polyploidy can provide a spare set of chromosomes where genes can mutate, without depriving the organism of its previous functions. It can also combine features of different related species where the polyploids are hybrids.In the percentage of individuals where the changes are detrimental to survival, natural selection will weed these out.

      Similarly other genetic conditions or mutations are more common than some meaning that DNA has the tendency to break / fault/ mutate in a particular way. Perhaps due to structural properties.

      Relatively simple mutations can affect numbers and sizes or organs, if these take place in genes controlling the switching on and off of other genes.

      I am sure you are all aware if the photon experiment – two slit exp I think – cant explain it well but it goes that when a photon goes through the slits instead of it ending up randomly on the plate you get these two lines. Totally not random and suggestive that one photon knows where the other photon went and ends up on the other slit.

      The reason for these effects, is that while described as “particles” for convenience, photons are not “particles”. They have properties of both particles and waves. While photons are relevant to photosynthesis in plants, gene replication works as a chemical process in their absence.

      Last point in summary – actually two- the 300 million year old fish (great article above thanks) that suggest that random mutations took place but they must all have been negative right?

      You seem to have misunderstood selection. In a very stable environment to which an organism is well adapted, random changes (as usual) make many individuals less competitive, but if the species is already evolved to near optimum for that stable environment, any changes will be down grading performance – and any individuals which leave the stable environment, will be selected for/against, in terms of their new habitats. – That is how related species diverge.

      Surely in 300 million years DNA could have done a bit better? Ok a bit harsh on DNA but this my point about external environmental forces acting on DNA it didn’t change over 300 million years as the environment didn’t change but we have to accept in light of the random argument that it did but couldn’t come up with anything?

      In a well adapted species, after the initial adaptations, there may be no small changes which will be beneficial. It is where the environment changes that some selected changes make diverging species more fitted to the new conditions. -
      For example, there were very large insects at times when the Earth’s oxygen levels were very high, but their respiratory systems cannot cope well enough for flight when oxygen levels drop, so smaller individuals out-compete and replace them in the fossil record.

  32. @ Steve Hopker etc

    There is an unbroken lineage (or lineages – chromosomal and mitochondrial) of DNA from, say, yourself (or from any cell in your body) to some pre-Cambrian ancestor, DNA to DNA to DNA… The actual organisms (e.g. you) are off-shoots of that line: no animal ever passed on its own phenome or even its own genome to a descendant, just the genes (or half of them, anyway) from its inherited germ cells, and therefore any heritable changes are strictly sequestred in the germ line. That’s the purely genetic sense in which the Central Dogma is often casually represented. The reality is that the germ line also includes cellular structures and machinery. There is an unbroken lineage of, say, cell wall from the earliest cellular ancestor to every cell in your body: those cell walls (etc.) are not off-shoots of the DNA lineage(s). No genome ever made a cell, nor can it completely specify a cell…

    @ Reckless Monkey

    …nor did any combination of proteins ever make a cell…

    @ Hardy

    …nor did any combination of bricks ever make a palace.

    @ Pabmusic

    I’m afraid you’re mistaken about TBW ch 9, which is a qualitative defence of gradualism. The only two clearly quantitative arguments in the chapter, I think, are R. A. Fisher’s microscope argument, which RD erroneously accepts, and Fred Hoyle’s 747 argument, which RD erroneously rejects. Neither argument involves signal-to-noise ratio (which is not mentioned in the book – information theory is nowhere considered, apart from a brief look at IT as an analogy for data storage in DNA).

    Ch 3 does include a quantitative argument, the Methinks-it-is-like-a-weasel, which is fatally flawed of course, precisely because it sidesteps the signal-to-noise problem.

    • In reply to #67 by logicophilosophicus:

      The actual organisms (e.g. you) are off-shoots of that line: no animal ever passed on its own phenome or even its own genome to a descendant, just the genes (or half of them, anyway) from its inherited germ cells, and therefore any heritable changes are strictly sequestred in the germ line.

      Oh dear! Are you seeking knowledge or just generating arguments with your erroneous assertions?
      We all know that genomes are passed on from gene-pools in populations and not just from individuals in sexually reproducing organisms.

      We also know that phenomes are passed on from the population and only approximate to parent individual phenomes in sexually reproducing organisms.

      no animal ever passed on its own phenome

      I suggest you read up full clones and Parthenogenesis

      I see you have nothing to say about my correction of your ridiculous claim @46!
      (@46 – And no genome ever made a cell, for example.)
      But have merely repeated the assertion!

      No genome ever made a cell, nor can it completely specify a cell…

      As I suggested earlier – You really should read up on asexual reproduction. (and on normal cell replacement in eukaryotes.)

      Asexual reproduction is a mode of reproduction by which offspring arise from a single parent, and inherit the genes of that parent only;

      ..nor did any combination of proteins ever make a cell…

      Did side-tracking questions and erroneous assertions ever make a contribution to knowledge in a discussion?

      the signal-to-noise problem.

      Your comments seem to have noise, but lack a coherent signal, apart from a gratuitous tendency to dispute established science from a viewpoint of ignorance.

    • In reply to #67 by logicophilosophicus:

      @ Steve Hopker etc

      There is an unbroken lineage (or lineages – chromosomal and mitochondrial) of DNA from, say, yourself (or from any cell in your body) to some pre-Cambrian ancestor, DNA to DNA to DNA… The actual organisms (e.g. you) are off-shoots of that line: no animal ever passed on its own…

      A few questions:

      What is the signal-to-noise problem, exactly? What answer would convince you that it is not a problem? Moreover, why is it compulsory that this answer be “quantitative” as opposed to the “qualitative” answers given above?

      Lastly, if genes don’t make cells, and proteins don’t make cells, then how does raw material end up as new cells during mitosis?

      • In reply to #69 by Zeuglodon:

        @ Zeuglodon
        69
        In reply to #67 by logicophilosophicus:

        What is the signal-to-noise problem, exactly? What answer would convince you that it is not a problem? Moreover, why is it compulsory that this answer be “quantitative” as opposed to the “qualitative” answers given above?

        In regard to the OP, a tiny genetically produced advantage is extremely likely to be swamped by other factors. For example, suppose that a new mutation arises which, all other things being equal, will increase an animal’s muscle mass by 1%, a fairly generous, rather than tiny, change. Nevertheless, this is a small advantage compared to variation in muscle mass due to any of the following: un/favourable environment in the womb (I know a pair of monozygotic twins one of whom is tiny), differential nutrition, differential exercise, disease, injury… Etc. The question is whether the new mutation, in a single individual, is likely to get the chance to make a difference, or is it a whisper lost in a tempest? The answer must be quantitative, though not precise of course – within a few orders of magnitude might be acceptable.

        Lastly, if genes don’t make cells, and proteins don’t make cells, then how does raw material end up as new cells during mitosis?

        Mitosis is the splitting of cells – the existing cell wall (like other parts, e.g. the nuclear membrane) is an essential template for growth/replication. The proteins are necessary but not sufficient conditions for this process.

        • In reply to #75 by logicophilosophicus:

          OK, that makes sense. You’re basically asking what is the probability that a mutation (i.e. a new allele) will survive its first generation or so, as in population genetics, when it runs the risk of being removed by sheer bad luck (say, if its phenotype was thwarted by unusual embryological complications and/or its host died)?

          Also, I’m not sure you understood my cell mitosis question: by what process do you think the raw material for new cells is converted into, say, the cell membrane or other structures like the libosome or the cytoskeleton? Cell division requires new material to make the resulting cells if they are to be the same size as the mother cell (otherwise, their volume would halve each generation). By my understanding, the new material is assembled when the RNA read the DNA and use it to assemble proteins, but I don’t think that’s what you’re getting at. For instance, your comment on the cell wall (did you mean cell membrane here, as they’re two different things?) seemed to imply the cell wall assembles itself. Would you please explain what you meant here?

        • In reply to #75 by logicophilosophicus:

          In regard to the OP, a tiny genetically produced advantage is extremely likely to be swamped by other factors. For example, suppose that a new mutation arises which, all other things being equal, will increase an animal’s muscle mass by 1%, a fairly generous, rather than tiny, change. Nevertheless, this is a small advantage compared to variation in muscle mass due to any of the following: un/favourable environment in the womb (I know a pair of monozygotic twins one of whom is tiny), differential nutrition, differential exercise, disease, injury… Etc. The question is whether the new mutation, in a single individual, is likely to get the chance to make a difference, or is it a whisper lost in a tempest? The answer must be quantitative, though not precise of course – within a few orders of magnitude might be acceptable.

          In a single event, it’s hard to say. Compared with the previous allele, it makes a difference in that the previous allele would have less of a result under the exact same conditions, though obviously a “1% bigger muscle mass” gene whittled down will have the same result as a “normal muscle mass” gene unexpectedly given a boost. In this hypothetical generation, the new allele would behave like a neutral mutation. But those are exceptions; over time, all the non-genetic factors regress to the mean, meaning that the allele’s effect will be obvious over more than one or two generations. Since both alleles face the same conditions in the long-term, the new allele’s phenotype gives it an advantage over its rival under those same conditions and can reach fixation. I don’t know how to represent that in numerical form, but once it passed through along Mendelian genetics, the noise normalizes and cancels itself out (due to regression to the mean) and the signal would become obvious, making selection biased in favour of the new allele.

          Also, I think you missed my question at Comment 79 about mitosis and cell membranes. If you can, would you please come back to those points?

          • In reply to #147 by Zeuglodon:

            In reply to #75 by logicophilosophicus:

            I don’t know how to represent that in numerical form, but once it passed through along Mendelian genetics, the noise normalizes and cancels itself out (due to regression to the mean) and the signal would become obvious, making selection biased in favour of the new allele.

            With some trepidation ie in the knowledge there are professional geneticists here, I agree. Indeed, am I right that Darwin himself had worried about the regression to the mean of inherited characteristics as undermining his theory, as the thought then was that inheritance was by a mixing of factors, so that new features might become diluted. It needed the belated awareness of Mendel’s work to show that genes are transmitted intact, so that new genes were inherited without dilution and thus without regression to the mean.

          • In reply to #149 by steve_hopker:

            In reply to #147 by Zeuglodon:

            Well, my point was more about the non-genetic factors around the phenotype regressing to the mean in the long term, not the phenotype itself. The very embryonic process is founded upon the recipes contained in the genetic code, so while unusual outside differences can arise in a particular case (e.g. a stray chemical gets in and makes some minor part of the process go wrong), over multiple generations they cancel each other out and don’t matter, allowing the rival phenotypes to compete unhindered on behalf of their respective alleles. I think the original point of contention was of an unusual non-genetic factor somehow “drowning out” the phenotypic effect, the problem with that idea being that such events not only effect pre-existing alleles to the same degree (which renders bringing it up as pointless), but are merely one-offs in the long run. As such, they can’t really be used to argue that new mutations’ phenotypes are blocked out or cut off by other factors.

          • In reply to #149 by steve_hopker:

            With some trepidation ie in the knowledge there are professional geneticists here,

            Access by those with literary skills to academic papers and scientific terminology, does not confer understanding of the science. That requires study from basics upwards, with an in depth understanding within a wider context. Those who do not understand, and contradict, basic definitions of subject areas, demonstrably lack such understanding.

            Do not be misled by these assertions which are being refuted by the biologists present (see151 and Zeuglodon). The trolling assertions, uninformed opinions, contradictions of evidenced science, false authority claims, and circular arguments, are derived from a lack of understanding of basic biology, accompanied by a Dunning-Kruger confidence, NOT by any understanding of advanced genetics. The uses of scientific terms and vague references to authors, are just a smoke-screen of complexity, in which to embed unsupported assertions – assertions which are reasserted – not corrected – (with refutations ignored, as on earlier threads), when biologists point out the errors!

            Alan4discussion @68 – In reply to #67 by logicophilosophicus:

            Oh dear! Are you seeking knowledge or just generating arguments with your erroneous assertions?
            We all know that genomes are passed on from gene-pools in populations and not just from individuals in sexually reproducing organisms.

            We also know that phenomes are passed on from the population and only approximate to parent individual phenomes in sexually reproducing organisms.

            Your comments seem to have noise, but lack a coherent signal, apart from a gratuitous tendency to dispute established science from a viewpoint of ignorance.

          • In reply to #147 by Zeuglodon

            In reply to #75 by Logicophilosophicus

            Your final point first:

            http://tuvalu.santafe.edu/~dirk/fluct/fluct.pdf (Analyses parts of the phenome – they are very limited – which can be passed on. Note that the three “heritable” cases are chromatin marking system [i.e. methylation], steady state system [self-perpetuating reactions] and structural inheritance system [three dimensional templates]. The second and third are precisely the non-genetic sources of information in cell machinery and structures which I mentioned. They are essential for cell construction.)

            Omnes cellula e cellula.

            Your main assertion is that (1) “over time, all the non-genetic factors regress to the mean” and thus “cancel out” so that the tiny genetic advantage (or disadvantage) (2) “will be obvious over more than one or two generations” allowing natural selection to operate.

            I don’t accept (1) at all. I’ll first try to give a simple analogy. You and I play a simple coin-tossing game. We agree to toss a penny exactly n times, and I keep a count of heads (I win) and tails (you win). At the end of the game the loser pays the difference d to the winner. Unfortunately, I cheat. If I owe you, say, 20 pence I fiddle the count, and give you only 19. If you owe me, say, 23 pence I tell you it’s 24. The game is the environment, and the little fixed (dis-)advantage is the mutation we are interested in. Suppose n=100. Assuming normal distribution, about half the time one or other of us owes about 7 pence. The advantage of 1 penny is not noticed in the noise of the environment. Try n=10,000. Now the likely debt is 70 pence, and the advantage is definitely irrelevant. If n=1,000,000 the likely debt is 700… Although d/n does get closer and closer to the mean, d gets further from the mean. Second, how are the various sources of noise from the environment expected to “cancel”? They’ll still be operating in 10 generations, or 20, much the same.

            Your (2) includes an order-of-magnitude estimate, “more than one or two generations”. Where did that come from? The tiny phenotypical advantage will never become “obvious”. It will have a tiny chance of influencing fertility (e.g. enabling survival to reproductive age). Taking the muscle mass example one stage further, suppose the mutant has a slightly increased running speed as a consequence than the hominid standing on his left. A sabre tooth approaches – from the right. All such life accidents add to the noise. How many generations might pass before the advantage was actually expressed in the phenotype, and a crucial situation arose where all the little accidents happened to balance out (almost) exactly? I don’t know, but my gut feeling is tens to hundreds, not “one or two”. In that case, the mutation might have to arise dozens of times before it became established. But that’s just my guess – you see, though, that only a quantitative treatment could answer such a question.

          • In reply to #154 by logicophilosophicus:

            I see. Thank you for answering the point about the cells.

            In reply to #147 by Zeuglodon

            In reply to #75 by Logicophilosophicus

            Your final point first:

            http://tuvalu.santafe.edu/~dirk/fluct/fluct.pdf (Analyses parts of the phenome – they are very limited – which can be passed on. Note that the three “heritable” cases are chromatin marking system [i.e. me…

            My (2) is based on the basic fact that, with a large enough sample from a population of events, extreme and anomalous incidents are much less likely to bias the overall results. It’s basically the Law of Large Numbers. In a given environment, factors will fluctuate and vary, but these variations which might distort individual cases by statistical law cancel out with a larger sample. An unusual runty development in the womb might effect an individual allele’s phenotype in one generation, but this exceptional case has less effect over more and more generations. This is a matter of statistical fact. As for my (1), that’s simply the corollary of (2).

            There are quite a few problems with your analogy. For a start, you don’t explain what role n is supposed to represent (steps in embryology? generations of offspring?), nor what the pay-off represents (leg length? number of offspring?), and it’s not obvious how the analogy takes into account a reproductive advantage that goes along with a phenotype. For the most part, I’m afraid you haven’t helped much in clarifying your point.

            Even ignoring these points, there are other issues I have with the analogy. A fair coin flip at any value n will tend to be 50/50, even if in any particular scenario it isn’t, so the payoff (in a non-cheating scenario) should be equal for both of us, especially the more times we play the game x number of times as that meets the criterion for the Law of Large Numbers. In a cheating scenario, the advantage is clearly yours, since a 1p extra is yours for the taking as opposed to if you didn’t cheat. This is especially so if the game is iterated (for instance, we play n=100 a thousand times, or x=1,000). I frankly don’t understand where the 7p difference is supposed to come from, and you neglected to explain it.

            Lastly, the original phenotypic advantage I postulated is supposed to be based on a ratio, not on an absolute value. My example was an increase in 1% of muscle mass. So, if an individual has a muscle mass of 100 grams, a mutant is expected to have 101 grams. If we adjusted your analogy accordingly, such that you got a 1% advantage, the result would be very different.

          • In reply to #155 by Zeuglodon:

            In reply to #154 by logicophilosophicus:

            I see. Thank you for answering the point about the cells.

            In reply to #147 by ZeuglodonIn reply to #75 by LogicophilosophicusYour final point first:http://tuvalu.santafe.edu/~dirk/fluct/fluct.pdf (Analyses parts of the phenome – they are very limited – whic…

            Rather, think of it like this. In two populations, there are two normal distributions for muscle mass, one for each. Their environments are equally chaotic, but in the long term are stable, like zig-zagging fluctuations on a graph staying close to a mean, so the only major difference is that one population’s graph is shifted slightly to the extreme end. For instance, if the mean muscle mass of Population 1 is 100kg, then the mean muscle mass of Population 2 is 101kg.

            Now, with such a tiny shift, the result is more individuals in the higher end for Population 2 and more individuals in the lower end for Population 1. The ratio of extreme individuals favours Population 1 over Population 2. Now consider the effect selection will have on them when combined. Selection is free to work on the difference, penalizing Population 1 more for having more low-end extremes and being biased in Population 2′s favour for the opposite reason.

            The point here is that the two environments are equally chaotic, since there is no probabilistic bias towards either Population, especially in the long run. Both have cases where individuals are born runty or oversized, both have cases where individuals die due to freak accidents, and both live in an environment which has an average to which these outstanding events regress, negating each other’s effects. They may fluctuate, but they stick to a mean. Since the environment hasn’t really changed, the difference comes down to the one between the two genes, since exactly the same argument applies to the regular allele.

            The only part needed is for the new allele, once it arises, to increase in numbers within the gene pool. Assuming nothing extreme happens to the original few mutants – and by its nature, this is unlikely – then the gene by simple Mendelian genetics will operate along selection lines over the generations and spread across the population. Even if a particular mutation has the bad luck of vanishing prematurely, the regular mutation rate will churn up another one at another time. Moreover, since a new allele’s frequency increases exponentially per generation, a premature death which would have nipped the process in the bud if it occurred to the first mutant rapidly loses its sting over surprisingly few generations.

          • In reply to #156 by Zeuglodon:

            In reply to #155 by Zeuglodon:

            In reply to #154 by logicophilosophicus:

            Bernouilli’s Law (dubbed “The Law of Large Numbers” by Poisson”) states that the statistic m/n tends to M/n as n tends to infinity, where M is the a priori expected mean and m is the mean of the observed values. In reality, M is only known in artificial situations like coin-tossing games, assuming a completely fair coin and toss; so in practical situations the Law seems useless. Of course it seems reasonable to deduce that the observed m/n for a large sample is a good estimate of M/n. Actually this is a statistical fallacy which has been much discussed in the Phlosophy/Methodology of Science. I remember having to do an in-depth undergraduate study of “The Inverse of Bernouilli’s Theorem” nearly 50 years ago. The counter-intuitive aspect is that while (m/n – M/n) tends to zero, |(m -M)| tends to infinity; hence my 7, 70, 700… (The 7 is a rough estimate based on the standard deviation of 5 for the binomial distribution, n=100; just under 50% of the normal distribution lies within + or -2/3 SD, so |(heads – tails)| exceeds 20/3 about half the time.)

            I suspect that when you say “The Law of Large Numbers” justifies your argument, you are actually referring to the folkloristic “Law of Averages” more correctly known as “The Gambler’s Fallacy”. Suppose you start out with a bankroll of £100 and play a coin tossing game, a pound a flip: your expectation is to end up with £100. Unluckily, after 20 flips you are, say, £10 down. All that has passed is irrelevant. Your bankroll, hence your expectation, is now £90.

            Since your (1) and (2) depend on a wrong application of “The Law of Large Numbers”, your argument fails.

            a new allele’s frequency increases exponentially per generation

            That might work for the Book of Genesis, but in a stable population limited by Malthusian constraints, the allele can only be expected to increase its frequency per generation if there is effective selective pressure per generation – the point at issue.

    • In reply to #67 by logicophilosophicus:

      @ Steve Hopker etc
      There is an unbroken lineage (or lineages – chromosomal and mitochondrial) of DNA from, say, yourself (or from any cell in your body) to some pre-Cambrian ancestor, DNA to DNA to DNA…

      I agree.

      The actual organisms (e.g. you) are off-shoots of that line: no animal ever passed on its own phenome or even its own genome to a descendant,…

      If I have understood this correctly, I agree with phenome point (I am too not a Lamarckian): but I don’t agree with the generalisation regarding the genome – genomes are exactly what is passed on. Of course any germ cell mutations are passed on, ie the genome is not always perfectly transmitted, but those are the exception – ie genes are generally passed on.

      … just the genes (or half of them, anyway) from its inherited germ cells, and therefore any heritable changes are strictly sequestred in the germ line.

      My point above (heredity in in the germ line) – so I agree with this and the observation of the mixing of parental genes. Which makes the previous statement that ‘no animal ever passed [on] … its own genome’ all the more puzzling. Perhaps I have misunderstood?

      That’s the purely genetic sense in which the Central Dogma is often casually represented.

      I have interpreted ‘Dogma’ to imply a strong rejection of neo-Darwinism. But why the capitalised word ‘Dogma’? If there is evidence for a reasonable alternative explanation to neo-Darwinism, ie an alternative scientific theory, there should be evidence and the related scientific reasoning. This is surely not a question of religious or political dogmas, ie unlike disputes over transubstantiation, if Marxist-Leninism was distorted by Stalin, etc. Or does this issue carry that kind of emotive force?

      The reality is that the germ line also includes cellular structures and machinery. There is an unbroken lineage of, say, cell wall from the earliest cellular ancestor to every cell in your body: those cell walls (etc.) are not off-shoots of the DNA lineage(s).

      What is the evidence for and the significance of this? Male cell structures in general are not included in the zygote (excepting the male gamete nucleus). But regarding the egg cell structures going forward into the zygote, they are replaced by cellular processes governed by genes. I am unaware of any evidence that cell walls, etc are capable of self-replication. I suppose some odd molecules might linger – but how would that matter? My understanding (as above) is that it is the genes which code for cell structures, or the enzymes involved in building them, which are inherited. If I am wrong, please say how.

      No genome ever made a cell, nor can it completely specify a cell…

      As per above: neo-Darwinism maintains the exact opposite, namely that it is the genome (nuclear plus mitochondrial) which does specify cells. The account is probably familiar, but in a nutshell: the nucleic acid sequences in chromosomes (genes) are transcribed to RNA, which is subsequently ‘decoded’ in ribosomes, wherein a triplets of nucleic acids are ‘read’ (as if a code) to link to the ‘coded’ amino acids which are sequentially polymerised into proteins. Some of the proteins are used directly in cell structures: many are enzymes that produce other molecules within the cell. I think these steps have been demonstrated many times in many species: indeed, are thought to occur in all known life. (Viruses and prions do not have these mechanisms but they are not I think generally regarded as life forms per se).

      Your post makes strong assertions (‘no genome ever, etc) that seem to contradict neo-Darwinism – indeed genetics as a whole. Well formulated new ideas are always welcome. But what is being proposed in place of neo-Darwinism: and what is the evidence to support it?

      • In reply to #77 by steve_hopker:

        In reply to #67 by logicophilosophicus:
        I am unaware of any evidence that cell walls, etc are capable of self-replication

        Prions (eg BSE / ‘mad cow disease’) are foreign cell fragments that provoke cells to replicate them (ie not exactly self-replicate). But in any case prions are a pathological infection: I do not think this is how normal cells structures are replicated

  33. A mutation to spread, does not need to make a life or death difference. If it makes you even a tiny bit sexier to mates, that is all it takes for the gene to spread.

    One of the amusing natural selections is an appearance similar to a celebrity. “Elvis-like” genes conferred an advantage, but the environment is changing so that constellation is not as powerful as it used to be, pushing always for streamlining.

    The difference can be something as seemingly insignificant as the ability to eat an additional food. In tough times that gives you an edge over your fellows in exploiting the standard foods.

    Any sort of efficiency in using food or water can give you an edge in tough times. This may be why we see the “use it or lose it” pressure in natural selection.

  34. I think part of the problem is people imagine a new gene gets tested in one individual, go no go. And that is all there is to it. If it is a go, there in no guarantee it will spread to the entire species. The gene gets retested in the next generation, and so on. It will eventually die out, or take over the species, or remain one of the species variants (like eye colour). It gets a lot of testing.

  35. @ Alan4Discussion

    We all know that genomes are passed on from gene-pools in populations and not just from individuals in sexually reproducing organisms.

    That must be the royal we. How do you collect a genome from a gene-pool? Note that “the genes (or half of them, anyway)” allows for both asexual and sexual reproduction. The clue is in the word “or”.

    We also know that phenomes are passed on…

    Rubbish. Behaviour, for example, is shaped by millions of experiences. How would you collect those up to pass them on?

    “no animal ever passed on its own phenome” I suggest you read up full clones and Parthenogenesis

    Animal cloning involves an egg cell, as does parthenogenesis. The orthodox view is that these cells have all been produced in the embryo, long before most of the animal’s phenotypic development is yet to happen, and that information cannot be added to the ova.You did say you were a biologist?

    Reckless Monkey @ Logicophilosophicus: “…proteins which make cells”
    Logicophilosophicus @ Reckless Monkey: “..nor did any combination of proteins ever make a cell…” (since, as pointed out in that post, to make a cell you ALWAYS have to start with a cell…)
    Alan4Discussion @ Logicophilosophicus: “Did side-tracking… ever make a contribution… in a discussion?”

    Strictly on point, then. So what’s your point?

    Your comments seem to have noise, but lack a coherent signal, apart from a gratuitous tendency to dispute established science from a viewpoint of ignorance.

    That’s one of those own-petard thingies.

    • In reply to #74 by logicophilosophicus:

      That must be the royal we. How do you collect a genome from a gene-pool?

      The same way organisms have been doing so for millions of years. – by looking at individual examples.

      Note that “the genes (or half of them, anyway)” allows for both asexual and sexual reproduction. The clue is in the word “or”.

      Thank you for demonstrating that you have not read up on asexual reproduction, and have no idea what you are talking about! – so we are wasting our time dealing with your erroneous assertions, which you have no intention of retracting or correcting. The clue is in the word “full”, in “full clone”. (100% diploid copy – not half. or haploid)

      We also know that phenomes are passed on…

      Rubbish. Behaviour, for example, is shaped by millions of experiences. How would you collect those up to pass them on?

      Learned behaviours – as distinct from instinctive inherited behaviours are not passed on genetically. They are not part of the phenome. They may be passed on as memes.
      (Why am I wasting my time correcting this Gish-Galloping rubbish?) The ignorant should ask questions rather than making foolish assertions.

      “no animal ever passed on its own phenome”

      I suggest you read up full clones and Parthenogenesis

      Animal cloning involves an egg cell, as does parthenogenesis. The orthodox view is that these cells have all been produced in the embryo, long before most of the animal’s phenotypic development is yet to happen, and that information cannot be added to the ova.

      That would just indicate that the phenotype was being passed from the grandparent via the parent. It is precisely because information cannot be added to the genetic material in the ova that they are clones!

      You did say you were a biologist?

      I am and you are not. That is how I can tell you that a full clone can be a 100% genetic diploid copy of its parent, and you have no idea what I am talking about. Not all clones start as eggs, but I should not have to explain that to anyone who had an understanding of biological diversity, or who had looked at the links I provided.

      I recall from an earlier discussion, that you have no scientific credentials, but like making “authoritative” assertions about scientific matters, while disputing the well evidenced science qualified people present to you!

    • In reply to #74 by logicophilosophicus:

      “no animal ever passed on its own phenome”

      I suggest you read up full clones and Parthenogenesis

      Animal cloning involves an egg cell, as does parthenogenesis. The orthodox view is that these cells have all been produced in the embryo, long before most of the animal’s phenotypic development is yet to happen, and that information cannot be added to the ova.

      Many of these features are better illustrated in organisms other than animals.

      I see you are playing at splitting hairs to generate arguments.

      We (scientists) also know that all the major features of the phenotype are passed on in genetically identical clones, but there can be minor variations due to phenotype plasticity. This phenotype plasticity is a feature of the genetics of the organism concerned. If there is little plasticity, the phenotype of an organism can be reliably predicted from knowledge of the genotype, regardless of environmental peculiarities during development.

      Your claim is very largely wrong, but may marginally correct in some species.

      Advantages of Asexual Reproduction

      • One parent is needed to complete the process of asexual reproduction.
      • In majority of the cases, one is sure an offspring will be produced.
      • The gestation period or growth period is very short.
      • The offspring has the same phenotype and genetic make up as the parent.
      • As there is no cross over or recombination of genes involved, chance of mutation is very less.
        http://www.buzzle.com/articles/asexual-vs-sexual-reproduction.html
      • In reply to #81 by Alan4discussion:

        In reply to #74 by logicophilosophicus:

        “no animal ever passed on its own phenome”

        I suggest you read up full clones and Parthenogenesis

        I see now I was wrong to agree with logicophilosophicus on phenotype transmission – the problems being lps’s liberal use of absolutisms – in this case ‘no’[animals] , which while dramatic, can be problematic academically and specifically scientifically. It is true (I think) for animals that sexual reproduction is the norm so an organism’s individual genotype is not passed on – half the genes are mixed with the other parent. But in asexual reproduction – which occurs in many plants and various animals on occasion – the genotype is passed on intact and so is much of the phenotype (though not all, since, I think the phenotype is the result of genes plus environment?)

        • In reply to #82 by steve_hopker:

          But in asexual reproduction – which occurs in many plants and various animals on occasion – the genotype is passed on intact and so is much of the phenotype (though not all, since, I think the phenotype is the result of genes plus environment?)

          The growth of the clone phenotypes can be influenced by environmental factors in some species in some situations, but it is difficult to argue for this in cases of animals budding off in divisions.

          http://oceanservice.noaa.gov/education/kits/corals/coral06-reproduction.html
          Corals can reproduce asexually and sexually. In asexual reproduction, new clonal polyps bud off from parent polyps to expand or begin new colonies (Sumich, 1996). This occurs when the parent polyp reaches a certain size and divides. This process continues throughout the animal’s life (Barnes and Hughes, 1999).

          Apart from their benefits from symbiosis, the increased numbers from asexual reproduction gives them the benefit of sexual and asexual reproduction when they eventually reproduce sexually.

  36. < When asked why it’s impossible to view evolution as it occurs, the answer is inevitably that it occurs on a very long time scale and that the individual mutations are too small to notice until they have had time to accumulate through many generations. If the individual mutations are so small, however, how can any of them actually contribute to the survivability or selection of the organism? >

    All children are slightly different from their parents. Have a look next time you go out, and you will see it with your own eyes. The differences are not too small to see with your own eyes. That’s what you can see within your lifetime.

    What you can’t see within your own lifetime is a new species arising as a result, because it takes a long time.

    My understanding is that birds are extremely like their parents. But there must be differences which are detectable because birds pair (I think it is their voices which allow recognition).

    There is another point which is much bigger. Natural selection explains how the current situation arose, but if most life is destroyed (again), the major evolution will start happening all over again. I don’t think we would be here if there had not been a major disaster.

      • In reply to #89 by bob_e_s:

        In reply to #87 by ClumpyMatter:
        I do have one question, however…

        The ‘footprint’ is in granite. How?

        The layer that the foot print is part of has turned on it’s axis due to plate tectonics, which means it is pretty darn old.

        • In reply to #90 by ClumpyMatter:

          In reply to #89 by bobes:

          The layer that the foot print is part of has turned on it’s axis due to plate tectonics, which means it is pretty darn old.

          I accept that, but my question still stands – how would you go about leaving a footprint in granite?
          Can you show me some other examples?

          • In reply to #91 by bob_e_s:

            In reply to #90 by ClumpyMatter:

            In reply to #89 by bobes:

            The layer that the foot print is part of has turned on it’s axis due to plate tectonics, which means it is pretty darn old.

            I accept that, but my question still stands – how would you go about leaving a footprint in granite?
            Can you show…

            What I think is interesting is the layer by the toes, it is squeezed up by the toes,which is common if you walk in muddy terrain. If some object that was shaped like a foot were dropped there, the toe-part of the object should be less in weight, yet the terrain is squeezed up where the toes are, which means it shows strong indications of someone walking there.

          • In reply to #92 by ClumpyMatter:

            In reply to #91 by bobes:

            In reply to #90 by ClumpyMatter:

            In reply to #89 by bobes:

            Ok, I’ll just cut to the chase; granite is an igneous rock. It is formed when molten rock rises from below the earth’s crust and cools, often as part of volcanic eruptions. It is extremely hard.

            Unless you’re suggesting the ‘giant’ trod in the molten lava and left his foot there while it cooled, there is no way a foot could make an imprint in that sort of rock. Fossils and footprints are left in sedimentary rocks.

          • In reply to #93 by bob_e_s:

            In reply to #92 by ClumpyMatter:

            In reply to #91 by bobes:

            In reply to #90 by ClumpyMatter:

            In reply to #89 by bobes:

            Ok, I’ll just cut to the chase; granite is an igneous rock. It is formed when molten rock rises from below the earth’s crust and cools, often as part of volcanic eruptions. It is…

            I can’t explain why it is in granite. I can only tell what is there. We must embrace what we can see with our own eyes. Here is what we know:

            1. It looks very much like a giant human foot print
            2. It is dated to be 200 – 3 billion years old

            Like Einstein said: “If the facts don’t fit the theory, change the facts”

            And by that, perhaps there are other ways in nature to form granite rocks that we don’t know of yet.

          • In reply to #94 by ClumpyMatter:

            I can’t explain why it is in granite. I can only tell what is there. We must embrace what we can see with our own eyes. Here is what we know:
            1.It looks very much like a giant human foot print
            2.It is dated to be 200 – 3 billion years old
            Like Einstein said: “If the facts don’t fit the theory, change the facts”
            And by that, perhaps there are other ways in nature to form granite rocks that we don’t know of yet.

            Did Einstein really say that?

            Sherlock Holmes also said, once you eliminate the impossible, whatever remains, however improbable, is the truth.

            It is impossible to leave footprints in granite.
            Therefore, we are left with the improbable, that it is a natural formation which just happens to look like a footprint.

            There is also another option, that it is a hoax.

            And anyway, what part of it has that date? The rock? it’s a pretty wide date range too, from 3 billion years to 200 million.
            Have you thought about this story at all before presenting it as fact?

          • In reply to #94 by ClumpyMatter:

            In reply to #93 by bobes:

            In reply to #92 by ClumpyMatter:

            In reply to #91 by bobes:It looks very much like a giant human foot print
            It is dated to be 200 – 3 billion years old

            So we can at least agree that young earth creationism ie the account of creation in six days less than ten thousand years ago is false.

            In reply to #90 by ClumpyMatter:

            In reply to #89 by bobes:

            Ok, I’ll just cut to the chase; granite is an igneous rock. It is formed when molten rock rises from below the earth’s crust and cools, often as part o…

          • In reply to #92 by ClumpyMatter:

            What I think is interesting is the layer by the toes, it is squeezed up by the toes,which is common if you walk in muddy terrain. If some object that was shaped like a foot were dropped there, the toe-part of the object should be less in weight, yet the terrain is squeezed up where the toes are, which means it shows strong indications of someone walking there.

            Amazing!!! Giant miners in fireproof pressure suits putting footprints in red-hot granite formed deep underground. With muddy rain penetrating the thick layers of rock which is covering the hot granite maintaining the pressure necessary for the crystal structure to form.
            Given that hot granite often takes thousands of years to cool and crystallise, after it has been intrusively squeezed between other rock layers, they probably needed quite a lot of supplies to stay there long enough for it to set hard, rather than hot-footing it back to the surface! Of course that sort of pressure would collapse mine tunnels in an instant – but hey! Why spoil a good story by letting facts get in the way! !

            Chronology of early Archaean granite-greenstone evolution in the Barberton Mountain Land, South Africa, based on precise dating by single zircon evaporation. – Some of the volcanic plutonic units contain zircon xenocrysts older than any exposed rocks. These indicate the existence of still older units, possibly stratigraphically lower and older portions of the greenstone sequence itself, older granitoid intrusive rocks, or bodies of older, unrelated crustal material.

            Of course you cannot leave footprints in rock-hard cold surface granite which is exposed after the overlying strata have been eroded away.

            This does not sound like mockery, he sound very serious here. He used the word “absurd”. Well that giant could have walked there and died from it, he doesn’t need magical lava proof feet to accidentially walk there and then later die from it.

            Lava is a surface volcanic material. Granite ALWAYS forms deep underground!

            … Probably enough silliness for one discussion! That’s the thing about creationist biblical tales. Not only are they clueless about biology, but they are also clueless about geology!

          • In reply to #118 by Alan4discussion:

            In reply to #92 by ClumpyMatter:

            What I think is interesting is the layer by the toes, it is squeezed up by the toes,which is common if you walk in muddy terrain. If some object that was shaped like a foot were dropped there, the toe-part of the object should be less in weight, yet the terrain is s…

            Thanks Alan, I’d been waiting for that!

            And I apologise for engaging with him and diverting the discussion.
            Couldn’t help myself.

          • Alan4discussion

            Water level can rise and lower over the years, especially considering that Africa had a different environment 200 million years ago.

            And rocks that appear on land can move in various ways, get from one position to another, and a whole variety of reasons for that to happen.

          • In reply to #124 by ClumpyMatter:

            Water level can rise and lower over the years, especially considering that Africa had a different environment 200 million years ago.

            And rocks that appear on land can move in various ways, get from one position to another, and a whole variety of reasons for that to happen.

            You are just making this up as you go along. It has nothing to do with the formation of granitic rocks.

          • In reply to #124 by ClumpyMatter:

            Alan4discussion

            Water level can rise and lower over the years, especially considering that Africa had a different environment 200 million years ago.

            So what was Africa’s environment like 200 million years ago, and how is it relevant?

            And rocks that appear on land can move in various ways, get from one position to another, and a whole variety of reasons for that to happen.

            Right. How? Give me some ways.

    • In reply to #87 by ClumpyMatter:

      Speaking of evolution, I wonder why there is a giant foot …

      Let me know your opinion.

      Claims about nature are not opinions. I understand a lot of people don’t get this.

  37. I can’t explain why it is in granite. I can only tell what is there. We must embrace what we can see with our own eyes. Here is what we know: It looks very much like a giant human foot print It is dated to be 200 – 3 billion years old Like Einstein said: “If the facts don’t fit the theory, change the facts” And by that, perhaps there are other ways in nature to form granite rocks that we don’t know of.

    You’re absolutely right, of course the way in which this applies to your footprint thing is that the FACT that granite is an igneous rock, does not fit with the THEORY that this is a real footprint.

    That there were no humans living at that time is not the problem, that theory could change. That we don’t know of any giants ever existing is not the problem, that theory could change. Granite being an igneous rock however, is a fact, not a theory.

    Change your theory, the facts don’t fit it.

    Edit: I misread your alleged Einstein quote as “…change the theory” however as I believe you mistyped and meant that anyway, my point still stands.

  38. If some object in nature caused that foot print, the object would have been lifted straight up, not rolling to any side. Judging by this, is probably not a hoax and probably not a natural phenomenon. It looks very authentic. The dark spot at the bottom is caused by tremendous pressure from the giant human and muddy rain probably caused it to darken, the sides are not as dark as the bottom part.

    If this foot print is true, then the evolution theory falls apart as it is presented today. But we need to study this further to say anything for sure.

    • In reply to #97 by ClumpyMatter:

      If some object in nature caused that foot print, the object would have been lifted straight up, not rolling to any side. Judging by this, is probably not a hoax and probably not a natural phenomenon. It looks very authentic. The dark spot at the bottom is caused by tremendous pressure from the giant…

      What part of ‘you can’t leave a footprint on granite’ is confusing you?

      It looks very authentic

      Like all the other proven giant footprints you’ve seen?

      If this foot print is true, then the evolution theory falls apart as it is presented today

      Let me guess, you’re a creationist? Either that or you’re trolling, and this is a wind up.

    • In reply to #99 by ClumpyMatter:

      You can leave a foot print in granite rock, and we have one.

      By what process? Magic?

      You’re irritating me by your refusal to engage your brain. You’re either having a wind-up (haha how funny) or you are being irrational.

      If you’re not having a wind up then please start thinking – it is not rational, logical or productive to start with what you’d like to be true and then bend everything else around it to fit. If you are genuinely interested in this, then do some reading into the way igneous rocks form and behave.

      if you’re not interested, then I’ll either assume you’re a troll, or you’re trying to push some creationist agenda, or you’re in on the hoax.
      Personally, I think it’d be too hard to carve granite to look like that, it’s probably just a natural formation where softer rock has formed a hollow and eroded away over time.

  39. This is the problem with creationists. Their understanding of science is SO poor, that their proposed “evidence” that contradicts evolution is often even more absurd than their original claims.

    The only way that footprint could have been left in granite, is if these giants had magical lava proof feet, which is probably the least absurd part of this, given that if biblical giants were around at that time then of course they’d have magical feet!

  40. With humans of that size, their skin would be very thick and they would have much greater tolerance for heat than modern humans. During the cooling phase the foot print could have been shaped. And it is shaped. We should not assume it is a hoax, but approach interesting findings in nature with curiosity, and not conclude that it is a hoax and then ignore it.

    I say we study it more.

  41. To say that they had to have had magical lava protection is basically silly philosophy. That giant could have walked there and died later. You are assuming he must have survived. (Silly philosophy)

      • In reply to #104 by bob_e_s:

        In reply to #102 by ClumpyMatter:

        To say that they had to have had magical lava protection is basically silly philosophy.

        He wasn’t making a philosophical point. He was mocking you.

        He said: ” if these giants had magical lava proof feet, which is probably the least absurd part of this, given that if biblical giants were around at that time then of course they’d have magical feet!”

        This does not sound like mockery, he sound very serious here. He used the word “absurd”. Well that giant could have walked there and died from it, he doesn’t need magical lava proof feet to accidentially walk there and then later die from it.

        Like I said, he presented silly philosophy. When hobby evolutionists want to try to do philosophy, it very often fails in the extreme.

        • In reply to #105 by ClumpyMatter:

          In reply to #104 by bobes:

          In reply to #102 by ClumpyMatter:

          I can’t speak for Seraphor but I’m pretty sure their comment was not an attempt and philosophy, but rather an attempt to highlight how ridiculous your claims are.

          Philosophy is irrelevant in this debate, in any case. What is relevant is that you have leapt to an extraordinary conclusion from a very ordinary piece of evidence. I use the word evidence advisedly, as the only thing it is really evidence for is that granite can form in strange shapes, which can sometimes look like things we recognise.

          That’s all. Footprints do not form in granite. If you’d like us to believe that they can, please find any other examples of human or animal footprints preserved in granite. That is basic scientific enquiry, which is slightly different from your scientific process of making-stuff-up, I know, but I think you could grasp the concept.

    • In reply to #107 by ClumpyMatter:

      as a matter of fact, the heightened granite at the toes indicates that the giant actually raised his foot quickly, indicating that he was in fact in pain.

      I’m going to use a quote from Blackadder:

      “The eyes are open, the mouth moves, but Mr Brain has long since departed…”

    • In reply to #107 by ClumpyMatter:

      as a matter of fact, the heightened granite at the toes indicates that the giant actually raised his foot quickly, indicating that he was in fact in pain.

      A quick search would show you that granite has a melting point ~1250 deg C, so I guess ‘he was in fact in pain’, even if supposedly ‘humans of that size, their skin would be very thick and they would have much greater tolerance for heat than modern humans.’ ROTFLMAO….

      Along with the facts that granite forms at 5 to 30 kms underground, at pressures of 4 to 7 kbar, while taking many years to cool, shows how ridiculous your beliefs are – which happens when you extrude ignorant assertions, while under great pressure to mould your thinking to your dogmas, from irrational GODDIDIT presuppositions….

      I am continually baffled, sad and embarrassed that adult humans can be so deluded that they cling to such nonsense, and blatantly demonstrate the Dunning-Kruger Effect…. Mac.

      • In reply to #144 by CdnMacAtheist:

        I like the geology, Mac, but we shouldn’t forget that 84% of the world population lap up the stupefying placebo effect of “goddidit”; rather like those who are released after a long sentence and wish desperately to return to prison where regimentation had become much more agreeable than the freedom to make their own difficult decisions.

  42. I was indeed making a mockery of the claim, because I, along with Bob here, am clearly frustrated at your stubborn inability to engage your brain in any productive way other than clutching at straws to ‘prove’ your giant fantasy and using clever-sounding words like “philosophy” in a clearly innapropriate context.

    You’re probably a troll, however as I have neither the evidence or conviction for that conclusion, then I suggest, if you are intent on participating in scientiofic debates, that you start small and work your way up once you’ve understood the basics.
    For starters, look for a blog on high-school geology.

    • In reply to #110 by godzillatemple:

      Wait a minute… Are we seriously debating a story that appears on a website called beforeitsnews.com (and apparently nowhere else)?

      It’s all over the web, if you search. Interestingly, it only appears on creationist/religious or conspiracy sites. And also interestingly, I can’t find any other reference to footprints in granite. Because it doesn’t happen.

    • In reply to #110 by godzillatemple:

      Wait a minute… Are we seriously debating a story that appears on a website called beforeitsnews.com (and apparently nowhere else)?

      Scientists keep it away from you by rejecting it. That is why you never hear of it.

  43. ClumpyMatter,

    Even if it looks like a footprint , it does not mean that there were giants and it does not mean its a footprint. If there were humanoid , bipedial fossils from this era , we’d have them. The fossil record shows life starting simple and becoming more complex.
    Not, ‘BANG! Giant Humanoids’. It does not work that way

    • In reply to #114 by Pauly01:

      ClumpyMatter,

      Even if it looks like a footprint , it does not mean that there were giants and it does not mean its a footprint. If there were humanoid , bipedial fossils from this era , we’d have them. The fossil record shows life starting simple and becoming more complex.
      Not, ‘BANG! Giant Humanoi…

      That’s true. Like I said in previous posts, we should study this further and not take lightly on this.

  44. Scientists keep it away from you by rejecting it. That is why you never hear of

    My how convenient, all those pesky scientists (with their inconvenient scientific facts) have banded together to censor all material on the subject of Proterozoicotriassic asbestos giants except for those posted on pioneering creationist websites (how could they? those websites are protected by god) and it’s up to you, the lone ranger, to expose the truth.

    • In reply to #120 by Seraphor:

      Scientists keep it away from you by rejecting it. That is why you never hear of

      My how convenient, all those pesky scientists (with their inconvenient scientific facts) have banded together to censor all material on the subject of Proterozoicotriassic asbestos giants except for those posted on pion…

      It doesn’t work like that. If you’re a scientist and you have the tremendous amount of evidence for evolution, you simply can’t go against the majority into land of speculation, too risky for a scientist, he could even lose his job, much more his reputation.

      Fear is a leading force for scientists, unfortunately and scientists does not like it much when their 8 year long study is suddenly rendered invalid, they don’t like that at all, many will protest silently.

      • In reply to #122 by ClumpyMatter:

        In reply to #120 by Seraphor:

        Scientists keep it away from you by rejecting it. That is why you never hear of

        My how convenient, all those pesky scientists (with their inconvenient scientific facts) have banded together to censor all material on the subject of Proterozoicotriassic asbestos giants…

        That’s right. After all we all know what happens when scientists appear with new evidence which conclusively overturns and established theory! They…err…well they get Nobel prizes, don’t they?

        • In reply to #123 by bob_e_s:

          In reply to #122 by ClumpyMatter:

          In reply to #120 by Seraphor:

          Scientists keep it away from you by rejecting it. That is why you never hear of

          My how convenient, all those pesky scientists (with their inconvenient scientific facts) have banded together to censor all material on the subject of Pr…

          At first, they get a thousand rocks thrown in their forehead, and 10 years later they usually get a nobel prize and an apologee.

      • In reply to #122 by ClumpyMatter:

        It doesn’t work like that. If you’re a scientist and you have the tremendous amount of evidence for evolution, you simply can’t go against the majority into land of speculation, too risky for a scientist, he could even lose his job, much more his reputation.

        This sounds like another creationist story!
        I take it you have never read scientific journals, where peer-reviewing scientists challenge dubious claims, or minor errors, – all the time.

        Fear is a leading force for scientists, unfortunately and scientists does not like it much when their 8 year long study is suddenly rendered invalid, they don’t like that at all, many will protest silently.

        Or reply defending their work loudly! Some of the exposed dishonest ones like Wakefield are still shouting about their claims where they can find a gullible audience.

  45. Well here we go again with the misdirected ad homs.

    I am aware that plant biologists in particular have taken the generic term “cell wall” and redefined it to refer to the cellulose outer wall of plant cells. Nevertheless my up-to-date Chambers Dictionary still states: “cell membrane (biol) the surface membrane surrounding a cell; a cell wall”… Since I referred to animals, yes, I do very obviously mean the outer membrane of animal cells. So do, for example, Houlihan (Professor of Zoology) and Jobling (Professor of Fish Biology) when they write (in 2008): “…the walls of animal cells are composed of protein and lipid.” That is unambiguous (and Googleable). If your zoological credentials are superior to theirs, take it up with them, not me.

    I was interested, nay amazed, to read that one of the “Advantages of Asexual Reproduction [is that] The offspring has the same phenotype and genetic make up as the parent.” On this planet? I was so interested that I looked up your source: Buzzle. I learned a lot at Buzzle. I learned that if I don’t Feng Shui my bathroom it will “drain away wealth” (as opposed to…) and that humans are “benumbed” by crop circles, which are created by aliens, and all sorts of other really cool stuff. Yet another of your embarrassing, bogus, erroneous sources. Still, you seem to have convinced Steve Hopker.

    I see now I was wrong to agree with logicophilosophicus on phenotype transmission – the problems being lps’s liberal use of absolutisms – in this case ‘no’[animals]… But in asexual reproduction – which occurs in many plants and various animals on occasion – the genotype is passed on intact and so is much of the phenotype…

    Of course I had a good reason for talking about animals, which was to avoid talking about plants and also unicellular organisms. Plants reproduce like animals, but they are also propagated by budding, suckers, grafts… That is sometimes called reproduction, but it is just vegetative growth. Meiosis is not involved. Take a tree. Saw it in half, vertically, in situ, roots and all. If both halves survive, which half is the parent? Now look at the phenotype, the pattern of branches and roots, and check whether it is identical in both halves. Not a chance. Layer half dozen runners from a blackberry bush and then cut them free and transplant them to different continents. What you have there, strictly speaking, is one plant with a very extreme phenome. (You could do the same with a planarian worm.)

    So I just wanted to talk about animals (not realising that there was some prohibition). I’m no expert, but I think it goes like this in humans. Start with a fertilized ovum, with genome A, implanted in the wall of the uterus. This divides a few times before differentiating into embryo and extra-embryonic tissues. After a couple of weeks a few dozen primordial germ cells leave the embryo and form a clump – on the wall of the yolk sac in humans. A couple of weeks later they are migrating back into the embryo, where those that are successful settle in the gonads. That few dozen has become some thousands, by cell division. Eventually an adult human being, comprising around a hundred trillion cells, is ready to be a new parent. Notice that apart from the first dozen or so days of embryonic development, the gametes are genetically independent of the body cells. The mutation rate, most of which is likely due to copying errors, is extremely low in such large animals, about one per base pair per hundred million generations. On the other hand, there are several billion base pairs in the human genome, so there may be dozens of copying errors at every cell division; and every cell, even the PGCs, has undergone dozens of divisions. So which cell do you pick to determine your genome? They’re all different. Having made your choice, you cannot then, as a prospective parent, expect to pass on a genome which doesn’t include dozens of differences – possibly all minor, causing only those tiny differences which are what neo-Darwinian evolution is all about.

    A couple of reputable sources:

    http://biology.about.com/od/geneticsglossary/g/phenotype.htm (Observable behaviour is part of the phenotype. See, for example, the next link.)

    http://tuvalu.santafe.edu/~dirk/fluct/fluct.pdf (Analyses parts of the phenome – they are very limited – which can be passed on. Note that the three “heritable” cases are chromatin marking system [i.e. methylation], steady state system [self-perpetuating reactions] and structural inheritance system [three dimensional templates]. The second and third are precisely the non-genetic sources of information in cell machinery and structures which I mentioned. They are essential for cell construction.)

    Your post makes strong assertions (‘no genome ever [made a cell] etc) that seem to contradict neo-Darwinism – indeed genetics as a whole. Well formulated new ideas are always welcome. But what is being proposed in place of neo-Darwinism: and what is the evidence to support it?

    Not in place of, but in addition to.

    • In reply to #125 by logicophilosophicus:

      Plants reproduce like animals, but they are also propagated by budding, suckers, grafts… That is sometimes called reproduction, but it is just vegetative growth. Meiosis is not involved.

      Oh! dear! As I said earlier, you are absolutely clueless about asexual reproduction and cloning, – even at school textbook level,

      http://www.biology-online.org/dictionary/Asexual-reproduction
      Asexual reproduction – Definition:

      A form of reproduction** that does not involve meiosis**, ploidy reduction or fertilization, and the offspring is a clone of the parent organism; because of no exchange of genetic material.

      Examples of asexual reproduction are:

      • Binary fission
      • Budding
      • Vegetative reproduction

      . . . . So you should stop making a fool of yourself with these ridiculous assertions and cherry-picked inappropriate examples.

      new clonal polyps bud off from parent polyps – http://www.richarddawkins.net/discussions/2013/9/12/the-central-paradox-of-evolution#comment-box-86

      I was interested, nay amazed, to read that one of the “Advantages of Asexual Reproduction [is that] The offspring has the same phenotype and genetic make up as the parent.” On this planet?

      It is not always the case, but you could learn something if you stopped posturing, sidetracking, and making ridiculous assertions! It is very common for offspring to have the same genetic make up as parents in asexual reproduction. I already explained FULL CLONES.

      The rest of your post has either been refuted or is irrelevant to my refutation of your sweeping generalisations and absolutisms about diploid phenotypes in asexual reproduction.

      The comically patronising ridiculous claims about your alleged total incidence of haploids in asexual reproduction have also been refuted.

      • In reply to #138 by Alan4discussion:

        Log: Plants reproduce like animals, but they are also propagated by budding, suckers, grafts… That is sometimes called reproduction

        A4D: (Quoting) “Examples of asexual reproduction… Budding, Vegetative reproduction”

        So you have merely confirmed the point I made: I had said that vegetative propagation is “sometimes called reproduction”. Of course, if all authoritative sources described it as “reproduction” then my “sometimes” statement would be wrong, and you would have a point, but they don’t, and so you don’t (e.g. http://www.biologie.uni-hamburg.de/b-online/ibc99/koning/vegpropn.html).

        That, as I very carefully explained, is why I particularly confined my points to animal reproduction. The OP concerns evolution; (near-) identical clones make no contribution to evolution.

        [In asexual reproduction] “The offspring has the same phenotype… as the parent.”

        You avoid defending this claptrap (it is not ever the case) which you lifted from the execrable “Buzzle”. Shrewd move.

        Your last two paragraphs attack statements which bear no resemblance to anything I have ever written. What’s that all about?

        The OP was about the potential difficulty of establishing very slight genetic advantages. I attempted to stay on thread. You clearly have no such intention or interest.

        • In reply to #145 by logicophilosophicus:

          You problem is your posturing with pseudo authority, when you do not even understand the definitions of basic scientific terms such as “asexual reproduction” and you also have a very limited perception of what constitutes an animal. Nevertheless you bluster on with ridiculous assertions, arising from ignorance of the subject and the misreading of biology papers resulting from your lack of understanding of the terminology.

          Log: Plants reproduce like animals, but they are also propagated by budding, suckers, grafts… That is sometimes called reproduction but it is just vegetative growth. Meiosis is not involved.

          It is ALWAYS CALLED ASEXUAL REPRODUCTION, and budding and binary fission, includes animals, as in the quote and link you ignored @138 .

          A4D: (Quoting) “Examples of asexual reproduction…{Binary fission} Budding, Vegetative reproduction”

          Quoting and linking!
          http://www.biology-online.org/dictionary/Asexual-reproduction

          Lphil – So you have merely confirmed the point I made: I had said that vegetative propagation is “sometimes called reproduction”. Of course, if all authoritative sources described it as “reproduction” then my “sometimes” statement would be wrong, and you would have a point, but they don’t, and so you don’t

          Rubbish! Science does not redefine its fields of study to accommodate your ridiculous assertions! An understanding of the scope of asexual reproduction is a basic school textbook level which you have not yet achieved, despite me giving you a biology dictionary definition in the post you are quoting.

          Lphil @74 -

          “no animal ever passed on its own phenome”

          I suggest you read up full clones and Parthenogenesis

          Lphi – Animal cloning involves an egg cell, as does parthenogenesis. The orthodox view is that these cells have all been produced in the embryo, long before most of the animal’s phenotypic development is yet to happen, and that information cannot be added to the ova.You did say you were a biologist?

          This is typical of your posturing ignorance! You clearly have no idea of the forms of asexual reproduction which do not involve ova, such as animals which reproduce by budding. I already explained this @76 ) You seem to be confused over yet another definition – not all animals are vertebrates!

          You did say you were a biologist?

          Alan @76 – I am and you are not. That is how I can tell you that a full clone can be a 100% genetic diploid copy of its parent, and you have no idea what I am talking about. Not all clones start as eggs, but I should not have to explain that to anyone who had an understanding of biological diversity, or who had looked at the links I provided.

          Lphil @145 – That, as I very carefully explained, is why I particularly confined my points to animal reproduction. The OP concerns evolution; (near-) identical clones make no contribution to evolution.

          This is more asserted rubbish. I gave an example and explanation @86 explaining how they contribute to expanding populations and improved survival of genes in corals. You have simply ignored this, and continue repeating silly assertions, thereby learning nothing!

          @76 -

          Lphil – Note that “the genes (or half of them, anyway)” allows for both asexual and sexual reproduction. The clue is in the word “or”.

          Alan – Thank you for demonstrating that you have not read up on asexual reproduction, and have no idea what you are talking about! – so we are wasting our time dealing with your erroneous assertions, which you have no intention of retracting or correcting. The clue is in the word “full”, in “full clone”. (100% diploid copy – not half. or haploid)

          ▬▬▬▬▬

          Lphil @145 – Your last two paragraphs [138] attack statements which bear no resemblance to anything I have ever written. What’s that all about?

          Really?????? Denial now!!!

          Alan @138 – The rest of your post has either been refuted or is irrelevant to my refutation of your sweeping generalisations and absolutisms about diploid phenotypes in asexual reproduction.

          The comically patronising ridiculous claims about your alleged total incidence of haploids in asexual reproduction have also been refuted.

          @67 by logicophilosophicus: – The actual organisms (e.g. you) are off-shoots of that line: no animal ever passed on its own phenome or even its own genome to a descendant, just the genes (or half of them, anyway) from its inherited germ cells, and therefore any heritable changes are strictly sequestred in the germ line.

          Perhaps “haploid” is another biological term you don’t understand as meaning half a diploid set of genes.
          Similarly your failure to read or understand my link on coral polyps, makes no difference to the refutation of your now debunked claims!

          I’m not going to bother with your ad-homs against Buzzle. They listed biological features at a simple level which I hoped you would be able to understand – but apparently you could not understand those, or the ones from the biology-online.org/dictionary.

        • In reply to #145 by logicophilosophicus:

          (e.g. http://www.biologie.uni-hamburg.de/b-online/ibc99/koning/vegpropn.html).

          Where you throw in some link which is claimed to support some ridiculous position as an “authority”, I am going to require a pasted quote of the section claimed to contradict established science – or in this case a well understood scientific definition.

          (asexual = not sexual)

          I have no intention of wading through lengthy documents trying to work out what you have misunderstood.

  46. I had a lot of fun reading the many clever and humorous comments here – massive imagination and a fair deal of confusion also. The definitions of gene and allele and the workings of mitosis (somatic cell division) and meiosis (germ cell division) is found in any basic textbook of genetics. The corner-stones of the Synthetic Theory of Evolution are not as easy to find today but I get the feeling that some of you here would be prepared to chew on them the next 2 years or so. Here they are from the Columbia Classics in Evolution Series Edts Niles Eldridge & Stephen Jay Gould, 1982
    1. Genetics and the Origin of Species by Theodosius Dobzhansky (originally publ 1937, but like Darwins work a bible for seriously interested). ISBN 0-231- 05475-0
    2. Systematics and and the Origin of Species by Ernst Mayr (also a bible). ISBN I don’t have at present.

    If these rather tough bits are not to your taste try
    3. The Growth of Biological Thought, Diversity, Evolution, and Inheritance by Ernst Mayr 1982, The Belknap press of Harvard University Press ISBN-0-674-36446-5/7

    There has been much discussion on point mutations and the time required to see a change. However, there are more dramatic changes that contribute to genetic changes of significance like chromosomal aberrations, and altered chromosome numbers. Consider the doubling of the chromosome number, not so uncommon among plants. The latter is a very interesting mechanism in that it opens up for prominent modification of extra copies of genes giving new functions without losing the original function because of simultaneous presence of unaltered ones. Actually we may ourselves be so called pseudopolyploids, meaning that early in our evolution ancestors “managed” to double their chromosome number by routes we don’t exactly know.
    I know the geneticist in me is a bit boring here, but seriously it is hard to enter this discussion because of the many jumps over gaps and the sometimes brave imaginative reasoning. Please excuse me.

    • In reply to #130 by Agge:

      Consider the doubling of the chromosome number, not so uncommon among plants. The latter is a very interesting mechanism in that it opens up for prominent modification of extra copies of genes giving new functions without losing the original function because of simultaneous presence of unaltered ones. Actually we may ourselves be so called pseudopolyploids, meaning that early in our evolution ancestors “managed” to double their chromosome number by routes we don’t exactly know.

      If you look at my link @65 you will see the tree of known polyploids in Eukaryotes. http://en.wikipedia.org/wiki/File:PaleopolyploidyTree.jpg – including those speculated as leading to mammals.

      • In reply to #132 by Alan4discussion:

        In reply to #130 by Agge:

        Consider the doubling of the chromosome number, not so uncommon among plants. The latter is a very interesting mechanism in that it opens up for prominent modification of extra copies of genes giving new functions without losing the original function because of simultaneo…

        Dear me – Alan4 – you had already clarified and discussed most of the most vital points in #65! I missed it. I will check the link. Thanks!

          • In reply to #135 by Alan4discussion:

            It never did any harm for people to independently present the same scientific conclusions!

            It doesn’t seem to do any good either :)

            There is a chap who calls himself “Born Again Christian” and who often visits me on Sundays to tell me that every dot and comma in the Bible is true, and that he doesn’t need any other book to tell him what he needs to know about life, the universe, and everything.

            Repeating calculations, graphs, physical laws, contradictions and condemnations of the bible by the bible itself, has never made a dent on my born-again friend, and probably never will. My conclusion is that either I don’t have any powers of persuasion, or that once certain beliefs are hard-wired into the brains of some humans, then nothing will unsolder their substandard circuits.

          • In reply to #136 by ZedBee:

            In reply to #135 by Alan4discussion:

            It never did any harm for people to independently present the same scientific conclusions!

            There is a chap who calls himself “Born Again Christian” and who often visits me on Sundays to tell me that every dot and comma…

            The odd but positive thing is that sometimes such people do change their minds. This site has such members – indeed I know someone who tells me he was an absolutely convinced Jehovah’s witness – which entailed evangelism such as you receive. But the doubts crept in and for some years he has been a convinced atheist. So strange as it seems, even the strongest dogmatism can yield.

  47. Hi Steve,

    I take your word for it; nevertheless, it seems to me that those who would venture into Richard Dawkins’ website (no less) probably have one toe in Aleppo on their way to conversion in Damascus (Oops, I think that is probably the wrong metaphor these days).

    • In reply to #141 by This Is Not A Meme:

      If Clumpy is a troll, they have my admiration. That was a lulzy read, especially bob-e-s’ posts.

      I’m still not sure if that was a wind up/troll or if he was just a…well, you know. A moron.

      I suspect he actually believed what he was writing as if he was trolling I probably would have continued biting. So he’s either extremely clever or extremely stupid.

      I actually found a debunking of the giant footprint story on Creation.com. That says a lot.

  48. In reply to #141 by This Is Not A Meme:

    If Clumpy is a troll, they have my admiration. That was a lulzy read, especially bob-e-s’ posts.

    Hi TINAM,

    LUL usually means ‘Lame Uncomfortable Laugh’, but also means penis in Dutch, and I think that ClumpyMatter looks like a dick…. 8-) Mac.

  49. In reply to #146 by ZedBee:

    In reply to #144 by CdnMacAtheist:

    I like the geology, Mac, but we shouldn’t forget that 84% of the world population lap up the stupefying placebo effect of “goddidit”. . . .

    Hi ZedBee,

    Although I fully understand that most folk were indoctrinated and forced to absorb lies and bullshit during their mind-sponge childhoods when so much reality, truth and thinking skills should have been shown them, I do have issues with their effects on others, both inside and outside of their ego-stroking, superiority-touting memeplexes.

    Those damaged should be allowed some respect, pity and concern, but I really get pissed when they grow up but won’t take responsibility for their mental activities, and harm our species and our future in so many ways by aiding, supporting and spreading ignorance, delusional thinking, and mind-slavery to one of many faith businesses.

    I realize that escaping the clutches of comforting / threatening families and peer groups isn’t easy, but the human race can’t afford to wait centuries for them to realize their many mistakes and harmful behaviors, since we are well into a population, economic, resource and climate crisis that requires big social changes, lifestyle sacrifices and behavior modifications, especially for those of us in ‘advanced, first-world societies’, since we consume and pollute so much more than ‘primitive, third-world societies’.

    We just can’t keep on doing the ‘same old, same old’ shit any more, and that primitive, old-time religious thinking just ain’t cutting it. I won’t be around for many more years, so I’m stridently calling out faith-heads while I can still rant, to start doing something positive for our species before it’s too late.

    Getting back to the Topic, it’s time to create more cultural evolution and make religions go extinct, since their supposed initial benefits have turned toxic, and long overstayed their welcome…. Mac.

    • In reply to #148 by CdnMacAtheist:

      Hi Mac,

      I will say this, hoping that the moderators will not consider it to be too far off topic: Ignatius Loyola gave the Jesuits their motto, “Give me the child until he is seven and I will give you the man.” So, although I agree with all the sentiments you expressed, nevertheless, those who benefit from docile ignorance – of the kind that prompted this topic – hold firmly in their hands the means of propaganda, and the minds and pockets of their international audience, aided by such as the lady who wrote comfortably from her castle:

      All things bright and beautiful, the Lord God made them all.

      The rich man in his castle, the poor man at his gate.

      etc., etc.

  50. The things that are opposed to the fixation of a beneficial mutation, are the other evolutionary forces: genetic drift (random gene frequency fluctuation), and migration. I don’t count mutation, because I’m focusing in a single mutation that is beneficial, compared to the rest of the possible mutations (or preexisting variants) in the same locus. In a sufficiently big, isolated population, genetic drift is very weak, so you can have SOME beneficial mutations of very small effect to start increasing in frequency. The only way to have zero genetic drift, and hence, no loss of beneficial mutations by chance, would be to have an infinitely big population. But in the case of quantitative traits, like height, claw length, etc, there are many loci (genes) involved, there are many chances of beneficial mutations arising in all of those loci, so even with a small amount of genetic drift, some/many beneficial mutations will pass through (there are many “lottery tickets”).

    Also, take on account that a small increase in chance of reproduction/survival only starts to make sense many generations later. You may not see a 1% increase in fitness (the term we biologists use for the amount of gene copies, a particular gene can leave in the next generation, given certain environment conditions, etc.) in one generation, but many generations later it gets translated in a certain number of individuals more, compared to the alternatives. Since reproduction is exponential in average (if you have two kids, and those two kids have two kids each, in two generations you can have four descendants – in four generations, sixteen descendants, etc), a small advantage may be noticeable in less generations than you may think.

  51. A good example of what I’m talking about can also be found in The Ancestor’s Tale, in which Dawkins recounts the findings of a longitudinal study of the Galapagos finches conducted by Grant et al, which includes both measurements and genetic analyses and evidence for beak efficacy under certain conditions. A difference in beak size of half a millimetre is sufficient to power natural selection during droughts, also effecting reproductive success in the aftermath. Since a Galapagos finch measures just a few centimetres in length (about 10 to 20), that’s a difference of about 0.5% total body length and about 5% of total beak length. Not 1%, of course, but still quite a small difference.

    In reply to #157 by Alan4discussion:

    In reply to #149 by stevehopker:_

    With some trepidation ie in the knowledge there are professional geneticists here,

    Access by those with literary skills to academic papers and scientific terminology, does not confer understanding of the science. That requires study from basics upwards, with an i…

    I’m flattered, but I am obliged to point out that I’m not really a qualified biologist. I just have an interest in the field, which I indulge in my spare time.

    • In reply to #159 by Zeuglodon:

      I’m flattered, but I am obliged to point out that I’m not really a qualified biologist. I just have an interest in the field, which I indulge in my spare time.

      The indications are that you have studied the subject in some detail with a scientific perspective.

      Likewise there are clear signs that some others have not, but are just picking subjects they think are sufficiently complex to “blind others with science”!

      The difficulty in offering evidenced explanations, is that peer-reviewed material will sail right past those who are cherry-picking bits of it to use as a badge of false-authority without understanding. They will also casually dismiss correct simple explanations, at a level they could understand, as being from sources lacking “authority”, while simply ignoring the information provided.

      This leaves them posturing, disputing the meaning of scientific terms, and ignoring and denying the evidence, with “irreducible incredulity”.

      It is very common in cherry-picked examples of “irreducible complexity”, where perceptions of evolution are centred on disputing its application to humans.

      Lphil, attempted to exclude the readily explainable features of cell evolution by specifying “animal evolution”, (apparently with humans or vertebrate sexual reproduction in mind), but this failed due to a lack of understanding of the biological definition of “animal”, and a lack of understanding of asexual reproduction.

      You will note, that while you have tried to explain the sidetracking into misunderstood complexities, I have challenged the unevidenced assertions and produced links and examples which refute these silly assertions, (while trying to shut down the side-tracking digressions which ignore and dodge my refutations).

      History suggests that neither of us will get recognition of the scientific points we have made!

    • In reply to #159 by Zeuglodon:

      A good example of what I’m talking about can also be found in The Ancestor’s Tale, in which Dawkins recounts the findings of a longitudinal study of the Galapagos finches conducted by Grant et al, which includes both measurements and genetic analyses and evidence for beak efficacy under certain conditions. A difference in beak size of half a millimetre is sufficient to power natural selection during droughts, also effecting reproductive success in the aftermath. Since a Galapagos finch measures just a few centimetres in length (about 10 to 20), that’s a difference of about 0.5% total body length and about 5% of total beak length. Not 1%, of course, but still quite a small difference.

      I have not read “The Ancestor’s tale”, but I am familiar with the example of Darwin’s Galapagos finches. Very small variations can indeed respond to selection pressure.

      I am not interested in playing with silly albsolutisms or further semantic side-tracking point-scoring games, which contribute nothing to scientific understanding.
      Lphil’s assertions have been refuted, but he simply ignores this, and is heading off into some sort of information theory gapology to blind the lurkers with (pseudo?)science. I asked for properly pasted quotes where claims are made of support from links. I suggest you do the same.

      Many key points I have made, (such as the relevance of asexual reproduction to the evolution of corals), refuting erroneous assertions, have simply been ignored by Lphil.

      Regarding Eukaryotic clones, – much of the work on environmental effects on phenotype development have been done on plants, as they are much easier to clone, and provide vastly greater numbers of accessible samples.

      Key research work was done by the East Malling Research Station.

      This station produced a numbered series of cloned apple root-stocks, which modified the phenotype development of cloned commercial varieties of apple (Cox, Golden Delicious etc) which were grafted on to them.
      This combination of commercial varieties with “Malling series” rootstocks, produced a range of predictable standardised sizes and phenotype of tree with standard quality fruits.

      Very occasionally sports arise (naturally or induced by radiation) in these clones, – with commercially desirable ones being reproduced by cloning on to these rootstocks. These variations are rare but are preserved where commercially useful.

      The whole of the world apple production industry depends on the production and phenotype predictability of these grafted, cloned, phenotype combinations, (which do not come true from their seed)

      • In reply to #167 by Alan4discussion:

        In reply to #159 by Zeuglodon…but also – boorishly – criticising Logicophilosophicus in the third person.

        OK. We’ve been here before. I will answer one point at a time.

        Many key points I have made, (such as the relevance of asexual reproduction to the evolution of corals), refuting erroneous assertions, have simply been ignored by Lphil.

        Your link was in comment #86, not actually even addressed to me but to steve_hopker; this apparently gave you licence to rant in #151 about my statement that “clones make no contribution to evolution”; you claimed this was “rubbish” which you had already disproved in #86, complaining “You have simply ignored this…”

        The link explains that corals are a sexually reproducing group. So-called asexual reproduction is also described in the link: “This occurs when the parent polyp reaches a certain size and divides.” You claim that this contributes to evolution – the point at issue.

        Back to basics. We assume, with Darwin (who made a special study of coral reefs, as it happens) that there is a stable population of coral fully utilising the available environment and limited by Malthusian factors. Two processes occur. (1) Larger corals divide, their fragments colonising any available space, and (2) corals release sperm and ova which combine with other ova and sperm leading to free swimming juveniles which eventually settle and metamorphose into new sessile adults. Since corals arising from processes (1) and (2) are in competition for limited resources, it is clear that division reduces opportunities for recombination, and is an anti-evolutionary factor, which is the direct opposite of your bizarre suggestion.

        This is universally known to evolutionary biologists: asexual reproduction in multicellular organisms is a surefire route to extinction. J. B. S. Haldane, many years ago, described the recurrent cul-de-sac dandelions encountered. Every so often an asexual stock emerges, and eventually dies out.

        When I studied biology we were taught that the Hydra was a good example of asexual reproduction by budding; years later I discovered that this was just part of a cycle of sexual reproduction; so much for the “basic school textbook level” of biology you promote (#151). In the hydrae, in the corals, in medusae, etc, the buds or fragments are only capable of sexual reproduction because in these types the gonads are distributed throughout the organism. The offshoot carries away the original germline. The reproductive cycle, despite your claim to the contrary, requires meiosis.

        (As far as I know the only obvious “exceptions” to this account are bdelloid rotifers. While reproducing asexually, they seem to have survived and evolved for tens of millions of years without the intrduction of genetic novelty by recombination. This was a mystery until very recently, when some of their genomes were sequenced, and it was discovered that, far from lacking genetic novelty, they had, by some as yet unknown mechanism, “pilfered” genes from many sources (i.e. not rotifer genes), which accounted for up to 10% of the genome.)

        That’s your one point.

        Many key points I have made, (such as the relevance of asexual reproduction to the evolution of corals), refuting erroneous assertions, have simply been ignored by Lphil.

        You were wrong, my assertion was not erroneous and your own source refutes your claim.

        • In reply to #169 by logicophilosophicus:

          The link explains that corals are a sexually reproducing group. So-called asexual reproduction is also described in the link: “This occurs when the parent polyp reaches a certain size and divides.” You claim that this contributes to evolution – the point at issue.

          Oh! dear! You still can’t understand BASIC biological terminology even after repeated explanations and a dictionary reference!
          The differences between sexual and asexual reproduction are school-book biology – learn some!!!
          Science is not interested in people with no scientific credentials, disputing standard definitions!

          Back to basics. We assume, with Darwin (who made a special study of coral reefs, as it happens) that there is a stable population of coral fully utilising the available environment and limited by Malthusian factors.

          No! WE don’t make silly assumptions!
          Yes! I know you can define special unrealistic situations to form the basis of your circular arguments. There is no reason to assume there is “a stable population of corals”. They are in constant competition between species, with factors like storm damage to reefs leading to new (re)colonisation of extensive areas.

          Like I said, you have absolutely no comprehension of basic biology, ecology, or biological definitions, even when they explained to you in the simplest of terms.

          Two processes occur. (1) Larger corals divide, their fragments colonising any available space, and (2) corals release sperm and ova which combine with other ova and sperm leading to free swimming juveniles which eventually settle and metamorphose into new sessile adults.

          That part is roughly right, apart from missing out the fact that polyps usually grow in colonies as they bud and divide , but that does nothing to support your contradiction of my evidence.

          Since corals arising from processes (1) and (2) are in competition for limited resources, it is clear that division reduces opportunities for recombination, and is an anti-evolutionary factor, which is the direct opposite of your bizarre suggestion.

          You just made that up that “bizzarre” assertion, from the basis of your silly unsupported assertion and own ignorance. The asexual reproduction greatly increases number of coral polyps by budding, which go on reproduce sexually, and then release greatly increased numbers of offspring into the ocean currents and often thousands of miles of new habitats. The assumption a stable population of coral fully utilising the available environment, is ridiculous.
          They are in constant competition between species, with factors like storm damage to reefs, leading to constant new (re)colonisations.

          My source clearly confirms that the asexual reproduction in corals greatly increases the numbers of sexually reproduced offspring – which anyone with even a basic understanding of evolution, would recognise as an evolutionary survival benefit!

          Many key points I have made, (such as the relevance of asexual reproduction to the evolution of corals), refuting erroneous assertions, have simply been ignored by Lphil.

          You were wrong, my assertion was not erroneous and your own source refutes your claim.

          Even when I give you links to science you look through bias-blinkers and can’t or won’t understand them , so simply make up ludicrous contrived contradictions. The post on corals is quite clearly a refutation of your claim that asexual reproduction is not of evolutionary survival benefit.
          You just keep making up these ridiculous assertions and dispute the science refuting them while you sit in the asserted ignorance of denial and irreducible-incredulity.

          • In reply to #171 by Alan4discussion:

            In reply to #169 by logicophilosophicus:

            Wrong. Malthus/Darwin. Here endeth the lesson.

          • In reply to #172 by logicophilosophicus:

            Just to be clear:

            “By observing different species, Darwin saw that there is variation in every population and that within these groups there is competition for limited resources such as food, water and shelter from predators.” (Open University) Without the limitation on resources there is no evolutionary pressure.

            The suggestion that a new allele will, by simple genetic drift, increase exponentially per generation in a population which has already reached its (Malthusian) limit, or that the repetition of past/on-going processes (whether vegetative or sexual) “greatly increases number of coral polyps” from what it was yesterday, or last year, or when the Beagle dropped anchor, in an ocean with a limited and already colonised environment, or that “reproduction is exponential in average” when resources are fixed and already fully utilised, has simply missed Darwin’s point. 150 years of evolutionary science ignored.

          • In reply to #172 by logicophilosophicus:

            In reply to #171 by Alan4discussion:

            Wrong. Malthus/Darwin. Here endeth the lesson.

            Ha! ha! ha! Falsely citing Darwin as an authority for your ignorance of the ecology of evolution is a comical fallacy!! That is why I asked you to provide pasted quotes from your cited links.

            Your demonstrated ignorance of school-book-level biology, and inability to understand simple scientific explanations, shows you have not even started your lessons in biology yet! – Indeed your posts indicate that your education lessons in biology ended before they started.

            “By observing different species, Darwin saw that there is variation in every population and that within these groups there is competition for limited resources such as food, water and shelter from predators.” (Open University)

            That is correct as far as the generality goes, but it does nothing to support your denial of my specific coral example .

            @173 Without the limitation on resources there is no evolutionary pressure.

            Rubbish! – There is strong competition to expand into the new areas and adapt to exploit new resources ! -

            when resources are fixed and already fully utilised,

            They are not, but may be in special situations.

            which has already reached its (Malthusian) limit,

            The Malthusian limit is about catastrophic collapse of populations in over-populated areas. It is yet another red-herring which shows you have no idea what you are talking about, but keep throwing in diversionary false authority claims for nonsense.

            It has nothing to do with colonisation of new areas, such as storm damaged reefs or shores of newly emerged islands.

            You just keep making up clueless assertions, which illustrate your lack of understanding of the subject! Scientists seek the facts and retract and correct their mistakes. Denier-trolls filled with Dunning-Kruger confidence – just keep on making up silly unevidenced assertions, and then dogmatically go through semantic contortions, trying to defend the indefensible!

            Science and nature do not care if you sit in troll-denial-ignorance and argue the hind legs off a donkey! They will continue to work as normal unaffected by your ignorance!

            http://animals.about.com/od/coralreefs/f/coralreefform.htm
            A stony coral colony begins as a single free-swimming founder coral polyp that attaches itself to a hard substrate such as submerged rocks. The founder polyp replicates itself repeatedly through asexual reproduction, producing a colony.

          • In reply to #176 by Alan4discussion:

            In reply to #172 by logicophilosophicus:

            In reply to #171 by Alan4discussion:

            Ha! ha! ha! Falsely citing Darwin as an authority for your ignorance of the ecology of evolution is a comical fallacy!!

            You do like to give orders. Here are the “properly pasted” quotations you require to show that, contrary to your abusively triumphalist claims, Malthusian limits are and always were fundamental to Darwinism:

            “In October 1838, fifteen months after I had begun my systematic inquiry, I happened to read for amusement Malthus on Population, and being prepared to appreciate the struggle for existence which everywhere goes on, from long-continued observation of the habits of animals and plants, it at once struck me that under these circumstances favourable variations would tend to be preserved, and unfavourable ones to be destroyed. The result would be the formation of a new species.” (Darwin)

            “The most interesting coincidence in the matter, I think, is, that I as well as Darwin, was led to the theory itself through Malthus – in my case it was his elaborate account of the action of ‘preventative checks’ in keeping down the population of savage races to a tolerably fixed but scanty number. This had strongly impressed me, and it suddenly flashed upon me that all animals are necessarily thus kept down – ‘the struggle for existence’ – while variations, on which I was thinking, must necessarily often be beneficial, and would then cause those varieties to increase while injurious variations diminished….I was lying on my bed (no hammocks in the East) in the hot fit of intermittent fever, when the idea suddenly came to me. I thought it almost all out before the fit was over, and the moment I got up began to write it down, and I believe finished the first draft the next day.” (Wallace)

            [Emphases added]

            Re your coral link from NOOA, you claimed:

            “My source clearly confirms that the asexual reproduction in corals greatly increases the numbers of sexually reproduced offspring – which anyone with even a basic understanding of evolution, would recognise as an evolutionary survival benefit!”

            Here is the “properly pasted” paragraph on “asexual reproduction” in corals from your source:

            “Corals can reproduce asexually and sexually. In asexual reproduction, new clonal polyps bud off from parent polyps to expand or begin new colonies (Sumich, 1996). This occurs when the parent polyp reaches a certain size and divides. This process continues throughout the animal’s life (Barnes and Hughes, 1999).”

            That’s less than 50 words from an article of several hundreds on reproduction in corals. They constitute the only mention of “asexual reproduction”. There is absolutely no suggestion that this process “greatly increases the numbers of sexually reproduced offspring” – so it is simply dishonest to claim that your key source “clearly confirms” your erroneous claim.

          • In reply to #181 by logicophilosophicus:

            In reply to #176 by Alan4discussion:

            You do like to give orders. Here are the “properly pasted” quotations you require to show that, contrary to your abusively triumphalist claims, Malthusian limits are and always were fundamental to Darwinism:

            This is totally irrelevant to the coral issue, for habitat reasons which I have already explained!

            BTW: I spent several months in my student days working on an ecology project studying the destabilisation of ecosystems by misguided, but well meaning early conservationists removing predators, and so causing population explosions followed by resource depletion and population collapse in nature reserves.

            You have as much chance of bluffing and blinding me with “science” or anecdotes on this issue, as the chances of a snowball thriving in Hell!

            That’s less than 50 words from an article of several hundreds on reproduction in corals. They constitute the only mention of “asexual reproduction”. There is absolutely no suggestion that this process “greatly increases the numbers of sexually reproduced offspring” -

            So you can’t understand how a colony of several hundred mutually defended polyps produce more offspring than a single polyp!

            so it is simply dishonest to claim that your key source “clearly confirms” your erroneous claim.

            Gazzooing!!!! – After a whole string of your false assertions followed by denials of evidence on links, you accuse me of dishonesty??????

            If you still can’t read and understand scientific articles

            “asexual reproduction”.

            . . .. . . .or the terminology, I can do nothing for you, until you go to school and learn some biology!

            You will find basic textbooks, and thousands of biology papers on “asexual reproduction” – if you stop making stuff up, and bother to look!

            In the meantime there is extensive information on asexual reproduction of corals @183, which anyone with scientific integrity or research skills, could have found for themselves.

          • In reply to #185 by Alan4discussion:

            Malthusian limits are and always were fundamental to Darwinism:

            This is totally irrelevant to the coral issue, for habitat reasons which I have already explained!

            I think I have indulged the side-track into Malthusian limits sufficiently.

            Such limits are totally irrelevant to the initial colonisation of cleared habitat by competing corals at the time of initial colonisation. (although they may come into play locally, later when the ecosystem is mature.)

            Numbers of mobile planulae (larvae) are the key competitive feature here, with offspring from clonal colonies out-competing any species relying on single heads by thousands in establishing claims to territory and consequently resources.

            Lphil @145 – That, as I very carefully explained, is why I particularly confined my points to animal reproduction. The OP concerns evolution; (near-) identical clones make no contribution to evolution.

            Your mistaken claim has been thoroughly refuted @ #183 where the evolutionary benefits of asexual reproduction, of genetically identical coral polyps and subsequent sexual reproduction by these, are clearly set out.

            I can see no benefit to readers in further elaborating on issues which should now be crystal clear.

  52. Ok I agree with a lot of this don’t understand some of it (not a great geneticist). – by the way I’m pretty sure plants do asexual and sexual repo. But one question – if 86 percent of our DNA is shared with frogs (don’t quote me on that!) how is that random change ? By the way @alan4discussuon thanks for that post I read the article- good. Please hear the beyond belief programme as some new evidence and let me know what you think. Pretty strange science? Also I know there are no photons on DNA whoever said that but I was referring to the quantum jitters- electrovalence in cell membranes – quantum enough ? Electron orbits etc – is the cell communicating at that level??

    • In reply to #160 by Subatomicmantra:

      . But one question – if 86 percent of our DNA is shared with frogs (don’t quote me on that!) how is that random change ?

      It would be the 4% which represents an accumulation over millions of years of beneficial random changes, picked out by natural selection since the species had a common ancestor.

      By the way @alan4discussuon thanks for that post I read the article- good.

      You might find this one – with some very familiar organisms – interesting! Parade of Polyploids

  53. I’m going to answer my own question! If 3 billion base pairs have to unwind and zip up again exactly there is bound to be a few random errors. Just like copying letters from a textbook. Dummy

  54. Then is thd key to evolution in my balls as my wife was born with a certain number of oovocytes . Are male permutations more likely to produce random error? Or are the human female’s complement more cafe fully thought out!!

  55. By the way @clumpy matter they always come at me with that bible giant quote as some lame attempt at a full explanation of the dinosaurs- which is it giant men or dinos ? Sorry about flogging this dead horse

  56. In reply to #166 by logicophilosophicus:

    In reply to #156 by Zeuglodon:

    In reply to #155 by Zeuglodon:

    In reply to #154 by logicophilosophicus:

    I suspect that when you say “The Law of Large Numbers” justifies your argument, you are actually referring to the folkloristic “Law of Averages” more correctly known as “The Gambler’s Fallacy”.

    Since your (1) and (2) depend on a wrong application of “The Law of Large Numbers”, your argument fails.

    Not even close. For a start, I made it explicit that the average would become clear the larger the number of opportunities for it to happen, which is precisely in line with the Law of Large Numbers. The Gambler’s Fallacy only applies for specific cases and small samples; for instance, predicting that a slew of heads inevitably means the next flip is a tails, rather than predicting that there will generally be an average result of 50/50 even if no one case actually meets it:

    What I think you confused for the Gambler’s Fallacy was my invocation of the regression to the mean, in which an extreme result (such as an unusual embryological development) will be followed by a result closer to the mean, as in the archetypal case of unusually tall parents siring a normal-sized kid (another genetic example). Daniel Kahneman talks about the phenomenon in his book, Thinking, Fast and Slow, and the conditions are met by the fact that extreme embryological events are both rare and have little to no causal effect on the embryological development of subsequent generations. One of my points with the two normal distribution graphs was that the introduction of a new allele was the only thing that could change the average for good, since it is from this average as a given that the non-genetic factors can deviate at all.

    I’ll explain that last part: the gene’s phenotype on a quantitative difference (as per our example, muscle mass being bigger than normal) as opposed to a qualitative difference (e.g. body colour or the presence/absence of a certain chemical) is its average result in a gene pool, given a certain environment. The gene’s input to the development of the organism is guaranteed with near certainty, given its necessary role in embryological and/or cellular development, and the only question is to what extent that quantitative phenotype can be modified by non-normal variations, such as embryological freak events. It’s modification past that point – and arguably even at that point, since the allele’s main phenotype is its synthesis of a protein strand – is generally just its meeting the environment and “being tested”, to a degree, and even though the details of any particular test will differ, overall they’ll be roughly the same for each generation of a population living in the same environment.

    The overall point is that the gene’s phenotype for a quantitative event, while probabilistic, is not randomly so. It will converge towards an average effect in a given environment because of the gene’s necessary role in building the body and therefore in setting up an average. Since the only major difference over more than a small sample of generations is the difference between the alleles and their phenotypes, we can therefore be confident that the “signal to noise” ratio – which is, strictly speaking, a bit of a stretch of that term’s meaning when applied here – is in the gene’s favour, given its near-certainty when transcribing the protein that starts the process.

    That might work for the Book of Genesis, but in a stable population limited by Malthusian constraints, the allele can only be expected to increase its frequency per generation if there is effective selective pressure per generation – the point at issue.

    No, you misunderstood my point here, and badly. I was referring to Mendelian inheritance and to how its mathematical logic would enable the gene to propagate among a population each generation, not to a literal population increase. Suppose our mutant arises with a new allele D, such that he is aD and everyone else is aa. Assuming nothing untoward happens to him, half his offspring will inherit his new allele purely as a matter of Mendelian genetics. They, in turn, will pass on the allele to half their offspring, and the result is genetic drift:

    Genetic drift or allelic drift is the change in the frequency of a gene variant (allele) in a population due to random sampling.[1] The alleles in the offspring are a sample of those in the parents, and chance has a role in determining whether a given individual survives and reproduces. A population’s allele frequency is the fraction of the copies of one gene that share a particular form.[2] Genetic drift may cause gene variants to disappear completely and thereby reduce genetic variation.

    When there are few copies of an allele, the effect of genetic drift is larger, and when there are many copies the effect is smaller. Vigorous debates occurred over the relative importance of natural selection versus neutral processes, including genetic drift. Ronald Fisher held the view that genetic drift plays at the most a minor role in evolution, and this remained the dominant view for several decades. In 1968, Motoo Kimura rekindled the debate with his neutral theory of molecular evolution, which claims that most instances where a genetic change spreads across a population (although not necessarily changes in phenotypes) are caused by genetic drift.[3]

    Even in the unlikely case that the new allele’s phenotype will be targeted and reduced by other factors, or negated, sheer genetic drift can increase its frequency in the gene pool even in such an event. However, there’s no particular reason to suspect that the new allele will be uniquely penalized in this way. While the loss of a carrier is catastrophic at this early stage (for instance, if the very first mutant gets killed unexpectedly with no descendants), it also becomes less likely to actually occur.

    • In reply to #168 by Zeuglodon:

      Without wishing to be rude, let me begin by indicating that this reply will be brief.

      Not even close. For a start, I made it explicit that the average would become clear the larger the number of opportunities for it to happen, which is precisely in line with the Law of Large Numbers. The Gambler’s Fallacy only applies for specific cases and small samples

      Your second sentence there actually falls into the trap I described.

      Your third sentence suggests you went to Wikipedia: you think that the fallacy only applies to small samples (short runs), and that given a long enough run there will indeed be “maturity of chances” as the jargon goes. Not so (hence the £90 example). The average will get closer to the expectation (but we can’t normally predict/define this in genetics), and yet the absolute value will wander further and further from the expected value (the “drunkard’s walk” in the jargon).

      Your claim about genetic drift is plain wrong. You are defending a claim of “exponential increase per generation” for a new allele, absent selection, based on genetic drift. Genetic drift giveth and gentic drift taketh away. As I said, there can be no expectation of increase. The allele is in competion with others. In a fixed population, a new allele reaches n copies only by displacing n other alleles as already explained (Malthus/Darwin…)

      • In reply to #170 by logicophilosophicus:

        In reply to #168 by Zeuglodon:

        Your second sentence there actually falls into the trap I described.

        Your third sentence suggests you went to Wikipedia: you think that the fallacy only applies to small samples (short runs), and that given a long enough run there will indeed be “maturity of chances” as the jargon goes. Not so (hence the £90 example). The average will get closer to the expectation (but we can’t normally predict/define this in genetics), and yet the absolute value will wander further and further from the expected value (the “drunkard’s walk” in the jargon).

        Your question was how a phenotype – specifically a quantitative one like an increase in size – is supposed to be reliably expressed amid a “noise” of confounding factors if a new allele’s phenotype is only slightly different from the old one’s. You gave examples such as an unusual growth difference in the womb.

        The answer- assuming that a phenotype is a quantitative variation in an existing structure, such as an increase in muscle mass – is that the new allele changes the value of the average, as in the case of overlapping normal distributions I mentioned. But the normal distributions tell you two things. The first is that the random walk has already been taken into account for it: that’s why there are a range of values from a few extremely small cases through the average ones in the middle to the extremely big cases at the other end. The second is that this is a scenario in which regression to the mean would occur. If half of the population have gene A and the other half have gene B, then if we separated them and measured, say, their muscle mass and plotted that against the frequency of particular values, then we would expect that gene B bearers would have an average bigger than that of gene A. That makes a difference because the ratio of extremes in each half of the population would be dramatically different.

        In such a scenario, the point is that the alleles are not fair but are biased, just in different directions, and the success of each allele depends on whether an environment favours one bias over another. Bearers of gene A will get penalized more because they are overrepresented in the case of extremely small muscle mass, meaning that they lose most of their members either to survival or to reproductive failure. It’s not equally probable that gene B will produce an extremely small muscle mass or its average muscle mass, which is why the Gambler’s fallacy does not apply.

        Of course there are differences in averages that would be negligible – for instance, if the only difference between one allele and another was a tiny, imperceptible extra muscle cell – but this is because of its impact in what the muscle is supposed to do in the first place (for instance, to subdue prey or fight off rivals), which determines the selection pressure. For instance, the Galapagos finches’ beak sizes mattered, and mattered in the millimetres, not because bigger beak size was prized for its own sake, but because their environment demanded finer tools with which to acquire food.

        Your claim about genetic drift is plain wrong. You are defending a claim of “exponential increase per generation” for a new allele, absent selection, based on genetic drift. Genetic drift giveth and gentic drift taketh away. As I said, there can be no expectation of increase.

        “No” expectation is plain wrong. While there’s no guarantee, there’s reasonable expectation based on Mendelian inheritance patterns and probabilities for a neutral mutation to increase in numbers over the generations, so long as the allele doesn’t vanish too early in the process. I did not mean to imply that it was a runaway process, as though it would instantly hit fixation in a matter of a few generations, but so long as it wasn’t unlucky in its first generation or so, it would enter the usual fluctuation of allele frequencies as regular genetic drift permits. Again, all of this is assuming the mutation actually is neutral.

        The allele is in competion with others.

        Actually, in genetic drift there is no competition. Genes just get randomly shuffled, with no pressure to overtake others as there would be in natural selection.

        In a fixed population, a new allele reaches n copies only by displacing n other alleles as already explained (Malthus/Darwin…)

        I already explained that I’m not talking about a population increase. A last common ancestor of everyone living today, who coincidentally was also the first mutant of a certain gene, could potentially have large numbers of that allele spread across the population despite its risky beginnings. Every generation, an aD mutant can pass on its D allele to half its offspring. They in turn can pass it on to half of their offspring, so long as their partner is an aa type. If an aD then gets to mate with another aD, that raises the possibility for DD variants to emerge, guaranteeing that all the young will have the D allele.

        Genetic drift relies on the introduction of new alleles to begin with, otherwise only one allele can ever be passed on. And, as I made clear previously, this is all assuming a beneficial new mutation somehow has its selective advantage systematically wiped out either most of the time or every time it appears, which is a stretch to begin with due to the argument I laid out above.

        Lastly, this is all depending on a phenotype which is quantitatively variable, such as muscle mass. An either/or phenotype (such as having an extra neck bone, one less digit on each foot, or an extra pair of ribs) would show an even more dramatic difference as a result, since there’s little to no overlap.

        • In reply to #174 by Zeuglodon:

          Zeuglodon commented on “RDFRS: The Central Paradox of Evolution”:

          In reply to #170 by logicophilosophicus:

          In reply to #168 by Zeuglodon:

          “Your question was how a phenotype – specifically a quantitative one like an increase in size – is supposed to be reliably expressed…”

          No – selected not expressed. Remember the sabretooth.

          “…the normal distributions tell you two things.”

          Let’s take them one at a time.

          (1) “The first is that the random walk has already been taken into account…”

          No. The “random walk” is the progression of the distribution through time. it is a stochastic process, inherently unpredictable.

          (2) “The second is that this is a scenario in which regression to the mean would occur.”

          There is no “regression to the mean“, for at least three reasons. One is that we don’t know the a priori mean, just the current distribution of values. Think of this distribution’s mean as the £90 in the example. There’s no particular reason for it to go anywhere, up or down. The second is that regression is only towards the mean in the sense that over the generations (or the increasing n in a coin game) the population mean should spend a lot of time close to the a priori mean, less time further away, etc. The third is that you are confounding a snapshot distribution with a process that “would occur.”

          “…the alleles are not fair but are biased… which is why the Gambler’s fallacy does not apply.”

          No. The “maturity of chances” fallacy doesn’t go away just because (for example) the casino has an edge of a couple of percent at the roulette table.

          “['Your claim about genetic drift is plain wrong. You are defending a claim of "exponential increase per generation" for a new allele, absent selection, based on genetic drift. Genetic drift giveth and gentic drift taketh away. As I said, there can be no expectation of increase.] ‘No’ expectation is plain wrong. While there’s no guarantee, there’s reasonable expectation…”

          Expectation is a technical term. Without selective pressure genetic drift tends up or down: the expectation is zero. As you’ll see below, for a single low effect mutation there is no reasonable expectation of surviving very long.

          “…in genetic drift there is no competition. Genes just get randomly shuffled…”

          No. There’s always competition. If a population contains n-1 genes of type A and 1 gene of type B in this generation, then assuming simple replacement the chances of random extinction of type B are 1/2 in generation 2, 1/4 in generation 3, etc. That series sums to 1, certainty, unless gene B is very lucky or very effective. Another way of looking at it is to point out that the random walk from 1 to 0 is much shorter – much more probable – than 1 to n. As I wrote, “In a fixed population, a new allele reaches n copies only by displacing n other alleles as already explained (Malthus/Darwin…)” That’s competition.

          You seem to think genetic drift favours variety. If I am right, it erodes variety. And I am:

          “…genetic drift refers to the expected population dynamics of neutral alleles (those defined as having no positive or negative impact on reproductive fitness), which are predicted to eventually become fixed at zero or 100% frequency in the absence of other mechanisms affecting allele distributions.”

          However the likelihood of 100% depends on first reaching 50%, which seems virtually impossible according to my analysis.. Well, that’s right. A single slightly advantageous mutation (except, for example, in a tiny immigrant population on an island lacking indigenous competion) has no chance.

          Nevertheless, multiple mutation cold do the job:

          “…one strong (and elegant) prediction of the neutral theory [genetic drift] is that at selectively neutral sites, the rate of substitution is equal to the rate of mutation…”

          But we were looking at a marginally advantageous genes:

          “It is important to note, however, that the impact of genetic drift is not limited to neutral mutations. Because of genetic drift, most advantageous mutations are eventually lost, whereas some weakly deleterious mutations may become fixed.” [Emphasis added.]

          You can Google phrases from those quotes to find the sources (not Wikipedia, definitely not Buzzle or somebody’s primary school project). Impeccable, and entirely relevant to the OP. Very small changes have a very slim chance of becoming established.

          BTW, since I have answered all your questions, could you quote me your version of “The Law of Large Numbers”?

          • In reply to #175 by logicophilosophicus:

            In reply to #174 by Zeuglodon:

            Zeuglodon commented on “RDFRS: The Central Paradox of Evolution”:

            In reply to #170 by logicophilosophicus:

            In reply to #168 by Zeuglodon:

            “Your question was how a phenotype – specifically a quantitative one like an increase in size – is supposed to be reliably expr…

            You could have just put up a link to that, you know.

            Well, I give up. To be honest, I’m losing track of what we’re discussing, and more and more, I’m coming to realize I’m not entirely sure I know enough to keep up.it looks like you’re right about the weaker advantageous alleles, but the only two alternatives I see are either a less undramatic form of gradualism – which would be consistent with the remarkable speed of evolution in laboratory experiments achieving dramatic change in only a few dozen generations (read, for instance, The Ancestor’s Tale on Galapagos finches, prologue included) – or saltationism, and the latter I see too many problems with. Linkage disequilibrium probably does play a role in giving new mutations a “hand”, so to speak, but in any case, I think I need to do more homework.

            And so I bow out of this particular discussion. I simply don’t know enough to continue, and don’t see any future in pretending otherwise. While I can’t say I enjoyed our chat particularly, you’ve given me a wakeup call, and in the long run it’s probably for my own good to know when best to back down and admit I’m out of my depth. I’ll give you credit for that much, at least.

          • In reply to #177 by Zeuglodon:

            What we were talking about was the OP’s concern how very small changes (extreme gradualism) would become established. The answer is with extreme difficulty, so, as I first remarked, I have tried to concentrate on very small advantageous mutations, and only gone into theory when asked; for example your #69. I don’t seek sidetracking or technical difficulty.

            I agree with you entirely that a solution may involve less extreme/doctrinaire gradualism. A clearly advantageous change – like a 5% increase in beak length (which may be a 15+% increse in beak mass?) may quickly spread.

          • In reply to #179 by logicophilosophicus:

            In reply to #177 by Zeuglodon:

            What we were talking about was the OP’s concern how very small changes (extreme gradualism) would become established. The answer is with extreme difficulty, so, as I first remarked, I have tried to concentrate on very small advantageous mutations, and only gone into t…

            So I was misunderstanding you. I had been wondering. I apologize for not seeing your point sooner, and for the resulting detour in our discussion.

          • In reply to #180 by Zeuglodon:

            In reply to #179 by logicophilosophicus:

            It wasn’t a fruitless detour – for example I had to locate http://tuvalu.santafe.edu/~dirk/fluct/fluct.pdf which I have now catalogued as a resource. Also I should apologise for reacting with irritation (notably at #125) on the assumption, which I realise was hasty, that you were acting in concert. My mistake.

  57. Induced evolution can give us a compressed view of the process if that is what you are after. Small changes can have a large effect over time, like a lever used to raise a great weight over a large distance.

  58. In reply to #159 by Zeuglodon:

    A good example of what I’m talking about can also be found in The Ancestor’s Tale, in which Dawkins recounts the findings of a longitudinal study of the Galapagos finches conducted by Grant et al, which includes both measurements and genetic analyses and evidence for beak efficacy under certain conditions. A difference in beak size of half a millimetre is sufficient to power natural selection during droughts, also effecting reproductive success in the aftermath. Since a Galapagos finch measures just a few centimetres in length (about 10 to 20), that’s a difference of about 0.5% total body length and about 5% of total beak length. Not 1%, of course, but still quite a small difference.

    As with many examples the evolution and rates of spread of alleles depends on various factors in the habitat, plus the fertility, position in the food-chain, and survival rate of offspring, which are specific to particular species and environments..

    157 by Alan4discussion:
    Access by those with literary skills to academic papers and scientific terminology, does not confer understanding of the science. That requires study from basics upwards,

    Elaborate mathematical constructs about evolution are meaningless without a detailed understanding of the basis of the inputs. A basis which anyone without an in-depth understanding of the ecology in a specific habitat, would be unable to assess.

    My example of coral polyps is a good illustration.
    **If someone cannot tell the difference in survival potential between the sexually produced offspring (microscopic larva called a planulae,) of a single polyp, and a colony of hundreds, or does not understand the nature of the habitat(s), – they have no chance of producing any credible mathematics on evolutionary outcomes. **

    Lphil @145 – That, as I very carefully explained, is why I particularly confined my points to animal reproduction. The OP concerns evolution; (near-) identical clones make no contribution to evolution.

    http://en.wikipedia.org/wiki/Coral

    While the coral head is the familiar visual form of a single organism, it is actually a group of many individual, yet genetically identical, multicellular organisms known as polyps. Polyps are usually a few millimeters in diameter, and are formed by a layer of outer epithelium and inner jellylike tissue known as the mesoglea. They are radially symmetrical, with tentacles surrounding a central mouth, the only opening to the stomach or coelenteron, through which food is ingested and waste expelled.

    Lphil – I was interested, nay amazed, to read that one of the “Advantages of Asexual Reproduction [is that] The offspring has the same phenotype and genetic make up as the parent.” On this planet?

    Yet another of your embarrassing, bogus, erroneous sources. Still, you seem to have convinced Steve Hopker.

    Asexual

    Within a coral head, the genetically identical polyps reproduce asexually, either via gemmation (budding) or by longitudinal or transversal division, both shown in the photo of Orbicella annularis.

    Budding involves splitting a smaller polyp from an adult.[19] As the new polyp grows, it forms its body parts. The distance between the new and adult polyps grows, and with it, the coenosarc (the common body of the colony; see coral anatomy). Budding can be:

    • Intratentacular—from its oral discs, producing same-sized polyps within the ring of tentacles
    • Extratentacular—from its base, producing a smaller polyp

    Division forms two polyps each as large as the original. Longitudinal division begins when a polyp broadens and then divides its coelenteron, analogous to splitting a log along its length. The mouth also divides and new tentacles form. The two “new” polyps then generate their missing body parts and exoskeleton. Transversal division occurs when polyps and the exoskeleton divide transversally into two parts. This means one has the basal disc (bottom) and the other has the oral disc (top), similar to cutting the end off a log. The new polyps must separately generate the missing pieces.

    Asexual reproduction has several benefits for these sessile colonial organisms:[23]

    • Cloning allows high reproduction rates, supporting rapid habitat exploitation.
    • Modular growth allows biomass to increase without a corresponding decrease in surface-to-volume ratio.
    • Modular growth delays senescence, by allowing the clone-type to survive the loss of one or more modules.
    • New modules can replace dead modules, reducing clone-type mortality and preserving the colony’s territory.
    • Spreading the clone type to distant locations reduces clone-type mortality from localized threats.

    Colony division

    Whole colonies can reproduce asexually, forming two colonies with the same genotype.

    • Fission occurs in some corals, especially among the family Fungiidae, where the colony splits into two or more colonies during early developmental stages.
    • Bailout occurs when a single polyp abandons the colony and settles on a different substrate to create a new colony.
    • Fragmentation involves individuals broken from the colony during storms or other disruptions. The separated individuals can start new colonies.

    . . .

    Alan4discussion@68

    In reply to #67 by logicophilosophicus:

    The actual organisms (e.g. you) are off-shoots of that line: no animal ever passed on its own phenome or even its own genome to a descendant, just the genes (or half of them, anyway) from its inherited germ cells, and therefore any heritable changes are strictly sequestred in the germ line.

    Oh dear! Are you seeking knowledge or just generating arguments with your erroneous assertions?
    We all know that genomes are passed on from gene-pools in populations and not just from individuals in sexually reproducing organisms.

    I think that my question has now been answered -albeit in a round-about way with many verbose twists, turns, and denials!

    • In reply to #183 by Alan4discussion:

      In reply to #159 by Zeuglodon:

      Ah, another does-he-take-sugar comment. I’ll reply anyway, which will at least avoid accusations of ignoring you…

      If someone cannot tell the difference in evolutionary potential between the sexually produced offspring (benefiting from recombination) of a single polyp, and a colony of hundreds of clones (same old same old) he or she has no chance of producing any credible comments on the mathematics of evolutionary outcomes.

  59. Sadly, neither Darwin nor Wallace is around to wither before the storm of your refutation.

    Anyway, one point at a time. As a “biologist and an ecologist” you wrote:

    Learned behaviours – as distinct from instinctive inherited behaviours are not passed on genetically. They are not part of the phenome. They may be passed on as memes. (Why am I wasting my time correcting this Gish-Galloping rubbish?) The ignorant should ask questions rather than making foolish assertions.

    “Learned behaviours… are not part of the phenome… rubbish… ignorant… foolish…”

    That’s me told!

    I was relying on the rubbish emanating from ignorant fools like these (please note the properly pasted quote):

    http://www.stanford.edu/group/CCB/Pubs/paulpdfs/2003_EhrlichandFeldman_whatcreatesour.pdf

    “A central theme of the flood of literature in recent years in ‘evolutionary psychology’ and ‘behavioural genetics’ is that much or even most human behavior has been programmed into the human genome by natural selection. We show that this conclusion is without basis… In fact, information from twin studies, cross-fostering, sexual behavior and the Human Genome Project makes it abundantly clear that most interesting aspects of the human behavioral phenome are programmed into the brain by the environment.”

    Luckily for you, both these wannabes (pretending to be preeminent biologists/ecologists for 40 plus years) are still alive, so you can personally abuse them rather than looking for a whipping boy.

    • In reply to #186 by logicophilosophicus:

      Sadly, neither Darwin nor Wallace is around to wither before the storm of your refutation.

      Oh dear! Still name dropping as a badge of false authority, where you have simply misunderstood their writings!

      Why not just read about corals on comment 183, and correct your errors the way scientists do.

      Anyway, one point at a time. As a “biologist and an ecologist” you wrote:

      Learned behaviours – as distinct from instinctive inherited behaviours are not passed on genetically. They are not part of the phenome…

      That’s me told!

      I was relying on the rubbish emanating from ignorant fools like these (please note the properly pasted quote):

      http://www.stanford.edu/group/CCB/Pubs/paulpdfs/2003EhrlichandFeldmanwhatcreatesour.pdf

      “A central theme of the flood of literature in recent years in ‘evolutionary psychology’ and ‘behavioural genetics’ is that much or even most human behavior has been programmed into the human genome by natural selection.

      I see you have managed to cherry-pick an example which contradicts “the flood of literature” from other academic sources, – as to the proportions in nature v nurture. – This has been a controversial subject in psychology for decades. – I did not however, mention proportions of inherited v learned behaviour in my comment.

      We show that this conclusion is without basis… In fact, information from twin studies, cross-fostering, sexual behavior and the Human Genome Project makes it abundantly clear that most interesting aspects of the human behavioral phenome are programmed into the brain by the environment.”

      Which is exactly what my comment “as distinct from instinctive inherited behaviours“, pointed out! (“Most interesting” is of course a selective subjective judgement in separating inherited from learned behaviours.)

      The capacity for environmental programming is inherited in the human phenome, but the subsequent programming modifying the phenotype behaviour is not passed on except as memes – as I stated.

      • In reply to #188 by Alan4discussion:

        In reply to #186 by logicophilosophicus:

        Sadly, neither Darwin nor Wallace is around to wither before the storm of your refutation.

        Oh dear! Still name dropping as a badge of false authority, where you have simply misunderstood their writings!

        They explicitly stated that the Malthusian limit was the necessary basis for natural selection. In fact you even missed that in your OWN source on the Malthusian limit, which you claimed referred only to a catastrophic collapse of population:

        “Malthus himself did not subscribe to the notion that mankind was fated for a ‘catastrophe’ due to population overshooting resources. Rather, he believed that population growth was generally restricted by available resources” (From A4D’s link – which claims to go to “Malthusian Limit” but actually goes to “Malthusian Catastrophe”.)

        You say I “managed to cherry-pick” one example of biologists stating that behaviour is part of the phenome. I had already cited two examples at #125.

        Since it would breach the Moderators’ strictures to draw any personal conclusions from the fact that both your statements are untrue, we’ll just have to leave it as a mystery.

        • In reply to #189 by logicophilosophicus:

          In reply to #188 by Alan4discussion:

          In reply to #186 by logicophilosophicus:

          Sadly, neither Darwin nor Wallace is around to wither before the storm of your refutation.

          Oh dear! Still name dropping as a badge of false authority, where you have simply misunderstood their writings!

          They explicitly stated that the Malthusian limit was the necessary basis for natural selection. In fact you even missed that in your OWN source on the Malthusian limit, which you claimed referred only to a catastrophic collapse of population:

          My comment clearly explained the limit, in balance, and the catastrophic run-away effects of imbalance.

          Of course it is when resource depletion is a limiting factor in what is basically a closed ecosystem.

          Coral reefs are not such a closed system. They have huge external resource inputs.

          “Malthus himself did not subscribe to the notion that mankind was fated for a ‘catastrophe’ due to population overshooting resources.

          The discussion was about animals in ecosystems, not mankind’s global abuse of the planet’s limited resources, which is an individual special case.

          Rather, he believed that population growth was generally restricted by available resources”

          It is where resources are the limiting factor, but many other factors are involved, so particular species may never reach that limit.

          The limit applies to the whole ecosystem, rather than individual species within it, although some may only be able to access particular resources, thus having an individual lower limit.

          Often resources become the limiting factor when other population restraints are restricted or removed (such as if predation of the potentially expanding population is holding the numbers in a fluctuating balance),.

          For example where predatory carnivores are removed from an isolated ecosystem, the herbivore population expands, overgrazing and reducing the vegetation, usually with an associated increase in disease, as crowding and starvation take effect. The herbivore population then crashes to well below the initial balanced level, until their food-chain recovers. This is very basic ecology. They have recently reintroduced wolves into Yellowstone to correct that sort of problem.

          (From A4D’s link – which claims to go to “Malthusian Limit” but actually goes to “Malthusian Catastrophe”.)

          My comment clearly explained the limit, in balance, and the catastrophic run-away effects of imbalance.

          The understanding of details of evolution of particular species and ecosystems, has, as a result of 100 years+ of research, moved on since the time of Malthus, Wallace and Darwin.

          Coral populations are always kept in balance by storm damage to reefs, competition with other coral species, and predation by reef fish etc. They may also be substantially reduced by environmental changes such as temperature. Coral reefs are one of the most productive ecosystems on the planet. They are resourced from oceans which are vastly larger than the areas of coral and they are also symbiotically resourced by sunlight.

          Malthusian resource limits, are generally irrelevant to the competitive colonisation by corals in the constantly changing environment of coasts, but may have effects of restricting more mature populations in local areas, where there is competition for space to grow.

          The evolutionary advantages of sexually reproduced offspring from asexually reproduced colonies of hundreds, compared to single polyps, in the recolonisation storm damaged reefs, or newly exposed rock, should be obvious.

          It is** very clearly explained** @183 and its link.

          Your problem in understanding is that you try to apply extreme and special situations, to the generality of ecosystems and life processes. Clearly by a lack of knowledge of the bigger picture. It is a common problem for those whose concepts of evolution are generally focussed on humans, rather than the full spectrum of life.

        • In reply to #189 by logicophilosophicus:

          You say I “managed to cherry-pick” one example of biologists stating that behaviour is part of the phenome. I had already cited two examples at #125.

          First of all these appear to be psychologists rather than biologists. They also in your quote, selectively pick (eg. sexual) features.

          There is in nature if not in studies, clearly a boundary between ephemeral features of the individual, such as posture, thoughts, and behaviour, – and what is generally considered to be an integral part of the inherited expression of the phenome.

          As I pointed out earlier there is also a long standing psychological debate as to the location of boundaries between instinctive inherited behaviour, and learned or environmentally (external) conditioned behaviour.
          I would suggest that any behaviour which can be changed, is ephemeral, rather than integral.

          I have in an earlier comment pointed out, that in your claim that phemomes are not passed from parent to offspring, you are very marginally correct in regard to a tiny percentage of the phenotype featured in some cases, but substantially wrong as most or all of the phenome is passed on in asexual reproduction in some species. (- for which I quoted the example of corals.)

          (In the case of vertebrate sexual reproduction, the genetic expression of the phenomes usually comes from a mix from both parents, – and that programmability is inherited.. – I also have already commented on phenotype plasticity. )
          In sexual reproduction the percentage or environmental modification of gene expression is also very tiny in comparison to the inherited component.

          • In reply to #191 by Alan4discussion:

            In reply to #189 by logicophilosophicus:

            You say I “managed to cherry-pick” one example of biologists stating that behaviour is part of the phenome. I had already cited two examples at #125.

            First of all these appear to be psychologists rather than biologists.

            You are “a biologist and an ecologist” and you think Paul Ehrlich and Marcus Feldman are psychologists? No further comment required.

  60. Moderators’ message

    Will all users please make a conscious effort to keep their comments non-aggressive and non-hostile to other users. Robust disagreement is welcome, but please keep it civil and avoid personal remarks.

    Thank you.

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  61. In reply to #192 by Alan4discussion:

    In reply to #185 by Alan4discussion:

    Malthusian limits are and always were fundamental to Darwinism:

    This is totally irrelevant to the coral issue, for habitat reasons which I have already explained!

    I think I have indulged the side-track into Malthusian limits sufficiently.

    A bit patronising, there. Re-read #169. Your two attempts at a get-out-of-jail-free card are

    1) Deny that Malthus was crucial to Darwin/Wallace – and claim that he is irrelevant to modern neodarwinism. (That pretty well proves you have never read, for example, the seminal works by R.A.Fisher, since the “Malthusian Parameter” could hardly have escaped your notice.)

    2) Claim that limited resources are only characteristic of “special unrealistic situations” and therefore irrelevant to evolution.

    Wrong.

    • In reply to #194 by logicophilosophicus:

      Malthusian limits are and always were fundamental to Darwinism:

      This is totally irrelevant to the coral issue, for habitat reasons which I have already explained!

      I should emphasise that your claim that there is competition in an evolutionary sense in the absence of this Malthusian threat to survival is completely at odds with evolutionary theory: all life evolves by the differential survival of replicating entities.

      • In reply to #195 by logicophilosophicus:

        If you can’t or won’t understand my comments explanations or read and understand the links I have provided, or the materials you claim to be citing, I am wasting my time discussing the matter further.

        I have already addressed your fallacious appeals to inappropriate and false authority.

        As I said earlier, your lack of any scientific credentials or knowledge of biology, is only too obvious. Comment 183 is quite specific and decisive, with my comments 190 and 192 dealing with the Malthusian issues. Your subsequent misquoting of my position on this @193 and @194, demonstrates that you are incapable of understanding basic ecology, and simply do not understand evolutionary processes.

        Your ignorant trolling is adding nothing to scientific knowledge for readers here!

        I am not interested in playing silly point-scoring games, so have nothing further to say on the subject.

        • In reply to #196 by Alan4discussion:

          In reply to #195 by logicophilosophicus:

          If you can’t or won’t understand my comments explanations or read and understand the links I have provided…

          The links you have provided…

          You complain that I rely on “False authority…” I’ll see your Buzzle + Wikipedia and raise you Malthus + Darwin + Wallace + Fisher + Haldane + Ehrlich + Feldman + Dawkins + …

          You previously jeeringly accused me of ignoring #86, which I pointed out was not addressed to me. Now you do exactly the same re #183, which was not addressed to me.

          The OP suggested there might be a problem with the fixation of very tiny genetic advantages. I noticed that no one here understood that this is a real problem, and commented. There are formulae for calculating the rate of evolutionary change, which you are unfamiliar with: this is clear because you deny the relevance of Malthus although all such formulae involve a Malthusian Parameter; also because you show no awareness of the key fact that evolution is primarily driven by INTRASPECIFIC competition for limited resources between different genetic strains. Instead you insist that apart from “special unrealistic situations” resources are unlimited, and yet there is some kind of competition (for what?) among genetic clones.

          You repeat your ad hom jeer (since this is not an argument for against any point made) that my “lack of any scientific credentials or knowledge of biology, is only too obvious.” Re knowledge, see for example the previous paragraph. Re credentials, I will remind you of this paragraph from a posting I made on another occasion:

          @Alan4Discussion: Well, I asked first, so here’s the deal: short CV. Real name, dates, places; education, qualifications, career history and any other relevant verifiable background or expertise. You first, and I guarantee to do the same immediately after your CV is posted. You have my solemn affirmation on this.

          You could have cleared the matter up in hours. You chose not to. The offer still stands – surely you have nothing to be afraid of.

          Your allegedly “specific and decisive” #183 is mainly a long cut-and-paste job from a Wikipedia article (the best part of 1,000 words, I guess), your usual authority-of-choice. Pasting is all very well, but cutting is by its nature selective. I had claimed that clones are, in evolutionary terms, basically extensions of a single individual (#125: and note the reference there to planarians – I was well aware that some lower animals can clone long before you allegedly proved my ignorance of this with your coral example).

          While the coral head is the familiar visual form of a single organism, it is actually a group of many individual, yet genetically identical, multicellular organisms known as polyps.

          That’s in your pasted extract. But what is an individual organism? This seems reasonable, taken from PubMed:

          Most biologists implicitly define an individual organism as “one genome in one body.” This definition is based on physiological and genetic criteria, but it is problematic for colonial organisms.

          Problematic, in genetic/evolutionary terms, because there is effectively only a single genome in, say, a coral colony. But also problematic in physiological terms, as in this paragraph from your chosen article which you chose not to include in your big cut-and-paste job:

          The polyps interconnect by a complex and well-developed system of gastrovascular canals, allowing significant sharing of nutrients and symbiotes. In soft corals, these range in size from 50–500 micrometres (0.0020–0.020 in) in diameter, and allow transport of both metabolites and cellular components.

          Of course, being a Wikipedia page, certain precautions are necessary: the reader should check the Talk and History tabs. This article has been given “Good Article” status by Wikipedia – that’s two grades below “definitive” on their scale. Why would a biologist use this as an authority?

          More to the point, these lengthy and repetitive perorations on coral have nothing whatsoever to do with the OP, and precious little to do with anything anyone else, including myself, has posted here.

          • In reply to #197 by logicophilosophicus:

            @196 If you can’t or won’t understand my comments, explanations, or read and understand the links I have provided, or the materials you claim to be citing, I am wasting my time discussing the matter further.

            I have already addressed your fallacious appeals to inappropriate and false authority.

            You complain that I rely on “False authority…” I’ll see your Buzzle + Wikipedia and raise you Malthus + Darwin + Wallace + Fisher + Haldane + Ehrlich + Feldman + Dawkins + .

            . + Duane Gish!!

            @196 -Your ignorant trolling is adding nothing to scientific knowledge for readers here!

            I am not interested in playing silly point-scoring games, so have nothing further to say on the subject.

  62. Say, for example, a bunch of monkeys climbed down from the trees and started walking on two feet. their skin, under their fur, is white.
    since white skin is more suseptible to skin cancer, then individuals with darker skin would survive longer– and breed more– than their whiter cousins.
    eventually this should lead to a whole branch of that species having dark skin.

    where they get big dicks and musical/dancing ability from; I don’t know

  63. in reply to Alan4discussion:

    fallacious appeals… Ignorant trolling… Duane Gish… false authority

    To avoid repeating myself, I demonstrated the immensity of the gulf between your insulting claims and the embarrassing reality here:

    http://www.richarddawkins.net/discussions/2013/4/4/evolution (see post #254 in that discussion)

    I notice your interest in scoring points stopped at the convenient point where you could ignore questions posed, such as how a self-proclaimed “biologist” discussing the mathematics of evolution has apparently never heard of the Malthusian Parameter, or how a self-proclaimed “ecologist” has apparently never heard of the author of probably the most well known ecological best-seller of all time, outselling even “The Silent Spring”. I first read Ehrlich’s “The Population Bomb” over 40 years ago – I still have that copy.

    You must realise that these matters undermine every point you have tried to make here. I urge you to reestablish your credibility by demonstrating your credentials as suggested:

    @Alan4Discussion: Well, I asked first, so here’s the deal: short CV. Real name, dates, places; education, qualifications, career history and any other relevant verifiable background or expertise. You first, and I guarantee to do the same immediately after your CV is posted. You have my solemn affirmation on this.

  64. The question:

    If the individual mutations are so small, however, how can any of them actually contribute to the survivability or selection of the organism?

    The answer:

    I think that the usual way to understand biological evolution is wrong :

    (1)
    First, Evolution is a fact than you can view whit your eyes in a “short period of time”: all animals and plants of farms are very different that their ancestors of ten thousands years ago, and it is very simply of understand: if for some reasons (in this case the human decision) the cow that makes more milk have more children, and this characteristic pass to the children, after many years you can have cows than produce a big amount of milk -the modern cows-)

    (2)
    An organism can survive due any reasons, and probably the 99% of mutations do not contribute to its survivality.
    But the mutations pass to the children, and they propagate them.

    (3)
    THE CAUSE OF SUCCESS IS A COMBINATION OF FACTORS, and a single mutation is only a passenger in this combination of factors, and the mutation is propagated BECAUSE the success (just the opposite of the usual way of thinking about this)

    (4)
    If the mutation contribute to an improvement of survivability, the mutation will be pass.
    But surely this kind of event is rare.
    And mutations are in 99,99999% irrelevants to survivality.

    (5)
    Individuals have an improvement of survivability DUE combination of factors.
    And THEN the mutations will be pass (traveling like passenger into this combination of factors).

    (6)
    If you think about that, and you are a mutation in a succesful individual into a successful group, your best way to propagate is to be a very little mutation, irrelevant, and do not cause a big change in the individual

    (7)
    The cause of success of an organism is a combination of factors
    Change happen.
    New combinations of factors happen.
    Some combinations of factors are more successful.
    Change pass to descendant.
    And a lot of little changes make a big change.
    The mutation is only a little passenger in this process.

    (8)
    The initial question again:
    “If the individual mutations are so small, however, how can any of them actually contribute to the survivability or selection of the organism? “

    (9)
    THE ANSWER:
    A single mutation do not contribute to survivability.
    The best way to “survive” if you are a mutation, is to be a very little mutation and do not affect the individual where you are.
    If you are lucky, and you are into a combination of factors that all togheter contribute to improve survivability, then you will be a successful mutation.
    The mutation only cause little changes in descendants.
    The mutation is the cause of little changes
    The acumulation of little changes (in all directions) cause new “combination of factos” (of all types).
    And some combinations of factors will propagate more than others.
    And the mutation will be propagate “into-the-combination”

    MORE INTELLIGENT ANSWER:
    At first, mutations are neccesary for change.
    But when exists a lot of “of-factors” the main way of new changes are “new combination of factors”
    And this cause the evolution (continuos new combinations in all directions, and the propagation of the more successful of them).
    And it happen also in the “cultural world of ideas”.

    Best regards
    LeoCano

  65. I think the stress on “tiny changes” via mutation is often grossly misunderstood. Remember that every organism has a large part of its genetic program devoted to instructions once active in its ancestors, but no longer in use. A very common mutation is a tiny one that changes “skip this section of code” to “read this section of code.”

    So, for example, human primate ancestors were almost certainly hairier than we are. But the instructions for making a coat of fur is almost certainly still in our genome (among what people mistakenly call the “junk DNA”). So, 10,000 years from now, if there is another ice age, and if a “tiny” mutation occurs that reactivates the “furry” genes in an individual, her descendants very well might enjoy a rather large adaptive advantage. A rather large change may result from such “tiny” mutations.

    • In reply to #202 by robbower:

      I think the stress on “tiny changes” via mutation is often grossly misunderstood.

      You are right that reactivation of disused genes is important, but it is not relevant here because the original supposed small-effect genes each needed to become fixed in the first place – the point at issue – before deactivation. (Also, you implicitly assume that a set of genes affecting a single trait may somehow be reactivated simultaneously, though that is less relevant.)

  66. I would suggest that any mutation capable of affecting an organism’s “fitness” (ability to survive find a mate and reproduce) does in fact have a detectable affect on the organism’s physical characteristics (its phenotype) – at least in principle. It may not be as obvious as an extra finger, but if one organism is making a selection from a group of very similar potential mates, then even very small differences in appearance, speed, behaviour etc. may cause significant differences in “fitness” – and hence the future success of a given mutation in the gene pool.

    So my main point is: small changes in phenotype that may be difficult to detect can have a very definite effect on fitness. (I’m mainly disagreeing with the premise that these changes are not detectable).

    The changes in phenotype that result from the immense accumulation of small changes from generation to generation hardly need any form of detection.

    • In reply to #204 by PaulDKirby:

      I would suggest that any mutation capable of affecting an organism’s “fitness” (ability to survive find a mate and reproduce) does in fact have a detectable affect on the organism’s physical characteristics (its phenotype) – at least in principle.

      That’s undeniable but needs quantification. An “ultragradualist” assumption might be, e.g., that if modern giraffes are 3m taller than their ancestors 3 million generations ago, then giraffes have benefited from 1 micron of increased height per generation. Certainly R. A. Fisher’s approach was along those lines. Such a tiny hint of an advantage would almost certainly be lost due to simple probability: “It is important to note, however, that the impact of genetic drift is not limited to neutral mutations. Because of genetic drift, most advantageous mutations are eventually lost, whereas some weakly deleterious mutations may become fixed.” [Emphasis added. Duret, 2008, Nature.]

      It seems on that simple approach that lucky leaps – “saltations” (not necessarily big ones) – may have been required.

    • In reply to #204 by PaulDKirby:

      I would suggest that any mutation capable of affecting an organism’s “fitness” (ability to survive find a mate and reproduce) does in fact have a detectable affect on the organism’s physical characteristics (its phenotype) – at least in principle.

      It can do but may be neutral . Quite often these sorts of changes are determined by genes controlling growth rates, timings or development of particular features. Things like fertility can be important.
      Immediately advantageous mutant genes are less likely to spread rapidly in a organism which produces one offspring every two years, than in organisms which produce thousands of offspring on a regular basis.

      If you want to see reliable science on this, I would suggest you have a look at some of the earlier posts on this discussion, and also bear in mind my more recent comments regarding the reliability of some postings here.

      I would also suggest looking at this thread which describes some of the pitfalls of internet discussions.

      @ robbower – likewise.

      BTW: If you are interested in “Malthusian Limits”, you could always read my detailed descriptions @190, @185, @183, @181, @176, @171, and earlier,. of the limiting factors relevant to the competitive establishment of coral populations in the context of potential competition between asexually expanded colonies and single polyps in their ecosystems.

      I have ceased explaining them to those who could not recognise the details of those limits when I explained them in earlier postings, but instead like to pretend that I, as an ecologist, cannot understand these fundamentals of ecology! It is a feature of the Dunning-Kruger effect, which I linked earlier.

      • In reply to #206 by Alan4discussion:

        Well now, we’re back to the third person, does-he-take-sugar approach, one of the numerous repetitive ways in which you break the Golden Rule of Netiquette. But then, you break it so many times. Glance back at your posts which you recommend for “detailed descriptions of limiting factors relevant to the competitive establishment of coral populations”, starting with #171: “Oh! dear! You still can’t understand BASIC biological terminlogy… school-book biology – learn some!!! …no scientific credentials… silly… no comprehension of basic biology… You just made that up… silly and unsupported assertions… ignorance… ridiculous… Even when I give you links to science you look through bias-blinkers and can’t or won’t understand them, so simply make up ludicrous contrived contradictions… You just keep making up these ridiculous assertions… you sit in the asserted ignorance of denial and irreducible-incredulity.” That was one of your more restrained efforts, with only around 20 jeers/insults. Your next (#176) is more characteristic: “Ha! ha! ha! Falsely citing… ignorance… comical fallacy!! Your demonstrated ignorance of school-book-level biology, and inability to understand simple scientific explanations, shows you have not even started your lessons in biology yet! – Indeed your posts indicate that your education lessons in biology ended before they started… Rubbish! …yet another red-herring which shows you have no idea what you are talking about, but keep throwing in diversionary false authority claims for nonsense… You just keep making up clueless assertions, which illustrate your lack of understanding of the subject! Scientists seek the facts and retract and correct their mistakes. Denier-trolls filled with Dunning-Kruger confidence – just keep on making up silly unevidenced assertions, and then dogmatically go through semantic contortions, trying to defend the indefensible! Science and nature do not care if you sit in troll-denial-ignorance and argue the hind legs off a donkey! They will continue to work as normal unaffected by your ignorance!” Hundreds of words of abusive jeering in posts you claim to be about “Malthusian limits” but which in fact deny the major relevance of limited resources to evolution, claiming that the expansion of corals by asexual propagation into virgin territory with unIimited resources is more representative of evolution. You exclaim:

        I have ceased explaining them [the limits] to those who could not recognise the details of those limits when I explained them in earlier postings, but instead like to pretend that I, as an ecologist, cannot understand these fundamentals of ecology! It is a feature of the Dunning-Kruger effect, which I linked earlier.

        However, you give a link describing “some of the pitfalls of internet discussions”. In fact the link describes only one pitfall of online discussion, and that is the problem of “fractious… uncivil… ad hominem comments” – in a word, abuse:

        The online content director for PopularScience.com announced Tuesday that the website will no longer accept comments on new articles, saying a small but vocal minority of “shrill, boorish specimens of the lower Internet phyla” were ruining it for everyone else.

        Your comment on those who “like to pretend that I, as an ecologist, cannot understand these fundamentals of ecology!” recalls that recent unexplained mystery when you did not recognise the name Paul Ehrlich:

        http://wiki.answers.com/Q/Who_is_the_most_famous_ecologist

        But my particular reason for bothering to answer your post is that I am fed up to the back teeth of this “Dunning-Kruger” business. “The Dunning-Kruger Effect” has a nice, scientific ring to it. Back in the 1990′s D & K, as university psychologists do, looked for a piece of research which cold be done using their university’s students. I’ve been involved in such cheap and cheerful research myself. They asked students who had done an exam to rate their performance on a percentile basis. Surprise, surprise, the lowest performing students were not good at this; yet nor were the highest performing. D & K suggested an explanation: “the miscalibration of the incompetent stems from an error about the self, whereas the miscalibration of the highly competent stems from an error about others”. Where most psychologists would diagnose boring old regression to the mean, Dunning and Kruger had sorted human beings into (at least) two cognitively distinct tribes: the thick kids understood the bright kids’ cognitive processes (but not their own); the bright kids were incapable of understanding the thick kids’ shortcomings… Also notice that the researchers were not analysing voluntary assessments from students who believed themselves competent to judge, but assessments from students put on the spot.

        This is from the abstract of the Dunning-Kruger paper:

        Across 4 studies, the authors found that participants scoring in the bottom quartile on tests of humor, grammar, and logic grossly overestimated their test performance and ability. Although their test scores put them in the 12th percentile, they estimated themselves to be in the 62nd.

        Students who were actually outscored by 7/8 of their peers guessed that they were only outscored by 1/3… hardly delusions of grandeur. (In my experience, students who are outscored by 7/8 of their peers have problems with any academic task.)

        And “humour, grammar, and logic”? What relevance has that to science? And, more intriguingly, where do you rate yourself on “humor, grammar, and logic”?

        Meanwhile, you owe it to yourself to lay the ghost (see #200). It is open to you to prove (you can, can’t you?) that you have scientific qualifications and that I have none.

  67. Hey, all!

    OP here. Man, this thread certainly ended up going on a lot longer (and stranger) than I originally anticipated…

    I just wanted to thank everybody who provided me with thoughtful responses instead of just chastising me for not having already read (and understood) all the books that Prof. Dawkins has written on the subject. I have learned a lot from the responses, and have actually been inspired to buy some of the aforementioned books. I’m currently halfway through “The Greatest Show on Earth” and have “The Blind Watchmaker”, “Climbing Mount Improbable” and “The Selfish Gene” queued up on my bookshelf. Some of it is still hard for me to grasp, but the information discussed in this thread has actually given me a better framework to understand it all.

    • In reply to #208 by godzillatemple:

      I’m currently halfway through “The Greatest Show on Earth” and have “The Blind Watchmaker”, “Climbing Mount Improbable” and “The Selfish Gene” queued up on my bookshelf. Some of it is still hard for me to grasp, but the information discussed in this thread has actually given me a better framework to understand it all.

      Hi GZT,

      Once you’ve read these books, you’ll have a far better understanding of the depth & breadth of the mechanisms & consequences of Evolution by Natural selection. Then you’ll be ready for some more excellent books that explore many other fascinating avenues on the subject….

      Then you’ll be ready to re-read these books and find deeper layers of understanding – you won’t get them all on the first couple of readings….

      Enjoy your journey of wonder, and afterwards you will have been greatly enlightened by reality as best we understand it so far…. 8-) Mac.

  68. It takes ages for ONE event to occur, so you’d have to watch the whole of one species for a really long time to see any ‘eureka’-style mega-win mutations. That’s why you can’t watch it, it’s not likely you’ll ever see one of the chance events. But if you’re willing to try, sit near an ante natal clinic (human) and wait for a new variant. It’ll be easier than another species, but good luck spotting one all the same. If they breed prodigiously, then there you go. If they fail and die, then there you go. Evolution in action! (it’s far more fascinating retrospectively)

    • In reply to #209 by toby.worth:

      It takes ages for ONE event to occur, so you’d have to watch the whole of one species for a really long time to see any ‘eureka’-style mega-win mutations. That’s why you can’t watch it, it’s not likely you’ll ever see one of the chance events…

      I think you may have misunderstood my original question.

      I understand that individual mutations are very hard to detect. And I also understand that these very slight mutations can, over time, aggregate until they do become much easier to detect (your “mega-win” mutation). What I was having trouble with was how such slight mutations could really have an effect on an organism’s survivability and/or chance of mating if they are, in fact, too slight to detect.

      Thanks to many of the helpful posts in this thread, however, I have now come to see how my fundamental understanding of the entire process was flawed. I’m sure I still don’t have it down perfectly (which is why I’m continuing to read up on the subject), but I now believe I have the gist of it, to wit:

      1. Small mutations are occurring all the time. Those that are not grossly harmful get passed along to future generations, which leads to diversity within a species. As long as the environment doesn’t change, however, these variations get dampened down and the species as a whole remains largely unchanged. This is why we have so-called “living fossils” in places where the environment has not changed noticeably for millions of years.

      2. Once a change in the environment occurs, however (whether because the environment itself changes or members of a species move to a different environment), those variations (which have been built up over many years due to many slight mutations) can get selected for and against. A variation that previously had no effect on survivability suddenly becomes crucial to survival (or, conversely, detrimental to survival). As a result, a relatively sudden and dramatic change may occur in the species as a whole as what was once a trivial difference literally becomes a matter of life or death.

      So it’s probably not the case that a mutation causes a particular bird’s beak to be one millimeter longer or a deer to have 1% more muscle mass and, as a result, that bird or deer has a better chance of living to pass on its genes. Instead, it is likely that a good deal of variety exists within the bird or deer population with respect to beak length or muscle mass due to many, many generations of small mutations that have been shuffled back and forth among the population. And then, let’s say, the flowers that the birds typically feed off of are all killed off by a blight and the only other flowers that are available for feeding upon require a longer beak than that possessed by the average member of the bird species. Or a new, slightly faster, predator is introduced to the deer’s environment. In this case, those who have the longer beaks or more muscle mass survive and those that don’t die off, leaving only the long beak or higher muscle mass gene to propagate.

      Or, to be more succinct, small mutations by themselves don’t really affect the survivability of an organism. Instead, small mutations accumulate in the gene pool until they are significant enough to be selected for or against by a change in environment.

      Hopefully, I’ve got that more or less right…

  69. We can see evolution happening and you must know this if you have studied the subject.

    Some examples: antibiotic resistance, Lrnski’s E. coli acquiring the ability to transport citrate across the cell membrane in an oxygen rich environment. If you want more examples then Google.

  70. Answering part of the initial post, survivability seems largely random in many cases. For instance, if two men come face to face with a Sabre Toothed Tiger, it won’t matter much that one has longer legs or one has sharper eyesight…they will both have to just run and which one gets eaten will be pretty much down to chance. Most real survival situations will be like this.

    • In reply to #212 by NordicAnna:

      Answering part of the initial post, survivability seems largely random in many cases…

      I agree, which is why I was having trouble accepting the idea that a very slight mutation could really have much of an impact on an an organism’s survival. But, as I discussed above, I think I now understand that slight mutations really don’t affect survivability until (a) they have a chance to accumulate to the point where they can have a noticeable effect and (b) there is a change in the environment which selects for or against that effect.

    • In reply to #212 by NordicAnna:

      Answering part of the initial post, survivability seems largely random in many cases.

      Remember that it is survivability of genes, not individual organisms. Producing a greater number of surviving copies is a major advantage. This is a major non-random factor in the number of offspring produced and the competitive survival of these. There will be other factors in survival, such as if a mutation is riding along on a gene with a positive survival trait. Also if a gene is dominant it is immediately subject to selection, whereas a recessive gene may be hidden from the effects of selection for generations.

      For instance, if two men come face to face with a Sabre Toothed Tiger, it won’t matter much that one has longer legs or one has sharper eyesight…they will both have to just run and which one gets eaten will be pretty much down to chance.

      Either of these traits could give advantage over individuals lacking them. The one with better eyesight would be much more likely to spot the threat at a distance and take early evasive action, and would also be a more successful hunter.

      Most real survival situations will be like this.

      It is more likely that counter balancing traits will not occur in such situations.

  71. Regarding the OP, when organisms are in a stable natural environment, there is very little evolutionary change even over long periods of time. Evolution occurs far more rapidly when a species finds itself in an altered environment. Here’s an exaggerated thought experiment:

    Imagine some members of a species of birds somehow find themselves on an island far from their natural home (doesn’t matter how). There are nuts to eat on the island, but they’re hard to open. One bird has a beak strong enough to open 10% of the nuts, whereas another very slightly stronger bird can open 12%. Importantly, the two birds are alive at the same time and this difference is due to variation within the same generation. If there were competition for the nuts, perhaps due to a poor harvest, which bird will more likely survive? The stronger bird has 20% more nuts available to it. In the next generation, then, the children are likely to inherit the slightly stronger beak, pushing the average beak-strength up just a little, thus changing the probability distribution of beak-strengths. So on to the next generation, where some offspring will be able to open 13% of the nuts.

    There are a couple of other interesting points. Strength may not be the only way to crack the nuts; some birds may just happen to be good at finding the nuts’ weakest point, again something that will be inherited by the offspring of these individuals. Another point is that the tree species now has another animal taking it’s nuts. If the birds’ consumption is significant, the trees will naturally be selected for those producing tougher nut cases. Thus the birds and trees will enter an evolutionary arms race.

    • In reply to #216 by Reason Saves:

      Importantly, the two birds are alive at the same time and this difference is due to variation within the same generation.

      Yes, I’ve come to realize that this is the key bit of information I was missing and it really does make all the difference. It’s not that a small change directly leads to an organism’s survival (or lack thereof). It’s that every species already has significant variation among its members due to small changes that have accumulated over time and it’s those larger-scale variations that contribute to (or detract from) survival when the environment changes.

      In your example, it’s not the case that a bird is born one day who can open 20% of the nuts compared to all the other birds who can only open 10% of the nuts. Instead, the species is comprised of a wide variety of birds with various abilities to open nuts — some can only open 5%, some can open 10%, some can open 15%, some can open 20%, etc. As long as nuts are plentiful, all the birds are able to open enough nuts to survive and pass on their genes and the various “nut opening” genes continue to be randomly distributed among the members of the species. But if there is suddenly a scarcity of nuts for some reason (or the existing nuts become harder to open), then suddenly those birds who can open 20% will have a huge advantage over those who can’t and they will be much more likely to survive to pass along their genes.

      Wash, rinse and repeat, but this time with the genes determining how well the birds can resist a particular disease, the genes determining how fast the birds can fly, the genes determining how well the birds can blend in with their surroundings, etc., etc., etc., and pretty soon we’ll have an entirely new species!

  72. Peter and Rosemary Grant have done an excellent work on Galapagos Finches that illuminates what you are asking. In short they have shown that a specific species responds very quickly to changes in the environment. Beak size abruptly enlarged from one generation to the next because of a drought that caused a strong selection on plants to produce larger and harder seeds. Ten years later beak size got smaller as a response to the invasion of a larger bird-species.

  73. One word answer, in my opinion, is ‘probability’. A minor mutation does not guarantee anything. There must be many times in the history of evolution that a mutation conveying a genuine advantage fails. The pint is that the gene always (in given circumstances) conveys an increased probability of reproduction so, over a long time, and in a large population, that gene will be selected for.

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