Jonathan McLatchie still doesn’t understand Dembski’s argument

Over at Uncommon Descent, Jonathan McLatchie calls attention to an interview that Scottish Christian apologist David Robertson did with him.  The 15-minute video is available there.

The issue is scientific evidence for intelligent design.  As so often occurs, they very quickly ran off to the origin of life, and from there to the origin of the Universe.  I was amused that from there they tried to answer the question of where God came from, by saying that it was unreasonable to push the origin issue quite that far back.  There was also a lot of time spent being unhappy with the idea of a multiverse.

But for me the interesting bit was toward the beginning, where McLatchie argues that the evidence for ID is the observation of Specified Complexity, which he defines as complex patterns that conform to a prespecified pattern.  He’s made that argument before, in a 2-minute-long video in a series on 1-minute apologetics.  And I’ve complained about it before here.  Perhaps he was just constrained by the time limit, and would have done a better job if he had more than 2 minutes.

Nope.  It’s the same argument.

His Specified Complexity argument is William Dembski’s pre-2005 argument.  It turned out that the argument required a conservation law to show that natural selection could not put this Specified Complexity into the genome.  Dembski did have such an argument, but it turned out not to work (see my 2007 article for the details).

In 2005-2006 Dembski changed the argument, by redefining Specified Complexity to have an additional condition.  Now you could only call a pattern Specified Complexity if it was not only complex and conformed to a prespecified pattern but also could not be brought about by natural evolutionary forces such as natural selection.  A number of people here and at Panda’s Thumb pointed out that this fails to show us how this condition is to be evaluated.  It makes SC something that comes in after one has somehow decided that an adaptation cannot have been achieved by natural selection.  In short, it has been safeguarded against the criticism that evolution could bring about SC by defining the issue away.  That makes SC a useless criterion.

But McLatchie has somehow missed all this history.  He is back where Dembski was in the book No Free Lunch: Why Specified Complexity Cannot be Purchased Without Intelligence, published in 2002.  McLatchie has totally missed both the refutations of Dembski’s original criterion, and the 2005-2006 fix that rendered the SC criterion useless.  In spite of having 15 whole minutes to clean up the mess, McLatchie and Robertson preferred to spend the extra time back at the origin of the Universe.

480 thoughts on “Jonathan McLatchie still doesn’t understand Dembski’s argument

  1. Adapa: Not just everything we see, everything we could possibly see as well. The Designer already did it, we just haven’t found it yet!

    Science!

  2. keiths:

    He [phoodoo] actually thought this was the entire paper.

    Unbelievable.

    phoodoo:

    No, Actually what I thought was, THIS IS WHAT HE FUCKING POSTED.

    No, you followed Robin’s link, copied the abstract — you know, that thing with the word “Abstract” at the top — and posted it thinking it was the entire paper:

    So I posted the part that answered the question? Because I posted the entire paper.

    That’s why we’re laughing at you.

    Let me help you out, phoo:

    abstract
    noun
    ˈabˌstrakt/

    1.
    a summary of the contents of a book, article, or formal speech.
    “an abstract of his inaugural address”

  3. phoodoo: This is why Patricks claim that different frequencies is evolution.

    Is it why Patricks claim different frequencies evolution?

  4. phoodoo: Its the same bullshit as you. Post a link, claim it says what you say it does. Then expect people to find its relevance to what you want to say.

    What a bastard!

    phoodoo: and the full paper is pretty certainly going to be the same

    That’s more like it! You need the abstract to trash a paper, not just a link to it!

    Your double standards are showing phoodoo. I’m embarrassed for you!

  5. I’m not a huge fan of defining evolution in terms of change in allele frequency, but it is, nonetheless.

    Creationists (and others) imagine a simple fluctuation process when they hear the expression, but initial mutation and allele extinction are also change in allele frequency, at the extremes. Then again, trying to get across the evolutionary concept of ‘allele’, and its relation to recombination … sheesh.

  6. phoodoo: But that is a specious claim, because they are all just wolves with different expressions of their alleles.

    Such ignorance and gibberish. Are detached houses closer to semi detached houses or igloos, or are they all just dwellings?

  7. keiths,

    Remember onlookers, Phoodoo is REAL. He’s not a P-A-R-O-D-Y or hoax. He reads UD “for educational purposes”.

  8. Phoodoo’s lack of answer is very revealing. We can now safely conclude that his ID “theory” has been falsified.

  9. Allan Miller: Creationists (and others) imagine a simple fluctuation process when they hear the expression, but initial mutation and allele extinction are also change in allele frequency, at the extremes. Then again, trying to get across the evolutionary concept of ‘allele’, and its relation to recombination … sheesh.

    They often say that natural selection can only eliminate variation, not create anything new. If you have a population with most individuals being of genotype aa bb cc dd ee but rare alleles that are A, B, C, D, and E, there may be few individuals that are genotype AA bb cc dd ee, or aa BB cc dd ee, and so on, and no individuals at all who are AA bb CC dd ee (etc.) then increase of the allele frequencies of A, B, C, D, and E will actually cause new multilocus genotypes to appear.

    So creationists and ID advocates are wrong that no new genotypes are created. They just don’t believe in recombination.

  10. phoodoo:
    Robin,

    The part of the paper that you referenced is useless (and the full paper is pretty certainly going to be the same) for the reasons I have been explaining.

    You haven’t explained anything. You haven’t referenced one quote from the abstract, let alone commented on anything actually noted in the paper as a whole, to demonstrate it’s useless.

    But in assuming that it’s useless, you do demonstrate the vacuousness of your position. You are effectively waving your hands and complaining that forensic science is “useless” because in your opinion (which appears to be all you are referencing) there’s no way to tell the relative relatedness of parents, grandparents, siblings, and cousins, which is just absurd on your part. You then continue (by analogy) to insist there’s no way to tell one’s relative relatedness to their European or African or Asian ancestry, which is equally absurd. But the kicker is, when someone actually provides you the basic methodology and the chemical and biological analysis, you get all butt-hurt rather than actually point out how the methodology, chemical, or biological analysis is wrong.

    So really Phoodoo…unless you have something constructive to your point to offer from the abstract or from the paper as a whole, basically all your whining amounts to is “I like ID because like masturbation, it makes me feel good.” Whatever…

    If you looked atdogs from around the world, you can also claim that one type of dog is more closely related to one than another.

    Absolutely. Here:

    http://www.dogbehaviorblog.com/2010/04/dog-breeds-and-genetic-relatedness.html

    But that’s not what you asked earlier. As I noted in reply upstream, St Bernards and Pekinese are likely equally related to wolves as both split off from wolves at roughly the same time, so they likely have the same genetic differences from wolves.* But there plenty of breeds that show closer relatedness to wolves than others. Why would you even think this wasn’t the case?

    But that is a specious claim, because they are all just wolves with different expressions of their alleles.

    This is just plainly false. Why not actually make an effort and look it up instead of just tossing out your obviously absurd opinions? If you’re so sure that evolution is nonsense, why not actually go and demonstrate how the current research is wrong?

    This is why Patricks claim that different frequencies is evolution.

    The above is incomplete.

    Dog breeds are not evolution.A poodle will always still be a wolf, just like Andre the Giant and dwarf Pygmies are still humans.

    Your opinions are just laughably erroneous Phoodoo.

    ETA: Note on the * above.

    I’m just going to post this for the record. I actually have no idea if Pekinese and St Bernards are equally related to wolves. My assumption that they are could be totally wrong. Really…dog breeds are not my area of study.

    But here’s the kicker for you Phoodoo: I’m fine with that. That’s what science is all about. Basically my assumption is a perfectly reasonable hypothesis. And given all the research into dog breeding and their genetic relatedness to wolves, I bet it’s already been tested. And if someone finds the actual research and notes that those two breeds actually have different relatedness to wolves, I’ll be happy to admit I was off base. Why? Because I’ll have learned something new. And I’m good with that.

  11. Joe Felsenstein,

    Yes, that’s true. My reference to recombination was in relation to its role in permitting gene pools though, and hence alleles which are quasi-independent subgenome fragments (per Williams). Alleles in the evolutionary sense are subgenome fragments when considered within a gene pool, entire genomes between such pools (or in asexual lines). Of course one can still talk of alleles in the subgenome sense when there is no gene flow. Though I think it can cause confusion.

    Even within a pool, how long is an ‘allele’ anyway? The lower-level units are sliced out by repeat rounds of recombination over extended generations. The real is much fuzzier than the ideal.

    As to phoodoo’s surprise that gene loss can be termed evolution, it is a variant of the ‘no new information’ idea. If a brand new gene – brand new info, with no corresponding locus occupying bits in the rest of the population – can be an allele of variants where it is absent, the reverse must also be true. A lost gene must be an allele of the variant in which it has not been lost.

  12. phoodoo:
    Change in allele frequency doesn’t give you novelty, so sorry, no that is not evolution.

    Your original statement was:

    Genome reduction is evolution?

    Interesting.I wonder how far that will take us.

    I simply pointed out that change in allele frequency over time is the definition of evolution, so yes, loss of an allele is an evolutionary process. Your failure to understand that demonstrates a profound lack of knowledge of the science.

    With respect to your new, non-responsive statement, if the reason for the change in allele frequency is a new mutation increasing in prevalence in the population then, yes, it can result in phenotypic novelty.

  13. phoodoo:
    This is why Patricks claim that different frequencies is evolution.

    It’s not my claim, it’s the definition used in the modern synthesis. If you had even a minimal understanding of what you are criticizing, you would know that.

  14. keiths,

    Let me help YOU out keiths.

    HE posted THAT link. I never thought it was an entire paper, because if he would have wanted to post an entire paper, that’s what he would have done. Instead he posts a link, says see, this is the answer, and then what? Then expects someone to go look for the paper, and just assume that somewhere, mysteriously in there will be the answer he wants to give, but for which he refuses to give himself?

    That is pretty much in line with your tactics keith. Just go say, oh well, read this, read Theobald, read Wagner…then get back to me. As if you are a teacher giving homework assignments.

    How about you go read a book keith. Then you can tell me which is more closely related to a wolf, a St. Bernard or a Pekinese. Then maybe you can learn why dog breeding is not an example of evolution in action.

  15. phoodoo,

    Then maybe you can learn why dog breeding is not an example of evolution in action.

    If you wish to exclude population processes (selection, drift) from your definition of evolution, then no it isn’t. If that’s what it hinges on for you. But if there are alleles in dogs that are not present in any wolf, then we must allow that something is going on, which is an evolutionary process as minimally accepted – descent with modification.

    Lineages change, populations adapt, might be one way of putting it. Not to be confused with adaptation of individuals.

  16. Patrick,

    But there are virtually no IDists that don’t accept that allele frequencies vary, so that is a stupid definition. In fact anyone who knows anything about biology knows that genomes are incredibly plastic, and flexible, and THIS is why we see so many variations and adaptations, which we know quite well will never in a billion years lead to a new, more capable animal. This is precisely what dog breeding has taught us, the further we get from the ancestral wolf, the more sick and debilitated the animal becomes. A chihuahua will never be as healthy as a wild wolf. It will never become a new animal, it is the dead end of the genome.

    This is also what Lenskis bacteria points to. As soon as we take away citrate, the bacteria very quickly reverts right back to its ancestral make-up. Why should that be? Because when you go down paths that destroy genes, just as Behe has written, you come to peaks that no longer can do anything. More dead ends. Its only possible to go back.

    WE have no examples in science, showing that this dead ends can open up to a new ray of light at the end of that tunnel. It is just pure speculation, that is not supported by evidence. Similarity of design, does not verify common descent.

  17. phoodoo,

    This is also what Lenskis bacteria points to. As soon as we take away citrate, the bacteria very quickly reverts right back to its ancestral make-up. Why should that be?

    Because when selection stops operating, there is nothing preventing loss of the genetic capacity.

  18. Joe Felsenstein: then increase of the allele frequencies of A, B, C, D, and E will actually cause new multilocus genotypes to appear.

    And alleles may interact in complex ways such that A and B together has a phenotype which isn’t the simple combination of A and B phenotypes separately

  19. Robin,

    I am taking issue with your entire concept of relatedness.

    Let’s take a Siberian Husky for example. Now a line of Siberian Huskies could have been created from wolves 10,000 years ago.

    Then you have a basset hound that was bred from wolves 100 years ago. Now the geneticist is going to look at the two’s genome and say that the Husky is more closely related to wolves, even though its ancestor goes back 10,000 years of generations to a wolf. Whilst the Basset Hound is only 100 years worth of generations from a wolf.

    So which is right? My contention is neither. They are all just wolves, because there is no one thing that is a wolf and isn’t a wolf. They are all wolves of varying shapes and sizes. They still can’t breed with tigers.

  20. Allan Miller,

    Right, but the contrary is true. There is not equal probability that the variant will remain, or will revert, it will revert. If the mutation did nothing to adversely affect the organisms fitness, it should be just as likely that it would remain. But invariably it is always a loss of fitness (don’t get me started about your sides ridiculous defintion of fitness).

  21. phoodoo,

    Right, but the contrary is true. There is not equal probability that the variant will remain, or will revert, it will revert. If the mutation did nothing to adversely affect the organisms fitness, it should be just as likely that it would remain.

    No. If the gene stops being adaptive, it cannot remain functional indefinitely, because of mutation. If nothing is preventing loss-of-function mutations, they will occur. [eta, of course, realising who I’m talking to, to be clear they will occur irrespective of selection, but without selection there is nothing suppressing their spread].

    But invariably it is always a loss of fitness (don’t get me started about your sides ridiculous defintion of fitness).

    OK, you did warn me … nonetheless, when you use the term ‘fitness’, a term with specific meaning in biology, how are you defining it? Have you merely defined it as ‘a quality which evolution cannot increase’? Have you an operational measure in mind one could verify?

  22. phoodoo: But there are virtually no IDists that don’t accept that allele frequencies vary, so that is a stupid definition. In fact anyone who knows anything about biology knows that genomes are incredibly plastic, and flexible, and THIS is why we see so many variations and adaptations, which we know quite well will never in a billion years lead to a new, more capable animal.

    That is literally self-contradictory. Everyone knows things can change a lot, but they will never change even more than that. That’s what you’re basically saying.
    It UNBELIEVABLY stupid to think like that. You are in effect saying that you can add up dollars but never earn a million, or take a few steps but never walk a mile, or…
    Seriously, how can you sit there and type out something so unfathomably idiotic? Don’t you get ticks or something from having to go through those torturous contortions of logic?

  23. Allan Miller,

    Just because a loss of function (actually a loss of loss of function), mutation is bound to happen again in the future of the bacteria, why should you expect that to then outnumber the bacteria that don’t get that loss of loss of function. Why not just a random mix of all variations then? Why did they retake the population?

  24. Rumraket,

    You would get the same kind of variation if you took photos of the skulls of all the different breeds in the world. So what?

  25. phoodoo,

    Just because a loss of function (actually a loss of loss of function), mutation is bound to happen again in the future of the bacteria, why should you expect that to then outnumber the bacteria that don’t get that loss of loss of function. Why not just a random mix of all variations then? Why did they retake the population?

    Because of drift. A lesson you failed to absorb in the ‘M&M wars’, so I’m wasting my time even saying it, but a population cannot remain indefinitely mixed. No es possible. This is how chemostats work, for example … yes, we’ve been here before. Many times.

  26. Allan Miller,

    That makes no sense Allan. This is the same reason the M&M game also makes no sense. Why would it continue to only drift in one direction? Does it ever drift towards the whole population being able to metabolize citrate, even when no citrate is present?

  27. phoodoo:
    Robin,

    I am taking issue with your entire concept of relatedness.

    Yeah, I get that…

    Let’s take a Siberian Husky for example.Now a line of Siberian Huskies could have been created from wolves 10,000 years ago.

    Then you have a basset hound that was bred from wolves 100 years ago.Now the geneticist is going to look at the two’s genome and say that the Husky is more closely related to wolves, even though its ancestor goes back 10,000 years of generations to a wolf.Whilst the Basset Hound is only 100 years worth of generations from a wolf.

    Actually, you have the analysis reversed. If the basset hound was bred 100 years ago from wolves and the husky 10,000 years ago from wolves, then the basset hound would be more closely related as it would have less genetic modification away from the parent source.

    It’s easier to understand this if you think of a tree with branches. The farther along a branch you go away from the meeting point (the node), the relatedness is reduced.

    So which is right?My contention is neither.They are all just wolves, because there is no one thing that is a wolf and isn’t a wolf.They are all wolves of varying shapes and sizes.They still can’t breed with tigers.

    Well, your contention would be wrong according to genetics and phylogeny. But you’re welcome to provide some evidence to support your contention if you have any.

  28. phoodoo: hey are all just wolves, because there is no one thing that is a wolf and isn’t a wolf.

    Are some humans more related to certain humans than are others?

    Even what we call a “wolf” is more related to some wolves than to other wolves. Call both basset hounds and huskies “wolves” and it still could be a fact that the “wolves” we call basset hounds may be more closely related to “wild wolves” than the huskies are (or vice versa). This isn’t about names.

    Glen Davidson

  29. phoodoo,

    That makes no sense Allan.

    Why not? Does the ecological principal of competitive exclusion make sense? This is a purely ecological principle, but based upon exactly the same population-level behaviour. Is ecology wrong too? I suspect you’d have no trouble with this if you didn’t have a problem with evolution.

    This is the same reason the M&M game also makes no sense. Why would it continue to only drift in one direction?

    It doesn’t. It drifts in both directions. But because fixation depends upon present frequency, small perturbations amplify, and one of the variants eventually disappears. Not necessarily the one that was initially dominant. But indefinite cycling round a mean 50% is much, much less probable than loss of one or other.

    Your intuition that all neutral alleles will remain in the population forever is not borne out, either computationally, mathematically or experimentally. And this has at least one practical application, to wit the chemostat, which you must think cannot work because pure strains can never come out of it.

    I realise that none of these things trumps your intuition, but we must work with what we can.

    Does it ever drift towards the whole population being able to metabolize citrate, even when no citrate is present?

    It is possible but unlikely. If it does drift in, it is as likely to drift out again. The long term expectation is ‘drifted out’, because nothing acts to keep it in without selection.

  30. Allan Miller,

    Oh my heavens. If drift was the only factor, then ANY outcome would be as likely as any other. Entire populations of citrate metabolizing bacteria, half populations of citrate metabolizing bacteria, entire populations of bacteria that can not metabolize bacteria, and everything in between. And yet this is NOT what happens. The populations revert back to the ones that can not metabolize citrate in absence of citrate. And they do it rather quickly.

    In your theory of drift, this is not at all what one should expect, if all mutations are equally fit in the absence of any pressure.

    You can’t get this?

  31. phoodoo:

    I posted the entire piece of paper that HE referenced!

    Geez!

    I see. So he referenced a physical piece of paper, and you posted that physical piece of paper on an electronic website. The entire physical piece of paper.

    That might just be the stupidest rationalization I have ever seen at TSZ.

  32. phoodoo,

    In your theory of drift, this is not at all what one should expect, if all mutations are equally fit in the absence of any pressure.

    You can’t get this?

    To repeat, if all mutations are equally fit, then all but one will eventually disappear. This has been borne out experimentally, computationally and mathematically, and is the fundamental principle behind at least one practical application, to wit the chemostat. It is also, I forgot to mention, borne out, complete with frozen history, in Lenski.

    This is what happens, your intuition notwithstanding.

    You can’t get this?

  33. Allan Miller,

    That’s not what happens Allan. In the absence of citrate there are not populations which have drifted to be able to metabolize citrate.

    It only drifts in one direction.

    How in the world are you calling it drift when the drift always goes only one way. That’s totally bizarre.

  34. keiths,

    Is it more stupid than you complaining about me commenting on an abstract you posted, to a paper you yourself hadn’t read, and then complaining that I hadn’t read the entire paper which you neither posted nor ever read yourself?

    If the abstract doesn’t contain the point you are trying to make, what in the hell is the point of referencing it? So that you could hope that maybe in the paper which you yourself hadn’t read it might say something useful?

    Is this better known as the “Swing and Hope Smokescreen Strategy?”

  35. phoodoo,

    Is it more stupid than you complaining about me commenting on an abstract you posted, to a paper you yourself hadn’t read, and then complaining that I hadn’t read the entire paper which you neither posted nor ever read yourself?

    I didn’t do that, but if I had, then yes — what you just posted about pieces of paper was far stupider.

  36. phoodoo,

    That’s not what happens Allan. In the absence of citrate there are not populations which have drifted to be able to metabolize citrate.

    No, of course not. Did I say that would happen? But in a population which can metabolize citrate, removal of that selective pressure is much more likely to result in loss of the gene than retention. There are more ways of not being able to metabolise citrate than to do so, for a start, and so in the absence of the selective pressure, one of them will eventually supplant citrate metabolism. You can actually see this in Lenski, FFS! He has freezers full of past populations! He can go back and check what happened, sequence the genomes or check fitnesses and so on.

    It only drifts in one direction.

    No, I explicitly said it drifts in both directions. But this does not equate to permanent cycling about the mean, with movements in one direction precisely cancelled out in the other. Eventually, there will be an excess of fluctuations in one (random) direction than another. It would actually go against probability for indefinite retention, like a razor permanently balancing on its edge. Once it starts to fall one way, it tends to keep going that way.

    How in the world are you calling it drift when the drift always goes only one way. That’s totally bizarre.

    Sure. Counter-intuitive, ain’t it? Nonetheless, this is what happens. Computationally, experimentally, mathematically, chemostat yadda yadda yadda.

  37. phoodoo:

    But there are virtually no IDists that don’t accept that allele frequencies vary, so that is a stupid definition.

    Yes, like other creationists, IDCists recognize that denying that evolution (change in allele frequency in a population over time) occurs would make them look even more foolish than they already do. That doesn’t change the definition.

    In fact anyone who knows anything about biology knows that genomes are incredibly plastic, and flexible, and THIS is why we see so many variations and adaptations, which we know quite well will never in a billion years lead to a new, more capable animal.

    Actually we got quite a few capable animals over the past four billion years or so. The evidence does not support your claim.

    This is precisely what dog breeding has taught us, the further we get from the ancestral wolf, the more sick and debilitated the animal becomes.A chihuahua will never be as healthy as a wild wolf.It will never become a new animal, it is the dead end of the genome.

    I’d bet even money on this thing vs a wolf:

    This is also what Lenskis bacteria points to.As soon as we take away citrate, the bacteria very quickly reverts right back to its ancestral make-up.Why should that be?Because when you go down paths that destroy genes, just as Behe has written, you come to peaks that no longer can do anything.More dead ends.Its only possible to go back.

    No, it’s because there is no longer any selective pressure preserving that gene in the presence of mutations. Standard evolutionary theory you should know before critiquing the entire discipline.

  38. Allan Miller: No, I explicitly said it drifts in both directions.

    Except it doesn’t drift in both directions! You can say it does, or that it could or that it should and all of that is meaningless. It only drifts in one direction-away from citrate!

    There ARE NOT populations that have drifted towards metabolizing citrate BEFORE they have ever been exposed to citrate. But if the drift you talk of was true there is no reason to think that it wouldn’t sometimes. But it does not.

    There are not even populations that remain able to metabolize citrate after the citrate is removed, but there most certainly are populations that remain unable to metabolize citrate.

    One direction Allan. One.

  39. Patrick,

    And there is also no selective pressure preserving the genes which don’t metabolize citrate. Yet they remain anyway. How bizarre.

  40. phoodoo,

    One direction Allan. One.

    Liam! Harry! Whatever you say phoodoo. There are, nonetheless, not likely to be populations that retain the ability to metabolise citrate indefinitely when the selective pressure is removed, nor is it true that neutral alleles will remain together in a population indefinitely. So I really don’t know what you are going on about.

  41. phoodoo:

    And there is also no selective pressure preserving the genes which don’t metabolize citrate.Yet they remain anyway.How bizarre.

    Now you’re just spewing incoherently. That doesn’t even rise to the level of nonsense.

    You don’t like science that contradicts your religious beliefs. We get it. E pur si muove.

  42. It is, I will grant, a curious and interesting fact that the gene for citrate metabolism (as opposed to transport) is retained by E coli from its fully citrate-metabolising ancestor. But there is no evidence that [aerobic] transport is turned on and off by environmental stimulus, and substantial evidence against.

    eta – to answer myself, it is retained because it is still used anaerobically.

  43. phoodoo: That makes no sense Allan. This is the same reason the M&M game also makes no sense. Why would it continue to only drift in one direction? Does it ever drift towards the whole population being able to metabolize citrate, even when no citrate is present?

    For fucks sake, the lower the frequency of the allele in the population, the more likely it will drift back out of existence. Particularly if the population is also huge (as bacterial populations almost always are). Yes, some times something drifts all the way from a single member carrying a mutation, to total fixation in a population, that CAN happen, it’s just much less frequent than the mutations drifting away again. Especially in bacteria.

    It’s a mathematical inevitability. You are literally questioning a fundamental principle in statistics. You would probably get this if you just tried to remove it from the whole “evolutionists hate god” subtext running through your head.

    Let’s try to make it super simple and say there’s a population of 10 individuals, one of which was born with a novel mutation that is neutral and is entirely subject to drift.
    That means there’s a 50% chance it will increase in frequency, and 50% chance it will drop in frequency (if the distribution was different than 50/50, it wouldn’t be neutral, but either beneficial or deleterious).
    Ok, what can happen now? There’s a 50% chance another individual will get the mutation in the next generation, and there’s 50% chance it will disappear.
    That means the mutation will basically behave like a fair coin, with heads being “increase to one more individual” and tails being “remove from one individual”.

    So you flip your coin and it goes heads, say. Cool, now it’s in two individuals. Try again, heads again. Oh, now it’s in three individuals. Flip again. Oh, now it was tails, it’s back down to two. And so on and so forth.

    As you can probably gather from this, having the mutation just randomly happen to keep rising in frequency every time is actually quite unlikely. Most of the time, it will rise a bit and then just fall back out, because that’s just the nature of a random equiprobable process. The bigger the population (bacterial populations are in their billions), the more unlikely it is for the mutation to drift to fixation, because that would entail a really really really really really long string of “heads” with comparatively few “tails”. That’s also why drift is stronger the smaller the population, because there’s a bigger chance there can be a string of “heads” or “tails” that will take something to fixation (or away, depending on the starting frequency).

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