172 thoughts on “YEC part 1”

1. stcordova:

   So diversification of subspecies (reproductively isolated descendants of a created kind) can happen after the flood, but I don’t expect new created kinds to appear but rather can go extinct.We already know many body plans no longer exist, they’ve gone extinct and the number of distinct plans has gone down.I expect this is true at many taxonomic levels.

   We have conclusive evidence there was no global “Noah’s Flood” only 4500 years ago. One of the major indicators is civilizations in China that lived right through this supposed all-life-killing Flood without ever noticing it. 🙂 Another conclusive piece of evidence is the DNA of millions of extant species including humans shows no genetic bottleneck at all in the last 4500 years.

   Your Gish Gallop isn’t helping you here Sal. This isn’t Young Cosmos where the average IQ of your posters was below room temperature Celsius.

2. Sal has convinced me of miracles. Mung has become a charming conversationalist. Perhaps this will carry over to issues where he disagrees with materialists and evolutionists.

3. stcordova,

   What really struck me is that it seemed all the languages emerged around the same time and it almost looked like humanity conspired in very diverse geographic locations to start having new written languages at the same time.

   Suggestive again that humanity is a relatively recent phenomenon.

   Paging Piotr.

   But there is the phenomenon of coalescence to deal with in any branching copying process. Looking backwards from the end of such a process, you get to a coalescent point because all other branches that don’t go through it have been rendered extinct, not because it is a ‘true’ origin. You have to control for that – it’s an artefact and you wouldn’t want to be accused of confirmation bias by ignoring that possibility, would you?

4. stcordova,

   Just as the Malthusian fitness model would almost suggest, the life form with the highest sustained exponential growth rate will swamp out competitors, and in this case, exterminate many of the competitors along the way. Bwahaha!

   And this is the organism – humans – that is currently in the process of genetic meltdown? Bwa and, indeed, ha! 🙂

   stcordova,

   Darwinian Deletion as a means of evolutionary diversification is a conceptually incoherent theory. If anything, absence of selection allows diversification.

   Absence of selection means Drift alone. Drift eliminates diversity too, just more slowly. Do you know why knowledgeable people aren’t even slightly troubled by the fact that the process of evolution involves a component that eliminates diversity?

5. stcordova,

   Observed present-day extinction suggests life is young.

   Not to me. It suggests that we have only recently started to screw things up on such a massive scale.

6. And this is the organism – humans – that is currently in the process of genetic meltdown? Bwa and, indeed, ha! 🙂

   Genetic deterioration, not necessarily reproductive deterioration. Here is Michael Lynch, National Academy of Sciences:

   Sanford’s pro-ID thesis supported by PNAS paper, read it and weep, literally

   Unfortunately, it has become increasingly clear that most of the mutation load is associated with mutations with very small effects distributed at unpredictable locations over the entire genome, rendering the prospects for long-term management of the human gene pool by genetic counseling highly unlikely for all but perhaps a few hundred key loci underlying debilitating monogenic genetic disorders (such as those focused on in the present study).

   Thus, the preceding observations paint a rather stark picture. At least in highly industrialized societies, the impact of deleterious mutations is accumulating on a time scale that is approximately the same as that for scenarios associated with global warming—perhaps not of great concern over a span of one or two generations, but with very considerable consequences on time scales of tens of generations. Without a reduction in the germline transmission of deleterious mutations, the mean phenotypes of the residents of industrialized nations are likely to be rather different in just two or three centuries, with significant incapacitation at the morphological, physiological, and neurobiological levels.

7. Sal: there is a really important point here that you seem unable to see:

   the selection coefficient of an allele is a function of the environment, and the environment changes.

   It blows yours, and Sanford’s, argument out of the water.

   stcordova: Genetic deterioration, not necessarily reproductive deterioration.

   If an allele does not affect reproduction, it is not deleterious. It is neutral.

   By definition.

   If you want to apply the word deleterious” to “an allele that would affect reproduction if it weren’t for modern medicine”, then you can’t use arguments from population genetics, which does not define the word in that way.

   Yes, as a result of modern hygiene and medicine, alleles that would in the past have been lethal, are now survivable, and so our genome is accumulating, overall, mutations that would be deleterious were we to find ourselves in a pre-technological environment, which remains possible, and if it arises, then we may well go extinct.

   But that tells us nothing about how old the earth is.

8. stcordova,

   From the Lynch abstract:

   “[…]a consideration of the long-term consequences of current human behaviourover the next few centuries in industrialized societies”

   You’re extrapolating a prediction applying to one species in a very specific environment to the entirety of global evolutionary history (not very long, in your view)? Do you really think that’s justified?

   Anyway, what about my other points?

9. As an aside, if genetic deterioration had the effect of reducing the human population without increasing death rates, I would not consider that a total disaster.

10. Allan Miller,

    Edit: *smiles and nods*

11. Anyone providing figures for how many new species evolving each year since say the history of pre-industrial man? The high rate of extinction has been thought to be going even before the human population explosion.

12. the selection coefficient of an allele is a function of the environment, and the environment changes.

    It blows yours, and Sanford’s, argument out of the water.

    Actually no, it shows the incoherency of using selection as a lens to identify function. In the world of Darwin, tay-sach’s disease, sickle cell anemia, high cholesterol, diabetes, blindness, loss of limbs and who knows what else can qualify as “fit”. It shows the conceptualization of biology in terms of reproduction rates goes against the engineering and medical notions of functionality. That was the point I made in Survival of The Sickest, Why We Need Disease

    Allen Orr critiquing Dennett told it like it was:

    When does adaptationism stop being a useful research strategy and start being a silly exercise in cleverness? Dennett never confronts these legitimate worries. It is far easier for him to ridicule Gould and Lewontin’s rhetorical excesses.

    I suspect Dennett fails to appreciate these concerns in part because his thinking is guided by a subtly misleading picture of adaptation. Dennett is fond of speaking of selection as leading organisms through “Design Space”: Selection “lifts” organisms along “ramps” of good Design. Although this imagery is often useful, it invites two subtle misconceptions about adaptation. The first is that natural selection cares about Design. In reality, selection “sees” only brute birth, death, and reproduction, and knows nothing of Design. Selection — sheer, cold demographics — is just as happy to lay waste to the kind of Design we associate with engineering as to build it. Consider the eyes of cave organisms who live in total darkness. If eyes are expensive to make, selection can wreck their exquisite engineering just as surely as it built it. An optic nerve with little or no eye is most assuredly not the sort of design one expects on an engineer’s blueprint, but we find it in Gammarus minus. Whether or not this kind of evolution is common, it betrays the fundamental error in thinking of selection as trading in the currency of Design.

    Second, hazy imagery of selection lifting organisms along Design ramps makes it hard to see that selection sometimes moves individual traits down ramps. But this surely occurs.

    This auto renormalization of selection coefficients leads to the perverse view that an organism can lose organ after organ and function after function and all the while keep getting “fitter”. What we actually observe in real-time lab and field observations is reductive evolution.

    Reductive evolution of complexity, square circle

    Just as I said, you think survival of the sickest is some genius insight. You revel in the loss of eyes (cave fish), the loss of stomachs (sharks), the loss of wings (beetles), the loss of legs (snakes), the loss of functioning blood (sickle cell anemia), etc. and think “Wow, Natural Selection is such a great theory to explain the evolution of complexity because we have so many examples of how selection destroys things for the sake of reproductive success.”

    Walter Remine told me of a parasite that essentially lost all of its functions and all that was left was essentially an anus. If someone knows what creature that was that suffered such a fate of reductive evolution, please post, that should be the poster child of Darwinian evolution.

13. Sal,
    Would you be more likely to pass your genes onto the next generation if

    A) You had sickle cell anemia
    B) You were dead

14. stcordova: What we actually observe in real-time lab and field observations is reductive evolution.

    Do you have anything to support that other then a link back to UD?

15. Sal, Your entire schtick reduces to variations on the “some=all, few=none” fallacy (I just made that up). It is not proposed that disablement is never adaptive, and you can’t extrapolate from the fact that adaptation is sometimes disabling to the conclusion that it always is.

    If disablement occurs and is adaptive, there are many ways to be disabled, so disabled sequences essentially drift, and they will display a lack of conservation. No-one proposes that lack of conservation is a marker for selection.

    OTOH, if there is conservation, this is a strong pointer towards function of some kind. It is not a symmetrical case. Both – loss and gain of function – can be adaptive. Only one results in conservation, and only one is searched for using the ‘lens’ of selection across taxonomic groups.

    And will you stop getting other people to do your arguing for you? Has Orr suddenly abandoned evolution or something? Does he now dismiss adaptation? I doubt it.

16. A simple test. If a person quotes a noted biologist or geologist against biology or geology, that person is almost certainly quote mining. But that would be dishonest, so no one here does that.

17. stcordova:
    Anyone providing figures for how many new species evolving each year since say the history of pre-industrial man?

    Did you ever respond to the request for your source on the number of phyla which have become extinct?

18. stcordova: Genetic deterioration, not necessarily reproductive deterioration.

    Yes, we understand. Your position is that the human population increased while still experiencing genetic deterioration.

    In fact, that’s basically the same position you have to maintain for all the species that were on the ark. They got off the ark and multiplied and diversified greatly, while deteriorating genetically.

    So your appeals to genetic deterioration are baseless and you admit it by trying now to separate it from reproductive deterioration [by which I assume you mean leaving fewer offspring and going extinct].

    You’ve just abandoned one of the pillars of your “young life” argument. What’s left?

19. stcordova: Actually no, it shows the incoherency of using selection as a lens to identify function.

    Sal, because “fit” has a very specific meaning in Darwinian evolution. The fact that it isn’t the normal English usage doesn’t make it “incoherent” – it just means you have to know the specific meaning it carries in order to make sense of it.

    And you are quite wrong about sickle cell anyway – first of all, it’s a special case, in that it only causes disease when you have two copies of the sickle cell allele – it provides immunity from malaria when you have one. So it’s an example (not rare, but not typical) where an allele approaches an optimum frequency in a population – in an environment in which malaria kills before reproductive age, it will tend to rise to the point at which the number of reproductive lives it saves is not exceeded by the number it damages (i.e. where a lot of people have one copy, but not may people have two – you have the right skill set for working out the probabilities!).

    Most new alleles, however, are near- neutral at the time when they appear in the population, and become advantageous or disadvantageous later, at a time when their frequency is already quite high.

    So the classic semi-hopeful monster picture is a straw man portrayal of how Darwinian evolution actually works. Better instead to picture a drip-feed of slight variation into the gene-pool of any given population, most of which is near-neutral at the time of appearance, but which allows a rich pool of variation, in which the frequencies of each allele can rapidly (within a generation) track small changes in the environment.

    Many people skeptical of Darwinian evolution reject evidence like the Grant’s finch studies by saying: oh, that’s just changes in allele frequency of alleles that is already there Sure it is – but the point is that there is always a rich range of alleles, precisely because of that constant drip-feed of near-neutral variation.

    Sanford completely misunderstood this.

    But you are also completely misunderstanding Sanford. Sanford wasn’t talking about disease-producing alleles – he was talking about what he refers to as Very Slightly Deleterious Mutations (VSDMs). And three answers to Kondrashov’s question are:

    • Those VSDMs may not be VSD but SD, or just D or even VSBM when found in combination (e.g. with another copy of itself, but often in combination with an allele of a different gene, aka “synergistic epistasis” – and we know this happens. It’s one of the many ways in which Behe is wrong./li>
    • Those VSDMs may well become VSBMs, or SBMs when the environment changes.
    • The selection coefficient in any case is in part of function of the allele frequency itself.

20. “Young life” seems to have suffered an early death.

21. YEC Part 2 addresses many of the other questions raised here outside the YEC 1 OP:

    YEC Part 2

22. Every day the earth gets older, and the young earth hypothesis becomes one day less believable.