The Reasonableness of Atheism and Black Swans

As an ID proponent and creationist, the irony is that at the time in my life where I have the greatest level of faith in ID and creation, it is also the time in my life at some level I wish it were not true. I have concluded if the Christian God is the Intelligent Designer then he also makes the world a miserable place by design, that He has cursed this world because of Adam’s sin. See Malicious Intelligent Design.

Jesus prophesied of the intelligently designed outcome of humanity: “wars and rumors of wars..famines…pestilence…earthquakes.” If there is nuclear and biological weapons proliferation, overpopulation, destruction of natural resources in the next 500 years or less, things could get ugly. If such awful things are Intelligently Designed for the trajectory of planet Earth, on some level, I think it would almost be merciful if the atheists are right….

The reason I feel so much kinship with the atheists and agnostics at TSZ and elsewhere is that I share and value the skeptical mindset. Gullibility is not a virtue, skepticism is. A personal friend of Richard Dawkins was my professor and mentor who lifted me out of despair when I was about to flunk out of school. Another professor, James Trefil, who has spent some time fighting ID has been a mentor and friend. All to say, atheists and people of little religious affiliation (like Trefil) have been kind and highly positive influences on my life, and I thank God for them! Thus, though I disagree with atheists and agnostics, I find the wholesale demonization of their character highly repugnant — it’s like trash talking of my mentors, friends and family.

I have often found more wonder and solace in my science classes than I have on many Sunday mornings being screamed at by not-so-nice preachers. So despite my many disagreements with the regulars here, because I’ve enjoyed the academic climate in the sciences, I feel somewhat at home at TSZ….

Now, on to the main point of this essay! Like IDist Mike Gene, I find the atheist/agnostic viewpoint reasonable for the simple reason that most people don’t see miracles or God appearing in their every day lives if not their entire lives. It is as simple as that.

Naturalism would seem to me, given most everyone’s personal sample of events in the universe, to be a most reasonable position. The line of reasoning would be, “I don’t see miracles, I don’t see God, by way of extrapolation, I don’t think miracles and God exists. People who claim God exists must be mistaken or deluded or something else.”

The logic of such a viewpoint seems almost unassailable, and I nearly left the Christian faith 15 years ago when such simple logic was not really dealt with by my pastors and fellow parishioners. I had to re-examine such issues on my own, and the one way I found to frame the ID/Creation/Evolution issue is by arguing for the reasonableness of Black Swan events.

I will use the notion of Black Swans very loosely. The notion is stated here, and is identified with a financeer and academic by the name of Nasim Taleb. I have Taleb’s books on investing entitled Dynamic Hedging which is considered a classic monograph in mathematical finance. His math is almost impenetrable! He is something of a Super Quant. Any way:

https://en.wikipedia.org/wiki/Black_swan_theory

The black swan theory or theory of black swan events is a metaphor that describes an event that comes as a surprise, has a major effect, and is often inappropriately rationalized after the fact with the benefit of hindsight.

The theory was developed by Nassim Nicholas Taleb to explain:

1.The disproportionate role of high-profile, hard-to-predict, and rare events that are beyond the realm of normal expectations in history, science, finance, and technology.
2.The non-computability of the probability of the consequential rare events using scientific methods (owing to the very nature of small probabilities).
3.The psychological biases that blind people, both individually and collectively, to uncertainty and to a rare event’s massive role in historical affairs.

Unlike the earlier and broader “black swan problem” in philosophy (i.e. the problem of induction), Taleb’s “black swan theory” refers only to unexpected events of large magnitude and consequence and their dominant role in history. Such events, considered extreme outliers, collectively play vastly larger roles than regular occurrences.[1] More technically, in the scientific monograph Silent Risk , Taleb mathematically defines the black swan problem as “stemming from the use of degenerate metaprobability”.[2]
….
The phrase “black swan” derives from a Latin expression; its oldest known occurrence is the poet Juvenal’s characterization of something being “rara avis in terris nigroque simillima cygno” (“a rare bird in the lands and very much like a black swan”; 6.165).[3] When the phrase was coined, the black swan was presumed not to exist. The importance of the metaphor lies in its analogy to the fragility of any system of thought. A set of conclusions is potentially undone once any of its fundamental postulates is disproved. In this case, the observation of a single black swan would be the undoing of the logic of any system of thought, as well as any reasoning that followed from that underlying logic.

Juvenal’s phrase was a common expression in 16th century London as a statement of impossibility. The London expression derives from the Old World presumption that all swans must be white because all historical records of swans reported that they had white feathers.[4] In that context, a black swan was impossible or at least nonexistent. After Dutch explorer Willem de Vlamingh discovered black swans in Western Australia in 1697,[5] the term metamorphosed to connote that a perceived impossibility might later be disproven. Taleb notes that in the 19th century John Stuart Mill used the black swan logical fallacy as a new term to identify falsification.[6]

The very first question I looked at when I was having bouts of agnosticism was the question of origin of life. Now looking back, the real question being asked is “was OOL a long sequence of typical events or a black swan sequence of events.” Beyond OOL, one could go on to the question of biological evolution. If we assume Common Descent or Universal Common Ancestry (UCA), would evolution, as a matter of principle, proceed by typical or black swan events or a mix of such events (the stock market follows patterns of typical events punctuated by black swan events).

If natural selection is the mechanism of much of evolution, does the evolution of the major forms (like prokaryote vs. eukaryote, unicellular vs. multicellular, etc.) proceed by typical or black swan events?

[As a side note, when there is a Black Swan stock market crash, it isn’t a POOF, but a sequence of small steps adding up to an atypical set of events. Black Swan doesn’t necessarily imply POOF, but it can still be viewed as a highly exceptional phenomenon.]

Without getting into the naturalism vs. supernaturalism debate, one could at least make statements whether OOL, eukaryotic evolution (eukaryogenesis), multicellular evolution, evolution of Taxonomically Restricted Features (TRFs), Taxonomically Restricted Genes (TRGs), proceeded via many many typical events happening in sequence or a few (if not one) Black Swan event.

I personally believe, outside of the naturalism supernaturalism debate, that as a matter of principle, OOL, eukaryogenesis, emergence of multicellularity (especially animal multicellularity), must have transpired via Black Swan events. Why? The proverbial Chicken and Egg paradox which has been reframed in various incarnations and supplemented with notions such as Irreducible Complexity or Integrated Complexity or whatever. Behe is not alone in his notions of this sort of complexity, Andreas Wagner and Joe Thornton use similar language even though they thing such complexity is bridgeable by typical rather than Black Swan events.

When I do a sequence lookup at the National Institutes of Health (NIH) National Center of Biotechnology Information (NCBI), it is very easy to see the hierarchical patterns that would, at first glance, confirm UCA! For example look at this diagram of Bone Morphogenetic Proteins (BMP) to see the hierarchical patterns:

BMP

From such studies, one could even construct Molecular Clock Hypotheses and state hypothesized rates of molecular evolution.

The problem however is that even if some organisms share so many genes, and even if these genes can be hierarchically laid out, there are genes that are restricted only to certain groups. We might refer to them as Taxonomically Restricted Genes (TRG). I much prefer the term TRG over “orphan gene” especially since some orphan genes seem to emerge without the necessity of Black Swan events and orphan genes are not well defined and orphan genes are only a subset of TRGs. I also coin the notion of Taxonomically Restricted Feature (TRF) since I believe many heritable features of biology are not solely genetic but have heritable cytoplasmic bases (like Post Translation modifications of proteins).

TRGs and TRFs sort of just poof onto the biological scene. How would we calibrate the molecular clock for such features? It goes “from zero to sixty” in a poof.

Finally, on the question of directly observed evolution, it seems to me, that evolution in the present is mostly of the reductive and exterminating variety. Rather than Dawkins Blind Watchmaker, I see a Blind Watch Destroyer. Rather than natural selection acting in cumulative modes, I natural selection acting in reductive and exterminating modes in the present day, in the lab and field.

For those reasons, even outside the naturalism vs. supernaturalism debate, I would think a reasonable inference is that many of the most important features of biology did not emerge via large collections of small typical events but rather via some Black Swan process in the past, not by any mechanisms we see in the present. It is not an argument from incredulity so much as a proof by contradiction.

If one accepts the reasonableness of Black Swan events as the cause of the major features of biology, it becomes possible to accept that these were miracles, and if Miracles there must be a Miracle Maker (aka God). But questions of God are outside science. However, I think the inference to Black Swan events for biology may well be science.

In sum, I think atheism is a reasonable position. I also think the viewpoint that biological emergence via Black Swan events is also a highly reasonable hypothesis even though we don’t see such Black Swans in every day life. The absence of such Black Swans is not necessarily evidence against Black Swans, especially if the Black Swan will bring coherence to the trajectory of biological evolution in the present day. That is to say, it seems to me things are evolving toward simplicity and death in the present day, ergo some other mechanism than what we see with our very own eyes was the cause of OOL and bridging of major gaps in the taxonomic groupings.

Of course such a Black Swan interpretation of biology may have theological implications, but formally speaking, I think inferring Black Swan hypotheses for biology is fair game in the realm of science to the extent it brings coherence to real-time observations in the present day.

775 thoughts on “The Reasonableness of Atheism and Black Swans

  1. colewd:
    Hi Cubist

    What new identified causes could reduce the grey swan population?

    You’re getting ahead of yourself. First establish that there are, in fact, such things as “grey swans”; only after that’s done will your question make sense.

    This is a very good point. What if we define grey swan as an event that we cannot model its cause mathematically?

    We could do that, sure. But according to the definition you’ve just provided, what qualifies an event as a ‘grey swan’ is not anything intrinsic to the event itself; rather, what qualifies an event as a ‘grey swan’ is human inability to create a mathematical model of its cause. So if a Creationist wants to base a scientific argument for Creation on the putative ‘grey swan’ status of some Event X (origin of life, say?), they’re pretty much arguing I don’t know! Nobody knows! Therefore, I do know—and what I know is, Creator done it.

    So, sure, you can define “grey swans” in terms of human ignorance if you really want to. You can identify an event as a ‘grey swan’ thanks to human ignorance of its cause(s). And if you do that, my next question will be, “So what?”

    Note that by defining a ‘grey swan’ in terms of human ignorance, you’ve provided an answer to your own question: Any and every “new identified cause” will “reduce the grey swan population”. So… just keep on trucking with mainstream science, I guess?

  2. stcordova: The multicellular creature is much much more fragile to slight variation in genetic change.

    This really is bullshit, you know. You can’t point to a single instance of any living population succumbing to genetic entropy, and when you try, you wind up naming populations that have been killed off by humans or asteroids or other environmental disaster.

    What you might say, and find some support for, is that populations adapted to narrow niches cannot reverse evolve to become generalists.

    Except that there are quite a few generalists– roaches, crocodiles, horseshoe crabs — that have survived for hundreds of millions of years without dying off from genetic entropy.

  3. petrushka:
    Except that there are quite a few generalists– roaches, crocodiles, horseshoe crabs— that have survived for hundreds of millions of years without dying off from genetic entropy.

    Uh, I wonder. If you were to take a sample population of any of these species back 100 million years, how similar do you think they would be? AIUI, all of these lineages have been undergoing genetic changes the whole time, if only from drift. So I think Sal is confusing genetic entropy (which apparently doesn’t exist) with genetic Brownian motion.

  4. cubist:We could do that, sure. But according to the definition you’ve just provided, what qualifies an event as a ‘grey swan’ is not anything intrinsic to the event itself; rather, what qualifies an event as a ‘grey swan’ is human inability to create a mathematical model of its cause. So if a Creationist wants to base a scientific argument for Creation on the putative ‘grey swan’ status of some Event X (origin of life, say?), they’re pretty much arguing I don’t know! Nobody knows! Therefore, I do know—and what I know is, Creator done it.

    Sometimes I meditate on the absurd sequence of preposterous coincidences leading up to me meeting my wife of lo these many decades. You could rerun time from, say, a week before I met her to the actual meeting, and repeat it forever, and it wouldn’t come anywhere close to happening again.

    It’s probably easier to shrug and consider it Divinely ordained, than to think “well, I had reached the point in my life where I was ready for such a relationship, and the probability of meeting a woman at the same point in her life was high enough to pretty much guarantee a connection within a year or so. We’ve simply been lucky to find ourselves compatible for so long.”

  5. Flint: Uh, I wonder. If you were to take a sample population of any of these species back 100 million years, how similar do you think they would be? AIUI, all of these lineages have been undergoing genetic changes the whole time, if only from drift. So I think Sal is confusing genetic entropy (which apparently doesn’t exist) with genetic Brownian motion.

    I’ve asked Sal about half a dozen times to explain the survival of cockroaches and crocodiles.

    I think what he said is this is evidence for a young earth, although he didn’t actually respond directly.

    We don’t have 200 million year old genomes, so we can’t directly observe genetic drift.

    What we can observe is creationists abandoning consilience. Sal inspired me to coin the term “excilience,” the practice of excluding consilience from any discussion of “best explanation.” Followed up by extensive mining of quotes and micro-thoughts from established scientists, for the express purpose of misrepresenting their arguments.

  6. Flint: Sometimes I meditate on the absurd sequence of preposterous coincidences leading up to me meeting my wife of lo these many decades

    I know my genealogy back a ways. I am descended from a line of guys who did things like hold the horses during famous battles. One of them wintered at Valley Forge and went home to help with plowing before any fighting. I think most of have points in our ancestry that might have changed things.

    A five minute delay in having sex, and we would be someone else. Or not at all.

  7. petrushka: I know my genealogy back a ways. I am descended from a line of guys who did things like hold the horses during famous battles. One of them wintered at Valley Forge and went home to help with plowing before any fighting. I think most of have points in our ancestry that might have changed things.

    A five minute delay in having sex, and we would be someone else. Or not at all.

    Let that be a lesson–don’t delay sex.

    Glen Davidson

  8. petrushka: I know my genealogy back a ways. I am descended from a line of guys who did things like hold the horses during famous battles. One of them wintered at Valley Forge and went home to help with plowing before any fighting. I think most of have points in our ancestry that might have changed things.

    A five minute delay in having sex, and we would be someone else. Or not at all.

    Yeah, this is the kind of thing I meant when I spoke of reality being contingent on an infinity of independent variables, making nearly all that happens “black swans”. Tweak just one of those variables, even slightly, and you’ll change whole slabs of history. Asimov addressed this in several of his novels (notably the Foundation series, and The End of Eternity).

    On one side, my family was building boats in New England since 1650, and continued doing so until about 20 years ago when the last of them (but me) died out. HOW could they be in this country so long, and be so industrious, and remain so poor?

  9. stcordova,

    Why should multi-cellular forms not be immortal like bateria if they have adequate nutrients and a nurturing environment?

    We are immortal like bacteria. What we aren’t is immortal in the sense we’d all like to be immortal: indefinite persistence of the soma (with health, wealth and the continuing interest of the opposite sex, of course!). The human germ line is a succession of cells in exactly the same way that a bacterial line is, albeit complicated by sex. It is wrapped in a diploid soma in us, naked in bacteria. But there is no obvious reason why somatic immortality should be advantageous in an evolutionary sense. And, indeed, long term diploidy carries its own problems. Such as cancer, a doomed attempt by a diploid line to become immortal.

  10. Petrushka,

    I don’t think we’ve seen extinction because of genetic erosion because:

    1. something else will finish off a compromised population

    2. auto renormaliztion to the best of the worst, i.e. a bad trait gets fixed and now the new genotype is the new standard of excellence (albeit functionally compromised like a blind cavefish). Jody Hey used auto renormalization to prevent mutational meltdown in his simulations, and I think that’s what happens in nature particularly in modes of reductive evolution. I like Hey’s “fix” better than Kondrashov’s synergistic epistasis.

    That said:
    http://www.jstor.org/stable/2410432?seq=1#page_scan_tab_contents

    Although it is widely acknowledged that the gradual accumulation of mildly deleterious mutations is an important source of extinction for asexual populations,
    it is generally assumed that this process is of little relevance to sexual species.
    Here we present results, based on computer simulations and supported by analytical approximations, that indicate that mutation accumulation in small,
    random-mating monoecious populations can lead to mean extinction times less
    than a few hundred to a few thousand generations.

    I think the problem with the computer simulations vs. the real world is that in the real world, there is auto renormalization.

  11. I’m waiting for the discussion of cockroaches and crocodiles. Why are they not extinct?

  12. stcordova: I don’t think we’ve seen extinction because of genetic erosion because:

    1. something else will finish off a compromised population

    You have no evidence from the real world that any significant extinction events were “something else” finishing off a “compromised population”.

    Why did passenger pigeons go extinct, Sal? How could you possibly support your fantastic claim that they were a “compromised population” before a new predator (humans, with guns) fatally disrupted their North American ecosystem? What’s your evidence?

  13. hotshoe_: What’s your evidence?

    Conservationists were ineffective in stopping the slaughter. A bill was passed in the Michigan legislature making it illegal to net pigeons within two miles (3 km) of a nesting area, but the law was weakly enforced. By the mid-1890s, the Passenger Pigeon almost completely disappeared. In 1897, a bill was introduced in the Michigan legislature asking for a 10-year closed season on Passenger Pigeons. This was a futile gesture. Similar legal measures were passed and disregarded in Pennsylvania. This was a highly gregarious species – the flock could initiate courtship and reproduction only when they were gathered in large numbers; smaller groups of Passenger Pigeons could not breed successfully*, and the surviving numbers proved too few to re-establish the species. Attempts at breeding among the captive population also failed for the same reasons. The Passenger Pigeon was a colonial and gregarious bird practicing communal roosting and communal breeding and needed large numbers for optimum breeding conditions.
    *my emphasis
    link

    It was the bird’s fault. They’d become gregarious, see.

  14. Keywords:

    Extinction;
    fitness;
    mutational meltdown;
    Saccharomyces cerevisiae

    Abstract.— In small or repeatedly bottlenecked populations, mutations are expected to accumulate by genetic drift, causing fitness declines. In mutational meltdown models, such fitness declines further reduce population size, thus accelerating additional mutation accumulation and leading to extinction. Because the rate of mutation accumulation is determined partly by the mutation rate, the risk and rate of meltdown are predicted to increase with increasing mutation rate. We established 12 replicate populations of Saccharomyces cerevisiae from each of two isogenic strains whose genomewide mutation rates differ by approximately two orders of magnitude. Each population was transferred daily by a fixed dilution that resulted in an effective population size near 250. Fitness declines that reduce growth rates were expected to reduce the numbers of cells transferred after dilution, thus reducing population size and leading to mutational meltdown. Through 175 daily transfers and approximately 2900 generations, two extinctions occurred, both in populations with elevated mutation rates. For one of these populations there is direct evidence that extinction resulted from mutational meltdown: Extinction immediately followed a major fitness decline, and it recurred consistently in replicate populations reestablished from a sample frozen after this fitness decline, but not in populations founded from a predecline sample. Wild-type populations showed no trend to decrease in size and, on average, they increased in fitness.

    http://onlinelibrary.wiley.com/doi/10.1111/j.0014-3820.2001.tb00608.x/abstract

  15. Alan Fox: It was the bird’s fault. They’d become gregarious, see.

    Overspecialization is a risky adaptation.

    Sal’s mistake is trying to tie this to genetic entropy. It’s stupid, sloppy thinking.

    If genetic entropy compromises populations, it would apply to bacteria, cockroaches, cycads, volvox, crocodiles.

  16. stcordova:

    The finding that a population, after being consistently and repeatedly forced into a severe bottleneck which greatly reduces the efficacy of selection, is in dire danger of extinction due to mutational meltdown seems entirely consistent with standard evolutionary theory to me.

  17. Dave Carlson:

    The finding that a population, after being consistently and repeatedly forced into a severe bottleneck which greatly reduces the efficacy of selection, is in dire danger of extinction due to mutational meltdown seems entirely consistent with standard evolutionary theory to me.

    Agreed. Some of my opponents in this discussion seem to question this standard aspect of evolutionary population genetics.

  18. stcordova: Agreed.Some of my opponents in this discussion seem to question this standard aspect of evolutionary population genetics.

    Now to support your “genetic entropy” nonsense all you need to do is show every species in the world was consistently and repeatedly forced into a severe population bottleneck.

  19. stcordova: Agreed. Some of my opponents in this discussion seem to question this standard aspect of evolutionary population genetics.

    No, we simply note that you apply it stupidly, and you cannot be bothered to learn anything.

    When are you going to explain the non-extinction of cockroaches, crocodiles, algae, and cycads?

    Nor explain why elephants and naked mole rats do not get cancer.

  20. stcordova: Wild-type populations showed no trend to decrease in size and, on average, they increased in fitness.

    At least you didn’t quote mine.

    Which goes to show that when creationist quote honestly, the quote completely undermines creationism.

  21. cubist,

    “So, sure, you can define “grey swans” in terms of human ignorance if you really want to. You can identify an event as a ‘grey swan’ thanks to human ignorance of its cause(s). And if you do that, my next question will be, “So what?”

    Is there a reason that we are ignorant to the cause of so many inflection points in evolution OOL Eukaryotic Multi cellular etc?

    “Note that by defining a ‘grey swan’ in terms of human ignorance, you’ve provided an answer to your own question: Any and every “new identified cause” will “reduce the grey swan population”. So… just keep on trucking with mainstream science, I guess?”

    Agree…maybe identification of the grey swans can help prioritize the journey.

  22. Adapa: Now to support your “genetic entropy” nonsense all you need to do is show every species in the world was consistently and repeatedly forced into a severe population bottleneck

    Noah’s ark, doncha know!

    Again, this is an example of what petrushka has already pointed out as excilience.

    In order for Sal to imply that article supports his fantasy, he has to ignore the words of the article itself – “Wild-type populations showed no trend to decrease in size and, on average, they increased in fitness.”
    [emphasis mine, from Sal’s quote above]

    And he not only has to ignore the words of this specific article, he has to cut out all the consilient evidence — from physics, chemistry, geology, ecology, microbiology — that our planet is old and that life has been established here for billions of years, radiated successfully, some lifeforms almost unimaginably old and some almost too new to recognize as separate species.

    But wait, there’s more. Sal also has to ignore the contradictions in his own position. According to him, evolution and natural selection cannot build new features or give rise to viable new species; he’s always raving about THE ANNIHILATOR and lately has been riding this hobbyhorse hard about genetic meltdown, weakening to the point of extinction (which obviously could only be true over a very short time frame, some millennia at most, or life would be extinct by now). And yet – YECcers must be the most hyper-mutationalists of all. There’s no other way we could have gotten 30000 species of beetles in 4k years from one pair on the ark unless every mutation is viable and none go extinct.

    Well, even then the arithmetic doesn’t work, even with hyper-mutation — but the point is that Sal has to use his excilience skills to deflect awareness of his own conflicting ideas and any awareness of the conflict between his bizarre timeframe and reality.

    So. It’s perfectly appropriate for me to give a sarcastic “Noah’s ark” answer to your question for Sal, because Sal can’t give you a real answer.

  23. petrushka:

    [stcordova cited article]: Wild-type populations showed no trend to decrease in size and, on average, they increased in fitness.

    At least you didn’t quote mine.

    Which goes to show that when creationist quote honestly, the quote completely undermines creationism.

    Yes!

  24. stcordova,

    Agreed. Some of my opponents in this discussion seem to question this standard aspect of evolutionary population genetics.

    ‘Seem’? I think you are misreading, at least if you refer to me.

    Small populations are in danger. I have acknowledged that on several occasions. But meltdown is but one aspect of that danger, and you can’t extrapolate it to every population, ever. That has been my contention.

    It’s like saying some infants die due to genetic disease, therefore all do.

    And let’s mention again the universally small populations off of the Ark.

    [eta – posted before I read down to find this had all pretty much been said by others!]

  25. hotshoe:

    There’s no other way we could have gotten 30000 species of beetles in 4k years from one pair on the ark unless every mutation is viable and none go extinct.

    <fifthmonarchyman>Jesus looked at them and said, “With man this is impossible, but with God all things are possible.”

    Matthew 19:26, NIV</fifthmonarchyman>

  26. Petrushka:

    Nor explain why elephants and naked mole rats do not get cancer.

    Another way of looking at this is that all other animals have genetic deterioration and elephants and naked mole rats got lucky. It demonstrates the inability of natural selection to purge out dysfunctional features of so many genomes. Thanks for the powerful data point confirming genetic erosion among so many animals. Millions of years of evolution hasn’t purged out cancer when it seems animal genomes could in principle function without cancers!

    I provided the yeast example because some here insist there is no evidence that genetic deterioration can result in extinction. That experiment falsifies that view.

    “Wild-type populations showed no trend to decrease in size and, on average, they increased in fitness.”

    Wild-type yeast that haven’t been through bottle necks and thus have bad mutants fixed have a chance. However, it is very very hard to evolve via selection a population that is gigantic and geographically spread out. But the experiment shows mutational melt down can cause a population to go extinct. The point being, there is no guarantee natural selection can weed out all the bad. That is a naive view.

    If genetic entropy compromises populations, it would apply to bacteria, cockroaches, cycads, volvox, crocodiles.

    Bacteria have suffered reductive evolution, I provided links earlier.
    For example:

    Reductive genome evolution at both ends of the bacterial population size spectrum
    http://www.nature.com/nrmicro/journal/v12/n12/full/nrmicro3331.html

    Bacterial genomes show substantial variations in size. The smallest bacterial genomes are those of endocellular symbionts of eukaryotic hosts, which have undergone massive genome reduction and show patterns that are consistent with the degenerative processes that are predicted to occur in species with small effective population sizes. However, similar genome reduction is found in some free-living marine cyanobacteria that are characterized by extremely large populations. In this Opinion article, we discuss the different hypotheses that have been proposed to account for this reductive genome evolution at both ends of the bacterial population size spectrum.

    Just because something is alive doesn’t mean it hasn’t suffered genetic erosion — look at wingless beetles for example.

    As to cockroaches, they can have 300 offspring each so they have more reproductive excess and thus can handle more mutational load. I did not say here that genetic erosion would cause them to die in 6,000 or so years.

  27. stcordova: As to cockroaches, they can have 300 offspring each so they have more reproductive excess and thus can handle more mutational load.

    No, this is stupid. The arithmetic of inheritance doesn’t work like that, and you should know better than to make up fairy stories about it.

    If cockroach parent Q has a hundred mutations and parent R has a hundred mutations, on average each of their offspring will have an assortment of 100 mutations (plus or minus a handful of brand new mutations or back mutations from the process of chromosome division). Having 3, or 300, or 30000 offspring doesn’t change that average.

    The survival value of reproduction having hundreds of offspring (and little or no parental care after egg laying/seed dispersal) vs having two or three offspring (and lots of family care after hatching/birth) has nothing to do with “genetic entropy” and has everything to do with the environment in which the species has evolved.

  28. stcordova: Another way of looking at this is that all other animals have genetic deterioration and elephants and naked mole rats got lucky.It demonstrates the inability of natural selection to purge out dysfunctional features of so many genomes. Thanks for the powerful data point confirming genetic erosion among so many animals.Millions of years of evolution hasn’t purged out cancer when it seems animal genomes could in principle function without cancers!

    (facepalm) Cancer isn’t a heritable trait Sal. Certain heritable genetic sequences may give you a higher susceptibility to certain types of cancer but you don’t inherit the cancer itself.

    I provided the yeast example because some here insist there is no evidence that genetic deterioration can result in extinction.That experiment falsifies that view.

    No it doesn’t. It shows extinction *may *happen in very small, bottlenecked population. It says nothing about larger populations with large genetic diversity.

    BTW Sal, we have sequenced the genomes of many animals that lived well before your claimed 6000 year old Earth. 40K year old manmmoth and brown bear DNA has been sequenced. We have horse DNA from 700K years ago sequenced, We even have Otzi the Ice man’s DNA from 5300 years ago. None show a “more perfect” genome that has severely degraded to what we see in similar extant species.

    Recalibrating Equus evolution using the genome sequence of an early Middle Pleistocene horse

    Abstract: The rich fossil record of equids has made them a model for evolutionary processes1. Here we present a 1.12-times coverage draft genome from a horse bone recovered from permafrost dated to approximately 560–780 thousand years before present (kyr bp)2, 3. Our data represent the oldest full genome sequence determined so far by almost an order of magnitude. For comparison, we sequenced the genome of a Late Pleistocene horse (43 kyr bp), and modern genomes of five domestic horse breeds (Equus ferus caballus), a Przewalski’s horse (E. f. przewalskii) and a donkey (E. asinus). Our analyses suggest that the Equus lineage giving rise to all contemporary horses, zebras and donkeys originated 4.0–4.5 million years before present (Myr bp), twice the conventionally accepted time to the most recent common ancestor of the genus Equus4, 5. We also find that horse population size fluctuated multiple times over the past 2 Myr, particularly during periods of severe climatic changes. We estimate that the Przewalski’s and domestic horse populations diverged 38–72 kyr bp, and find no evidence of recent admixture between the domestic horse breeds and the Przewalski’s horse investigated. This supports the contention that Przewalski’s horses represent the last surviving wild horse population6. We find similar levels of genetic variation among Przewalski’s and domestic populations, indicating that the former are genetically viable and worthy of conservation efforts. We also find evidence for continuous selection on the immune system and olfaction throughout horse evolution. Finally, we identify 29 genomic regions among horse breeds that deviate from neutrality and show low levels of genetic variation compared to the Przewalski’s horse. Such regions could correspond to loci selected early during domestication.

    How do you square all this directly refuting genetic evidence with your “degrading genome” claims?

  29. Adapa:How do you square all this directly refuting genetic evidence with your “degrading genome” claims?

    When a highly congenial speculation produced ex rectum is flat contradicted by an enormous amount of consistent and unambiguous observation, something has to give. For the creationist, it can’t be the doctrine, so what else is left but exciliance?

  30. stcordova,

    Hi Sal
    Cancer can occur without mutation in the genome. An example is vitamin d deficiency as measured in our blood. Vitamin d is a small molecule that is mostly obtained from exposure to the sun. It is a reaction that starts with sunlight modifying cholesterol in our skin and then being additionally modified in our liver and kidney. The molecule is part of the nuclear transcriptional protein complex that is involved in cell adhesion and division. When cellular levels of vitamin d are too low our cell cycle can go out of regulation, produce stem cells, and ultimately a cancerous tumor.

  31. colewd: Cancer can occur without mutation in the genome.

    But there are animals that don’t get cancer.

    Obviously they are violating the Tard Law of Thermodynamics.

  32. Looking at the Amazon reviews it seems that Sanford is aware that genetic entropy should have wiped every species out by now. I guess that means he’s a YEC.

  33. stcordova,

    However, it is very very hard to evolve via selection a population that is gigantic and geographically spread out.

    No, you just need to produce an average of more than one offspring per individual (2 in a sexual population). No selection required.

    Of course it’s hard to expand into a colonised niche. But what’s it colonised by? A resident species. How did that get there…?

    It can’t be genetic entropy all the way down. At some point, expansion must be possible, unopposed by species-level competition (selection of a sort) since competition can only occur when there is a competitor.

    This is where ‘universal meltdown’ falls down. One of the places, anyway.

  34. colewd:
    cubist,

    So, sure, you can define “grey swans” in terms of human ignorance if you really want to. You can identify an event as a ‘grey swan’ thanks to human ignorance of its cause(s). And if you do that, my next question will be, “So what?”

    Is there a reason that we are ignorant to the cause of so many inflection points in evolution OOL Eukaryotic Multi cellular etc?

    Yes: The earliest signs of life on Earth date back to around 3.5 billion years ago.

    Note that by defining a ‘grey swan’ in terms of human ignorance, you’ve provided an answer to your own question: Any and every “new identified cause” will “reduce the grey swan population”. So… just keep on trucking with mainstream science, I guess?

    Agree…maybe identification of the grey swans can help prioritize the journey.

    Again: You’ve defined ‘grey swans’ in terms of human ignorance. Which is all well and good, but it means that anything you regard as a “grey swan”, is a thing some scientist will regard as “a promising area of research”. Why, then, bother with the ‘grey swan’ label in the first place? So far, said label perfectly pointless and redundant to me.

    Perhaps you can firm up your definition, so that there’s some way to tell the difference between a “grey swan” and a “promising area of research”?

  35. stcordova,

    Another way of looking at this is that all other animals have genetic deterioration and elephants and naked mole rats got lucky. It demonstrates the inability of natural selection to purge out dysfunctional features of so many genomes. Thanks for the powerful data point confirming genetic erosion among so many animals. Millions of years of evolution hasn’t purged out cancer when it seems animal genomes could in principle function without cancers!

    Be nice if the Designer had sorted that one out then, wouldn’t it?

    You can’t assume that, because one organism has characteristic X, all organisms should. We don’t have trunks either. It all depends on strength of selection, which is not a universal for any factor.

    Elephants do get cancer, but only about 5% die of it as opposed to humans at 25%.

    Selection against cancer varies. It tends to be deferred rather than eliminated – eventually, if you live long enough, you’ll get it, whatever species you are. Selection is most strong against early-onset – particularly those occurring prior to the end of reproduction. The link of that to evolution should be obvious. So if we took cancer deaths prior to menopause, or within the lower 90th percentile of age-when-last-child-spawned in men, we’d see much lower rates in people too. The data are skewed by our carrying a significant number of older members, Plus if we stopped sunbathing and eating and breathing carcinogens we’d do even better; these have nothing much to do with population-level genetic deterioration. Our stats are bumped up by circumstance, and surviving ancients.

  36. stcordova,

    I provided the yeast example because some here insist there is no evidence that genetic deterioration can result in extinction. That experiment falsifies that view.

    A view no-one has expressed.

    But still, genetic deterioration was elevated in the yeast by having different mutation rates between the two strains. Sure, there is a rate of mutation that will cause extinction pretty reliably. What mutation rates will remain among non-extinct strains?

  37. stcordova,

    Just because something is alive doesn’t mean it hasn’t suffered genetic erosion — look at wingless beetles for example.

    True enough – my gills are worse than useless, for example.

  38. Perhaps the stupidest concept in this discussion is the notion that loss of morphological features, or reduction in size, is genetic deterioration.

    It’s a bit like a hoarder arguing that throwing stuff away is an unacceptable loss, because you might need it some day.

    I have a tendency to keep broken things for spare parts, and I find I sometimes need something I have recently thrown away.

    But the math Sal is quote mining is applicable to bacteria as well as to humans and elephants. I’m sure the sums are done correctly, but it is a flawed model of life.

    Odd, that IDists can see where GA simulations of evolution don’t model living things, but abstract equations do?

  39. Hi Sal
    Cancer can occur without mutation in the genome. An example is vitamin d deficiency as measured in our blood. Vitamin d is a small molecule that is mostly obtained from exposure to the sun. It is a reaction that starts with sunlight modifying cholesterol in our skin and then being additionally modified in our liver and kidney. The molecule is part of the nuclear transcriptional protein complex that is involved in cell adhesion and division. When cellular levels of vitamin d are too low our cell cycle can go out of regulation, produce stem cells, and ultimately a cancerous tumor.

    That was very informative. Didn’t know that about Vitamin D. TSZ is such a great forum to learn things! Thanks. And petrushka just taught me about cancer-free elephants. Those data points were worth the price of admission.

    But, how do we know we (all cancer capable organisms) don’t have defects already that make such creatures vulnerable to cancer, We may find the elephants have a working model of what we don’t have.

    I spoke to a cancer researcher at an NIH sponsored event. She says the incidence of juvenile cancer is occurring at earlier and earlier ages. I suspect some of it may be statistical sampling bias and some due to environmental poisoning, but as we hope to track many more genomes through generations we may be able to isolate how much is genomic.

    We may find out the human race is slowly eroding genetically. The thesis follows from this principle:

    1. most variation is not creative of function, it is at best of no effect and more damaging than creative. The usage of the words “beneficial” and “deleterious” in evolutionary literature is misleading.

    2. For every bad mutant purged by drift or selection, more new mutants emerge.

    This is true especially for large functional genomes, low excess reproduction rates, high mutation rates.

    Here is a data point:

    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.

    Michael Lynch
    http://www.uncommondescent.com/darwinism/sanfords-pro-id-thesis-supported-by-pnas-paper-read-it-and-weep-literally/

  40. stcordova,

    But, how do we know we (all cancer capable organisms) don’t have defects already that make such creatures vulnerable to cancer, We may find the elephants have a working model of what we don’t have.

    Elephants have multiple copies of a gene TP53, a tumour suppressor gene. That appears to be one of the keys. It’s harder to break them all than just one. And it appears that elephants gained them rather than we lost them.

    Will you be declaring this a data point against your theory? Or are counter-facts not possible? 😉

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