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:
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.
Dave,
http://sandwalk.blogspot.com/2014/04/a-creationist-tries-to-understand.html
The 130 figure is based on measured mutation rates and Chimp/Human divergence. That’s Larry’s figure not mine. Larry’s argument depends on ENCODE being really really wrong and proteins not being that specific.
If 80% of the genome is optimized for function, 80% of 130 is 104 ~ 100.
But even 2% functional would still be 2.6 bad mutation per individual per generation, still beyond Muller’s limit of 0.5 and Moran’s of 1 – 2.
cubist,
“I apologize; I thought that a person as interested in “why is that?”-type questions as you, might look at the bare assertion of it’s old and go on to think about why the age of Event X might be relevant to the question of why we are or are not ignorant of the causes of that Event X. I see that I was wrong about that.”
What I am interested in is why we can model physics more easily then biology. If we can make a mathematical model that can predict outcome, and test the model then the challenge of historical evidence is less relevant to finding cause.
For someone who prides himself on math, you seem to have missed
2% of 130 – 2.6
25% of 2.6 = 0.65
25% are for seriously detrimental. The other 75% may be mildly but still detrimental. I said Larry is assuming most proteins aren’t that specific in terms of the space of functional forms for a given interactome. I think that is mistaken.
Do you think someone in general can tolerate having 75% of the amino acids in their protein coding regions mutated? How about 75% their introns?
So my original calculation of 2.6 stands.
Larry can’t afford much room to be wrong since 0.65 is already past Muller’s limit of 0.5 (and Muller has a Nobel Prize, Larry doesn’t). He’s having to strain and imagine a lot of tolerance to mutation.
Ok, so let’s take the 0.65 figure. That is 0.5% of the genome. Does anyone think we can mutate 99.5% of the genome and not suffer some serious damage? Well, Larry has to at some level believe something in that ball park. Even 80% seems outrageous to me. E. Coli might survive that, not humans.
One thing worth pointing out is DNA coils and changes in DNA in one spot affects DNA a million base pairs away because the coiling brings parts of DNA in close proximity.
https://en.wikipedia.org/wiki/Enhancer_%28genetics%29
Stuff like this can’t just be mutated willy nilly without functional compromise.
stcordova,
Typically one-eyed. Deleterious ones are fixing but beneficial aren’t? You have it wrong.
Even if the human race is dying out (not proven by some shaky math and a touching faith in ENCODE), this says nothing about the historic progression to the species.
stcordova,
And yet there are polymorphisms. How strange.
stcordova,
No (although 75% of bases does not equate to 75% of amino acids).
Such people tend not to exist. That leaves the remainder to soldier on.
I’m using your words.
You have variously claimed 130 detrimental mutations, 100, and 2.6.
We know from actual evidence that 90 percent of the genome is indifferent to mutations. It isn’t conserved. Functional or not, it is insensitive to mutation.
Let’s take the 2.6 coding mutations per human. If 0.65 are serious, they are unlikely to fix.
So maybe two per human. But humans have mostly pairs of genes, so effectively we are down to one.
Not a lot to hang YEC on.
You haven’t even mentioned that some of that 2.6 are going to be beneficial or compensating. You haven’t mentioned that some mildly detrimental mutations can lead to otherwise unreachable beneficial mutations.
Where’s the math?
Adapa,
“Those who preached hatred and fear and guilt and who ruined innumerable childhoods should have been thankful that the hell they preached was only one among their wicked falsifications and that they were not sent to rot there.”
— Christopher Hitchens
stcordova,
Is there a functional spec or actual source code for ANNIHILATOR available for inspection?
Some interesting stats:
Between one and tree percent of humans are born with a genetic defect.
About 19 percent of men and 13 percent of women do not reproduce.
Since the population (prior to the advent of birth control) grew steadily, one might be forgiven for assuming that seriously detrimental mutations die out due to purifying selection. It’s not a matter of differential reproduction. Nearly 15 percent of humans simply never reproduce.
Is it unreasonable to assume that individuals who have accumulated a large number of detrimental mutations are among that percentage?
How about it Sal? You have any numbers?
Does ANNIHILATOR include purifying selection? What numbers do you use?
For the record, even the ENCODE folks seem to have largely stopped defending that initial 80% claim. For instance, it is conspicuously absent from their 2014 follow up (http://www.pnas.org/content/111/17/6131.full).
Also, asserting that a sequence is functional is not at all the same thing as asserting that it is completely intolerant of mutational change. Sal, if you want to argue that the immense degree of genetic polymorphism seen in nature is mostly deleterious, you’re going to have to work a lot harder than this.
ENCODE’s problem is claiming there can be functional sequences that are completely tolerant of mutation. Moran has admitted this is within the realm of possibility, but if true, it makes the “detrimental mutation” label moot.
Based on my understanding, it seems like there is a fairly wide continuum when it comes to the degree of mutational tolerance a functional sequence can have. Some proteins are extremely conserved, others show a much lower degree of conservation outside of certain domains or active sites. Four-fold degenerate sites in protein coding sequences are often (though not always) relatively free of constraint. The functional lncRNAs I posted about last week seem to be perfectly tolerant of mutations except in certain regions. That’s why the authors had to look for “microhomology” to even identify them in different organisms.
All the more reason why — when you are quibbling over two
percentor 0.5percent— you don’t hang a YEC hat on genetic entropy.Post edited.
Agreed.
Actually, it should be two or 0.5.
Not percent.
stcordova,
Kondrashov posed a question regarding effective neutrality on the detrimental side and offers a couple of possible answers – synergistic epistasis and ‘soft selection’. I was offering another. If you multiply up any approximation over many allele trajectories, you will end up with an erroneous view. It’s like saying 1/100th of the population is small, so an allele fixed in that 1% is effectively neutral, and the next 100th is small too so it still is, and the next … for sure, multiple mutations affect multiple loci not one, but it remains the case that the neutral approximation cannot be used on the wider set of all alleles, as if small selection coeficients are never effective regardless how many times they are fed in.
The tenure of any detrimental allele is less secure than a beneficial one of approximately equal distance from neutral, regardless of population size, when many alleles are considered.
The overall tendency for any population is the accumulation of beneficial alleles and the removal of detrimental ones. That’s not universal – there are things that can counteract this tendency – but it does not have to be to account for extant and thriving species 3.8 billion years on. Because we have a set of populations, not just one. They can’t in total be subject to the variance that affects one considered in isolation. The Law Of Large Numbers operates.
Please share how you observed genetic entropy. Did you build a genetic entropy meter? What are the units?
You got that right!
Hard to measure imaginary concepts. Can you weigh fairy dust?
Open source project!
https://github.com/annihilator
Complex phenomena are intrinsically more difficult to model than simple phenomena. Biology is a lot more complex than physics. ‘Nuff said?
True, and so what? Cordova’s ‘black swan’ is still a uselessly ill-defined not-quite-a-concept-yet, and your ‘grey swan’ extension of Cordova’s term is still redundant & pointless.
Anyone want to wager it has the same basic function as Sanford’s hopelessly cooked “Mendel’s Accountant”? Where a population would rapidly crash to zero no matter what inputs were provided?
cubist,
Complex phenomena are intrinsically more difficult to model than simple phenomena. Biology is a lot more complex than physics. ‘Nuff said?
Biology includes both chemistry and physics. What makes it more complex? Is it more complex than quantum mechanics?
You are confusing difficulty with complexity.
Chemistry is more complex than physics; biology more complex than chemistry.
That doesn’t imply that biologists are smarter than physicists. Just that it is more difficult to find regularities in biology.
cubist,
True, and so what? Cordova’s ‘black swan’ is still a uselessly ill-defined not-quite-a-concept-yet, and your ‘grey swan’ extension of Cordova’s term is still redundant & pointless.
I understand thinking this is pointless right now. The overall theme is the difficulty in modeling biology and the cause of this. I understand you agree here that biology is complex and difficult to model but lets work through the WHY of this is a problem and then I think the swans will make sense.
I explained why a bacteria can have a lot of polymorphisms but a human with it’s complex multicellular structure and developmental mechanisms can’t tolerate as many. I provided evidence with the HeLa cells. E. Coli has only 20% conservation, that means it might tolerate a lot of polymorphism. You think a human can tolerate having 80% of its DNA scrambled?
You apparently missed the explanation. Your viewpoint is as bad as supposing that since the unicellular HeLa cell can be so badly damaged and still keep reproducing, that surely the originator of Hela can also be as badly damaged and live — but she didn’t. So much for your polymorphism argument.
That’s nothing compared to you Sal. You apparently missed the 99.9% of the scientific data that directly refutes your idiotic YEC genome degradation claims.
At least 80 percent of the human genome is indifferent to scrambling. Most of the rest is more tolerant than you assume.
You toss around numbers with abandon. Could we ask you to pick one and stick with it?
No code, but I provided the outline.
1. Interspecies competition resulting in extinction of species.
Don’t you think it’s kind of absurd you’re demand for a simulation when we have real world evidence of “Elimination of Species by Means of Natural Selection?” What more accurate model is there than what we see in recorded history. And how many new species to replace the one gone or going?
Here is list of over 7000 for starters.
http://www.iucnredlist.org/search
How many news ones? No one here at TSZ has much of counter.
2. Genetic Load overwhelmed. I provided numbers and analysis here:
No one here in this discussion has refuted the logic with anything but misrepresentaitons — like Petrushka insinuating I said genetic erosion is necessarily leads to extinction.
Species extinction causes genetic extinction, not necessarily the other way around. See:
Genetic deterioration isn’t the major cause of mass extinction, but mass extinction is a component of genetic extinction — 100% functional loss. Selection doesn’t arrest that, in fact it helps speed the elimination. Said it again, 4th time at least.
Genetic deterioration isn’t the major cause of mass extinction, but mass extinction is a component of genetic extinction — 100% functional loss. Selection doesn’t arrest that, in fact it helps speed the elimination. Said it again, 5th time at least.
Genetic deterioration isn’t the major cause of mass extinction, but mass extinction is a component of genetic extinction — 100% functional loss. Selection doesn’t arrest that, in fact it helps speed the elimination. Said it again, 6th time at least.
So how many times does Petrushka intended to keep insinuating that I’m making the argument that genetic entropy is necessarily leads to extinction?
3. Reductive evolution. Natural selection may select against functional compromise, but it also can select for it. I provided papers that show this. Did you just decide to ignore them? In fact Lenski made a simulation for the Black Queen hypothesis. Then Koon said reductive evolution is the dominant mode of evolution with (not-at-all-explained) spurts of accumulation — (aka poof).
All 3 elements were listed in as part of the ANNIHILATOR model. But why do we need a simulation, I’ve provided references to data points in the real world.
So how many new features does the Darwinian model predict will fix into the human genome per generation by natural selection? 1,2,3? How about zero.
If zero, the human race is stuck in neutral at best, going in reverse at worst. Anyone here think the human race is improving genetically? If not, my point stands.
On what basis do you make that assertion? But even if off by a factor of 10, that’s 8% of the genome, which is 10.4 mutations, which is 20.8 times bigger than Muller’s limit.
But do you think the human genome (gene pool) is improving? If not, my point stands.
Weasel can be created in a single line of Perl. Your confidence in your “model” is outstanding.
Wow. You actually answered your own question before you asked it.
Mu.
stcordova,
So how come there are many polymorphisms in the human population?
20 % comparing what to what? I asked this already.
Is that happening? Should we be concerned? 90%+ of the DNA appears to be unable to suffer a deleterious point mutation. But if you actually changed 80% of the DNA all at once it would be infertile due to inability to perform a successful meiosis with the wild type. But it doesn’t change all at once. It changes at c130 per individual. Any damaging ones get filtered out by selection, leaving the rest.
You seem to have missed my discussion of all these points upthread, shortly after you raised them.
stcordova,
You do realise that, when a species has been eliminated by natural selection (competition with another), there is a species left, with a bigger range? It’s little different from elimination of an allele by selection.
Do you envisage ALL species being eliminated in this way, and the last one just kind of jumping off a cliff?
stcordova,
How about zero for alleles fixed by genetic entropy too, then? How is deterioration more likely, if even beneficial alleles can’t fix?
There is no requirement for humans to evolve one single step further for evolution to be true, by the way. You’re picking a poor model species to apply to the entirety of evolutionary history. So far, we’ve had populations that are too small and populations that are too big to adapt! Is there nothing in the middle?
stcordova,
What if someone else said something else? I mean, why is Koonin the only authority that matters on this? Mainstream science discusses both the positive and the negative evidence for one’s theory.
And yet, humans are chock full of polymorphisms. As are most other complex multicellular species that we have observed. What’s up with that?
Fair enough, I haven’t paid especially close attention to the discussion. But your HeLa point seems to be entirely irrelevant to to the broader discussion. Do you think that the tumor cell line would still proliferate outside of a laboratory setting? What does this have to do with what’s going on in nature?
More specifically, what does somatic cell mutation have to do with evolution?
Sincere apologies, Allan. Didn’t mean to diss you, I’m out numbered with some determined guys to take my OP down.
If I weren’t a creationist I’d say it will all definitely end when the universe burns out — the 2nd law of thermodynamics guarantees the end.
The Designer got busy with E.coli.
We know all those variations couldn’t have been invented via evolution.
Because
Since “improving” can only be measure by reproductive fitness in the current environment and since in our current environment the average human life span has increased from 30 years to over 80 years in the last two millennia I’d say yes, it is improving.
Your point is refuted.
See, I think this is extremely cool. It’s quite the testament to how ecologically diverse and hyper abundant some bacteria are. What the term “species” evens means in a bacterial context is an interesting problem.
FWIW, I made a superficial (I mean really really superficial) look at the aaRS genes of E. Coli strains that may suggest 100% conservation in those genes. Unfortunately I had to drop the project temporarily. I’m hoping JohnnyB, myself, and some new found friends will take it up.
The reason this is of interest to me is that aaRS has been a phylogenetic marker by evolutionary biologists. Why is there inter-species variation of aaRS but no INTRA-species variation of aaRS. I could be totally reading the sequence comparisons wrong, but at the very least this all says something about E. Coli’s aaRS clock.
The study can be carried out, it’s just a matter of tedium. If you find that my preliminary findings on the aaRS genes (about 20 plus a few) in E. Coli are all wrong, I would still be grateful for the correction. Whatever the outcome, JohnnyB and I would be happy to advertise your findings.
stcordova,
I’m intrigued but don’t really have the time at the moment to give a firm commitment. If I do find some time, I’ll try to give it a look.
stcordova,
You have to be a bit careful about your species concept. Bacterial species don’t sit very well in the species concept applied to eukaryotic populations. But the broad answer is simply comparative rate of change. If speciation (bifurcation and divergence) happened (say) every 500,000 years, but fixed change to an AARS in a lineage happened every (say) 5 million years, you would expect to see very little inter-species variation except when the change was in the process of fixing, a shorter portion of the whole. It would be polymorphic for a relatively short time. But you would still get variation within a higher taxonomic group than species, as we do.
AARSs and evolution – review
I have no problem with that on principle, but it would mean the E. Coli we all know and love (cough) was a relatively new strain from a single parent in a single host!
And what about all the other genes that are the 20% core? If there is low intra-species divergence then E. Coli as we know it is a relatively new phenomenon, it sort of appeared recently on the scene, eh?
Now what if we find the same intra species patterns for all other bacterial species? 🙂
But I’m getting way ahead of myself. We don’t know if my very very preliminary analysis is even correct. The NIH NCBI gene banks are open for business, but so many genes, so little time….