by Joe Felsenstein
http://www.gs.washington.edu/faculty/felsenstein.htm
Over at Uncommon Descent Sal Cordova has opened a dramatic new thread “Gambler’s Ruin is Darwin’s Ruin“. Apparently improvement of a population by natural selection is now shown to be essentially impossible. He invokes the example of Edward Thorp, who developed the winning system for blackjack fictionalized in the movie 21.
Cordova uses the stochastic theory of gene frequency change of citing Motoo Kimura and Tomoko Ohta’s well-known 1971 monograph “Theoretical Aspects of Population Genetics”, and argues that
Without going into details, I’ll quote the experts who investigated the issues. Consider the probability a selectively advantaged trait will survive in a population a mere 7 generations after it emerges:
if a mutant gene is selectively neutral the probability is 0.79 that it will be lost from the population … if the mutant gene has a selective advantage of 1%, the probability of loss during the fist seven generations is 0.78. As compared with the neutral mutant, this probability of extinction [with natural selection] is less by only .01 [compared to extinction by purely random events]. (bracketing is by Cordova)
This means is that natural selection is only slightly better than random chance. Darwin was absolutely wrong to suggest that the emergence of a novel trait will be preserved in most cases. It will not! Except for extreme selection pressures (like antibiotic resistance, pesticide resistance, anti-malaria drug resistance), selection fails to make much of an impact.
The Kimura/Ohta quote in question is on page 1 of their book, and describes a mutant with a selective advantage of 1%.
This would be a shocking disproof of decades of work in population genetics—if it accurately reflected the ultimate fate of those mutants. Fortunately, we can turn to an equation seven pages later in Kimura and Ohta’s book, equation (10), which is Kimura’s famous 1962 formula for fixation probabilities. Using it we can compare three mutants, one advantageous (s = 0.01), one neutral (s = 0), and one disadvantageous (s = -0.01). Suppose that the population has size N = 1,000,000. Using equation (10) we find that
- The advantageous mutation has probability of fixation 0.0198013.
- The neutral mutation has probability of fixation 0.0000005.
- The disadvantageous mutation has probability of fixation 3.35818 x 10-17374
In other words, yes, in this case there is a lot of loss of advantageous mutations, about 49 being lost of every one that makes it to fixation. But they are each nearly 40,000 times as likely to fix as are individual neutral mutations, and deleterious mutations are essentially never going to fix in such a case.
Why does this give such a different result than the comparison of 0.78 to 0.79? It is because after 7 generations the surviving mutants in the case of selective advantage are at a higher frequency than are those in the neutral case, and the result is a much greater chance of fixation.
In fact, the Gambler’s Ruin shows a similar behavior—its mathematics is similar to (but not identical to) the population-genetic case. If you toss coins with a stake of $1 against a house which has $1,999,999 to wager, and you both keep playing until one holds the whole $2,000,000, if the game is fair you will be the ultimate victor one time out of 2,000,000, and the rest of the times the house will win. But if you have a 1% advantage, so that on each toss you have a 50.5% chance of winning, you will be the ultimate victor nearly 1% of the time. Mostly you will be ruined, but you will bankrupt the house 20,000 times as often as you would if the toss were fair.
So yes, the mathematics of Gambler’s Ruin speaks to the issue of natural selection—but it confirms its effectiveness.
(The other issue raised by Cordova, that of interference between mutations at different loci, is the well-known Hill-Robertson effect. If the loci have more than a tiny amount of genetic recombination between them, the interference largely vanishes. Cordova and the other commenters there have forgotten this.)
Basically then, he’s pretending that mutations are rare events?
It is always amazing how creationists, and Sal in particular, can see one thing in a text book that seems to support their presupposition and completely miss the majority of the lesson which indeed shows that their conclusion is wrong. The clue should be that the book Sal quote-mined deals with an integral part of evolution theory, namely population genetics. Also if this book was printed in 1971 and wasn’t an earth shattering refutation of “Darwinism” then, why should we now expect it to be?
Prof. Felsenstein (sir), I must disagree with you about the Hill-Robertson effect - I’m not sure Sal is that advanced. I suspect he’s assuming a (roughly) constant total variance in fitness so that having more genes involved reduces the average effect of each one. But I haven’t pushed him on it, because I forgot to check the literature when I was at work.
I don’t have access to the book in question. Do they provide an equation to calculate the odds that a mutation with s=.01 will be fixed out of a population?
Is it, by chance, the remaining 98%?
It hardly seems meaningful to infer the effectiveness of natural selection by comparing the rate of fixation in advantaged vs. neutral mutations, when in fact you are comparing “tiny” to “much tinier.”
Rather, the most meaningful conclusion appears to be that genetic drift reduces the the odds of fixation of an advantaged trait by 98% in an s=.01 scenario.
I noticed in that UD post that Sal said he’d seen both “21” and “Expelled” the same day. Does he have like a job or something?
Some comments on the comments:
J. Biggs wrote:
No, they are rare. He’s noticing that even advantageous ones very often get lost, and arguing that this refutes the effectiveness of natural selection.
unglss asked:
I’m not sure what you mean by fixed “out of” a population. You can use Kimura’s 1962 formula for fixation probability of a single copy of a mutant that has selective advantage s and population size N, and it is (1-exp(-2s))/(1-exp(-4Ns)). So for s = 0.1 that is 0.181269 if N = 1,000,000. But that’s what I’d call fixation “in” a population. What do you mean by “out of”? By the way, Kimura’s original 1962 paper is in Genetics and is freely available there by web. More equations available in my own population genetics free e-book.
unglss again:
If by “it” and “out of” you mean the probability of getting ultimately lost rather than fixed, yes, it is 1 - Prob(fixation).
unglss again:
It’s a matter of the overall rate of fixation of advantageous mutations and of deleterious mutations, and these have very different probabilities of fixation, as you can see from the probabilities.
You’d be right. Either the mutant fixates or goes extinct, so with s = 0.01, the extinction probability is 1 - 0.02 = 0.98. However, the thing to note here is that if the mutant fixates, then that’s it, it’s “taken over” the population. Considering the timescales of evolutionary change, if advantageous mutants appear time and again, each successful fixation would only increase the population’s fitness (even if it only happens 1% or 2% of the time). This is basically natural selection, and shows how mutation and selection drive evolution, improving populations over time. Isn’t it great?
Replying to the first part of your comment, “tiny” vs. “tinier” isn’t really a good way to look at things. Even a tiny selective advantage can push up the fixation probably several orders of magnitude. This just means that a single mutation doesn’t always lead to “improved” populations, but over time, many mutations (which on long enough timescales, are not *rare*) do.
Sal really stepped into my world on this one, since I counted Blackjack for several years. I take him apart here:
http://scienceavenger.blogspot.com/[…]ero-sum.html
He doesn’t even understand the basics of the issues, making statements like:
“If he has a 1% statistical advantage, that means he has a 50.5% chance of winning and a 49.5% chance of losing.”
Which reveals either that he is completely ignorant of the rules of blackjack, or he doesn’t understand the difference between probability of victory and expected winnings.
I would also note that it is highly unlikely that Thorp’s system was the one used in the movie. Blackjack counting systems improved dramatically in the 70’s and 80’s as computing power allowed for simulations for the first time, and his would no doubt have been surpassed in efficiency by more modern systems.
bump
Sir:
Thank you for your response. By “fixed out of” I meant eliminated as a variant. I apologize for my lax use of words.
Thanks for the equation itself, also. I greatly appreciate your time.
I agree with you that this certainly does not “refute” natural selection. However, I don’t think it’s “Darwin’s gain,” either. An s=.01 mutation may have a 40,000x better chance of fixation than a neutral one, but the more relevant fact is that the s=.01 mutation has only a 2% chance, and the neutral and disadvantageous mutations have virtually no chance at all.
The problem becomes even more severe in smaller, isolated populations (where genetic drift becomes more severe), and in the context of sexual reproduction (where each child receives only 50% of the collective genetic diversity of its parents).
I don’t think this is any meaningful “gain” for Darwin at all. Rather, it’s a significant hurdle that mutations have to get over to get fixed. It may be surmountable, over significant periods of time, but it is a hurdle, nonetheless.
Of course such a theoretical discussion cannot ever prove that evolution by natural selection is impossible anyway. There are always a host of other factors operating in the real world that can drastically alter the probabilities. For example, what is the dominance of the newly arisen mutation? How many offspring are produced carrying the new mutation and what is the rate of inbreeding? Are there other considerations such as hitchhiking, pleiotropy, density dependent selection, sex-linkage, etc. All these factors and many more can help to determine the initial and ultimate fate of mutations no matter how selectively advantageous they are. And then of course there is population size, environmental heterogeneity etc.
Leave it to creationists to find the end of “Darwinism” in everything they read. Why is this guy reading 37 year old papers anyway? No matter what he quote mines he will always find that science has moved on in the last thirty years anyway. How come these guys never seem to notice that? It’s almost as if they as just trying to find things that someone might take the wrong way instead of really trying to learn anything about science.
I am afraid I can’t take credit for that comment. I believe you were referring to Henry J.
AAHHHHH.…The Cordova.…standard with fine Corinthian Bullshit.
Dr. Felsenstein,
Thank you for responding to our discussion at Uncommon Descent. I appreciate that you would take time to respond. I have provided links from Uncommon Descent to your response here. I encourage those reading Uncommon Descent to read your response.
Many thanks for taking time to read what I wrote and offering a response here at PandasThumb.
Salvador T. Cordova
unglss said:
In small populations the chance of fixation of an advantageous mutation will still be about 2s (Haldane’s approximation from 1927). For N = 1000, for example, fixation probability of an advantageous mutant with s = 0.01 is still about 0.0198013. The probability of fixation of a neutral mutant is now up to 0.0005, and that of a deleterious mutant is bigger than it was but still below 10-19.
And sexual reproduction is no problem because that calculation was for sexual reproduction. Each child receives half of its genes from each parent, but also each child has twice as many parents as in the asexual case.
Sal Cordova argued that there was little difference in outcome between advantageous and neutral mutations. He was wrong about that, and I assume that he will admit that.
At least I have to say that Sal is probably the most polite ID/Creationist that comments here.
Mr. Felsenstein:
I greatly appreciate the explanation. Thanks.
Forgive my abject ignorance, but I’ve been wondering whether s=.01 is typical. I gather that if this number were even slightly larger, the probability of fixation would go up dramatically. So is s=.01 conservative? unglss seems to be saying that for evolution at this level of selective advantage, the loss rate implies that evolution will be slower than actually observed in some cases. So my guess would be that some beneficial mutations offer better than a 1% improvement. And those would be a LOT more advantageous than neutral mutations.
So where did the 1% number come from? Is it realistic?
Flint:
Seems like that’s going to depend on the mutation at issue. Certain mutations (like antibiotic resistance) are going to be significantly higher than .01. The S of other mutations (like gradual changes to anatomy) are going to be much lower. Seems like you’d actually have to observe the effect of the mutation to determine the S. Yes?
J. Biggs:
Oh, Sal’s a peach, alright:
His “politeness” here is merely convenient. The above comment is typical of his rhetoric.
I specifically said:
I was taking issue with Darwin’s statement:
However, Kimura and Ohta noted:
Darwin was responsible in large part for the false assumption that “every advantageous mutation that appears in the population is inevitably incorporated”. But Kimura and Ohta demonstrate this claim is false by several orders.
You are correct that selective advantage leads to a stronger probability of fixation, but how many traits can be fixed over time seems not very clear, especially if we are talking multiple traits simultaneously…
I alluded to the problem of selection interference. It has been discussed, but I think it needs to be more fully explored and better known than it is today. John Sanford of Cornell indirectly postulated there is a limit to the value of selective advantage “S” depending on how many traits are viewed as selectively advantaged in the population. He suggests selection in human populations can only be effective for 700 traits simultaneously under a multiplicative fitness model. I have not been able to independently confirm his calculations.
I presume the work of Robertson-Hill might have bearing. It was mentioned in Kimura and Ohta’s work page 13. It appears Sanford follows the line of reasoning of Robertson-Hill in his book Genetic Entropy.
In anycase, I felt your rebuttal was for the most part well argued. I hope I have at least clarified my position, even if you disagree.
regards, Salvador T. Cordova
(my highlighting)
There appears to be a conflation of Hemoglobin S (Human genetic resistance to Malaria) with drug resistance in parasites.
So we have 4 examples of positive evolutionary selection being waved away, rather than just 3.
@ Flint and ungtss:
Here, S is usually taken as “small” so is quite close to zero. This is because selection in nature is “weak”, or has only a small contribution to fitness. If S was “large”, like say S = 1 or S = 2, the biology just doesn’t make sense. It’d be like a human giving birth to Wolverine from the X-Men. Advantageous mutants are typically only a little advantageous. And even in antibiotic resistance or related ideas, selection is usually still weak.
What false assumption? Made by whom? No one with a triple digit IQ would read that passage and think that Darwin literally meant that 100% of advantageous mutations would be passed on. What utter tripe.
Sal, we aren’t in 1859 anymore.
ungtss, yes, the chance of a beneficial mutation spreading throughout the population (using the numbers posited here) is 2%. The chance of the mutation going extinct is 98%.
So how many times would the same mutation have to arise to ensure that it gets fixed in the population, again assuming the numbers we are using here?
1 mutation: 2% chance of fixation 2 mutations: 4% chance of fixation 3 mutations: 6% chance of fixation 4 mutations: 8% chance of fixation 5 mutations: 10% chance of fixation 6 mutations: 11% chance of fixation .…. 33 mutations: 49% chance of fixation 34 mutations: 50% chance of fixation 35 mutations: 51% chance of fixation .…. 207 mutations: 98% chance of fixation 208 mutations: 99% chance of fixation
So if just 1 animal in a population has the beneficial mutation, there is a 98% chance the mutation will not spread and a 2% chance that the mutation will spread. Many/most mutations likely start in just this manner, with a single mutation in a single individual.
Now imagine that a 2nd animal (at some other point in time) has the same mutation. In other words, I am not saying that two animals at the same time have the same mutation (which is certainly possible); I am saying that the first mutation died out and has now re-arisen in a different animal. This mutation has the same 2% chance as the original animal, but the overall chance that the mutation fixates (either from the first or the second individual) is 4%.
The numbers above speak for themselves. Each number assumes that only a single individual has the mutation at a given time. How many times would the mutation have to “independently arise” before it is likely to fixate in the population?
Once the same beneficial mutation appears 35 separate times, it is more likely than not that it will spread through the population.
Again, I think these numbers may underestimate how easy it is because more than one individual can have the same mutation.
Mutations are rare? That’s not what one hears at Sandwalk.
No, Sal is literally correct. Darwin did indeed say in that particular quote that selection is preserving ALL that are good. Not some, not most, ALL. But of course, it would be a perverse misreading to think Darwin was making such a case literally when it seems pretty obvious he was describing the general sweep of selection. Elsewhere, Darwin makes it clear he understands that individuals born with potentially beneficial characteristics commonly do not survive to breed for reasons entirely unrelated to that characteristic. I vaguely recall Darwin illustrating this with moths and candle flames.
What Sal has done here is (gasp) quote mined Darwin.
Consider J Biggs’ carefully choreographed astonishment:
I could only ask that people READ the material surrounding Sal’s quote, to see exactly what sort of case Darwin is making at that point.
Dan,
What simulation are you specifically referring to
What simulation are you referring to? Can you point to the specific page in his book where he say’s its his simulation? Or that he used a simulation in the first place to reach his major conclusions? Do you have Sanford’s book? :-)
By the way, for the readers benefit, state some realistic ratios of beneficial to harmful according to the magnitude of s.
1. s greater than .05
2. s less than .05 but greater than .01
3. s less than .01 but greater than .000001
or some detailed distribution.
Better yet, tell me if you agree with Kimura’s s-values for the “no-selection box”. If you don’t agree, provide s-values for the no-selection box described in Sanford’s book. Tell us if you agree with the no-selection box hypothesis.
Regarding heterozygous advantage, are you saying this will solve the problem of mutational meltdown. It didn’t seem to work so well in those cases, did it? :-)
Heterozygous advantage has been involved in the persistence of Sickle Cell anemia and Cistic Fibrosis. I’m sure you’ll feel just peachy if you discovered you were heterozygously advantaged with Sickle Cell and Cystic Fibrosis recessives in your personal gene pool or that of your family members.
In anycase, it’s ability to rescue from mutational meltdown is dubious. Why is heterozygous advantage any better than any other advantage. For the readers benefit, can you affix a generalized s-value to it? :-)
But of course, one merely needs to redifine what is “good” to argue Darwinism works. One merely needs to label Sickle Cell anemia and Cistic Fibrosis as examples of the effectiveness of selection in weeding out the bad. Survival of the Fittest is now being relabeled Survival of the Sickest.
If the sickest survive, one has to wonder if selection is that effective at evolving seriously innovative solutions. Sickle Cell anemia seems to be a bit of bridge-burning strategy, not one of real large scale innovation.
Wow, 360 comments later and my disdain for lawyers remains unchanged.
Considering creationists willingness to equivocate on words like “science” and “theory”, why would they feel obligated to avoid equivocating on a word like “entropy”?
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Salvador T. Cordova said:
You know Sal is losing an argument when he suddenly starts pretending he can’t respond to you unless you provide exact page numbers (which he never does himself). He’s run away from losing arguments this way at least once before, so I guess he’ll be gone from this thread soon as well.
So once again, he probably won’t admit he was wrong to equate my arguments with the (alleged) surgical mutilation of innocent children. (Hey, Wormtongue, which organ did I just cut out of a baby with this post?)
Well, since he isn’t in the habit of providing exact page numbers, I don’t see why anyone should go to that much trouble for him. Once again, a creationist fabricating arbitrary rules for other people, but never following them himself.
And of course the asshat will never apologize for slander. He’s Lying For Jesus™, and that somehow makes it okay.
Maybe someone should just start spreading a rumor that Slimy Sal rapes babies and drinks their blood. It’s as honest as his own tactics. It’s not our fault Slimy Sal’s moral compass points straight to the gutter.
In anycase, it’s ability to rescue from mutational meltdown is dubious.
Well, if we observe that “mutational meltdown” is not taking place, then we can safely conclude that either: a) it’s not happening; or b) something is indeed rescuing us from it. So your argument isn’t exactly relevant in the real observable world.
But of course, one merely needs to redifine what is ”good” to argue Darwinism works.
…says the guy who redefines any word on the fly at any time in order to make his arguments sound credible.
One merely needs to label Sickle Cell anemia and Cistic Fibrosis as examples of the effectiveness of selection in weeding out the bad.
Well, yeah, parasites that can beat a host’s immune system survive better in said host than those that can’t.
Survival of the Fittest is now being relabeled Survival of the Sickest.
And “labeling” is relevant…how?
If the sickest survive, one has to wonder if selection is that effective at evolving seriously innovative solutions.
What are you talking about – the sickest germs, or the sickest host-creatures? Either way, this statement makes no sense: even when “the sickest” survive, they tend not to reproduce as much as the healthiest.
Sickle Cell anemia seems to be a bit of bridge-burning strategy, not one of real large scale innovation.
That does nothing to disprove evolution; it’s merely an example of an adaptive response that confers a lot of short-term gain (the ability to thrive within a host) with little long-term loss (the ability to keep itself alive via a host for longer periods of time than a mere germ can anticipate). As long as the germ can spread to another host before the first dies, the species and its adaptive trait survive.
To be fair, Sal is saying that the TOE predicts (or his version of the TOE, whatever) evolutionary breakdown, and since this is not happening, reductio ad absurdum the TOE is wrong.
And along these same lines, physics must be wrong since bumblebees are observed to fly. Divine Bumblistic Antigravity is the only possible explanation. QED.
Re: Salvador
It’s kind of lame to imply that evolution only stipulates fixed “good” or “bad” mutations and cannot look at such things in relative terms. “Good” or “bad” does indeed vary by environmental condition. If you look at the survivors after extinctions due to, say, human encroachment: they are rarely the specialists supremely adapted to survive in a particular environment. Rather, they are the generalists who are moderately well adapted to a lot of different circumstances. Rats, cockroaches, coyotes, and so on.
If anything, the difficulty of fixing advantageous traits argues why generalists remain in a population that according to naive evolutionary theory should favor super specialists. Super specialists should out-compete generalists every time, but generalists remain: divine intervention, or inertia plus environmental change? Sharks, horseshoe crabs, cockroaches; generalists who have retained a set of features through geological eras. It is apparent some examples exist of stable phenotypes despite silent neutral mutation fixation. Species may explode, but they do not “melt down,” nor is it implied anywhere in evolutionary theory that they do so. Is 200 million years long enough to demonstrate persistence despite mutation?
These forms also argue against the supposition that “advancement” is the rule, something that evolution doesn’t presuppose, but is flung about as if it were foundational to evolution at large. A straw-man, of sorts. Population genetics demonstrates that, in theory and through mathematical extrapolation, forms can persist and do not melt down, and that advantageous mutation is possible but not a foregone conclusion, or rule.
test
Hey, Sal. What’s this then?
mendelsaccountant dot info (apologies for the awkward URL. The PT software won’t take stuff from that domain apparently)
I can see how you might have missed it, considering it’s only linked to from Sanford’s home page at Cornell, and that can only be found through his entry on Wikipedia if Google is too hard (as it so often is). Plus, as everyone knows, Wikipedia is just wicked obscure, so who could fault you on your research, given all that?
Super specialists? I love the gepard, such a beautiful running machine! But oh so vulnerable - it needs to catch something to eat before spending too much energy. Not quite so beautiful but much better chances of survival for the hyenas.
One does not need to be particularly smart to realize what a genetic trapdoor the super specialists have gone through. Rats are among the most successful animals. As are Homo sapiens, for the time being. We have no guarantee that man ever will overcome his predicament.
This information comes from:
J. Sanford, J. Baumgardner, W. Brewer, P. Gibson, and W. Remine. Using computer simulation to understand mutation accumulation dynamics and genetic load, in Y. Shi et al. (eds.), ICCS 2007, Part II, LNCS 4488, Springer-Verlag, Berlin, Heidelberg, pp. 386-392.
You can find it also at the home page for Mendel’s Accountant.
I have only skimmed his book for a general audience, but I get the impression that these serious flaws are not mentioned there.
These flaws are a shame, as a lot of work went into the programming. I’m a computer programmer myself, as well as a physicist, and I recognize the work that goes into programming. But I also recognize that a simulation based on faulty assumptions will give faulty output.
I’m not sure why you think that my feelings, my peachyness, or my family is relevant to this discussion, but for the record both of my children are adopted, so whatever genes I happen to possess stopped with me.
Obviously not, it is a description of what your claims consists of, and why they are inconsistent:
This is predicting observations from an hypothesis freely, without regard to existing data.
This is constraining prediction to existing data, focusing on existing facts to derive predictions to test with.
It is inconsistent and wrong - you want to test as many predictions of a theory as possible, regardless of already existing data, to be able to reject false theories. This is why creationism is a barren pseudoscience, it is satisfied with what is known and don’t care for empirical theories.
It should be obvious from the description that there isn’t “three aspects” of falsifiability, and why your claim of them is false as I described falsifiability in that comment.
Obviously you cling to dogma, as you want to use “facts whose significance does not depend on the assumptions of the paradigm”, while empirical testing amounts to using observational facts and prediction of facts based on theory so that their significance depends on the later.
Dogma amounts to a religious text, whether it is explicitly written down or passed on as an oral tradition.
That isn’t what I claimed. As I described with falsifiability, we test predictions of a theory, so of course those tests are theory-dependent.
Obviously observations are repeatable and robust under a specific test.
Those links go to the evidence. As I said, work it, to find out.
Nope, the claim is that organisms that look like the first population have been fully designed. While in fact all what we do is to recreate organisms shaped by later evolution.
You don’t have any, as I have explained several times in the previous and this comment. At least science have the sensibility to claim that we don’t know, while we proceed to work the problem.
Meaningless pareidolia, added with the spice that you gloss over the gaps in it. Why is Ceres a planet (it isn’t)? And how do you explain Pluto (you don’t)?
Doesn’t Muller’s Ratchet only apply to populations that reproduce asexually?
I will reiterate part of my comment on your repeated claim:
So as observationally selection is effective in some populations, and according to Hawks now perhaps the most powerful evolutionary mechanism among humans, your question is a moot point.
As it happens, the paper I linked to on work on E. coli gives an example of a distribution of observed selectable fitnesses.
I think it’s also a problem for sexually reproducing populations. See:
http://www.jstor.org/pss/2410432
and also:
Kondrashov, A.S (1995) Contamination of the genome by very slightly deleterious mutations: why have we not died 100 times over? Journal of Theoretical Biology, 175, 583-594.
Crow, J.F. (1997) The high spontaneous mutation rate: a health risk? PNAS, 94, 8380-8386.
I’d be interested in seeing Joe’s thoughts, or basically anyone better qualified than me!
ok, i’ve been lurking long enough.
Ungtss has claimed(in all seriousness) that in two separate instances, life has been ‘created’ from ‘scratch’.
apart from being patently untrue(and indicating things about ungtss which DO make it difficult for me to believe that he and I share a common ancestor…hey, he may have falsified common descent after all :p ), i see another very large problem with these claims(for ungtss): if MEN, the Scientists that ungtss and his ilk despise so much, were to CREATE life in the labratory…wouldn’t that, um…what’s the word…RUIN the creo/IDiot notion that life is too utterly spooky and mysterious to ever be understood by Science? just a thought…
oh, and another thing: if you people(creo/IDots)are going to continue to withhold your earth-shaking evidence of design from us, can you AT LEAST stop using stupid and trite analogies like Airplane and Car engines to attempt to get your point across? A 747 is not comparable to a living organism in any meaningful way. Thanks, guys. we appreciate it.
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