LONG WINDED VERSION AT UD:
Darwin’s Delusion vs. Death of the Fittest
CONCISE VERSION AT TSZ
From Kimura and Mayurama’s paper The Mutational Load (eqn 1.4), Nachman and Crowell’s paper Esitmate of the Mutation Rate per Nucleotide in Humans (last paragraph), Eyre-Walker and Keightley’s paper High Genomic Deleterious Mutation rates in Homonids (2nd paragraph) we see that by using the Poisson distribution, it can be deduced that the probability P(0,U) of a child not getting a novel mutation is reasonably approximated as:
where 0 corresponds to the “no mutation” outcome, and U is the mutation rate expressed in mutations per individual per generation.
If the rate of slightly dysfunctional or slightly deleterious mutations is 6 per individual per generation (i.e. U=6), the above result suggests each generation is less “fit” than its parents’ generation since there is a 99.75% probability each offspring is slightly defective. Thus, “death of the fittest” could be a better description of how evolution works in the wild for species with relatively low reproductive rates such as humans.
I’d like a straight answer to a simple question. If your equation precicts something at variance to what is observed, does it really make sense to posit fairies as the cause of the discrepancy?
Sal seem to think if evolution can’t be modled with a simple first year algebra linear equation, therefore magic.
No possibility that fitness space isn’t modeled correctly. No possibility of compensating mutations. No possibility of random drift.
For sure, the dynamics of genotypic and phenotypic change are of absorbing interest to all those interested in evolution and how she works.
But this thing about “genetic entropy”? What the heck does it matter?
So far as we know, all species now extinct have become so because their food and homes disappeared (or effectively became unavailable) – or because they became prey to a species new to them (per the dodo and hungry sailors)
But if that were NOT the case, and the human race were on a long slide to some kind of drooling incapacity to cope – then what?
It’s apparent that there there is nothing we can do to stop it, so it seems that Sanford and Cordova are, in the absence of evidence that it actually happens (and in the presence of very many fast-breeding species that have not apparently suffered), simply wagging an admonitory finger at us.
“All we can do is sing as we go”
I actually had some correspondence with John Sanford (who was charming) to settle a dispute I was having with with Mung at UD, and he gave me permission to post it.
He replied:
Of course there is a third view (which of course I hold), which is that the Genetic Entropy thesis is simply wrong, for a great many reasons, not least of which is the notion that deleteriousness is a fixed property of a variant, not one that varies depending on genomic and environmental context.
Lizzie, it is simply blindingly stupid to argue that smaller genomes are less susceptible to genetic entropy that genomes having many duplications and lots of non-coding sequences.
The less fat, the worse the problem would become.
Unless the characterization of functional space is simply wrong.
Now I wonder which is more likely: reality differs from Sal’s simple model, or Sal has stumbled upon an error in theory overlooked by generations of scientists.
The chimpanzee genome paper presented pretty strong evidence for selective constraint on synonymous mutations — much weaker than on nonsynonymous changes, to be sure, but still present. I suspect that the constraint results from a modest number of highly constrained sites, rather than broad but weak constraint. (The paper gives the example of mutations that would alter splicing.)
Hi Lizzie and keiths, and thanks. I ended up here because I’ve run into Lizzie on my occasional forays into Talk Rational (where I am sfs, and where there is maybe more talk than rationality).
There is indeed, unfortunately. I can’t make head nor tail of the place any more.
But now I know who sfs is 🙂
Apologies in advance for my lack of responses to many of the good criticisms fielded in this discussion. I will take them in to consideration, and also pass them on to Dr. Sanford, Walter ReMine and other members of the Mendel Team if I have the chance. I hope the readers at UD and TSZ will be motivated to ponder these topics.
Muller’s Nobel Prize winning research led to Muller concluding if U=0.5 for humans, then meltdown was inevitable. I suggested that if U=1 or higher, then Muller’s argument for meltdown becomes much clearer and has more force, but fundamentally, I’m not expressing a concern that hasn’t been expressed before.
The claims I’ve put forward may lead to testable observations. What little we can agree on is that continued gathering of genetic statistics on the emergence of new diseases in the present and very recent past (say 100 years) is a worthy enterprise. ID proponents, creationists, and evolutionists pretty much agree more observations and measurements of our genes is a good thing. That is perhaps the one thing we can agree on.
Sal, can you cite an instance of a species going extinct due to accumulated deleterious mutations? If not, do you have any theory as to why?
Has it occurred to you that if a simple algebraic formula doesn’t match observation, than perhaps reality might be a bit more complex?
I think it’s worth noting a couple of points about two arguments that have been mentioned in this thread, the genetic load argument (which seems to be called the “U Paradox” in the present context) and the genetic entropy argument, which involves the accumulation of very slightly deleterious mutations.
The first is that the phenomena in question do not overlap: genetic load is the result of deleterious mutations that will eventually be eliminated by natural selection, but that harm their possessors in the meantime, while genetic entropy concerns mutations that are too weakly deleterious to be affected by natural selection, and that therefore can fix in the population.
The second difference is that genetic load is a phenomena that affects real species, with the only question being the severity of the effect, while genetic entropy is almost entirely imaginary, the result of extrapolating a mathematical model into a regime where it makes no physical sense.
The model in question is one that describes the distribution of fitness effects. Researchers (well, Kondrashov, at least) observed that the frequency of deleterious mutations declines with severity, starting from the least severe ones that we can detect and declining to the much less common lethal mutations. Extrapolating this distribution down to even lower selection coefficients leads to the prediction that there should be tons of very slightly deleterious mutations. The interesting point about these is that their fitness effect is so small that natural selection cannot weed them out, and so their sheer number will inevitably degrade a species’ genome until it goes extinct. There is no reason to think that these VSDMs actually exist, however, and good reason to think that they don’t.
Take a simplified but concrete case, one that has already been mentioned: codon bias. It is clear that some synonymous codons have a slight selective advantage over others, and that mutations from the optimal codon will have slightly deleterious effects. Let’s use some semi-realistic numbers for, say, chimpanzee. Assume sub-optimal codons have a disadvantage of 10^-8. Chimpanzees only have an effective population size of a few tens of thousands, and that means that purifying selection in chimps can’t eliminate deleterious mutations with disadvantages of much less than 10^-5. Nothing will prevent mutations from changing optimal codons to suboptimal ones in chimpanzees, then. If there are ~10 million possible synonymous mutations in the chimpanzee genome, then eventually chimps must lose ~10% of their fitness (10^7 * 10^-8) just from this one class of VSDMs. Inevitable decline, right?
Obviously, this is nonsense. There is no fitness decline in chimps due to loss of optimal codon usage because codon usage was never optimized in chimps in the first place. Their ancestors haven’t had large enough population sizes for detectable codon usage bias for hundreds of millions of years, which is the span during which many of their genes (and almost all of the rest their genome) came into existence. As Lizzie alluded to, you can only have this kind of decline if you’re starting with a perfect genome, and evolutionary biology has no mechanism for producing such a genome in the first place. Arguing about genetic entropy is literally arguing about nothing at all.
In one sense, to be sure, genetic entropy is real and has indeed occurred. Our long-ago ancestors were bacteria, and they did have something very close to perfect genomes, because they were subject to the ruthless selection that a very large population brings. Since then our population size has repeatedly dwindled, first to single-celled eukaryotes, then to simple metazoans, and then through the lineage of increasingly large-bodied mammals. In the process, our genomes have indeed accumulated a large number of slightly deleterious mutations, things that would have been weeded out of our bacterial ancestors. Compared to bacteria, our cells replicate very slowly (and our overall rate of replication is simply pathetic), our genomes are large and sloppy, we carry a heavy genetic load of deleterious mutations and we’ve lost the ability to synthesize key nutrients. We are, in fact, lousy bacteria. Along the way, however, we’ve also picked up a number of other capabilities that offset the losses — new modes of exploiting ecological niches, reproducing, obtaining nutrients and energy. As Michael Lynch has pointed out, it is only the permissiveness of small populations that has permitted our lineage to develop its complexity. Personally, I kind of like it this way. (Although I do wish something could be done about the human back — that bit of suboptimality is bugging me these days.)
stcordova,
Can someone supply a reference for Muller thinking that U=0.5 would be fatal for humans?
Not exactly what you asked for:
petrushka,
Note that this is for the Y chromosome, which is non-recombining and therefore thought to be where Muller’s Ratchet might have a role. Presumably the comment about u=0.5 referred to the whole-genome mutation rate, not just the non-recombining portions.
I read this to mean that the ratchet would be most likely to affect non-sexual organisms having fewer genes or shorter genomes.
Am I wrong about this?
The ratchet is thought to affect non-recombining genomes, with longer genomes more likely to be affected because they imply a higher mutation rate. (Non-sexual is not quite the same as non-recombining. Bacteria are asexual, but manage to exchange a fair amount of DNA anyway, while mitochondria, chloroplasts and the Y chromosome all occur in sexually reproducing species, but do not recombine.)
Okay, I’m just trying to get a grip on the relevance of this concept. So far it seems like one of those things that is conceptually true, but so what?
Sal seems to be taking the word of a young earth creationist. the ratchet, on the other hand, seems not applicable on scales of thousands of years, and possibly not on scales of millions of years.
SC @ UD,
No, I don’t think that’ll happen actually. And even if the best answer to why the universe is here at all turns out to be “let there be light” then that’ll still have had nothing to do with the 100% human written bible.
Would those be the same observations and measurements that might “break down” in 30 or a thousand years.
Salvador, don’t you think it’s more likely that just as when you learnt more about physics the possibility of a YEC universe has (as you yourself admit) diminished considerably, so as you actually learn more about biology these “problems” you point out will also diminish?
The world is not 6000 years old, Adam and Eve are a fairy tale for when humanity was as a child, not a yardstick to measure back to via your spurious “genomic degradation” idea and it’s disgraceful how you pretend that your YEC has nothing to do with your promotion of “Darwin’s Delusion”.
Why don’t you write up this idea and send it off for publication? There are plenty of ID/YEC zero impact journals desperate for content.
This is pretty much the response I’d give to the various “what if you’re wrong”-type questions:
http://www.youtube.com/watch?v=QXzlMblBQpQ
Not necessarily – there are too many mechanistic distinctions between us and viral sequence to allow too much inference about what might be a problem in one kingdom applying to another. Meltdown could be a problem for an organism with a very large genome packed with function, and relatively low fecundity, while not being an issue for species elsewhere on the scale for some or all of those parameters.
Meltdown could conceivably be a problem with appreciable frequency, but we don’t see much of it because by its very nature it causes demise, and the world is populated by the mutationally robust.
Whether we are susceptible is unproven – I think the lack of functional density in our genome is the undoing of Sal’s argument, along with substantial doubt about the fraction of mutation which is nonlethal in early development but fitness-depressing.
In any case, there are more likely threats queuing up to do us in.
Don’t be daft. ‘Deleterious’ and ‘beneficial’ have long been defined by biologists with respect to differentials in mean reproductive success of carriers, and for many reasons, those differentials can shift – today’s deleterious can be tomorrow’s beneficial, and vice versa. The ‘problem’ lies with people who choose to misunderstand. The terms are relative – if one allele is beneficial, its alternative is de facto deleterious. I know you don’t like relative concepts. Perhaps there is an ultimate source of Objective Benefit you wish us to appeal to.
Nice! Threat of an afterlife in hell.
Cordova, I probably won’t be around 30 years from now, and absolutely none of us will be around here 1000 years from now. So the only possible interpretation of your given time frame is an after-life interpretation. The only possible way in which you could believe and state that “[we will] really regret it” is if you (yes, you personally, Cordova) see us experiencing an afterlife of regret. Note, this afterlife of regret is otherwise known as hell, since in an afterlife of heaven there will be no regret, even if we had happened to be wrong in our previous earthly existence.
Cordova, that’s disgusting. Good thing you didn’t try that around me physically as I’d wash your mouth out with soap for that kind of foul language. Yeah, you didn’t use any bad words, but you used a bad heart and a filthy mind when you chose to imply that I am going to experience hell in my future because I accept the current best consensus of science.
Actually I should thank you for showing your true colors as a Abrahamic gangster who publicly threatens scientists with hell if they don’t believe some bible interpretation.
Sal makes the usual neophyte mistakes that, despite his claims of having taken “advanced” science courses, indicate that he doesn’t pay attention to what he is learning.
I suspect that, like all ID/creationists, he takes courses merely to learn jargon in order to bend them to fit preconceived sectarian beliefs.
But this error is far more basic; it comes before physics, chemistry, or biology. It is an elementary/middle school mistake.
Whenever one proposes that there is a probability that something will go wrong, one minus that probability is the probability that it will not go wrong.
But there is something even more basic that Sal is missing here. In a collection of multiple events going on within the same time frame, there are probabilities associated with each of the events. They don’t all have to go “wrong” at the same time, and they don’t all have to go “not wrong” at the same time. In short, not all events have to be proceeding in the “same direction” at the same time.
The ability to recognize this is a matter of intellectual maturity; and it isn’t limited to just biological mutations. The first notion that should cross the mind of a person who has achieved this level of understanding when confronted with a specific case should be to ask whether a particular type of event taking place is the ONLY type of event that is taking place.
In complex organisms, experiments usually involve control groups. High school students in biology learn about control groups and why they are necessary. The ability to understand the need for controls requires a level of maturity that recognizes that multiple events taking place within the same time frame are not necessarily locked together and going in one direction.
One doesn’t have to know any biology to know that; one only has to be sufficiently mature or without an agenda aimed at making everything come out to fit a preconceived set of beliefs.
And throwing in “math” doesn’t cover up the mistake.
And would this be the sfs1 on theologyweb?
OMagain,
I agree with your assessment of the odds, but when Cordova says, “You’ll really regret it”, I don’t think, even then, there’s cause for regret, on the merits of the question, at least. Being, uh, how does that go, again — burned eternally by an unquenchable fire — would be cause for lamentation at one’s own suffering at the hands of this god, of course. But this is like telling a blackjack expert that he will regret not hitting with a “19” in his hand, and a “6” showing as the dealer card.
There are ways to lose by standing in that scenario. It’s not the smart assessment of the odds and probabilities from a fair deck of cards, but it could and it does happen. Sal says I must “hit” on 19, despite the probabilities and the evidence in front of me. If the hand plays out and the card I would have drawn was a 2 and it was needed to avoid losing the hand, Sal’s demand that I hit on 19 against that dealer’s 6 card up was correct in hindsight, but only in hindsight.
Given the same or similar circumstances in a subsequent hand, I would stand again on 19 vs a dealer’s 6 up. We don’t have certainty available, but we can apply our experiences and knowledge, and all of that runs against Sal’s recommendation. If, on the eventuality that Sal’s demon-god obtains, suck to be me, I guess, but given the same overwhelming evidences and experiences available, I’d be a fool to embrace the ideas Sal advances.
I’d sooner hit on with a hard 20 in hand.
Agree. I think Cordova’s last several years and going forward are a good real-life example of the disingenuous nature of many YECs pursuing scientific credentials. One can see the cynicism in action here, in slow motion, as Sal picks up familiarity with terms, concepts, studies and domain-internal controversies. But the fideism and fundamentalism remain, incorrigible. It’s just a gloss that provides cover for the same pre-conceptions he went into this with.
A student learning how best to turn the system against itself, where that’s possible through misdirection, obfuscation and deception.
Too bad. Sal has had some nice opportunities to actually develop some knowledge and skill in this space. I have in the past wondered from glimmers of skepticism and doubt, faint but detectable, if Sal might shed the subterfuge and benefit from the resources available to him. I think not, based on recent evidence.
Before I can respond to this, I have to ask you and Sal some questions at this point as to what you actually believe we see.
Does DNA exist?
Is the arrangement of base pairs inherited from parents?
Do mutations happen?
Are deleterious mutations permanently deleterious, for all time?
Is a deleterious mutation one that decreases fitness to reproduce? If no, then what is a deleterious mutation?
Is the proportion of deleterious mutations in the population increasing per generation?
[makes note of WJM’s blatantly obvious “They did it first, Mom!” tu quoque fallacy]
[makes note of the perfect and absolute absence of even so much as a pretense of an attempt to criticize Mr. Cordova for not defining Mr. Cordova’s terms]
[makes note of the perfect and absolute absence of any indication that WJM might think it’s a Bad Thing when terms are not clearly defined]
[nods and goes on about his business]
This may interest you, Lizzie:
http://www.antievolution.org/cgi-bin/ikonboard/ikonboard.cgi?s=51ad54a990d6daa1;act=ST;f=14;t=7297;st=0
Think of the puppies!
Yeah, so SC’s model(or actually, his interpretation of his model) is wrong. All it really says is that no population ever skirts around at “optimality” in terms of the fitness of it’s total complement of genes. Many loci will have slightly deleterious mutations in them. Occasionally, an individual will be unlucky and get a lethal mutation(which we know happens, many spontaneous abortions happen early in development and you have to “try again”). So we just keep having plenty of children(there’s 7 billion of us now) and natural selection will fix the rest.
So in essenec the real issue is a standard ID-creationist fallacy of arguing from overgeneralizations and engaing in black and white, dichotomous thinking while the real world is much more nuanced.
There is a reason the 3 amino-acid assumption is generous.
When proteins act through binding (think lock-and-key methapor), if specificity were low (let a variety of keys open the same lock), then proteins would be interacting and binding with all sorts of things they shouldn’t and there results a conflict.
To conceptualize the problem, if the human has 30,000 proteins, the body needs to discriminate 1 from the other, hence the address space must be at least 30,000 large, and preferably just for safety. To discriminate between 30,000 proteins one needs more than 3 amino acids (20^3.44 = 30,000). It is reasonable to suppose more are needed to ensure sufficient discrimination between proteins.
By way of analogy, a 32-bit computer has more addressable space than a 16-bit computer. High specificity (high improbability) isn’t an option, it’s a requirement for a complex system. Hence, a smooth gradient for selection from one protein to the next isn’t reasonable even in principle when dealing with systems that require high specificity.
But, that’s not even the end of it. Locks are usually far more complicated than keys, and a single protein specificity is nowhere near the complexity of the structure that must integrate it. If proteins are the basic building blocks, then the infrastructure that integrates it is more complex just like buildings are more complex than the building blocks that integrate the building blocks. Changing 3-amino acids and finding a way to use it is like creating a new sized brick and trying to integrate it into an existing building…the few times we see this works out in organisms, where 3 amino acid changes are significant, is the rare exception, not the rule.
Though we might have an exception to this once in a while where change in 1 or 2 amino acids is significant, it is the exception rather than the rule. To extrapolate such isolated cases as some sort of general principle, is the fallacy of hasty generalization.
William,
Salvador said:
When Salvador repeats the claim in the OP without having responded to any of the “good criticisms” or having changed any of his claims will that give you pause as to how ID views science? He will, he’s been doing the rounds with this one for several years now.
I mean, he’s had plenty of time to write the comment above this one, comment at UD and so on. But respond to the specific points that, basically, collapse his “argument”?
No, all we get in response to those are apologies and excuses. And, perhaps, if he “has the chance” he’ll pass them onto some other creationists who’ll also ignore them and continue to repeat the same claims.
I could go through this thread and note a dozen good questions of which Salvador obviously has no answer, and if he were to attempt an answer the flaws in his “argument” would be immediately apparent. Yet for some reason he does not even try to respond, preferring to throw red herrings like the above comment instead.
You seem like an intelligent person William. Can’t you see through this “cargo cult” science? If somebody responds to a claim you make with a good criticism that you can’t answer, is that how you behave? Pretend that the point was never made or brush it off with “I’ll take it into consideration”?
In short this thread demonstrates why people like Salvador and KF are unable to participate in the peer reviewed world. The claims they make are not designed to be defended, they are designed to be made to give the appearance of science to whatever is being claimed. When it comes to the point of defending those claims they either retreat to the ivory castle (UD) or run for the hills (Dembski/Dover).
William, perhaps if you picked a question you considered relevant from this thread and asked Salvador you might get a different type of brush off? I know you won’t get an answer responsive to the question asked!
I think the 64/32/16 bit computer analogy fails on many levels. My 60 bit chip can emulate an 8 bit processor.
Try reading The Soul of a New Machine to get a glimpse of how a new computer architecture can evolve without losing the ability to execute old code natively.
If you are trying to say the specification cannot evolve, I think you need to read some more.
Regarding Muller’s value of 0.5
see page 155 paragraph 3 of
Our Load of Mutational
“if Ut should rise above 0.5, the amount of selective elimination required for the maintenance of equilibrium, would as we have seen, be greater than the rate of effective reproduction…[for reprodcution of 2 per couple] the upper or critical mutation rate, that beyond which any equilibrium is impossible, must be much lower than 0.5 and, a we have seen, perhaps lower than 0.1”
This pertained to Muller’s research on the effects of radiation on the next generations. That was his immediate concern and for his related work in understanding x-ray mutagenesis, he won the Nobel prize. He unwittingly gave creationists a lot of ammunition.
and also see paragraph 2 of page 1344
Mutational Load by Kimura and Mayurama
If U=.5 then even for fruit flies, the load is too much as Kimura showed, if so, then for U=1 or greater this will be even more true.
The cartoon model attempted to show that for U=1 or higher, the derivations become simpler, and for U=6, selection becomes pretty much irrelevant because one would have to presume selection is 99.75% accurate in eliminating the new bad mutations for every generation, which is unreasonable as Sanford’s former Cornell colleague, Kondrashov, demonstrated.
Sal. In the vicinity of Chernobyl the observed mutation rate in mammals is three times the rate observed elsewhere, and populations are stable.
Why do you suppose that is?
This is relevant because the paper you cite is not about natural mutation rates, but about the hypothetical effects of global nuclear war and severe fallout.
We now have a living wild laboratory in which these consequences are being tested.
Sanford worked with Kondrashov at Cornell?
That actually does happen, in varying degrees. The system isn’t that specific, it can’t GET that specific on well-known physical grounds. Specificity is gradual, it’s not fully dichotomous. Weak binding exists everywhere, the question is only about how long and how tight, and whether it is enough to disrupt the system completely. Again, there’s isn’t a black-and-white answer to this and it’s a matter of degree.
Some proteins proteins will clump together regardless of shape and sequence given even quite small changes to ionic strength and salinity of solution. For example, adding salt to extracted cell cytoplasm causes most fat-soluble proteins to clump together easily. This fact is directly exploited by many protein purification techniques.
But that’s simply demonstrably false. Jack Szostak used selection to isolate RNA sequences from a randomly generated mixture, which had the ability to bind a specific substrate while discriminating against another: It worked remarkably well, see here:
http://molbio.mgh.harvard.edu/szostakweb/publications/Szostak_pdfs/Sazani_et_al_2004_JACS.pdf
Well, it has to step aside the fallacy of blind assertion.
Thanks. Muller is correct within the model he’s using, but that’s precisely the model I previously criticized. It’s an inadequate model — which is to say, it’s wrong. It assumes only a small number of deleterious alleles present in any individual, so that each new mutation ultimately causes a “genetic death” (that is, a failure to reproduce because of the deleterious allele). As I wrote earlier, that’s not how real deleterious alleles operate in humans. Instead, each genetic death removes an individual who is heavily loaded with many deleterious mutations. This is possible because humans (like any successful complex species) tolerate quite a high ongoing load of deleterious mutations just fine.
As always, bad model = invalid conclusion.
Do you have a reference for Kondrashov on this point? I was aware that he’d muffed the very slightly deleterious mutation issue, but didn’t know (or had forgotten) that he’d used this model as well. It wouldn’t be at all surprising if he did — lots of geneticists get this point wrong.
To be fair, Sal’s reference is 63 years old. That seems fairly typical of ID references.
And the lock-and-key analogy is completely stupid when you look at the real world of actual locks and keys.
I have a truck key which opens the door and turns on the ignition switch of a completely separate car – but won’t open the trunk of that same car. Meanwhile the car key as cut by the factory works every lock on the car, of course, but only unlocks the door of the truck, not the truck ignition. And note: these are keys made out of stiff metal, which actually do have to fit specifically within some tight tolerance; the pins have to contact with a sufficient mechanical pressure; they cannot stretch at all nor barely compress. But they don’t have to be too specific …
Now take another look at the supposedly-analogous lock/key in a binding site on a catalytic protein. What’s the tolerance? Mechanical pressure, no. They bind chemically – which doesn’t requite even as little precision as a typical door key – “close” is almost certainly close enough. The chemicals jiggle, partially widening or elongating in response to magnetic force of other molecules jiggling nearby. They compress. They stretch. How long do they have to hold on for? Just long enough … jiggle, jiggle …
So even if the lock/key example of “Gotcha – Amazing Specificity” were valid in our known-designed (ID!) machines – and it’s not valid even there – it’s certainly a stupid metaphor to use in trying to prove that “Darwinian random mutation” can’t possibly work because biological molecular lock-and-keys are too specific to have evolved.
Creationists are so in love with what they assume must be (Because. Bible god.) that they are blinded to what actually is, in the real world. It’s all airy-fairy pie in the sky to them, all of it, even when they pretend to be engaging in specificity,
You can dress up a pig with pretty arithmetic but it’s still a pig.
Meanwhile, back in the real world, we have actual catalytic protein “lock/key” systems which have evolved while we were watching. If your equations say it can’t happen, but it does happen anyway in the real world, that’s a clue there’s something wrong with your equations. Not something wrong with reality.
Get a clue, Cordova.
Yeah, but in this case much more recent references work from the same model, without realizing there’s any issue with it. I think the Nachman and Crowell mutation rate paper does. I also have a highly competent colleague who works on deleterious mutations, and still uses that model (or at least did the last time I talked to him about it, which was a couple of years ago).
Heh. That’s older than I am, and I already think I’m older than dust.
To be fair, Nachman and Crowell’s paper cited Muller’s 1950 paper in 2000, and Michael Lynch referenced it in 2010 Proceedings of the National Academy. Rate Spectrum in a way favorable to Muller’s hypothesis of grave challenges for the human genome.
Lynch went to the trouble of defending Muller. Does that Lynch’s paper suggest humans are getting progressively healthier? No. It describes the failure of Natural Selection.
If you say, “NS no longer operates because of industrialization”, it only goes to prove the point Nature is under no obligation to make populations behave according to a Darwinian model, there are tons of counter examples starting with those identified by Raup to the present day. NS works, except when it doesn’t.
But as I said, we’ll all know the answer in far less than geological time if the human genome is indeed deteriorating….no need to settle the issue in this discussion, the facts could tell us in the next couple of decades (they already have, but some haven’t caught on).
Michael Lynch:
“it is difficult to escape the conclusion that the decline in fitness is at least %1 in humans and quite possibly as high as 5%”.
And this is telling:
“a full reassertion of the power of natural selection would be incapable of returning the population to a state better than that represented by the least loaded chromosomal segment”
Criticize what I’ve said, but the data will be the final judge. We’ll know the answer in due time. Blame the problem on industrialization, but it goes deeper than that. If U=6, even with 99.75% effective selection and each female giving birth to 807 kids, the genome won’t get better.
I’ve given what I think is true. No need to try to settle the issue by more debate, observation and testing will judge who is right.
Cordova –
You do realize that Lynch’s paper is about the future problem faced by modern human society since we have interfered with natural selection, given our compassionate care of less-than-perfect humans, don’t you?
Please don’t tell me that your use of Lynch is just another creationist quotemine and that you didn’t even read his paper.
Unless, you actually are advocating a return to the bad old days of prayer and charms instead of medicine; starvation instead of golden rice; men just like you dying young in attempting to fight off wolves instead of keeping safe within our solid homes and vehicles.
We know your god would be okay with that. God’s plan, no matter what.
What about you? Are you okay with that?
Indeed, for example simply by observing dead organisms you’ve worked out that the dead stay dead!
Sal@UD
I once read a sci-fi story about the last few steps of someone on a planet they just landed on. It was much like ours, but totally free of life.
He managed to make it to the sea before he died….
Sal writes at UD:
Sal, you still don’t understand the “Darwinian model”! Seriously. Leaving aside the claim that “NS no longer operates because of industrialization” (with which I disagree), it is perfectly true that in a benign environment, populations will be more tolerant of mutations – in other words that mutations that would otherwise be generally deleterious, will not be deleterious in a generally benign environment. But this isn’t NS “not working” and it certainly isn’t “prov[ing] that ature is under no obligation to make populations behave according to a Darwinian model”, “Nature” is under no “obligation” anyway, but the Darwinian model will operate as long as some heritable variations result in variation in reproductive success. It can’t not.
What would be true would be to say that “Nature is under no obligation to maintain human beings on this planet”. She isn’t. However, they still seem to be doing worryingly well, regardless.
But to think that NS is no longer “working” is absurd. There are huge selective pressures on us right now, especially in “developed” nations with access to fertility control. Darwinian theory predicts that female fertility peak will move later.
Already there are data (sorry don’t have access to the citation here in Milan) that support that prediction.
What’s with the overemphasis on natural selection and “Darwinian” adaptationsm here anyway? You’re citing neutral theory (which is a theory of evolution) as evidence against Darwinism (adaptationist theory of evolution) in order to insinuate that, I gather, we should discount both. It doesn’t follow, and I think most population geneticists have accepted neutral theory.
Natural selection works until it doesn’t. Also known as the argument from irrelevant trivial tautology.
It seems you forget how fitness is defined 😛
The irony of which is that most of them actually believe that for a particular person ~2 millenia ago, the dead came back alive.
Rumraket,
Don’t forget Lazarus of Bethany.
Still waiting on your answers to my questions, Mr. Cordova:
What definition of ‘deleterious’ are you using when you refer to ‘deleterious’ mutations?
What definition of ‘beneficial’ are you using when you refer to ‘beneficial’ mutations?
The gene for sickle-cell anemia, which confers resistance to malaria when inherited from one parent, but confers sickle-cell anemia when inherited from both parents: ‘Beneficial’ according to your definition of ‘beneficial’, or ‘deleterious’ according to your definition of ‘deleterious’?
A mutation which puts white fur on its possessor: ‘Beneficial’ according to your definition of ‘beneficial’, or ‘deleterious’ according to your definition of ‘deleterious’?
If you’ve answered my questions and I missed your answers, perhaps you could provide the URL(s) which point to your answers, please?