Nachman’s Paradox Defeats Darwinism and Dawkins’ Weasel
| November 14, 2009 | Posted by scordova under Creationism, Darwinism, Evolution, Intelligent Design, Video |
The following is a crude 1-minute silent animation that I and members of the IDCS Network put together. God willing, there will be major improvements to the animation (including audio), but this is a start. Be sure to watch it in full screen mode to see the details.
http://www.youtube.com/watch?v=SrIDjvpx7w4
The animation asserts that if harmful mutation rates are high enough, then there exists no form or mechanism of selection which can arrest genetic deterioration. Even if the harmful mutations do not reach population fixation, they can still damage the collective genome.
The animation starts off with healthy gingerbread men as parents. Each spawns ginger kids, and the red dots on the kids represent them having a mutation. The missing ginger limbs are suggestive of severe mutations, the more mild mutations are represented by ginger kids merely having a red dot and not severe phenotypic effects of their mutation. The exploding ginger kids represent Selection doing its thing and removing the less functionally fit from the population. The persistence of red dots on the ginger kids represents persistence of bad mutations despite any possible mechanism of selection.
Nobel Prize winner HJ Muller (of Muller’s ratchet fame) suggested that the human race can’t even cope with a harmful rate of 0.1 per new born. The actual rate has been speculated to be on the order of 100-300.
The animation uses a conservative harmful rate of 1 and argues (with some attempts at humor) that deterioration would thus be inevitable even with a harmful rate of 1 per new born.
I save discussion in the comment section the relevant but technical topics of truncation selection, sexual reproduction, recombination, synergistic epistasis, compensatory mutations, relief from Muller’s ratchet etc. These highly technical topics should be addressed and were not included in the animation. We can discuss them in the comment section.
However, the essential problem of mutation rates and deterioration is depicted by the animation. How this cartoon is illustrative of reality (when we consider the technicalities such as recombination, sexual reproduction, synergistic epistasis), can be discussed in the comment section.
In light of such problems Kondrashov posed the rhetorical question, Why have we not died 100 times over?. Kondrashov attempted to answer the question, but I don’t think the problem has been solved. The animation expresses my skepticism of the long term benefit of “synergistic epistasis”.
And if the conclusion symbolized by the animation is true, then on what grounds can we believe Darwinism is true?
The animation was inspired by a paper by Nachman and Crowell. Two years ago I wrote: Nachman’s U-Paradox. This animation helps illustrate the problem of Nachman’s paradox.
I recommend we should build a non-partitioned WEASEL to feature how Nachman’s paradox will trump Dawkins conclusions that somehow Darwin found the answer to appeance of design. One can get an idea of what it would look like given the animation.
[ Admins, I can't seem to embed the video, can you embed it for me? I think embedded video requires higher privilege than my account has.]
Notes:
1. We could have done the drawings differently to emphasize the mutations are unique and novel and different for each ginger kid, but I save that work for later (including audio).
2. There is a refinement to the animation that is in order based on Nachman’s calculation of average removal rates of harmful mutations assumng trucation selection, “U”=3, and a conservative reproduction rate for humans, but I didn’t get around to it. That is yet another modification for future animations. We’ll need also some technical research on the matter.
108 Responses to Nachman’s Paradox Defeats Darwinism and Dawkins’ Weasel
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I think it’s fair to call it an imaginative piece of work.
The project of tracking the rise of SNP’s and other mutations is being done independent of ID. It is done because of the intense medical interest in tracking hereditary diseases.
And unlike Darwinism which is quick to mislable something as “beneficial” so long as it makes more babies, the medical community is more inclined to view mutations as a bad thing. See my objection to characterizing things as “fit” when by any other standard, they are diseased: Survival of the Sickest, Why We need Disease.
Consider:
Number of Rare Genetic Conditions on the Rise
Is this merely more recognition? We’ll see.
The enigma is, why have these diseases persisted (selection ain’t working so well). Thousands upon thousands of hereditary diseases persisting for centuries.
We’ll see.
In the mean time there is another area of research that could cast doubt on Darwinism, purifying selection, the enigma of Ultra Conserved Sequences.
More in a subsequent comment on this thread.
And you don’t think statements like the following by Nachman aren’t handwaving by the same standard?
Just invoke “synergistic epistasis” and mutations magically become damaging enough to weed it out the population. Just invoke “positive epistasis” and magically the bad mutations become good. This line of deduction is known as circular reasoning.
No model for viability, selection coefficients, fecundity (all the complaints you and Mung lodge against me).
Fine.
But I will make a subsequent comment about this regarding ultra conserved sequences and the potential for an unabated rise in SNP’s and the impotence of purifying selection.
By the way, thank you for agreeing that there is likely a point where there are enough mutations when no amount of selection can be of help. Muller said for humans, 0.1, Nachman (if there is no Synergistic Epistasis), 3.
I will argue reasons empirically why synergistic epistasis is unlikely based on results of ultra “conserved” sequences between mice and humans.
Prediction: The ultra “conserved” regions will experience an unabated rise of SNP’s (single nucleotide polymorphisms).
This will be inconsistent with the claim purifying selection (the purging of “bad” mutations”) has been operating on the genome of mice and men for the last 100 million years.
So much for synergistic epistasis.
Synergistic epistasis would predict instant death or ill effects. Hardly a dent eh? Maybe Nachman’s “fix” to his own paradox is no fix at all, but rather circular reasoning refuted by hard nosed empiricism.
If these ultra-conserved regions are not being purified and purged via purifying selection, then why does it seem they have been arranged like a bunch of coins oriented to all heads?
These knockout experiments are prima facie evidence that selection can’t see these regions, yet somehow they appear to be magically ordered like a bunch of coins oriented heads, or plagiarism, or (gasp) common design.
Unabated rise of SNP’s in this region would confirm selection has a hard time seeing these regions.
Finally, Kimura showed by cost arguments (comparable to the ones presented in the animation), that 90% of molecular evolution is non-Darwinian. This is symboliized by the much celebrated and widely accepted “Neutral Theory of Molecular Evolution”. If 90% of the molecules in the genome are functional, and 90% of the molecules are not subject ot selection, the implication is that most of the functioning in the genome was totatlly originated independent of Darwninian blindwatchmaker processes. This is not “argument from ignorance” but rather a brutal proof by contradiction.
Thus we have found design and function not attributable to natural selection. Where then is the source of this design and function? Whatever the source, we can have good reason to remove Darwinism as a plausible explanation.
Continued degeneration of function will be evidence selection can’t arrest deterioration. If selection can’t arrest deterioration, circumstantially speaking, it would cast doubt that it had anything to do with the creation of such function.
And in light of Kimura’s work and Sternberg’s hypothesis, it should seem painfully evident that selection doesn’t account for the creation of most function in the genome, and perhaps most of the rest of the human body.
For the readers’ benefit, not all designs need to be “functional” in the sense of reproductive success.
In the world of human affairs, if one came across a configuration of coins that were all heads, or like the configurations (where H=heads, T=tails):
or
etc.
These are recongizable linguistic type designs. Whether they have function or not, they are recognizable designs.
The ENCODE project discovered comparable linguistic architectures in the genome. When I examined some of the sequences myself using data mining tools, the design was astonishing, definitely non-random (the above coin examples were non-random). These designs are especially found in the regions often thought to be expendable junk, hence not subject to selection (like those ultra conserved sequences).
These designs are subject to deterioration. If they are non-functional, they will be especially immune to the mechanisms of selection to purge them even if we assume sexual recombination mechanisms.
The haploid animation that I put forward can then be modified to deal with the diploid case, and it can be seen that selection will not arrest the deterioration of these designs.
So these linguistic designs could be powerful designs that can’t be attributed to selection, if there is a rise of SNP’s in these regions in the present day, real time.
Also, even on the assumption these are regions not subject to selection (from the prejudicial view that they were Junk DNA), how then do they have linguistic structure?
Linguistic structures are recognizable designs. I gave some illustration with coins what linguistic designs could look like.
Now, what would be especailly bad for the Blindwatchmaker argument is if these linguistic regions are both functional and invisible to selection. I’ve provided arguments above why I think that is the case based on Kimura and Sternberg.
Further, testing of the real-time rise of SNP’s in these regions would be empirical confirmation that selection is mostly impotent save a few exceptional cases.
The animation would thus be materially correct provided it were modified to illustrate the diploid case and say Nachman’s number of U=3 (U=number of mutations per individual). The work published in 2009 on human mutation rates using solexa technology suggests U = 100.
There are several differences. Nachman isn’t trying to “prove evolution.” It’s already well-established, hence he is interpreting his finding in the light of the known facts, and in the light of plausible mechanisms. In addition, he’s not claiming to have demonstrated synergistic epistasis, but suggesting it as an avenue of additional research.
That’s Nachman’s number of deleterious mutations. The total number of mutations is much higher. What recent study indicates that deleterious mutations are that high in humans?
You keep repeating falsehoods zach.
Model: Haploids, 1 new harmful per newborn.
Analogous Diploid case:
Mentioned in the OP at UD.
U=3, 3 harmfuls per newborn
Result:
Kid gets about 1 or more harmfuls from each parent. Kid gets 3 additional.
Why is this. With 40 kids, 2 might have no mutations from parents carrying 3 mutations. If parents have fewer than 40 kids, then, it’s likely all the kids have 1 mutation or more!
See the resemblance now to the haploid model.
Did I get the chance to make these clarifications? Maybe, but I was so distracted by the strawmen and derailments being put forward I didn’t get the chance to add these. I make amends now.
But the data was right there in Nachman’s paper.
Comprende?
I made the inference several times in this thread.
The nature paper said about 100 new mutations. Sternberg said about 90% functional. This would strongly suggest U = some number around 100.
Whether this leads to meltdown is another story. The issue is whether selection can police these functional regions. Which it obviously does not (in light Kimura’s work). Ergo: Selection doesn’t create most of the function in the genome.
Is that the average mutations per individual? What is the distribution of effects of the harmful mutations? How often do reversions occur? How frequent are beneficial mutations and what is their distribution? What is the population? The size of the genome? What about recombination which is common in haploid organisms?
You still didn’t point to any such study. What specific research has Sternberg done to support the claim?
Minimum. See the discussion above.
How about trying to model it with the other parameters to your choosing.
Feel free to report the results.
Do you think that Jistak’s provisional agreement with me is generally well founded regarding 1 harmful per newborn in haploids?
See the Evolution and News Report for a bibliography. Disagree with Rick? Do you needed peer-reviewed by Darwinists before you can even consider the conclusions.
Feel free to express on what grounds specifically Sternberg is wrong.
We’ll know in the coming decades if junk DNA is junk.
PS
I do express my thanks that you’ve tried to stick to the topics at hand and you’ve never attacked me personally despite the fact that I’ve not always been so nice to you.
For that I salute you.
Unlike myself, who has apparently expressed a revulsion for Salvador that can only be expressed as contempt and repugnance.
Now I’ve been charged of making the claim here at UD that I find Sal repugnant, even though I cannot recall the occasion.
See my response to Sal here:
http://telicthoughts.com/mutat.....ent-248736
I repeat what I said there: Sal, If I called you repugnant, I apologise.
I can’t find anyplace in this thread where I have done so.
Sal, this is not a model.
Perhaps you mean to model the case of haploid organisms who experience 1 new harmful mutation per newborn.
If that is the case, you need to develop such a model.
Let us say that each newborn dies, as a result of the harmful mutation.
GREAT! Now that is something we can actually model.
For each newborn that enters the population, add one harmful mutation to that individual.
For each harmful mutation in an individual in the population, remove that individual from the population.
Are we making progress yet?
Well, to answer that, we need to ask how well our model tracks with observations of actual organisms.
Care to comment?
Mung,
It wasn’t in this thread, it was 2 years ago here at UD.
Baloney. Look at the animation. The seleciton model doesn’t matter. Who gets killed doesn’t matter. With haploids, the number of offspring doesn’t matter.
The model is minimally simple to drive home the theme: if there are enough harmfuls mutations, no model of selection can prevail against deterioration. Therefore with respect to haploids,the other details are moot. Do you understand what the word “moot” means.
I just did. Do you understand what the word moot means with respect to the matter at hand.
Hint: moot means with respect to any other possible modeling parameters or details, the parameters and details don’t affect the final outcome. Thus it doesn’t add anything to the clarity of the model.
Look at the friggin animation!!!! It illustrates visually what will happen!!!! Sheesh.
Zach has yet to run it with those specifications. He’s been running the diploid model. I’ve objected, and Zach, who’s been quick to provide sim work, has been noticably quiet to run the simulation that is consistent the animation.
Why the silence?
scordova at 102,
“Is that the average mutations per individual?”
Minimum. See the discussion above.
How about trying to model it with the other parameters to your choosing.
Feel free to report the results.
Now you’re just teasing.
Why so coy? I’d really like to understand your underlying model, possibly to the extent of being able to implement it in software. Could you please describe it at the level of detail suggested by Zachriel?
Haploids: 1 new harmful per new born
Try implementing that. Are you having problems counting up to 1?
scordova at 107,
Haploids: 1 new harmful per new born
Try implementing that. Are you having problems counting up to 1?
Ah, it could be worse, I could be having problems demonstrating common courtesy.
Zachriel at 101 politely detailed the additional information required to understand your model:
Is that the average mutations per individual? What is the distribution of effects of the harmful mutations? How often do reversions occur? How frequent are beneficial mutations and what is their distribution? What is the population? The size of the genome? What about recombination which is common in haploid organisms?
Without knowing those kinds of parameters, it is not possible to replicate your model. I am more than willing to go to the effort of doing so; I hope you are willing to provide the additional information.