So you’re saying that either your simulation is faulty or everything we know about geology and physics is wrong, and you pick the latter. Is that not megalomania?
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No, but what you’re doing definitely is elephant hurling.
I could provide more details if that would help.
If the world is only 6000 years old and there was a global flood 4000 years ago, then all radiometric dates are wrong, which means that what we know of radioactive decay is wrong, which means that our basic theories of particle physics are wrong. Would you agree?
And most of what we know of geological processes is wrong. There has been no significant plate motion or subduction, ever. The continents have occupied their current positions from the beginning. What we know of remanant magnetism is wrong. Seismic data interpreted as subducting plates are inexplicable. Earthquakes are inexplicable. Volcanoes are inexplicable. The Hawaiian Islands are inexplicable. Ophiolites are inexplicable. Essentially, nothing in geology is explicable.
The geological column is not a temporal sequence (or was, in geological terms, deposited simultaneously, worldwide). Correlation of strata can’t be done, not by lithology, not by sequence stratigraphy, not by index fossils, not (see above) by radiometric dating. There is no biotic succession.
There was no Permian or Cryogenian glaciation. There is no K/T boundary clay and no Chicxulub impact.
Phylogeny, both molecular and morphological, is illusory. The so-called nested hierarchy does not exist. Except when it does, and there’s no way to tell the difference. Two species of Drosophila really are related by common descent, but two species of primates with equal divergence are not.
Would that be enough elephants for you?
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Thanks, and I’m beginning to see I had a slight misunderstanding of terms. I was using ‘diminishing returns epistasis’ interchangeably with ‘antagonistic epistasis’, but apparently DRE is a more broad concept that includes the suggestion of a shifting DFE. The phenomenon of DRE as you’re describing it is very much an artifact of reductive evolution in microbial cultures selecting for fast-reproducing strains in the laboratory environment.
Microbes adapt to specific lab conditions, and only with very narrowly-defined fitness parameters like growth rate. This is not really applicable to LMEs in any meaningful way.
In LMEs, the parameters we see strongly imply fitness decline, which is the exact opposite of what you’re discussing here. You’re appealing to evidence that fitness stops increasing, and then you’re appropriating that evidence in favor of the exact opposite idea: that fitness will start increasing. Bait and switch. It’s right there in the name: diminishing returns. Not “suddenly increasing returns”!
I have. Apparently you and Masel referenced the same paper? In the paper regarding the mechanism, they state this about so-called “global epistasis”.
The global epistasis hypothesis asserts that the benefit of a mutation depends solely on the fitness of the background genotype instead of the genotype per se.
That is extremely wrong-headed thinking that ignores what the genome is, which is a set of highly complex instructions for life in a code we are only beginning to fully understand. So yes, the effect of a mutation will depend entirely on the genome and not at all on background fitness. The results of these yeast experiments are being greatly misinterpreted, putting the cart before the horse.
Dr. Masel states on her website “we still don’t have an answer”. Her preprint is a proposed solution, not an accepted or final one. And this particular solution (mega-beneficial mutations) is a non-starter and is nothing new. As I said, Kimura already suggested it back in 1979. It makes zero sense and is nothing but sophistry. Damage spread throughout the genome is not going to be undone by a small number of large-effect mutations. Fitness is not a substance.
Nobody has demonstrated anything of the kind. Quite the opposite. They have demonstrated that there is a limit to how much mutations can cause microbes to increase in replication speed in a lab.
Backwards as usual. You don’t have a mechanism to explain the phenomenon yourself (since you’re ignoring the obvious one that these changes are genetically reductive in nature).
I do have a mechanism that explains why this wouldn’t apply to LMEs, though, and it’s staring you right in the face already, right there from the paper. The biological architecture of organisms. Increasing complexity. Randomly changing complex functional machines is not likely to improve upon them.
Saying that low fitness increases the chances for beneficial mutations is like saying a pile of trash is easier to improve upon than a Corvette, since it’s got further to go. Or it’s easier to jump to the moon the further you get away, since there’s so much more room to jump! In other words, it’s sophistry.
You’re making the same mistake that Hancock did. You’re quietly assuming that the problem of near-neutrality somehow doesn’t apply to beneficial mutations just as it does to deleterious ones. Of course it does. There is no significant difference in probability of fixation for a near neutral beneficial compared to a near neutral deleterious mutations. In LMEs, the vast majority of beneficial mutations will fall below the drift barrier just the same as the deleterious ones.
And this is why microbial experiments are so often misleading with respect to GE (as Sanford identified). Because the stochastic mutation load paradox doesn’t apply to microbes the same way it does to LMEs.
The irony of me having to explain the mechanics of the stochastic mutation load paradox to you once again.
The fact that it’s due to entropy is both obvious and already acknowledged in the literature. Gerrish admitted it, but you have closed your mind to this because it breaks your worldview.
One would need to actually demonstrate this in the positive direction you’re suggesting, not just the negative direction (diminishing). Stop trying to bluff your way through this problem, it won’t work.
We already know it can’t. It has been extensively modeled, and that’s why we have Kondrashov’s Paradox.
I’m just shaking my head because this is the same old sickle cell anemia bait-and-switch all over again. Reductive evolution being paraded around as “beneficial” because of extenuating circumstances. Reminder: sickle cell anemia is ALWAYS a debilitating disease in every environment.
This is actually what Michael Lynch is banking on. He thinks lots of deleterious near-neutral mutations can accumulate and then join together, form functional complexity, and then suddenly become beneficial. The problem there is that with realistic parameters in LMEs, we will be dead long before anything like that has any chance of happening. It beggars belief, but this is the lengths that evolutionists must now go in order to make it seem, if only to themselves, that there is some plausible mechanism for their theory.
I already addressed this claim. Go read what I already wrote about back mutations.
Did you happen to read the title? You are quotemining the article! It said “any single mutation”. They are talking about mutation accumulation.
By the end, the Wrangel Island mammoths were genetically screwed.
If sign epistasis works to rescue LMEs from fitness decline as you suggest, then this should not have been possible. You’re weaving a fairy tale.
Yes, what I meant there was “antagonistic epistasis”. But diminishing returns doesn’t do what you claim it does in any case. It acts to stop fitness increase, not stop fitness decline.
If so, you’ll be the first one. None of the population geneticists on here have had one word to say about it, including Hancock strangely enough. That should probably tell you something. But there’s nothing hidden about it, you can look at it for yourself.
Yes, I did, thanks. It turns out that diminishing returns epistasis and antagonistic epistasis are related but slightly distinct concepts, so thanks for helping me figure that one out. The terminology in population genetics is a black box.
You mean “phase”? No, it’s not a bare assertion. Fitness is not a substance you can pile up in one place to offset the loss of it in another place. That whole concept is reductive and wrong-headed. I’m sorry to see that so many smart people cannot understand that, but the reason is obvious. They will not question their worldview so this is all they can come up with.
No, it would not help if you were to change the subject and start delving into a completely different set of debates about different claims you’re making.
That won’t help.
In your earlier post, you said “or everything we know about geology and physics is wrong”.
Given the context, the “we” could mean you and @UncensoredPilgrims . Or could could mean the whole of society.
That’s the real mistake. @UncensoredPilgrims doesn’t know that (because he has decided to not allow himself to know that). And the whole of society doesn’t know it either, for the whole of society included the YEC, who have decided to not know that.
In your later post, you again use “we” in the same way.
Yes, his accusation of “elephant hurling” is silly. But that’s how YECs see it.
So you hand wave away her statement, but you really liked that quote mine for the opening of your debate. It is clear that is a problem statement to direct research and not intended as end conclusion.
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I’d extend this that in the Young-Earth creationist framework, the entire universe is illusory.
There is a great article published in 2019 about a young Earth creationist who deconverted from YEC when they couldn’t reconcile their belief in a young universe with observations in the universe.
In particular, it was the light trail hundreds of thousands of light-years behind the galaxy ESO 137-001 that they couldn’t reconcile. It didn’t make sense than in a universe only 6000 years old that a galaxy would have travelled for hundreds of thousands of years.
After first reading this article, I would occasionally point other YECs to it to see what they made of it. Invariably the only responses I got to explain this observation is that “God made it that way”.
In my view, this nullifies any observations about the universe. Any contradictory observation can be explained away with an appeal to the supernatural.
Organizations like CMI and AIG even take this a step further and bake this right into their faith statements.
This is further why I don’t understand why Paul Price or any creationist is attempting to model anything. Since there is no way to take into account an unbounded supernatural source interfering with the fundamental nature of the universe, trying to model anything in a creationist universe is irrelevant.
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That’s a strawman argument. The Christian God is not capricious our random, trying to foil our experiments with his random miracles. That’s why Christianity birthed modern science. Christian men like Isaac Newton believed in a God which upholds the universe in an understandable way, and the miracles he does he does for understandable reasons (and the really big ones are recorded for us so we can study the effects).
Rather, trying to model anything in an atheist universe is pointless, since you have no way of knowing that 1) human brains are evolved properly to understand truth and 2) that the universe will behave in the next millisecond the same way it behaved previously. Appealing to past experience to justify this belief (known as the uniformity of nature) is simply circular.
Is it? Are you talking about fitness or your idea of genetic entropy? There are many ways to achieve fitness so it seems obvious that loss of fitness in one area can be compensated for by a gain in another. Fitness is the question in Kondrashov’s paradox so work attempting to address that will naturally be talking about fitness.
That;s a bit rich coming from a Young Earth Creationist.
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With respect to “Genetic Entropy”, one small loss in fitness is just like any other, so it is essentially all one thing. A more realistic view of fitness would have multiple factors and possibly multiple survival strategies.
This does not improve the situation for GE, because now fitness needs to degrade in multiple domains simultaneously and equally. At best it becomes increasing unlikely with an increasing number of factors.
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My original statement stands. The YEC notion of heterozygosity to explain the multitude of animals is contrary to the same plain reading of scripture that underpins creationism to begin with. It is a massive interpretive dissonance.
Breeding population plays a role. Conservationists have long been acutely aware it is challenging to maintain genetic diversity in shrinking and siloed habitats.
Empty verbiage or projection; I’m not sure which.
Just because your model fails to encompass a reality does not make such aspects to be sophistry.
Everybody has been trying to tell you this. Traits. Biological architecture of oganisms are traits, and those play a role in selection. You seem to prefer “functional complexity” because that is a creationist dog whistle, and avoids dealing with the immense data supporting the evolution of adaptive traits.
For a self proclaimed expert on Genetic Entropy, you demonstrate a far superior grasp of rhetorical apologetics than either the scope of population genetics or entropy.
Further, you abuse the place of models in science - they are not used to disprove an observed phenomena - they point the way to develop more comprehensive research. You have not shown interest in refining the range of the model because your objective is apologetics. Protein folding is still not perfectly modeled, although great strides have been made. That does not mean that proteins do not fold any more than your model means life is doomed.
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No, it isn’t. Once again your posts reveal you don’t read the papers I link with any comprehension, merely to look for ways to dismiss them and the things I say.
They have tested it directly even on single genes. Why do mutations even in single enzymes that improve their enzymatic rate, during adaptive walks, show diminishing returns, and the corollary that when their catalytic effiency is very low, the same beneficial mutations have larger effect sizes, and mean beneficial effect size is larger? Your ad-hoc fantasy excuse cannot explain this.
They have tested many different types of mutations affecting many different cellular functions in this way.
Why does the same beneficial mutation confer a larger fitness benefit in a less fit genetic background, or a poorer environment, than it does in fitter backgrounds and better environments? That is to say, when background fitness goes down, beneficial effect size goes up for the same mutation. So the same beneficial mutation becomes more visible to selection in a lower fitness background.
Why does the same deleterious mutation have a larger fitness cost in a more fit genetic background, or in a better environment, than it does in a less fit background and poorer environment? That is to say, when background fitness goes up, deleterious effect size goes up for the same mutation. So the same deleterious mutation becomes more visible to selection in a higher fitness background.
The implication, which you are working desperately to avoid acknowledging, is that when fitness gets lower and lower, the beneficial mutations gain larger effects (true even for the same mutations, therefore not caused by new “reductive” mutations) and the same deleterious mutations gain smaller effects (as a direct consequence, when fitness gets lower those beneficial mutations can now compensate for many more deleterious ones both because the beneficial mutation gained more beneficial effect, while the deleterious mutation became less deleterious). Conversely, when fitenss gets higher and higher, deleterious mutations gain larger effects (become more visible to selection) and beneficial mutations gain smaller effects (therefore slowing the rate of adaptation). This phenomenon has been measured on multiple forms of life including viruses, bacteria, and multicellular eukaryotes, and even mutations in the same gene.
The same mutation has a different effect-size that depends on background fitness. This what you’re not getting. Think about what this means.
Your ad-hoc excuse that this has to do with “reductive evolution in microbes”, or that the effect would mysteriously disappear just because and organism gets more complex, simply doesn’t work as an excuse here. It has no power to explain these observations. This does: Patterns and Mechanisms of Diminishing Returns from Beneficial Mutations - PMC
This completely destroys your entire post.
You could have erected the same ad-hoc nonsense at the level of single proteins and insisted viruses are much too complex for the phenomenon to show up there.
You could have erected the same ad-hoc nonsense at the level of viruses and insisted bacteria are much too complex for it to show up there.
You could have erected the same ad-hoc nonsense at the level of bacteria and insisted eukaryotes are much too complex for it to show up there.
You could have erected the same ad-hoc nonsense at the level of single-celled eukaryotes and insisted multicellular-eukaryotes rae much too complex for it to show up there.
But since it’s yet to be directly measured in an animal because model organisms are usually small and easy to work with, here we are. It is only a matter of time before someone goes and documents diminishing-returns of this type in C. elegans, or Drosophila, or Arabidopsis thaliana, etc.
What is your excuse going to be then Paul?
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Oh look! Here’s a paper for those who actually believe in reality rather than magic, demonstrating diminishing-returns epistasis for large multicellular eukaryotes (Drosophila, and A. thaliana):
It’s inferred using comparative genetics between species Paul will no doubt reject common ancestry for and therefore to him this study will simply be question begging. But there it is, what he says isn’t real.
Someone will eventually directly measure it in species Paul believes it can’t exist in. What will his excuse be then? Place your bets now.
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LMAO. Yeah those whales sure did increase fitness universally across all environments when adapting to an aquatic lifestyle didn’t they?
According to Paul Price’s model of evolution, when whales beach, they should get up and sprint further inland. And when they don’t, that means evolution is false for reasons that don’t make sense in any reality.
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He also puts a hilarious emphasis on the values of quotes he can lift off websites, offhand remarks in pop-sci articles, casually mentioned in the discussions of papers, etc.
His obsession with what they write on the Hasel lab website is just the latest example. Proposing a solution isn’t the same as having “solved” the problem. Apparently you need to literally declare it in those same words. “We solved the paradox!”
You can’t just write something like “we are pursuing models where X acts to suppress the effect of Y” or something like that.
The literalist mind at work.
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Yes, my point is that genetic entropy is not identical to fitness. If genetic entropy is taken to be an irreversible loss of information then it would not be unreasonable to argue that it couldn’t be so easily reversed. But the subject is fitness which is clearly different in that respect.
So it comes down to confusion on the part of the promoters of genetic entropy. Which hardly helps a claaim that genetic entropy is science. Especially as they don;t seem interested in clearing it up.
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No? It’s the opposite. Fitness is a metric which acts as a rough proxy for total genetic function. It is not a substance than you can just lump together from any place in the genome. The genome is an instruction manual. Many mistakes all throughout cannot be compensated for by a few big helpful mistakes thrown in.
That’s exactly what does happen. The genome is hit by mutations all throughout, and the population is hit with mutations all throughout, being spread roughly evenly, creating a generally homogenous loss of average fitness with Ohta’s Ratchet.
This is what’s necessary to argue for YEC, and YEC is necessary for GE. When you’re trying to upset all of science, all of science is relevant.
How do you know that? And why did he fake so much data, like the light from distant supernovae that never actually happened?
How does theism solve this problem? Of course it doesn’t.
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I, being but one man, cannot explain all the mysteries of biology to you. But here is my question for you: why do you keep equivocating between diminishing returns and increasing returns? Why do you keep pretending that a process which stops fitness increase somehow also magically stops fitness decline with no mechanism or observation to support it?
I guess for the same reason that an ice cube is more helpful when you’re hot than it is when you’re cold. But this is all just a red herring since you’re talking about microbes adapting to test tube environments with one very specific and narrow definition of fitness. This is not applicable to genome-wide changes in LMEs.
That’s not ad hoc.
Oh look! Here’s a paper for those who actually believe in reality rather than magic, demonstrating diminishing-returns epistasis for large multicellular eukaryotes (Drosophila, and A. thaliana)
Both of these examples may be multicellular eukaryotes, yes, but they are not large. They are on the opposite end of that spectrum. They have small genomes and fast replication times – the very things that make them least affected by genetic entropy. These are not LMEs. LMEs are things like wooly mammoths (dead from GE), humans (dying from GE), monkeys, Komodo dragons, and the like.
Thanks, can you please refute your own arguments more often? It saves me the trouble.