Kondrashov's Paradox: Why We Haven't Died 100 Times Over

Conversation
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Sure. Absolutely. Never said anything else. But duplicating a chapter does not alter the plot, does it? The point is still and always that genotype, expression, and phenotype cannot be teased apart, and that fitness effects are not intrinsic to the genotype but are measured by the differential success of the living, breathing, organism. This is elementary. Once again, I’m not denying anything, not the role of the genome, and not the roles of phenotype and environment on fitness outcomes. Its you that has problems with where life and death and reproduction actually happen.

This is all about GE. Your model does not capture all the complexity that exists in nature, and is empirically falsified, which is why you reject factors that are real but not captured in your model. For all your talk of functional complexity, you dismiss the role of function in a complex and dynamic environment. You still cannot even answer if a mutation changing color is deleterious, neutral, or beneficial.

The reason you have zero interest in the actual biological limits on your model is that GE is just a dogma of dispensational theology; as I stated before, a quixotic denial which “is religiously motivated by some notion of plenary inerrant inspiration of the archetype genes of Eden.”

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So survival is a component but only for the offspring, not for the parent? That still just boils down to reproduction only. No, survival is an inherent part of the definition of fitness (meaning mutations that harm survival without affecting reproduction can still be said to be reducing fitness).

The truth is, the word fitness is foggy but it acts as an imperfect proxy for total genetic function. You won’t get anybody who isn’t a creationist (that I’ve heard at least) come out and openly admit that, but Gerrish’s statement is an implicit admission that functional complexity lies at the heart of fitness effects. Fitness is not purely relative or subjective, far from it.

In the vast majority of cases it is. That’s why Gerrish et al openly acknowledged that fact. It’s not just any complexity though, it’s functional complexity.

Yes, that’s an example of an edge case where the artificial lab environment created conditions where part of the robust function that is needed in nature became unecessary or even detrimental in the lab. Exceptions don’t overturn the rule.

Again we hear what “everyone” would agree with. Not sure I buy it. In any case, if someone wants to claim some other DFE besides the ones we have published evidence for, then the burden of proof is on that person.

Fixed? Not strictly fixed, but it’s never going to change so much that suddenly thermodynamics starts running in the wrong direction and functional complexity starts assembling itself without a designer.

The more I explore this, the more it becomes clear that GE is an absolutely unbeatable problem for evolutionists, and when confronted with it they can only resort to redefining words and ignoring the obvious facts of life.

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It’s hard to carry on any sort of civil conversation when you constantly insult the intelligence (in two meanings of the phrase) of everyone here.Why not try leaving all that out and responding to what people actually say? One obvious fact of life is that there are many millions of extant species. If there really were widespread GE, why wouldn’t most of them be extinct by now?

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It’s really rich to see you saying this to me in the context of this thread (or more broadly, this whole board, or more broadly again, the whole internet). Pretty much everybody engaging here has at one point or another attacked my intelligence, my ability to read, my education, my credentials, my honesty, and so on and so forth. If you can’t take it then don’t dish it. I have been responding to what people say extensively. Most of the time my responses are ignored or misconstrued.

Take for example this very post I’m responding to. You ignored almost all the content of my post and responded only to the last paragraph, and then only to get offended, and you had the gall to suggest that I should actually respond to what people say (the very thing you were not doing in the process of making that post).

As I’ve already stated many times on here and also in the livestreamed debate:

GE is independent evidence that enough time has not yet elapsed for most LMEs (not all!) to go extinct. Many of them already have gone extinct. Some of them, like the wooly mammoth, we can directly identify mutational meltdown as the cause of extinction.

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Wikipedia - Fitness (biology)

Fitness … is a quantitative representation of individual reproductive success.

That is perfectly clear and integrates all other factors including survival, given that not surviving is strongly correlated with not reproducing. There is nothing foggy about it except the incoherence in your dissonant mind. There is nothing to admit. Its a matter of DEFINITION. You are welcome to coin a word with a different meaning, but get your own special little creationist blitherin word, this one is taken.

Says the person who seeks to redefine fitness and ignores the obvious role of traits.

And yet, elephants which YEC consider to be the same kind, are still very much with us 4000 years later.

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No, survival is only important in so far as it contributes to the number of offspring reaching reproductive maturity. Some species produce vast numbers of offspring, where only a few survive. Others have few offspring but take care of them, helping them survive the early stages of infancy, or even beyond that.

Fitness in population genetics is not foggy - it is very clearly defined. And you’re calling that definition a “redefinition”, which is clearly absurd.
There are two issues here. First there is the fact that there are many ways to achieve fitness and survival may or may not be a component. Consider the giant pacific octopus - each breeds only once, the female may produce hundreds of thousands of eggs. The female cares for the eggs, not taking any time to eat - and will die after the eggs hatch. The vast majority of the hatched larvae will not survive - only two need to reach adulthood to sustain the population.

Second you are still trying to make the concept fit your own ideas - and it doesn’t. You want fitness to be an inherent quality of the individual - but it can’t be. The definition does not allow it.

Indeed it is really clear that within-species competition is a part of fitness. All members of a species require the same resources - and if there are not enough to go around some must do without. When a species is expanding mean fitness must be > 1.0, when it reaches the limit of expansion mean fitness must fall to 1.0 even if the species is unchanged. Within-species competition for the limited resources explains this.

And yet parasites typically lose complexity. Complexity is not fitness - it may contribute to fitness but it may also detract from it.

Yes this is a typical reaction in apologists when a much-loved idea is shown to be untenable - becoming more convinced of it and embracing obvious falsehoods to prop up that conviction. Tell me how can using the standard definition of fitness in population genetics when discussing a work of population genetics possibly be a redefinition?

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No, why would you say that? Why do you give such uncharitable readings constantly?

John Harshman keeps telling you to read what people write and this is a perfect example of why.

Gee, I wonder why I wrote “When we say fitness is about reproductive success, it is to be implicitly understood that the survival component is part of what reproductive success means.”?

That’s just wrong. Just flat out wrong. Now YOU are the one redefining fitness.

Already explained why complexity is not a proxy for fitness.

And nobody here claims it is. Neither are the traits (phenotypes) that are the underlying physical causes of fitness. The goat in the picture really does have those horns, and it doesn’t matter where you personally think the top of the skull ends and the horn begins. The trait is a concrete, objective, physical reality. So is the density of it’s fur, the length of the hairs, the hair diameter, how fast they grow, and so on and so forth.

It isn’t, and he didn’t. Complete misrepresentation of his words. He wrote it is more likely that mutations are deleterious than beneficial, not that increasing complexity increases fitness, which is what you are trying to imply. He has stated no such thing anywhere and it doesn’t follow from his words.

There is no such rule. You made it up and none of your sources support it.

Besides, streamlining (the shedding of excess genetic material that does not contribute to fitness) happens constantly in nature. Again since microorganisms are much easier to work with (see more evolutionary change within human timeframes, are easier to collect and sequence), there are plenty of good examples there. For one, bacteria will routinely expel plasmids containing new genes that were beneficial for a time, but turned detrimental in a changed environment.

Heck, even in our own geneome we have innumerable pseudogenes that are both inactive and degraded. Genes for making egg-yolk protein (we begin developing a yolk-sac in development, but the process is aborted), hundreds of pseudogenes for olfactory receptors, the classic GULO pseudogene for the enzyme in vitamin c biosynthesis, which is totally unnecessary when you can just eat a few plants. And so on and so forth.

So, to be sure, lab environments are typically much simpler than natural environments, but the same processes are known both by observation and inference to occur in the wild.

No, the burden of proof is on those who want to convince others that their simulation correctly reflects observational reality.

Since you are the one who presents your SLiM simulation to the readers/watchers of your debate, to convince us that we should go extinct due to GE and that life could not have evolved, you are the one who has the burden of supporting the parameters you used in your simulation.

Since your simulation had a fixed DFE, and since the realism of that idea is disputed, you must shoulder the burden of showing that the DFE doesn’t change but remains fixed regardless of what the fitness level of the population is.

Get to work.

Oohhh, really? It was in your simulation. So how much is it not fixed? Evidence please!

Nobody claims the DFE reverses thermodynamics. Another silly misrepresentation from you Paul. Do better.

Rich coming from the guy who makes up ad-hoc rationalizations why DFEs observed changing even in multicellular eukaryotes somehow magically wouldn’t also apply or happen to “large”(a measure you’ve yet to rigorously define and delineate) multicellular eukaryotes.

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If GE is the reason woolly mammoths went extinct then why haven’t elephants also gone extinct?

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You guys (and I can say that about this group because you act as a block and basically only ever criticize me, never one another) – you guys cite wikipedia, while I cite peer-reviewed papers.

Yet you claim that I have no credibility. That’s about all that needs to be said here. I’ve already shown from Dr. Orr that 1) the word is fuzzy (countless definitions have been proffered) and 2) it entails both survival and reproduction. It is not as simple as counting offspring that survive, and as you get more complex that gets more and more true.

In my simulation, the fitness is used to cull the population prior to reproduction, deciding which individuals reproduce at all. Reproduction happens with fixed numbers of offspring per set of parents (I chose 8 total per pair of parents). This is very realistic for LMEs like humans. Genetic factors rarely play a role in the number of children we have. Socioeconomic factors are the prime determinant of number of children, not genetics.

No simulation will be perfect, and all will entail simplifying assumptions. You can certainly change the method and use fitness to directly determine the number of offspring had. It will change the internal dynamics a bit, but fitness decline will still be inevitable as long as you keep the parameters within Kondrashov’s danger zone. Population geneticists who are in the know, like Dr. Masel, will tell you this. “Fitness keeps declining no matter what”. It’s because of Ohta’s Ratchet.

You cited wikipedia, I cited peer reviewed sources. I don’t think you’re on the high ground here. I do my homework, you sit on the sidelines and parrot the propaganda you learned in school.

Here is Orr from the same paper I already cited:

“…the word ‘fitness’ has been used to mean subtly different things.”

This is why I say it’s ‘foggy’.

Here’s another peer-reviewed source talking about the definition of fitness, emphasis mine:

‘… the concept of fitness was born from the original notion of evolution by natural selection, and fitness is a critical component of how adaptive evolution proceeds. Yet biologists have disagreed about the formal definition of fitness since the term was first introduced (Dobzhansky 1968; Stearns 1976; Cooper 1984). Indeed, in his glossary, Stearns (1976, p. 4) defined fitness as “something that everyone understands but no one can define precisely.”’

Wadgymar, S. M., Sheth, S. N., Josephs, E. B., DeMarche, M., & Anderson, J. (2024). Defining fitness in evolutionary ecology. International Journal of Plant Sciences,185(3), 218–227. https://doi.org/10.1086/729360

Of course, I’d say Stearns perhaps assumed too much when he assumed everyone understood it. It seems most do not because they oversimplify it.

Here’s a peer-reviewed example of fitness describing survival only, with reproduction not even considered, emphasis mine:

“Fitness curves were computed to examine changes in survival with different trait values …”

Byars, S. G., Papst, W., & Hoffmann, A. A. (2007). Local adaptation and cogradient selection in the alpine plant Poa hiemata along a narrow altitudinal gradient. Evolution, 61(12), 2925–2941. https://doi.org/10.1111/j.1558-5646.2007.00248.x

I’ve noticed you tend to make bold claims you cannot back up, then when I challenge you on those claims, you just drop it and act like it never happened (such as when you claimed that created heterozygosity is contrary to a plain reading of scripture).

Implicit in what you said above is a claim that if any member of a created kind goes extinct due to mutational meltdown, we should expact all members of that kind to go extinct at the same time. Can you perhaps back up this claim?

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Did you somehow miss my post #62?

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And these authors clearly show, using empirical evidence, that traits affect fitness and in relation to the local environment.

The fitness analysis indicates that selection coefficients change between low- and high-altitude sites, and that they are in opposite directions for the two traits measured. The graphs suggest that selection is toward the extreme values of the range, reflecting strong directional selection on both traits that seem directly related with survival at different altitudes in the alpine zone. Other studies that have incorporated local adaptation experiments and selection analyses have demonstrated that traits in a population can be selected in opposing directions across environmental gradients.

Empirical demonstration that environmental selection can push a trait in a certain direction. Thanks for that paper Paul.

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Of course it is fixed in my simulation, and as far as I know that’s all SLiM is capable of in the first place. You might be able to write custom code to change the DFE mid-simulation, but out of the box it is not set up for that. Why, I wonder?

The reason I said “not strictly fixed” is just that there is so much stochasticity involved in real biology and real environments. The fixed DFE is just an approximation of what would actually be observed in real life.

It’s important to remember why there is a DFE in the first place. Why is it that scientists go to the trouble of publishing DFEs if they don’t believe they remain reliable through time?

The answer is that they obviously do think they are describing a reliable estimate of a DFE over time. DFEs have the shape they do because of two factors:

  1. Random probability applied to errors in replication

  2. The specifics of the genome of the particular organism

More complex genomes will tend to have DFEs that are even more skewed towards zero compared with simpler organisms. That’s the princess and the nucleotide paradox at work.

None of these two basic factors is expected to vary with respect to average fitness in the population, as you are claiming it does. So please be specific: what mechanism are you proposing that can act to shift the DFE in some meangingful sense as a population changes in average fitness?

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In the entire history of this forum I have never seen two creationists or ID proponents who have been active here at the same time, disagree or argue against each other (and there have been multiple-year-long periods where several creationists/ID-proponents were active at the same time).
Gilbert Till and now Bill Cole has dropped in for a few drive-by comments here and there in these recent threads and it’s companions and offshoots, and it sure as scheisse wasn’t to rebut you or disagree with each other.

Both of them ostensibly support some form of OEC, and more widespread common descent than you do (in Bill’s case, it seems to fluctuate as randomly as radioactive decay, Shrödingers descent-suppoter that he is, but I digress), and even if the topic is the question of the age of life or the age of the Earth they dare not push back on you. You will never find a more wretched hive of monolithic groupthink than creationism-supporters.

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Yes, I did miss that post. In it, you change your original claim from “it’s contrary to scripture” to “scripture doesn’t teach it”. Which of course I would agree with. I never said scripture had anything to say about zygosity, but when we combine our modern knowledge of genetics with the historical foundation that scripture provides, it becomes a very reasonable inference in how God must have engineered life with the ability to diversify and occupy different niches.

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In debating creationists over 20+ years, I’ve found it’s extremely rare to see creationists publicly disagree or criticize each other.

The only times I have seen criticism is if a creationist starts asking too many questions and/or appears in danger of leaving the flock. These instances can often invite a hostile response from fellow creationists. Again, this is just based on what I’ve seen over the years.

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Except it’s not even remotely consistent with what we observe in human populations today.

I know, you’re not willing to look at actual, direct observations to see if they show your claimed “very reasonable inference in how God must have engineered life” is in any way reasonable.

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… anonymous claims that were removed from Wikipedia for being unreferenced.

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Evidence please.

You get a DFE when you record the fitness effects of a sufficiently large number of different mutations.

To determine whether the DFE changes with organismal fitness, you need to record the fitness effects of large numers of different mutations in genetic backgrounds with different fitness levels (which implies you need to record the organismal fitness of the individuals in which you then go on to collect data on a DFE). Scientists can even record the fitness effects of the same mutation in different genetic backgrounds and see how the magnitude of effect of that same mutation changes as a function of the fitness of that genetic background. A phenomenon you have no explanation for with your empirically unjustified assumption that the DFE remains fixed.

I think the truth here is it strongly depends on the types and scopes of the questions they are trying to answer, and different scientists come to these questions with different backgrounds and ways of analyzing them. As you can see further down, plenty of scientists think diminishing returns epistasis (and a number of related phenomena) are widespread, if not universal.

That’s just the answer you would like to believe, nothing more Paul.

In all cases where scientists did the work to assess whether and to what extend the DFE changes with organismal fitness, it did change, and substantially so.

None of the DFEs you’ve found were from articles where scientists explicitly set out to determine the magnitude of diminishing returns epistasis, and you only have poor excuses for why you don’t accept those studies where they change.

You outright ignored the paper I referenced where they showed diminishing returns epistasis in a multicellular eukaryote.

This is just an assertion on your part that simply begs the question.

You don’t speak for the people working in this field at all and there’s no reason to think your statements here reflect their views.

It’s also ultimately irrelevant since all the empirical data we have on this question shows the DFE changes with fitness, with lower fitness opening up more numerous avenues for compensatory beneficial mutations, and of greater magnitude of effect.

I largely agree with these authors on the cause of diminishing-returns epistasis:

Interestingly, that paper also suggests that it is commonly believed that fitness effects of mutations increase in stressful environments:

Our observation supports the common belief that the fitness effects of mutations tend to increase in stressful environments (Agrawal and Whitlock 2010) and further demonstrates that this increase also occurs even when the background genotype fitness is controlled for.

In this paper analyzing data from the LTEE (still on the bioXriv), the authors suggest that diminishing-returns epistasis might be a universal phenomenon of life (and suggest it is “key rule of evolution” even in the abstract):
https://www.biorxiv.org/content/10.64898/2026.03.17.712273v1.full

Diminishing fitness gain in biological evolution has been widely observed across different groups, including bacteria5,26, viruses27, and yeast28. This indicates that diminishing fitness gain in biological evolution is a universal phenomenon29,30. Collectively, these studies suggest that as the level of adaptation increases, the fitness gains conferred by later beneficial mutations tend to diminish.

My bold.

In this paper, they even suggest the possibility that I have, that diminishing returns epistasis can potentially help protect small isolated populations from extinction:

Regardless of the biological mechanisms that underlie global epistasis, further work is needed to establish its generality. If it holds broadly, several important implications are conceivable. In genetics, our model can improve predictions of the phenotypic effects of mutations. In conservation biology, the possibility that low-fitness genotypes have access to large supplies of beneficial mutations gives hope that evolutionary rescue may prevent some species extinctions. In evolutionary biology, our results point to the existence of a universal class of distributions of fitness effects of mutations, which could explain why evolutionary dynamics of fitness are so similar and predictable across systems (25, 36, 42, 52). More broadly, our model may help us better understand these dynamics, including how the DFE changes during evolution (see (45), Section 2.2), how adaptation to one environment affects fitness in another (26), how pan-genomes evolve (see (45), Section 2.3), etc. More fundamentally, our results suggest that epistasis reduces the effective dimensionality of genotype-to-phenotype maps (8, 43, 44, 51). What biological constraints cause this dimensionality reduction, how it emerges and when it breaks down are exciting open questions in systems biology.

My bold.

The future doesn’t look good for GE.

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I claim that you have chosen to shred your own credibility which is rather a different point. And I note that you evade the real question. According to you including within-species competition is a “redefinition” of fitness. Obviously arguing that the definition is foggy does nothing to help that.

Indeed, Orr mentions mating success as a component of fitness - can it be denied that there is competition for mates in many species?

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GE isn’t evidence. It’s a claim about what the evidence (data) ought to show. And since we know that billions of years have elapsed, this claim is obviously false. But let that aside for now and assume we accept your timeline of 6000 years. Have you tried any simulations to see what sorts of species ought to be extinct now if your claim were true? In other words, have you tried a range of effective population sizes, per generation mutation rates, and generation times to see what portions of that space should still be viable? Have you compared this to the data for extant species? I suggest that if you did this, you would find that lots of extant species should have been extinct by now, even on your short timeline, if the simulations were accurate.

And it wasn’t “the wooly mammoth” that suffered the mutation meltdown, it was a tiny remnant population on Wrangel Island. Did you read your source?

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