Different kinds of gaps

[Vanengelen (Erik van Engelen)]

@T_aquaticus

This also leaves the question of how many “coordinated” mutations are possible in a given genome, how many coordinated mutations are needed in a given evolutionary relationship, and how that would interact with sexual recombination.

How many “coordinated” mutations are possible? I would say: Three?
How many coordinated mutations are needed? For a chimpanzee-common ancestor to create a human I would say: a million times 50 mutations coordinated? But you may call this a sharpshooter fallacy and you think that potentially millions of different “human” species could have evolved from our common ancestor, but sadly, it did not happen.
Of course, sexual recombination would have influence, but it is not easy to understand what this influence would be.

Dear Taq, there seems to be a fundamental difference in our basal intuitions about how easy mutations lead to new functions. You think that the possibilities are many, and I think that they are very scarce. Already the origin of one protein with completely new function is difficult. In ‘normal’ biology except evolutionary theory, I don’t see scientists that seriously take the appearance of new functions into account. It is mostly loss of information, loss of regulation, damage and so on. Selection is continuously busy to get rid of that noise. We see that in bacteria. If we see the presence of a new type antibiotic molecule or (at the other side) an antibiotic degrading molecule, nobody thinks that it originated recently and we don’t expect that raising in our laboratory, it was already there at one place on earth (soil in China), but we only discovered it recently.

In our lab, some years ago, colleagues wanted to use aptamers for creating tests to detect animal diseases. Publications with regards to aptamers were promising. We used a protocol for generating random oligo nucleotides aimed to bind certain molecules. You produce huge numbers of random oligo nucleotides and then go through an iterative selection process to select the molecules that bind the target. The only function needed was: binding. The results were very disappointing. And after some years, we stopped the project.

[Klax (The only thing that matters is faith expressed in love.)]

So what’s the gap in rationality that only irrationality can fill again?

[T_aquaticus]

@Leyton

What you’re trying to do is ignore what we’ve learned about the genetic and molecular mechanisms of embryonic development.

I’m not ignoring anything. I am asking for specific examples of DNA differences that result in differences in embryonic development, and why you think those DNA differences can not be produced by evolution. I’m actually asking to see the information, not ignore it.

@Leyton

What is your evidence to support that?

One example:

From extrapolations we estimate that 8.2% (7.1–9.2%) of the human genome is presently subject to negative selection and thus is likely to be functional, while only 2.2% has maintained constraint in both human and mouse since these species diverged.
8.2% of the Human Genome Is Constrained: Variation in Rates of Turnover across Functional Element Classes in the Human Lineage

There are several studies that have looked at sequence conservation and signals of selection within the human genome, and they all seem to come in at ~5-10% of the human genome.

Yes it is. In the section you quote it might only be implicit, but later (penultimate para) they say explicitly:

They say explicitly that neutral mutations only evolve neutrally in 5% of the genome. It isn’t saying that neutral mutations can only occur in 5% of the human genome. Neutral mutations and evolving neutrally are two different things.

What the article explicitly states is that neutral mutations will not evolve neutrally due to many different mechanisms. Again, it is NOT saying that only 5% of the genome can have neutral mutations. For example:

A mutation will not evolve neutrally if it provides a direct fitness advantage, but the converse does not apply. A mutation can appear to evolve non-neutrally if it is merely located close to a mutation that affects fitness. In sexual organisms like humans, each child inherits DNA from its parents in big, continuous chunks. Even distant cousins will share large chunks of DNA that were inherited from recent common ancestors. If that part of DNA happens to contain a beneficial mutation, hundreds of nearby mutations might hitchhike along for the ride as the beneficial DNA spreads quickly through a population (Smith and Haigh, 1974; Charlesworth et al., 1993). These hitchhikers confer no fitness advantage but, equally, they do not behave the way we expect neutral mutations to do.

It explicitly states that neutral mutations can evolve non-neutrally.

@Leyton

But what you’re relying on is that neutral mutations will work in this way and have a constructive effect. In theory it can happen, but only with a probability of something like 1 in 10^18 if two specific bases are involved, in 10^27 if three, etc. You are relying on good luck (or magic).

Why would it have to be two specific bases? Do you think there is only one such interaction possible in the human genome? If so, I would love to see that evidence.

For example, how many combinations of two mutations in the modern human genome can result in a beneficial phenotype? Don’t you have to know this number before you can calculate probabilities of one such interaction being found?

@Leyton

No, what I was illustrating with the dice is that as the probability decreases you need to roll more dice or more often.

The problem is your calculated probability. You are also ignoring the parallel nature of sexual reproduction which can combine beneficial mutations from separate genetic backgrounds into the same genetic background. For example, let’s say there are 100 possible beneficial mutations that are not linked (i.e. are far enough apart in the genome to allow recombination). The odds of getting these 100 mutations is not 100 times the probability of getting 1 of them. Rather, these 100 mutations will occur in different individuals within the population. As these beneficial mutations increase in frequency you will start to get an accumulation of beneficial mutations due to sexual reproduction. This greatly increases rate at which evolution occurs.

@Leyton

For the example of resistance, there are only a few possible beneficial mutations, all in the same gene so far as I’m aware.

Is that true for every single adaptation? I see no reason why it would be.

@Leyton

For the vertebrate genome there will of course be many locations where beneficial mutations could in theory occur. Eg current estimate is up to 25,000 genes for humans, and quite likely there’ll be several possible locations for each of these. But to get a constructive change to embryonic development, at a minimum you’d need to make a constructive change to an existing control sequence, probably to several and/or the genes of corresponding transcription factors. This would require many coordinated mutations.

Examples?

If none of these coordinated mutations for development can even be cited, then what’s the point?

@Leyton

I think you may misunderstand what fixation means in population genetics. It only means that a mutation becomes a normal part of a population’s genome (close to, if not at 100%).

I know what it means. What I was replying to is your insistence that neutral mutations can only be lost. I am pointing out that they can also be fixed.

@Leyton

‘Permanently established’ is wrong. If a specific location presents an advantage then natural selection will offer some protection. But a neutral location will not benefit from this, and will be as susceptible to change as any other location.

Neutral mutations can also reach fixation.

[T_aquaticus]

@Vanengelen

How many “coordinated” mutations are possible? I would say: Three?

There are only three possible combinations of mutations in a given genome that can produce a beneficial phenotype? How did you calculate that?

@Vanengelen

How many coordinated mutations are needed? For a chimpanzee-common ancestor to create a human I would say: a million times 50 mutations coordinated?

How did you determine that they are coordinated?

@Vanengelen

Dear Taq, there seems to be a fundamental difference in our basal intuitions about how easy mutations lead to new functions. You think that the possibilities are many, and I think that they are very scarce. Already the origin of one protein with completely new function is difficult.

What brand new proteins do humans have that chimps do not?

Why can’t you get a completely new function from a limited number of mutations in an existing functional protein? How do you determine if a function is completely new to begin with?

@Vanengelen

In our lab, some years ago, colleagues wanted to use aptamers for creating tests to detect animal diseases. Publications with regards to aptamers were promising. We used a protocol for generating random oligo nucleotides aimed to bind certain molecules. You produce huge numbers of random oligo nucleotides and then go through an iterative selection process to select the molecules that bind the target. The only function needed was: binding. The results were very disappointing. And after some years, we stopped the project.

I’ve done the same thing to test protease specificity using FRET peptides with random amino acid sequences, so I’m familiar with the general use of these types of libraries.

Of course, DNA binding is just one function out of millions of possible functions. There are many functional proteins in humans that don’t bind DNA. You would also have to qualify the level of binding that you were looking at, and compare that to what might be functional in early life or even in modern life.

[Klax (The only thing that matters is faith expressed in love.)]

In other words can anyone point to an actual gap in the four billion years of evolution aka life, nature, that evolution, aka life, nature can’t fill?

[Dale (evolutionary providentialist)]

(Beyond cosmic rays providentially altering DNA and embryonic development, there doesn’t appear to have been any mention of epigenetic change here.) The Christians arguing here for some kind of capital ‘I’ ID and irreducible complexity and any other ‘gap’ are only arguing from incredulity as far as I can tell.
 

“…the most common mutations, transitions, are not really ‘copying errors,’ because the keto-enol transition of the base is driving them and the polymerase is working correctly. So if you’d like, that can be seen as providence more than chance.”
– a Christian Molecular Biologist

Not having accepted evolutionary science since youth and YECism, and having endorsed OEC (old-earth creationism) for a long time (decades), that statement was highly influential in the change in my thinking (another was my nephrectomy not a very long time earlier). I’m okay with God being sovereign over abiogenesis as well, with no exceptions to the natural order required – all laws intact, just exceptional and extraordinary timing and placing. Kinda like the same person winning five independent lotteries and being the only one to have bought any tickets, and only one ticket in each, right? (I won’t tag those who know the rhetorical question is directed to them, although I started to for one of you. ; - )

[adamjedgar (adam james edgar)]

@pevaquark

It seems like your main argument is that in this one case, explanatory gaps appear to have gotten larger with more scientific inquiry - therefore it makes sense to consider alternative explanations for gaps in the explanation of natural phenomena. Would you say that in certain cases, it makes more sense to be open to supernatural explanations but in other cases, it makes less sense to be open to supernatural explanations? After all, the general rule seems to work the other way around, where explanatory gaps are closed or narrowed by scientific mechanisms - like with the evolution of bacterial flagellum for example or with the stability of the solar system.

how can you quote the biologos article on bacterial flagellum when Michael Behee (as one of an ever increasing number of creation scientists) exposed this problem in the evolutionary theory and have shown that its a very problematic example for evolutionists?

[Klax (The only thing that matters is faith expressed in love.)]

No it’s not. It’s entirely his problem and he utterly fails to make it evolution’s, life’s, nature’s problem. Apart from nature having come up with Michael Behe. And you. And Layton and Erik the Vet. Which is normal in evolution.

[pevaquark (Matthew Pevarnik)]

@adamjedgar

how can you quote the biologos article on bacterial flagellum when Michael Behee (as one of an ever increasing number of creation scientists) exposed this problem in the evolutionary theory and have shown that its a very problematic example for evolutionists?

Because my Bayesian priors led me to put up blinders to comprehend anything contradictory to the oath I took to worship at the altar of evolution.

[Dale (evolutionary providentialist)]

I couldn’t possibly be detecting any irony, could I?

[Dale (evolutionary providentialist)]

@adamjedgar

how can you quote the biologos article on bacterial flagellum when Michael Behee (as one of an ever increasing number of creation scientists) exposed this problem in the evolutionary theory and have shown that its a very problematic example for evolutionists?

The idea of exaptation and the similarities of the bacterial injectisome to the bacterial flagellum helped me to accept biological evolution after having been a YEC for a sizable chunk of my life. Learning about the neutral theory of evolution and neutral drift and that evolution can and does produce complexity were factors as well.

Sorry, you have not cited any real problems, just interesting puzzles at best.

[Daniel_Fisher]

@T_aquaticus

You can include God and intelligent agency.

These are the types of data you would need to explain:

1. The twin nested hierarchy of morphology and DNA sequence
2. The pattern of transition and transversion mutations when comparing genomes. See here: Testing Common Ancestry: It’s All About the Mutations - Article - BioLogos
3. Why exons have more conserved sequence than introns when comparing genomes between species
4. The pattern of orthologous and non-orthologous endogenous retroviruses
5. The pattern of transitional fossils, why they follow the same nested hierarchy as living species
6. Genetic equidistance

Those are just a few off the top of my head.

I’m not familiar with each of the above, and don’t have time to research further at present… but briefly, can you clarify for me…

• which of the above are direct evidence of common descent?

versus

• which are direct evidence of the mechanism of unguided natural selection working on unguided natural variation?

This goes back to the point toed above… “evolution” can refer to the process of common descent, or the Darwinian mechanism… the core difference that sets ID and others apart from the bio logos/“evolutionary” position is not dispute about common descent, (hence why a common-descent-affirming, “evolution” believing scientist like Behe and others are fully supported and embraced by the ID side, but whose ideas are more or less persona non grata at Biologos.)

But from my amateur and cursory glance at your list, they all appear to be arguments for common descent, which is not my dispute.

[Leyton]

@T_aquaticus
I’m not ignoring anything. I am asking for specific examples of DNA differences that result in differences in embryonic development, and why you think those DNA differences can not be produced by evolution.

As I said in my previous response, we may not be in a position to do this yet. But even if we were and showed it was highly improbable to occur, you’d likely plead sharpshooter fallacy. But what we know already about gene regulation shows any constructive changes are extremely unlikely to arise opportunistically.

From extrapolations we estimate that 8.2% (7.1–9.2%) of the human genome is presently subject to negative selection and thus is likely to be functional, while only 2.2% has maintained constraint in both human and mouse since these species diverged.

So from this you infer that approx. 90% of the genome is evolving at a rate consistent with neutral mutations. However, how did they derive their estimate? By comparing genomic sequences of different mammals. Most of their 10% is focused on protein-coding sequences, so it is not surprising that there is relatively little changes in sequence, even between different species. However, they then assume that the differences between mammals in non-coding sequences implies that these sequences are subject to ‘turnover’, which you imply (I don’t think the authors actually say so) means susceptible to neutral mutation. But this extrapolation is based on assuming that eg humans and mice have diverged from a common ancestor. And, the question to ask is: much of the non-coding sequences are repeats; wouldn’t repeats have been randomised by neutral mutations? (Another indication that their rationale is unsound is that, because they conclude these non-coding sequences are mutable, they conclude that a large proportion of this could be deleted without impacting on fitness (p8). Whereas we know that much of non-coding regions are required for eg packing of DNA.) So, I’m going to look into this further, but I think these differences between the non-coding regions of different mammalian (and other vertebrate?) groups may provide further genomic evidence against common ancestry. So thank you for drawing it to my attention!

@T_aquaticus
They say explicitly that neutral mutations only evolve neutrally in 5% of the genome. It isn’t saying that neutral mutations can only occur in 5% of the human genome. Neutral mutations and evolving neutrally are two different things.

It explicitly states that neutral mutations can evolve non-neutrally.

Agreed. But even taking this into account (and the paper discusses various examples) she still concludes that only about 5% of the human genome is susceptible to neutral evolution, as my previous quote, and this is from the subtitle of her paper

Just 5% of the human genome is subject to neutral evolution,

So it’s hard to maintain as you do that she doesn’t mean it.

@T_aquaticus
Why would it have to be two specific bases? Do you think there is only one such interaction possible in the human genome? If so, I would love to see that evidence.
For example, how many combinations of two mutations in the modern human genome can result in a beneficial phenotype? Don’t you have to know this number before you can calculate probabilities of one such interaction being found?

Based on what we know about the length of control sequences for genes, which I mentioned last post, how many two-specific bases do you think will lead to a beneficial phenotype, and why?

@T_aquaticus
The problem is your calculated probability. You are also ignoring the parallel nature of sexual reproduction which can combine beneficial mutations from separate genetic backgrounds into the same genetic background. For example, let’s say there are 100 possible beneficial mutations that are not linked (i.e. are far enough apart in the genome to allow recombination). The odds of getting these 100 mutations is not 100 times the probability of getting 1 of them. Rather, these 100 mutations will occur in different individuals within the population. As these beneficial mutations increase in frequency you will start to get an accumulation of beneficial mutations due to sexual reproduction. This greatly increases rate at which evolution occurs.

What you then need to take into account is the probability of those specific 100 coming together within a population of a given size (and without others that might counter the effect of some of them).

@T_aquaticus
If none of these coordinated mutations for development can even be cited, then what’s the point?

Taking account of what we do know, rather than relying on what we don’t (evolution of the gaps).

@T_aquaticus
I know what it means.

If you know what fixation means then you’ll agree that ‘fixed’ mutations are susceptible to change. And if so, then why do you keep repeating that fixation will happen. That’s not in question.

[T_aquaticus]

@Daniel_Fisher

I’m not familiar with each of the above, and don’t have time to research further at present… but briefly, can you clarify for me…

• which of the above are direct evidence of common descent ?

versus

• which are direct evidence of the mechanism of unguided natural selection working on unguided natural variation ?

They are all evidence of both. #3 would need to be fleshed out to cover common descent a bit better.

@Daniel_Fisher

But from my amateur and cursory glance at your list, they all appear to be arguments for common descent , which is not my dispute.

That isn’t the case. For example, a designer could take an adaption from a mammal species and add it to a bird species, or vice versa. This would violate a nested hierarchy. So the nested hierarchy is both a piece of evidence for common descent and unguided natural evolutionary mechanisms. The pattern of transitions and transversions is the same because it is the fingerprint of unguided mutations that we see happening in modern life. The pattern of endogenous retroviruses evidences the unguided insertion of viral sequences and the pattern of inheritance consistent with common descent. The pattern of transitional fossils links in with the nested hierarchy, so again both common descent and unguided natural processes. Genetic equidistance links in with unguided accumulation of mutations resulting in genetic distances consistent with both a nested hierarchy and common descent.

[T_aquaticus]

@Leyton

As I said in my previous response, we may not be in a position to do this yet. But even if we were and showed it was highly improbable to occur, you’d likely plead sharpshooter fallacy.

And I would likely be correct.

Let’s say I had a deck of cards. I shuffle them and then deal them out one at a time face up. The probability of getting that specific order of cards is 1 in 52!, or 1 in 8x10^67. That is an extremely unlikely outcome, and yet I got it on the very first try. In fact, I will get an equally improbable outcome every time I do the same experiment.

The same for mutations. Any time mutations occur it will result in an extremely improbable outcome. Every. Single. Time. And for the same reasons that my card example produces improbable outcomes.

@Leyton

But this extrapolation is based on assuming that eg humans and mice have diverged from a common ancestor.

It’s not an assumption. It’s a conclusion based on mountains of evidence.

@Leyton

And, the question to ask is: much of the non-coding sequences are repeats; wouldn’t repeats have been randomised by neutral mutations?

Not if those repeats are from relatively recent transposon insertions which make up a large chunk of the non-coding intergenic DNA sequence.

@Leyton

But even taking this into account (and the paper discusses various examples) she still concludes that only about 5% of the human genome is susceptible to neutral evolution,

That’s not what I understood. You seemed to be saying that neutral mutations could only occur in 5% of the genome which is not what the paper said.

@Leyton

Based on what we know about the length of control sequences for genes, which I mentioned last post, how many two-specific bases do you think will lead to a beneficial phenotype, and why?

I have no clue of how that could even be calculated which is why I am extremely skeptical of those who claim they can, which is most of the ID/creationist crowd.

@Leyton

What you then need to take into account is the probability of those specific 100 coming together within a population of a given size (and without others that might counter the effect of some of them).

If they are all beneficial, it’s extremely likely. As each beneficial mutation increases in frequency it will be more and more likely to be found with the other 99 beneficial mutations that are also increasing in frequency.

@Leyton

Taking account of what we do know, rather than relying on what we don’t (evolution of the gaps).

What coordinated mutations for development do we know of?

@Leyton

If you know what fixation means then you’ll agree that ‘fixed’ mutations are susceptible to change.

All mutations are susceptible to change.

When a mutation occurs there are 3 general results. The mutation can almost immediately disappear from the population. The mutation can increase in frequency a bit and circulate at a low or medium frequency. The mutation can increase in frequency to the point where it is found in all individuals in a population. You seem to think that only the first situation happens.

[Daniel_Fisher]

Appreciate the thoughts as always; i’m tight on time at present, but briefly one quick observation…

@T_aquaticus

The pattern of transitions and transversions is the same because it is the fingerprint of unguided mutations that we see happening in modern life.

if i understand rightly, this is true only for those sections of otherwise similar sections of DNA. Orphan genes unrelated across species can’t even be claimed as having such patterns, no? as such, the pattern of mutations between homologous sections of DNA are evidence that mutations in those sections are indeed explicable by said natural processes… a process that no ID proponent denies to my knowledge.

In other words, if i understand rightly, an ID proponent that supported common descent, but who hypothesized that humans were intentionally designed at a specific point in time through specific larger non-homologous modifications of DNA in a proposed CHLCA, while keeping the other ~95-98% of the genome untouched, would expect just such a pattern of mutations to occur along the homologous DNA over the corresponding ages as the species continued to diverge.

So again i’m not sure how this demonstrates the efficacy or mechanism of unguided variation/selection regarding those parts of DNA that are actually under discussion?

[T_aquaticus]

@Daniel_Fisher

if i understand rightly, this is true only for those sections of otherwise similar sections of DNA . Orphan genes unrelated across species can’t even be claimed as having such patterns, no?

You are making the assumption that orphan genes are not in regions with otherwise similar sections of DNA. There are many cases where orphan genes are the product of just a handful of mutations that produce a new transcript. Two species can share the same stretch of DNA with just a few differences while only one of those species will have a gene within that stretch of DNA. When they say that it is a new gene they are saying that the DNA is only transcribed in one species.

There are also cases of orphan genes that are due to indels (the portmanteau of insertion and deletion). In this case, we would not be comparing substitution mutations which are the transition and transversions. However, the distribution of indels is also as random as the substitutions.

@Daniel_Fisher

In other words, if i understand rightly, an ID proponent that supported common descent, but who hypothesized that humans were intentionally designed at a specific point in time through specific larger non-homologous modifications of DNA in a proposed CHLCA, while keeping the other ~95-98% of the genome untouched, would expect just such a pattern of mutations to occur along the homologous DNA over the corresponding ages as the species continued to diverge.

They would need to explain why those modifications are inconsistent with unguided mutations and why we don’t see those same modifications in other more distantly related species. This is where the nested hierarchy comes in.

[Daniel_Fisher]

@Leyton

I don’t know what prompted me to try to work out the specificity / improbability of a typical protein, but I chose cytochrome c which at just over 100 amino acids (aas) is fairly short. An obvious question I realised from quite early on is how specific does the sequence need to be? One approach is to look at what aas are the same across all the sequences we know, which span a wide range of plants and animals for cytochrome c. But there’s still the possibility – I would guess likely - that a completely different structure, with completely different aa sequences, could work. How can we quantify this? Maybe, with our increasing ability to model protein folding, and knowledge of how aas work at an enzyme’s active site, one day we’ll be able to answer this. However, with our present knowledge I think there are 2 strong reasons against an evolutionary origin to biochemical mechanisms.

Very appreciated, thanks. this was somewhat similar to when i started exploring… early in my life i was exposed to a creation science proponent saying something to the effect of, “what are the odds that even one protein could form…” or the like. at the time, i dismissed this observation entirely, i simply retorted (in my mind) that, sure, the odds may be astronomical, but we’re not talking a single opportunity… but potentially billions and billions of attempts over billions of years…

it wasn’t until i actually did the math, and understood exactly what ~10^130 possible combinations actually meant that i began to understand how irrelevant billions and billions of opportunities over billions of years were when were talking that level of magnitude…and how prohibitive the numbers are we were talking.

On a completely different topic, you may have the background to help discuss something particularly interesting to me regarding the design behind the tRNA molecules in the protein synthesis process… would you have the time/inclination/expertise to discuss further? if so i can start a new thread and/or private discussion, so as not to derail this present thread.

[T_aquaticus]

There has been some discussion of mutations that lead to changes in gene expression. I decided to quickly look at what the literature is saying about lactase persistence in humans. This is the condition where humans continue to produce the lactase enzyme into adulthood instead of stopping production during childhood.

It turns out that there are a lot of different mutations responsible for this phenotype. It’s not a case of one lucky mutation and only one mutation that can produce this phenotype. Also, these mutations cluster to a region well upstream of the gene for lactase, about 13-14,000 base pairs upstream. At least 6 mutations have been thoroughly studied and are verified to functionally change lactase expression, and their geographic distribution is pretty interesting.

Interactive map exploring worldwide allele frequencies for the most studied lactase persistence (LP)-associated genetic variants (http://bionit.ugr.es/pages/investigacion/software/bioinformatics-methods-software). Data for each SNP are represented by a different color. It also offers a detailed description for each included study (incorporating information related to geographical location, ethnicity, frequency of LP-associated alleles, and literature references). The figure presented here represents a static capture of the interactive map.
Genetics of Lactose Intolerance: An Updated Review and Online Interactive World Maps of Phenotype and Genotype Frequencies - PMC

This is why I am very skeptical of claims that these types of mutations are extremely rare and almost impossible for evolution to produce.

Also in the paper:

On the other hand, the persistence of LPH activity throughout adulthood (LP) seems to be a genetic trait following a dominant inheritance pattern, and involving the action of cis -element mutations. Particularly, it has been described that the effect of several SNPs leads to an alternative path for LCT expression that is not downregulated, as the original pathway is [4]. The molecular mechanism for these SNPs is the creation of new binding sites for specific transcription factors, such as the octamer-binding protein 1 (Oct-1) [65].

[Klax (The only thing that matters is faith expressed in love.)]

@Daniel_Fisher

it wasn’t until i actually did the math, and understood exactly what ~10^130 possible combinations actually meant that i began to understand how irrelevant billions and billions of opportunities over billions of years were when were talking that level of magnitude…and how prohibitive the numbers are we were talking.

You’re still trapped by meaningless numbers which have absolutely nothing to do with nature whatsoever. No matter how good the science is, you utterly ignore it for the sharpshooter fallacy, after following every rational step. Ah well, that’s evolution for you. There was obviously survival value in that kind of flawed, superstitious reasoning, or the larger cognitive mechanisms that have that as a by product.