I’ve skimmed it. It’s great (and indeed, more or less is an extended thesis inspired by my 2004 paper; yet he does the subject much better than I did). But I have no plans to review it in particular. If anyone asks for a suggestion on the subject, though, he tops the list.

You are making a large number of factual, mathematical, and epistemological mistakes here. I address them all in Biogenesis and the Laws of Evidence.

And as I’ve repeatedly stated, I have read them.  I simply disagree with your assessment.  I will say it again: The 1 in 10^41 odds you give is for (‘toy model’) assembly of a single, self-replicating molecule, NOT for the origin of life.  Your claim that the odds are actually far better than this due to putative ‘countless other initial self-replicators’–only one of which need arise–that ‘must necessarily’ have existed is likewise irrelevant and misses the point entirely, because that still only deals with a single molecule, NOT the origin of life.  It doesn’t matter how many supposed ‘countless’ different self-replicators you think could theoretically achieve the same result, because no single one of them can achieve all the results that are needed.  As I said, a single molecule does not life make.  A single self-replicating molecule is neither living, nor sufficient in itself to originate (or evolve) life.  It may be entirely necessary, but it’s nowhere near sufficient.  Even if more than one type of self-replicating molecule can perform the same type of function, no one molecule can perform every function that is needed for life (which for even ‘simplest, first’ life is believed to require the functional integration of at least three key components: metabolism, compartmentalization/encapsulation, and replication–not of a single molecule, but of the entire autopoietic entity).  This is one of the many problems that all single polymer scenarios–which try to avoid the astronomical improbabilities associated with the independent random assembly of multiple different polymers (with different functions) on the early earth in sufficient proximity during the same window of time–ultimately run into: you still have to eventually somehow derive all these other components, either independently or from a putative single self-replicating polymer.  And the single self-replicator of the ‘RNA First’ hypothesis is not even part of life as we know it, which regardless of whether other types of life are possible is still where we need to get to on earth in only a few hundred million years.
  
The appeal of ‘RNA First’ is that at first blush it seems to solve the chicken-or-egg paradox of ‘DNA is needed to make proteins/catalytic enzymes, and proteins/enzymes are needed to make DNA, so which came first?’  The discovery of catalytic RNA seems to circumvent this problem, but only temporarily, because we still must somehow separate this combined informational-catalytic polymer into separate informational (DNA) and catalytic (proteins) polymers and cooperatively integrate them into a sophisticated transcription-translation information processing system for protein synthesis in only a few hundred million years.  The ‘RNA First’ hypothesis glosses over these immense difficulties by simply assuming that somehow the ‘RNA World’ transitioned to this ‘DNA-Protein’ world.  But no one really knows how to plausibly accomplish this, even in theory.  Even logically, there are immense hurdles.  There is no straightforward trajectory from a self-replicating system that selfishly outcompetes and chemically ‘evolves’ by ‘Darwinian natural selection’ into separate informational and catalytic biopolymers related through an arbitrary, semiotic code that are functionally integrated and work together cooperatively, not competitively.  And it is further difficult to explain how a single self-replicator that was so successful (in terms of fitness), would then be replaced, so as to leave no vestige of its prior existence (i.e., we see catalytic RNA, but we don’t see self-replicators in living things that catalyze their own synthesis.  Those functions are segregated in life).  ‘RNA First’ proponents postulate an initial self-replicator (that was subsequently replaced and left no physical evidence of its prior existence) in an attempt to solve only one small piece of the greater puzzle.  ‘Metabolism First’ proponents reject the scenario.  You treat it as if it is a foregone conclusion, when it remains a contentious, hotly debated issue.

Thus, you haven’t proved the origin of life by random chance to P —> 1, you’ve simply moved the goal posts by reducing the problem of life’s origin to just the origin of a single self-replicating molecule, while ignoring a host of other problems and assuming that if we can just generate an initial self-replicator then any and all subsequent problems will magically solve themselves, and life will automatically emerge via ‘Darwinian’ chemical evolution.  But that is an enormous leap that no one has empirically demonstrated can happen, or even how it plausibly could happen in theory.  It reminds me of a 2011 NewScientist article entitled, ‘First Life: the search for the first replicator’ that similarly relates: ‘Once the first self-replicating entities appeared, natural selection kicked in, favouring any offspring with variations that made them better at replicating themselves. Soon the first simple cells appeared. The rest is prehistory.’  But that’s like saying, ‘Hitler failed his entrance exam for the Academy of Fine Arts Vienna.  One thing led to another.  And the US dropped an atomic bomb on Japan.’  It explains nothing and leaves out most everything.

And that brings us full circle to what is really my main point: namely, that unlike biological evolution and universal common ancestry–for which we enjoy substantial, definitive evidence–we do not possess the same for the origin of life and cannot speak in such definitive, emphatic terms.  Abiogenesis is our working hypothesis in science and assumed to be true, but unlike biological evolution it still remains an empirically unverified working assumption.  That is not an argument for theism or ‘super ghosts’–which have no consideration or place in science–nor the rantings of a ‘delusional apologist’ as you erroneously presume (I’m an evolutionary biologist).  It’s simply a statement of fact about our current level of scientific knowledge on the subject. While biological evolution has been empirically demonstrated, abiogenesis has not, and it would be misleading to suggest otherwise.

In the interests of thoroughness and to dispense with any further accusations that I haven’t read the article, I will also take time to comment on selected portions of said article.  In addition to the main problem I see of reducing life’s origin to the origin of a self-replicator, I feel there is some inconsistency and/or selective application/criticism in your article.  You are very good at spotting others’ assumptions, but I feel like you do so selectively and inconsistently, and don’t always recognize some of your own assumptions that you make in turn.  I believe you have also conflated some issues, and I disagree with you that Totani has committed ‘fatal flaws’ in his article.  I find that Totani’s work is exactly what it purports to be; no more, and no less.  I will start with some of your ‘fatal flaws’:

“4.  Confusing the winner with the players: Assuming that only exactly our life is possible (or that there is only one possible self-replicating molecule), when in fact many other kinds of life are possible” [In theory.  But that is an assumption, too.  Maybe there are, maybe there aren’t.  We simply don’t know.  Certainly no one has demonstrated that ‘many other kinds of life are possible’, and the phrase ‘many other kinds’ is ambiguous.] “(and there must be many different self-replicators that could start it off),” [Again, supposition.  Why ‘must’ there have been?  Where is your indisputable empirical evidence to make such an emphatic claim?  The truth is we don’t know.  We don’t have definitive empirical evidence to demonstrate that any single self-replicating molecule–much less the examples you discuss–are sufficient to ‘start it off” (which I take to mean a pathway that inevitably and unavoidably leads to life via ‘Darwinian’ chemical evolution).  It is a popular idea.  It is often presumed.  But even proponents recognize that scenarios invoking self-replicators, autocatalytic sets, and the like may be necessary, but are still not sufficient.  For example, the authors of the ‘Autocatalytic Networks at the Basis of Life’s Origin and Organization’ article you cite make this plain in the abstract: ‘We argue that autocatalytic sets are a necessary (although not sufficient) condition for life-like behavior.].   

What the empirical and experimental evidence does indicate is that cells with minimal genomes of only a few hundred genes and proteins can exist.  But these are parasitic obligates or synthetic organisms that can only exist in controlled environments within a narrow range of tolerances and which are dependent on artificially or host supplied nutrients.  By contrast, the ‘simplest’ free living cells have genomes with upwards of a thousand genes.  Of course, it is assumed that the very first life had to be far simpler–some suggest 30-40 genes–and maybe it was so, but again this is still conjecture and speculation.  No one has demonstrated this empirically.  But regardless, if estimates are correct, then we had only a few hundred million years to not only originate a putative self-replicator and ‘first life’, but also the Last Universal Common Ancestor (LUCA), with an estimated 400 genes. 

“5.  Begging the size of the protobiont: Not deriving a sound evidence-based estimate for how small (i.e., how structurally simple) a self-replicating molecule can be.”

This is a conflation.  A self-replicating molecule is not a protobiont.  A protobiont is encapsulated/compartmentalized (i.e., ‘membrane’-bound) by definition. 

Regarding Totani, you write, ‘His only Type 5 error is ignoring pre-RNA worlds and over-estimating even the minimum RNA size based on some faulty logic’.  No, it isn’t.  You have this tendency to make emphatic, rigid, black-or-white claims, and to frame others’ work in similar ways, when they have not done so themselves.  Totani’s article is very speculative and rife with uncertainties, as many theoretical works are.  But there’s nothing wrong with that, because his work acknowledges this and doesn’t purport to be definitive ‘proof’.  He continually qualifies his remarks and acknowledges that there are many uncertainties in his calculations.  These are the marks of a meticulous, careful scientist who doesn’t inflate the significance of his conclusions but properly tempers them in accordance with the inherent uncertainties that exist.

You write: “Totani’s second argument is more defensible, but still flawed: there are no currently known ‘RNA molecules shorter than 25 nucleotides’ that exhibit ‘a specified function,’ whereas ‘there is a reasonable hope to find a functioning replicase ribozyme longer than 40-60’ nucleotides.  In other words, we haven’t observed anything in nature so small that even has a function much less the function of self-replicating, so if we stick with what’s been experimentally accomplished so far, the minimum we can argue is 40 nucleotides….The problem is that ‘must be larger than 25’ does not get you to ‘must be at least 40.’  The early earth had millions of years to randomly sequence molecules; scientists do not.  So replicators of, say, 30 nucleotide length are beyond our ability to discover by merely random mixing. So we cannot actually rule them out.”—But neither can we ‘rule them in’.  You’re just speculating.  Regardless, Totani is not ruling them out either.  He’s simply basing his figures on what the empirical, observational evidence he cites actually supports, as opposed to speculating.

You write: “This is the one point where Totani overstates what his sources actually say. He only cites two: a 2012 paper by Robertson & Joyce that only has this to say on the point:

“It is difficult to state with certainty the minimum possible size of an RNA replicase ribozyme. An RNA consisting of a single secondary structural element, that is, a small stem-loop containing 12–17 nucleotides, would not be expected to have replicase activity, whereas…[something] containing 40–60 nucleotides, offers a reasonable hope of functioning as a replicase ribozyme.”

“So Totani’s “40-60” number is actually just speculation. It is not any actual evidence-based argument for a minimum size.”

No, you are mistaken.  It’s not ‘just speculation’. It shows a lack of understanding of molecular biology. You omitted significant parts of the quote.  It’s not just ‘something’ containing 40-60 nucleotides, but a specific, structural feature at issue:

“An RNA consisting of a single secondary structural element, that is, a small stem-loop containing 12 –17 nucleotides, would not be expected to have replicase activity, whereas a double stem-loop, perhaps forming a “dumbbell” structure or a pseudoknot, might just be capable of a low level of activity. A triple stem-loop structure, containing 40–60 nucleotides, offers a reasonable hope of functioning as a replicase ribozyme.One could, for example, imagine a molecule consisting of a pseudoknot and a pendant stem-loop that forms a cleft for template-dependent replication.”  

You seem to misunderstand.  It’s not the length by itself that’s significant, but the secondary structure stem-loop needed for catalytic activity.  Multiple stem loops are needed for meaningful catalysis that outpace naturally occurring decomposition reactions.  The nucleotide numbers simply reflect the number of nucleotides needed to structurally form a stem-loop.  It is common knowledge that a small stem-loop (‘containing 12-17 nucleotides) does not exhibit catalytic activity.  The reasons for this are well-understood.  When it comes to a putative ‘RNA World’ ribozyme that specifically catalyzes RNA replication (i.e., a replicase), ‘it is difficult to state with certainty the minimum possible length’.  But based on extant ribozyme correlates that catalyze non-replication reactions we would not expect replicase activity to occur with a single stem-loop, because we don’t observe catalytic activity with single stem-loops in extant ribozymes; and even if we did, the activity level would be negligible and not sufficient to outpace decomposition.  

You then write: “And this, mind you, is solely for an RNA-first scenario. It is now known RNA might [yes, might, it is conjecture] actually be an evolved, not an original, feature of life. Which gets us to Totani’s biggest mistake: he only ever considers RNA protobionts [No, not a ‘protobiont’.  Totani doesn’t consider membrane-bound protocells; except only to note that ‘the highly uncertain’ Pev parameter–the probability an active polymer once produced proceeds to Darwinian evolution to complete abiogenesis–which he assumes with 100% certainty (Pev = 1) ‘as a baseline’–that consideration of ‘Any other essential factors involved in the origin of life, e.g., encapsulation by membrane vesicle formation, may significantly reduce this parameter’].  Nowhere in his paper does he even mention, much less account for, PNA-first models of biogenesis. [That’s not quite true.  Totani notes that ‘Non-RNA nucleic acid analogues may have carried genetic information before the RNA world emerged’ and says his formulations ‘can also be applied to such cases’, but that is not ‘the aim of this work’, which focuses specifically on RNA polymer assembly.  Non-RNA analogues are beyond the scope of his work.  You can’t fault research for being no more or less than what it purports to be].  Yet these are increasingly more likely [No, that does not follow.  The experiments simply demonstrate that PNA-based replicators as short as 32aa can be produced.  They don’t prove (and can’t prove) that that’s what actually happened historically, nor is there any vestige of such actually existing in the history of life.]…. Totani, in other words, is reading the wrong literature. [No, he’s aware of it, it’s just not the focus of his research]. He is looking for the smallest self-replicating RNA molecule, when what we should be looking for is the smallest PNA molecule [No, not necessarily (see below)], because we have already experimentally proven that PNA self-replicators exist that are much simpler than anything we know from RNA. [But again, that doesn’t prove a PNA-World preceded an RNA-World.] Indeed, if we apply Totani’s own highly conservative math to the smallest empirically known PNA self-replicator [but not empirically known as an actual stage in the history of life] then his own conclusion would be that life has already originated on average once per Hubble volume, not less than once. And again, his math is already overly conservative on that point, as I explained earlier.”

The problem here is that you have latched onto a ‘PNA-First’ scenario because in your mind it seems to be a ‘slam dunk win’ that makes abiogenesis all the more certain, when it’s actually not necessarily so.  This is because you have to factor in the actual chemistry.  The greater ease with which PNA self-replicators form implies greater thermodynamic stability, which is great for PNA, but not for subsequent ‘chemical evolution’.  The rule is chemical reaction systems run toward lower energetic, equilibrium states and then stop.  The more stable, the more difficult it is to get products to participate in further reactions.  Thus, instead of a slam-dunk win, PNA could be a chemical dead-end.  Like the problems with transitioning from an RNA- to DNA-World, it is not clear that transition from a PNA- to RNA-World could be an easily accomplished feat   It’s easier to get PNA nucleotides than RNA nucleotides, but not necessarily as easy to then go from PNA to RNA.  Such may ultimately be more problematic than the problems with RNA nucleotide synthesis.  That is why not everyone has jumped on the PNA ‘bandwagon’.  And that is why it’s not significant that Totani doesn’t address PNA-First scenarios, and why it isn’t his ‘biggest mistake’ or any mistake at all.”

So we can actually be sure life is more common than Totani concludes. It still must be extraordinarily rare; just not that rare.”

No, we can’t actually conclude that, because of the numerous assumptions and uncertainties that you don’t address.  You selectively focus on factors that you believe increase the probability of abiogenesis, while ignoring the factors that don’t.  Like the Pev = 1.0 assumption that once we have a self-replicator, chemical evolution will proceed to the origin of life with 100% certainty.   An enormous leap that is assumed without empirical demonstration.  Why do you ignore such a huge assumption?  By contrast, Totani recognizes the probability that this would actually happen is ‘highly uncertain’, and further notes that his study does not consider ‘other essential factors involved in the origin of life’ that ‘may significantly reduce this parameter’.

Another example of this selective criticism is where you make much of Totani’s statement that the possibility of abiogenesis occurring more than once inside the observable universe should not be overlooked, which you then claim he overlooks. You write, ‘It’s like saying “if we disregard all the things that make life frequent, we get a result that life is infrequent.” Being practically a useless tautology, this isn’t a very meaningful scientific result.”  But Totani’s discussion is more nuanced than this and than you give him credit for.  You fail to point out that Totani also disregards many things that make life infrequent in his same discussion of this possibility, and that he is not claiming his calculation is an accurate reflection of all these realities, but that he is doing ‘toy model’ chemistry (i.e., ‘As a toy model to consider this…’) that does not factor in ‘RNA oligomer destruction’ by processes like ‘hydrolysis or UV radiation during the dry phase’ that may limit ‘such a polymerization process’.  Why do you not similarly take him to task for his failure to consider empirically known processes that would reduce the likelihood of abiogenesis?

The truth is Totani has done nothing grievous nor made any ‘fatal flaws’ in reasoning or methodology.  To the contrary, he has been exceedingly transparent about his methods and the assumptions and uncertainties therein, as well as the limitations of his work. There is also nothing wrong with ‘toy domain’ chemistry, which is routinely employed in probability estimates like this.  A grievous ‘sin’ would be to use ‘toy domain’ models, but fail to disclose this in one’s methods, because that would falsely imply the results are closer to reality than they actually are.  And it seems that you have done similarly here by giving readers the false impression that abiogenesis has been proven with 100% certainty, when in fact, these are ‘tinker toy’ assembly models that do not accurately reflect physico-chemical realities.  It is not just a simple matter of ‘rolling the dice’ enough times like you said in an earlier comment, because that is not how mass action chemistry actually works.  And yet you don’t take Totani to task for this.  Totani assumes a sufficient supply of activated RNA nucleotides, but you don’t take him to task for this either (Do you know how difficult it is to generate just the building blocks of the building blocks of RNA and then activate them?  Extremely.  It further requires a reducing atmosphere which didn’t exist on the early earth, so a temporary, transient impact-induced one has to be postulated, and on and on and on).  These, and countless other real-world problems for abiogenesis are not factored into Totani’s toy domain chemistry.  But you don’t object to that. 

For a general discussion of such problems in life origin research, see, e.g., Bains (2020), “Getting Beyond the Toy Domain.  Meditations on David Deamer’s ‘Assembling Life'”:

“In my view, almost all the OOL chemistry that I see is Toy Domain chemistry. It is making single types of biochemicals in a controlled laboratory setting using pure chemicals that might, just might, have been present in trace amounts in a complex mixture of thousands of other chemicals at OOL, under conditions that might have existed and might have persisted long enough, and then stopping the reaction at exactly the right time to maximize the yield of what you want. It neglects that many of the postulated starting materials are themselves unstable. It neglects that they will react with other chemicals present. It neglects that the intermediates will all react with each other, and with the products.”

I also take issue with some of the things you say in ‘fatal flaws’ #6 & #7, but I grow tired….

By the Lords of Kobol you are now talking in a circle. I just gave you a summary of all those converging facts and links covering the rest. Since you refuse to actually learn or read anything I will summarize what I am saying one last time.

Pick any “fact” that has to be the case for any of the dozen or so evidence-based theories of biogenesis on Earth, and it has been extensively documented to be actually or inevitably ubiquitously occurring in the entirety of the known universe.

Therefore, nothing else is needed to explain what happened. Abundant evidence establishes every model would work given enough time; abundant evidence establishes there was enough time; and abundant evidence establishes every required element of every model is absurdly frequent in the known universe.

Yes, that means there are any of a dozen ways it could have happened, because the evidence has been destroyed by time, so we cannot zero in on which one was the one that happened here. But the probability on present evidence it was one of them approaches 100%, given all the facts I just summarized.

If you want to explore those facts, you have an article and links. Go to it.

Richard Carrier wrote: “All the other converging conditions are established facts (we know for a fact that they existed on the early Earth)”

And in your view, these ‘converging conditions’ are? Please clarify.

Yes, and for all the reasons stated. The article (and linked material) explains:

(1) The chance of that single self-replicator is not the probability of biogenesis, because there must necessarily be countless other initial self-replicators, so the probability of any one of them arising by chance is the sum of them all, which will be many times higher (this is the third law of probability). Yet even just that one probability will be met 1,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000,000 times in the known universe. Ergo, any other factors that need converge can have no significant effect on the fact that P(random biogenesis) —> 1. This is fact.

(2) All the other converging conditions are established facts (we know for a fact that they existed on the early Earth; so their epistemic probability of their having been conjoined here is essentially 100%; this includes time: 200 million years is an outrageously long time, especially for single-chain and single-cell replicators, who double their populations in minutes, not years). And none of those conditions are anywhere near as unlikely as self-replicator chaining; we know for a fact that all of those conditions will be extremely common across the known universe. Not a single one is even unusual, statistically, in terms of its causal inevitability given such an enormous pool of randomized worlds and the established laws of physics and chemistry. It is in fact only self-replicator chain assembly that could have been too improbable; but facts now establish, it is not. And we need nothing more than these things to explain biogenesis.

(3) The hypothesis that biogenesis was a random event is verified factually by the observation of all the necessary concurrent conditions (whereas no intelligent design scenario is), e.g. random biogenesis (not intelligent design) predicts a vast universe of vast age with vast content (to make the improbable self-replicator chain a likely outcome, owing to such vast numbers of available attempts) and a universe almost entirely lethal to life (this universe, by both mass and volume, is 99.9999…% lethal to life, and thus is as near to being incapable of hosting life as a universe can be and still randomly generate life). Both observationa are predicted by random biogenesis. Neither is predicted by intelligent design. And nothing uniquely predicted by intelligent design is observed. The conclusion follows. See §2 in Bayesian Counter-Apologetics.

All of this you would already know, if you would simply read the articles you’ve been told to read, before commenting on them.

Sigh. I told you. The article you are commenting on already explains this. Please READ the article you are commenting on.

You will then learn you are asking for the wrong probability. The relevant probability is of this happening within a 200 million year window on ANY planet in the ENTIRE UNIVERSE. Which will always be some particular planet. There is no reason it “had” to be Earth. Earth is just where the dice rolled the boxcars. But those dice were being rolled billions and billions of times across all the biophilic planets and moons there are and ever have been.

As to what the correct probability is, my entire article you are commenting on goes over how we know roughly within a margin of error what it is. So READ. THE. ARTICLE.

No one is ignoring or pretending. You have not directly answered my question. I will repeat it: “What is the probability of life ‘spontaneously’ arising on earth within a 200 million year window?” And to save time and avoid continued back-and-forth tedium, I will also answer the question myself: NO ONE KNOWS. The probability is currently incalculable and involves too many unknowns. And to save more time I will further note that based on what you have written here, in your article, and elsewhere that it would seem we are BOTH in AGREEMENT on this!