Two kinds of complexity: why a sea anemone is not a Precambrian fossil rabbit

The British biologist J.B.S. Haldane is said to have remarked that the discovery of fossil rabbits in the Precambrian would falsify the theory of evolution. Over at Evolution News and Views, Dr. Cornelius Hunter has argued in a recent post that the sea anemone (whose genome turns out to be surprisingly similar to that of vertebrates) is “the genomic equivalent of Haldane’s Precambrian rabbit – a Precambrian genome had, err, all the complexity of species to come hundreds of millions of years later.” Apparently Dr. Hunter is under the impression that many of these ancestral genes would have been lying around unused for much of that time, for he goes on to triumphantly point out that “the idea of foresight is contradictory to evolutionary theory.” RIP, evolution? Not by a long shot.

An unfortunate misunderstanding

Dr. Hunter seems to have missed the whole point of the report that he linked to. A sentence toward the end of the report would have set him right, had he read it more carefully (emphases and square brackets are mine – VJT):

It’s surprising to find such a “high level of genomic complexity in a supposedly primitive animal such as the sea anemone,” [Dr. Eugene V.] Koonin [of the National Center for Biotechnology Information (NCBI) in Bethesda, Md.] told The Scientist. It implies that the ancestral animal “was already extremely highly complex, at least in terms of its genomic organization and regulatory and signal transduction circuits, if not necessarily morphologically.

That’s right. Genomic complexity and morphological complexity are two completely different things. That was the take-home message of the report. It was also the message of the other report cited by Dr. Hunter:

It is commonly believed that complex organisms arose from simple ones. Yet analyses of genomes and of their transcribed genes in various organisms reveal that, as far as protein-coding genes are concerned, the repertoire of a sea anemone — a rather simple, evolutionarily basal animal — is almost as complex as that of a human. (Emphases mine – VJT.)

As if that were not clear enough, Figure 1, on the opening page of the report, spells it out:

Figure 1: Animal miRNAs and morphological complexity. Grimson et al.3 (data along red lines) reveal the evolutionary origin of animal miRNAs by examining organisms at the base of the animal tree. Combining their data with previous work, three different measures of complexity become apparent: the number of protein-coding genes, total number of neurons and number of miRNAs. There is relatively little correlation between morphological complexity and the number and diversity of protein-coding genes. However, miRNA number correlates well with the organism’s total number of neurons. Indeed, a large proportion of vertebrate miRNAs are expressed in the nervous system. These data also show the dynamic nature of the miRNA complement in each lineage, particularly visible in rapidly evolving species (Oikopleura and fruitfly).

Morphologically, the ancestral animal was a very simple creature – so simple that the only real debate going on at present is whether it was more like a comb jelly (a creature with muscles, a nerve net and sensory organs, but no brain or central nervous system, pictured above, image courtesy of Kevin Raskoff) or a sponge (which is sessile and which lacks a nervous system altogether). Certainly it was nothing like as complex as a fly or a worm.

Genetically, however, the ancestral animal seems to have been in some respects better endowed than a fly or a worm. As the report cited by Dr. Hunter puts it (emphases mine – VJT):

The genome of the sea anemone, one of the oldest living animal species on Earth, shares a surprising degree of similarity with the genome of vertebrates, researchers report in this week’s Science. The study also found that these similarities were absent from fruit fly and nematode genomes, contradicting the widely held belief that organisms become more complex through evolution. The findings suggest that the ancestral animal genome was quite complex, and fly and worm genomes lost some of that intricacy as they evolved… The researchers also discovered that exon-intron structure is very similar between modern vertebrates and sea anemones. Both have intron-rich genomes and about 80% of intron locations are conserved between humans and anemones. Fly and nematode genomes, on the other hand, have lost between 50 and 90% of the introns likely present in the animal ancestor.

Building the Precambrian genome – was foresight required?

And what were these genes doing in the original ancestor, anyway? Is there any evidence to suggest that they were placed there in an act of foresight, to be used only by the ancestor’s distant descendants? I’m afraid there isn’t. Dr. Hunter has made an inferential leap here. He isn’t the only one: Dr. Stephen Meyer makes a similar criticism in a 2001 paper which he co-authored with P. A. Nelson and Paul Chien, The Cambrian Explosion: Biology’s Big Bang. Referring to Dr. Susumu Ohno’s now-famous paper, The notion of the Cambrian pananimalia genome (Proceedings of the National Academy of Sciences, Vol. 93, pp. 8475-8478, August 1996), in which Ohno proposed that “all those diverse animals of the early Cambrian period, some 550 million years ago, were endowed with nearly identical genomes, with differential usage of the same set of genes accounting for the extreme diversities of body forms,” Dr. Meyer objects that Dr. Ohno “envisions the pananimalian genome arising well before its expression in individual animals. Specific genes would have arisen well before they were used, needed or functionally advantageous” (pp. 31-32). However, in his paper, Dr. Ohno makes it clear that the ancestral genome he is envisaging was “rather modest in size,” and he points out that all of the five genes which he argues were “certain to have been included in the Cambrian pananimalia genome” were in fact useful to organisms back in the Cambrian period: indeed, it was possession of these genes that “made the Cambrian explosion possible.” Finally, I would like to pass on a rather blunt but factually accurate observation made by Dr. Nick Matzke, in a comment on an Uncommon Descent post I authored back in 2015:

…[B]ecause he’s not a paleontologist, one thing Ohno misses, IIRC, is that there is clear evidence of bilaterians in the Precambrian — trackways and burrows indicating bilateral symmetry, a coelom, etc., and these continually increase in complexity through the small shelly fossils, only reaching the “classic” Cambrian Explosion tens of millions of years later. This is all true regardless of one’s interpretation of the Edicarans etc. Thus, it’s idiotic to say, as Meyer does, that Ohno’s hypothesis means “the pananimalian genome ar[ose] well before its expression in individual animals.” Fossil traces of bilaterians are there before the Explosion, they had worm-level complexity, all of those common genes between all the phyla basically are what is required to specify a bilaterian body plan, which is what worms have.

In a follow-up comment, Dr. Matzke added:

There was, in fact, not a huge amount of origination of genes and proteins required to produce the Cambrian phyla, and we know this because they all have the same basic complement of genes and proteins. The differences that they have are basically due to differential duplication of genes and subsequent modification of genes, and sometimes rearrangement/recombination of pre-existing gene chunks.

A mea culpa

At the time, I was prepared to concede that Dr. Meyer was “probably wrong” on the the question of when these genes and proteins originated, and that they may have arisen long before the Cambrian period. I was even prepared to allow that the genes in the ancestral pan-animalian genome, back in the Precambrian, may have originally had functions of their own, that were later co-opted or ex-apted by their Cambrian descendants, giving rise to new functions. But it seemed to me that Dr. Meyer’s larger point – that the likelihood of even one functional protein fold originating on the primordial Earth was vanishingly low – was still valid. In the end, I thought that Dr. Douglas Axe’s 2010 paper, The Case Against a Darwinian Origin of Protein Folds, clinched the matter, since at least some new protein folds would have had to have come into existence during the Cambrian explosion, even if (as Dr. Matzke pointed out) there were only a few folds that were actually unique to bilaterian animals (the group of animals in which the Cambrian Explosion occurred), with just 17 new domains at the root of bilateria, (sponges and cnidarians having originated earlier).

How wrong I was. Last year, Rumraket wrote an excellent post debunking Dr. Axe’s claim that only about one in 1077 sequences of 150 amino acids was capable of folding and thereby performing some function — any function. There are, at the present time, no good grounds for accepting such a claim, and there are several grounds for treating it with skepticism. In my review (written last year) of Dr. Axe’s book, Undeniable, I describe how my own confidence in the much-vaunted one in 1077 figure was shattered, when I emailed some scientists in the field who kindly set me straight. I would therefore like to offer my belated apologies to Rumraket and to Dr. Matzke. They were right and I was wrong.

If you’re going to argue for design in the genome, this is not the way to do it. Here’s a better way, which doesn’t even use the word “design.” The facts speak for themselves.

Two questions for Dr. Hunter

Finally, I’d like to pose two simple questions to Dr. Hunter, regarding the papers he cited:

(1) Do you agree with the claim that humans are scarcely more complex (genetically speaking) than sea anemones?

(2) Can you cite a single proponent of either Intelligent Design or creationism who predicted this discovery, prior to 2005?

Complexity – good and bad metrics

Regarding (2), I can attest that leading ID proponents fought against the claim, tooth and nail, appealing to the “fact” that human beings have 210 cell types, while Cambrian animals had about 50 and sponges, only 5 (see this paper, for instance), and arguing that new genes and proteins would have been required to generate these additional cell types. However, the oft-repeated assertion that humans have 210 cell types turns out to be a myth, which has been roundly debunked by Professor P.Z. Myers. What’s wrong with this assertion?

The short answer: this number and imaginary trend in cell type complexity are derived entirely from an otherwise obscure and rarely cited 60 year old review paper that contained no original data on the problem; the values are all guesswork, estimates from the number of cell types listed in histology textbooks. That’s it.

And here are the original references cited to back up those figures about the number of “cell types” (a term which has never been explicitly defined) in various kinds of animals (emphases mine – VJT):

5. Andrew, W. 1959. Textbook of Comparative histology. Oxford Univ. Press, London

13. Borradaile, L.A., L.E.S. Eastham, F.A. Potts, & J. T. Saunders. 1941. The Invertebrata: A manual for the use of students. 2nd ed. Cambridge Univ. Press, Cambridge.

85. Maximow, A.A. & W. Bloom. 1940. A textbook of histology. W. B. Saunders Co., Philadelphia.

126. Strasburger, E., L. Jost, H. Schenck, & G. Karsten. 1912. A textbook of botany. 4th English ed. Maximillian & Co. Ltd. London.

Further comment is superfluous.

I’d also like to draw readers’ attention to a 2007 post by Professor Larry Moran, titled, The Deflated Ego Problem, in which he gently pokes fun at scientists who clung to the belief that the complexity of the human genome was far greater than that of “primitive” animals like flies and worms, and listed seven proposals (all invalid, in his view) for redeeming the complexity of the human genome.

Dr. Hunter’s statement that “we repeatedly find early complexity” when investigating the history of animals suggests that he would answer question (1) in the affirmative: our genes are about as complex as a sea anemone’s. As for morphological complexity, I can only state that as far as I can tell, there isn’t any straightforward way of measuring it, although I have no doubt that I’m structurally far more complex than a worm or a sea anemone. (Insects I’m not so sure about – see below.)

I understand that a recent paper in Nature (which unfortunately I cannot access) has finally addressed the origin and evolution of cell types in a rigorous fashion, and that Steven McCarroll’s Lab at Harvard Medical School and the Broad Institute is attempting to map the different kind of cells in the body, using micro-RNA.

I’d like to conclude with a quote from P.Z. Myers’ 2007 post, Step away from that ladder, on the subject of complexity, which is well worth reading (emphases mine – VJT):

I’m fairly familiar with the insect neurodevelopment literature, so when I saw papers saying arthropods only have 50-60 cell types, alarm bells started ringing...

I’m also familiar with some embryonic vertebrate nervous systems, and I can say that they tend to have many more cells in them — but they don’t seem to be as precisely identified at the single cell level as the invertebrate CNS. We have large populations of cells with similar patterns of molecular specification, rather than this kind of precise, cell-by-cell programmatic identity.

Now, from a genetic perspective, which pattern is more complex? I don’t know. They’re both complex but in very different ways — it’s basically impossible at this point to even identify a quantifiable metric that would tell us how complex either of these kinds of systems are. How many cell types are present in this whole animal? I don’t know that either… I bet it’s many more than 60, though.

I’ll go out on a limb and make a prediction: any difference in the degree of complexity, assuming an objective method of measurement, in the triploblastic metazoa [basically, all animals except sponges, placozoans, cnidaria and possibly comb jellies – VJT] will much be less than an order of magnitude, and that the vertebrates will all be roughly equivalent… and that if any group within the vertebrates shows a significant increase in genetic complexity above the others, it will be the teleosts. I’ll also predict that any ‘extra’ complexity in members of these groups will not be a significant factor in their fitness, although it might contribute to evolvability.

What do readers think? Over to you.

319 thoughts on “Two kinds of complexity: why a sea anemone is not a Precambrian fossil rabbit”

  1. PaV

    Acartia: I would also argue against HIV deniers, astrology and bible literalists. That doesn’t make any of those issues relevant.

    So, IOW, you don’t want to be bothered with logic and facts? Disdain, somehow, is proof of something?

  2. PaV

    GlenDavidson,
    Oh yeah, you can just see “design” in life without actually showing intelligent choice, but we can’t reliably observe developmental pathways that served a different function yet are modified at some point to serve another one.

    The bones of bird wings are a fine example of the latter.

    Only if you equate change and the theory of evolution, and, by extension, neo-Darwinian processes, only then does any of your argument have standing. But, you simply “assume” this to be the case, and then turn around and use it as a “proof” of the case. What’s at stake here is an explanation of “how” the changes came about, not, that they did, or did not, occur. We KNOW they occurred. So, now, HOW did they occur?

    ” . . . it is simply the case that evolution may produce highly complex organisms, often more complex than necessary due to old development steps not being easily lost.”

    Now, to press the simple argument I made up above, what you are saying here is this: “At some point in the past, the organism we’re discussing had to overcome certain obstacles that required the ‘evolution’ of a number of traits, traits which no longer are needed. However, these traits are hard to get rid of. It takes time. And so what it looks like now is that something developed that has not fitness value, when, in fact, somewhere in the past this organism DID need these traits to maintain its fitness.”

    And, so, it is obvious that you’re positing that things happened in the ‘past’ which we can in no way prove, or disprove, since we can’t ‘rewind’ the tape.” Ergo: pseudoscience!

  3. PaV

    petrushka: Behe’s calcs are the poster child for bumblebees can’t fly engineering analysis.

    petrushka:

    Wake up. The numbers that vjt is using are theoretical. The numbers Behe used come directly from nature.

    But, alas, the theme of evolutionists is: don’t believe your lying eyes.

  4. OMagain

    PaV: And, so, it is obvious that you’re positing that things happened in the ‘past’ which we can in no way prove, or disprove, since we can’t ‘rewind’ the tape.” Ergo: pseudoscience!

    Like what? Name such a thing.

  5. GlenDavidson

    PaV:
    GlenDavidson,
    Oh yeah, you can just see “design” in life without actually showing intelligent choice, but we can’t reliably observe developmental pathways that served a different function yet are modified at some point to serve another one.


    The bones of bird wings are a fine example of the latter.

    Only if you equate change and the theory of evolution, and, by extension, neo-Darwinian processes, only then does any of your argument have standing.

    If we don’t make up shit, that is. Of course we explain using processes known to exist, not your fantasy Designer.

    But, you simply “assume” this to be the case,

    Complete BS. Evolution by known processes has entailments, such as the derivative nature of organisms undergoing it. That’s what we look for to see if it indicates that known evolutionary processes occurred, and that is what we find. You prefer making up shit.

    and then turn around and use it as a “proof” of the case.What’s at stake here is an explanation of “how” the changes came about, not, that they did, or did not, occur.We KNOW they occurred.So, now, HOW did they occur?

    Look at what is left by the processes and match them up to observable causes. You know, science, what your side constantly fails to accomplish.

    ” . . . it is simply the case that evolution may produce highly complex organisms, often more complex than necessary due to old development steps not being easily lost.”

    Now, to press the simple argument I made up above, what you are saying here is this:“At some point in the past, the organism we’re discussing had to overcome certain obstacles that required the ‘evolution’ of a number of traits, traits which no longer are needed.However, these traits are hard to get rid of.It takes time.And so what it looks like now is that something developed that has not fitness value, when, in fact, somewhere in the past this organism DID need these traits to maintain its fitness.”

    Yes, it’s common throughout life. You lack any sort of reasonable explanation for that, and, well, anything at all.

    And, so, it is obvious that you’re positing that things happened in the ‘past’ which we can in no way prove, or disprove, since we can’t ‘rewind’ the tape.”Ergo: pseudoscience!

    They’re called clues and evidence, and no one is claiming “proof” like a strawman-attacking IDiot pseudoscientist does.

    The fact of the matter is that with common descent without magic or intelligence simply has to produce the pattern of commonality and lack thereof that we happen to see in organisms. That’s how we establish the facts, not unlike how geology and astronomy discover what happened in the past. If we get certain results, certain processes occurred, in the absence of magical mystery agents made up by IDiots.

    Why does the rooster not have a penis? It isn’t because it doesn’t start to grow, it’s that apoptosis prevents its growth into a useful organ. Completely stupid from a design standpoint, as the rooster expends the energy and material making cells for the penis, while also expending the energy to break the cells down again. By contrast, it fits with evolutionary contingency and lack of choice of various alternatives, so happened to work is what is used, apoptosis.

    But you want your made-up fantasies to prevail, so you don’t care about the evidence, even denying its ability to point to the processes that made the evidence. Pure pseudoscience, but that’s what’s to be expected from adherents of the pseudoscience of ID.

    Keep your projector beaming bright, though. It’s all you have, being bereft of any evidence for your claims across the board.

    Glen Davidson

  6. PaV

    AhmedKiaan,

    Ahmed: remember when I asked you to write an OP explaining just how HIV brings about AIDS you demured?

    Let’s assume that HIV is the cause of AIDS.

    Those who propose all of this say that there are about 24 or 25 separate diseases that are caused by HIV. (BTW, have you ever heard of any other virus doing anything like this at all?)

    Let’s task the case of South Africa. The president there would not allow anti-retrovirals to be used. What should we expect IF the HIV virus does in fact bring about AIDS?

    Well, as HIV spreads–and we are told that HIV is an ‘epidemic’ in all of Africa, with South Africa being no exception–then HIV will infect more and more people, who will then die of these 25 or so deadly diseases. Right?

    Further, with time you would expect the population to decrease given this ‘epidemic’ and its deadly outcomes. Right?

    But what happened in South Africa?

    The population GREW. That’s funny, isn’t it? And what about the number of cases let’s say of pneuomonia, tubercolosis, and so forth?

    While the number of persons having HIV steadily increased, the number of those having the diseases associated with HIV stayed about the same from year to year. How is that possible?

    Well, here’s how it’s possible. If HIV is no more than a carrier virus, causing no harm to the person having it, then the MORE you TEST for HIV, the more you will find it. Why? Because it is a harmless virus that gets passed on from one person to the next WITHOUT anyone knowing it.

    Now, here’s the “definition” of AIDS: you have one of these 25 diseases,
    AND, you are detected as having HIV.

    Thus, the more you test, the more HIV virus you will find. Given that the level of people contacting or developing these 25 other diseases STAYS the SAME, then you will have roughly the same number of people dying each year of these same 25 diseases, BUT, the number of people diagnosed as having AIDS will continue to increase each year.

    This is what you will find there. And, if you look for World Health Organization statistics, you’ll find that they’re simply MADE UP. Yes, that’s right: MADE UP.

    This is all about political correctness and Big Pharma, along, of course, with crony capitalism.

    These are facts. They need to be refuted before I can accept the HIV-AIDS connection.

    (You realize, of course, that the way in which AIDS is “defined” makes it impossible to disprove the connection. Why? Because they are connected from the start simply through assumption. It’s a lot like how evolutionists first assume evolution took place, and then use the evolution on display to “prove” evolutionary theory. If you don’t know already, you can’t pull yourself up by your bootstraps.)

  7. FrankieFrankie

    GlenDavidson: Evolution by known processes has entailments

    Nice equivocation. The question is are those known processes design processes or blind and mindless processes?

  8. FrankieFrankie

    PaV:
    Frankie,

    Frankie:

    I hadn’t seen that open letter of Behe’s before.I guess we’ll just have to wait for their calculations, eh?

    Huh? Contingent serendipity doesn’t need any steekin’ calculations!

    But anyway I just thought it was funny because they were attacking Behe for “his numbers” and how irrelevant they are, when in fact the numbers come from peer-reviewed work on antimalarial drug resistance (Behe had no part in it)

  9. PaV

    Rumraket: That would be about 225 amino acid substitutions that have accumulated over 50.000 generations.

    That’s nice that you’re using “generations.” Tell me, though, how many “cells” are we talking about? I can’t remember exactly what Lenski’s group does, but I sort of remember that they start a colony each day, renewing the medium, and then letting it grow. Now, I don’t know how many “generations” there are in a day ( 24 hrs.), but is it around 2^12? I would say that’s a fair guess, meaning around 4,000 cells, with EACH cell susceptible to mutations. Now, that means the true number of mutational opportunities would be more like (2^12)^50,000/12 = (roughly) ~(2^12)^4,200, or 4,000^4200 cells produced, and a like number of mutational opportunities. The probability of an amino acid change is then, what , 225/(4000)^4200, or, roughly 225/ 10^42,000. Now, take 1 in 10^20 as the number for producing TWO mutations. Then, (10^-20)^225/2 = (10^20)^114 = roughly, 10^2250, which is hugely greater than what your numbers calculate out to.

    And, BTW, all these 225 non-synonymous mutations later, and we still have a bacteria doing just about what it started out doing. What do you make of that?

  10. dazzdazz

    Mung:
    Some people are too dumb for words.

    Considering how utterly stupid your last response to me was, you should probably consider whether that applies to you

  11. PaV

    Rumraket:PaV:
    He settled on the malarial parasite. And, guess what: the probability of even a two-amino acid substitution turned out to be extremely low.

    Yet roughly 225 accumulated in about 20 years in the LTEE.

    Two hundred and twenty five.

    10^20 replications is far less than (2^12)^50,000/12, right?

  12. PaV

    Allan Miller: How’s that work? He calculated a probability, which demolishes all subsequent arguments against his probability calculation?

    His method is awful. Simple, but awful.

    He didn’t calculate a probability. And I didn’t state that he did. The calculation was made by someone else.

    And Behe issued a challenge. Frankie has already posted it.
    Here it is again.

    Is his method “awful” simply because you can’t refute it? Is that it?

  13. J-Mac

    Torley,
    Are you an experimental scientist as are J.Coyne, Larry Moran, D.Grawler, Richard Dawkins, D Axe and A Gauger and so on?
    If you happen to be one of them, just post the data of your experiments that prove your faith speculations at least worth 10%. . .. I’m sure you can pull this off..

  14. DNA_Jock

    PaV,
    You are correct that your numbers don’t line up with Rumraket’s.
    I think you have made a mistake in your math.
    By way of illustration, you state that the LTEE generated “4,000^4,200 cells, and a like number of mutational opportunities.”
    I sincerely doubt it. 4,000^4,200 equals 10^15,128.
    The number of particles in the observable universe is a mere 10^80, so you are claiming that Lenski produced over 10^15,000 bacteria for each particle in the observable universe.
    Exponentiation, you are doing it wrong.

  15. J-Mac

    Torley, When you find time, please post just as long post about the origins of life and endosymbiosis fact and how you were convinced to believe them. Please don’t forget to mention how you have been awestruck by the endosymbiosis theory. You must’a cried….

  16. RumraketRumraket

    PaV: That’s nice that you’re using “generations.”Tell me, though, how many “cells” are we talking about?I can’t remember exactly what Lenski’s group does, but I sort of remember that they start a colony each day, renewing the medium, and then letting it grow. Now, I don’t know how many “generations” there are in a day ( 24 hrs.)

    The generation time now today, is about 20 minutes. When the experiment started it was about an hour.

    but is it around 2^12?I would say that’s a fair guess, meaning around 4,000 cells, with EACH cell susceptible to mutations. Now, that means the true number of mutational opportunities would be more like (2^12)^50,000/12 = (roughly) ~(2^12)^4,200, or 4,000^4200 cells produced, and a like number of mutational opportunities.

    Where did you learn math?

    4000^4200 is more cells than have ever existed in the entire history of life on this planet. It’s more than the total number of elementary particles in the cosmos. They couldn’t fit in the visible universe.

    Dude, what the actual fuck?

    Let’s get some basics straight. Just setting the generation time to 30 minutes, gives us 48 generations in a 24 hour day. But who cares? We already know the total generation time for those 225 amino acid substitions: 50.000

    The experimental protocol: Overview of the E. coli long-term evolution experiment

    So there’s 10 ml of growth medium, from which 0.1 ml is transferred to a new flask every day. Typical growth densities for bacteria reach about a billion (10^9) for a ml. So about 10 billion bacteria is the population size in a flask. Each lineage has their own flask. The above given mutation numbers from the paper are for a single typical lineage.

    It’ll drop every day to a hundreth of that (100 million) during transfer (0.1ml of 10 ml is a hundreth), but get back up relatively quickly. Let’s just put it at a nice constant 10 billion to make the calculation simple (this simplification is in your favor).

    10 billion times 50.000 = 500 trillion. Or 5.0×10^14
    That’s the total number of bacteria in a lineage for the duration of 50.000 generations of the experiment.

    In 5×10^14 bacteria, 225 amino acid changes accumulated.

    That’s about a hundred times more mutations than two, in a population roughly six orders of magnitude smaller than Behe’s estimated 10^20.

    Conclusion: You’re fucked.

    And, BTW, all these 225 non-synonymous mutations later, and we still have a bacteria doing just about what it started out doing.What do you make of that?

    Bacteria are still bacteria after almost 4 billion years of evolution. Just like Homo Sapiens is still a mammal, a vertebrate and a eukaryote. Bacteria is a domain of life. Saying “after 20 years, they still belong to the bacterial domain” is as meaningless as saying “after 6 million years, the ancestor from which Chimpanzees and Humans evolved is still made of eukaryotic cells”.

    What the fucking hell else would you think was gonna happen? The fact that the still belong to the bacterial domain doesn’t mean no evolution took place.

  17. AcartiaAcartia

    PaV: So, IOW, you don’t want to be bothered with logic and facts?Disdain, somehow, is proof of something?

    Where did I say that? If you can present any valid evidence for any of these, I will listen. But, so far, everyone with AIDS has HIV. Astrology has never been demonstrated to be causative of anything. And bible literalicy? Good luck with that one. Arguing against these is not acknowledging their relevancy. It is an argument against ignorance.

  18. RumraketRumraket

    J-Mac: Torley,
    Are you an experimental scientist as are J.Coyne, Larry Moran, D.Grawler, Richard Dawkins, D Axe and A Gauger and so on?
    If you happen to be one of them, just post the data of your experiments that prove your faith speculations at least worth 10%. . .. I’m sure you can pull this off..

    So what experiments do you perform where divine creation of complete living organisms, is something that happened?

    If observing something directly by way of experiment, is the critieria that justifies belief, then it’s a criterion you yourself and your beliefs can’t meet. You weren’t around to observe divine creation by spoken word, from nothing, of anything at all. It is wholly removed from experience. Nobody has ever seen anything like it take place. Yet that’s what you believe happened. IOW, you are failing to live up to the standard you demand of others to justify beliefs.

    To put it blunt: You are a hypocrite.

  19. RumraketRumraket

    PaV: 10^20 replications is far less than (2^12)^50,000/12, right?

    Yes PaV. That is correct. The number 10^20 is far less than 2^12^50.000. I wonder how in the hell you can type it and not immediately think to yourself “maybe I did something wrong here?”.

  20. AcartiaAcartia

    PaV,

    Those who propose all of this say that there are about 24 or 25 separate diseases that are caused by HIV. (BTW, have you ever heard of any other virus doing anything like this at all?)”

    You do realize that HIV affects the immune system? If you have a compromised immune system, you are prone to numerous diseases. I would be surprised if it is only 24 or 25.

  21. J-Mac

    Torley,

    If you keep objecting Larry Moran’s theory of the explaining everything in the evolution theory as per Larry’s authority… you just missed the best part of your life…

  22. AhmedKiaan

    “Ahmed: remember when I asked you to write an OP explaining just how HIV brings about AIDS you demured?”

    No, I don’t. Where’s that?

    (That would be stupid to ask anyway–would you ask a chemist to write up a description of Wolf-Rayet stars? No, you’d go find an astrophysicist. If you want to know how HIV/AIDS works, you’d go find a researcher who works in the field.)

  23. RumraketRumraket

    J-Mac: If you keep objecting Larry Moran’s theory of the explaining everything in the evolution theory as per Larry’s authority… you just missed the best part of your life…

    Hey J-mac, are you some how in your own psychotic way trying to say you are the one holding the keys to salvation and eternal life?

    If God really exists, isn’t that up to Him, not you?

  24. DNA_Jock

    Acartia: But, so far, everyone with AIDS has HIV.

    And, curiously, everyone who experiences a sustained viral response to anti-HIV drugs does not progress to AIDS. Weird, innit?
    I would love to see an explanation for the curious behavior of hemophiliacs. When the supply of FVIII/FIX was contaminated, they were infected with HIV and developed AIDS. Before and after this tragedy, no HIV and no AIDS. What about their “lifestyle” changed so dramatically in one direction, and then back again?

  25. MungMung

    Acartia: But, so far, everyone with AIDS has HIV.

    LoL. I swear I read PaV saying the exact same thing earlier. Post a parrot pic!

    If you don’t have HIV, then you don’t have AIDS. Isn’t that what PaV said?

    ETA:

    Now, here’s the “definition” of AIDS: you have one of these 25 diseases,
    AND, you are detected as having HIV.

  26. keithskeiths

    vjtorley:

    In my review (written last year) of Dr. Axe’s book, Undeniable, I describe how my own confidence in the much-vaunted one in 10^77 figure was shattered, when I emailed some scientists in the field who kindly set me straight. I would therefore like to offer my belated apologies to Rumraket and to Dr. Matzke. They were right and I was wrong.

    I appreciate your willingness to state this so forthrightly and publicly, Vincent.

  27. keithskeiths

    J-Mac:

    Torley,

    If you keep objecting Larry Moran’s theory of the explaining everything in the evolution theory as per Larry’s authority… you just missed the best part of your life…

    J-Mac,

    Your syntax is a bit tortured and hard to parse, so I can’t say for sure, but it sounds like you are accusing Vincent of making an argument from (Larry’s) authority.

    On what basis? I see nothing in the OP or in the comments to back up your accusation.

  28. PaV

    Rumraket,

    Thank you for your numbers—but not your sarcastic, snarky, venal tone.

    Now. 500 trillion reproductions. 225 mutations. Population size of chimps/apes: what, 200,000 at most. 6 million years. How many years per generation? 2, or 3. Use 2. Then 2 x 10^5 x 3 x 10^6 = 6 x 10^11 total chimps that had a shot at bringing about human ancestral line.

    Yet, per your calculation, that means that in all those reproductive events, only (6 x 10^11/500 x 10^14) x 225 = (approximately) ZERO mutations (0.003).

    Oops. Now what?

  29. PaV

    Acartia: You do realize that HIV affects the immune system? If you have a compromised immune system, you are prone to numerous diseases. I would be surprised if it is only 24 or 25.

    And amyl nitrates and drug usage weakens the immune system.

  30. PaV

    Rumraket: Bacteria is a domain of life. Saying “after 20 years, they still belong to the bacterial domain” is as meaningless as saying “after 6 million years, the ancestor from which Chimpanzees and Humans evolved is still made of eukaryotic cells”.

    So, you’re saying that all the mutations in the world aren’t going to get you from bacteria to eukaryotic life. Right?

  31. MungMung

    PaV: Thank you for your numbers—but not your sarcastic, snarky, venal tone.

    It’s what passes as “discourse” here.

  32. PaV

    AhmedKiaan,

    It was over at UD. I’m sure you remember. And it’s interesting that you don’t feel qualified to write the OP, but qualified enough to critique any OP that I write. Interesting.

  33. dazzdazz

    PaV: So, you’re saying that all the mutations in the world aren’t going to get you from bacteria to eukaryotic life.Right?

    Are you one of those dumbasses who think that because one species evolved from another, the latter can’t exist anymore?

  34. MungMung

    PaV: And it’s interesting that you don’t feel qualified to write the OP, but qualified enough to critique any OP that I write. Interesting.

    Reminds me of petrushka, who is always plugging Andreas Wagner’s Arrival of the Fittest, but will never post an OP on it for discussion.

    But don’t ever post your own OP to discuss a book that might be friendly to ID. God no. People froth at the mouth. Admit they have no intention of reading it. Accuse you of failing to give proper attribution, all kinds of BS. Anything but discuss the issues.

  35. MungMung

    dazz: Are you one of those dumbasses who think that because one species evolved from another, the latter can’t exist anymore?

    Are you one of those dumbasses who thinks humans evolved from apes?

  36. MungMung

    dazz: Irony. Meter. Blown. OUT

    You and I were discussing saltations, until you quit. Then we were discussing common descent, until you quit.

    Is symbiogenesis saltational or not?

  37. FrankieFrankie

    PaV: So, you’re saying that all the mutations in the world aren’t going to get you from bacteria to eukaryotic life.Right?

    Rumrat will tell you the “right” mutations are the key. Seriously.

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