These Weeks in Intelligent Design – 18/05/11

Intelligent design news from the 28th of April to the 18th of May, 2011.

Finally! It’s back again, your fix of ID news and discussion. To make up for my three-week-long absence, this post will cover five of the top ID blog posts from the past three weeks. Lucky for me then that it hasn’t been an especially busy time for the ID community during my break – otherwise I’d have a much bigger job on my hands.

Anyway, enough grovelling, let’s get into it.

Today’s posts are about Osama bin Laden and junk DNA, Oxford University and evolutionary mathematics, dissent in the evolutionary ranks, enzyme evolution, and, of course, junk DNA.

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First up this week, David Klinghoffer plunged headfirst into newsploitation mode, trying to somehow link Osama bin Laden’s recent death with intelligent design. It’s masterful, it really is. Trust me:

President Obama is said to have known the whereabouts of Osama bin Laden since September but chose to wait until May to authorize action against him. Why the delay? Could it perhaps have been to provide a super-timely news hook for the rollout of Jonathan Wells’ new book, The Myth of Junk DNA? If so, an additional note of congratulation is owed to Mr. Obama.

How do you think OBL’s body was identified? By a comparison with his sister’s DNA, evidently those non-coding regions singled out by Darwin defenders, among the pantheon of other mythological evolutionary icons, as functionless “junk.” Indeed, the myth has featured in news coverage of Osama’s death. Reports the website of business magazine Fast Company:

Because your parents give you some of their DNA, they also give your siblings some of the same genetic code — which is why sibling DNA tests work. They sometimes concentrate on areas of the genome called “junk DNA” which serves no biological function but still gets passed along to offspring. By testing for repeat strands of DNA code in these areas, it’s possible to work out if two individuals are related as siblings.

The Toronto Star strikes a similar note:

When testing against a relative’s DNA, scientists often look to parts of the genome described as junk DNA which are passed on to all offspring.

Readers of this space and of Dr. Wells’ book, published this month, will know how thoroughly the myth has already been debunked in peer-reviewed scientific literature. Unfortunately, the news hasn’t yet reached the general interest media, and it continues as what Richard Dawkins might call a powerful “meme” in the public’s thinking about evolution. In fact, in Daniel Dennett’s book Darwin’s Dangerous Idea, junk DNA is given as one of the scientific predictions made for Darwinian evolution by Dawkins himself.

If Darwin is right, there ought to be huge swaths of ancestral garbage cluttering the genome, serving no purpose other than to identify otherwise unidentified forensic remains. So if those huge swaths turn out after all to be vitally important to the functioning organism, what does that say about Darwin’s theory? Ah, that’s exactly the question addressed in Jonathan Wells’ book.

Let’s see how many Darwin lobbyists have the guts and honesty to acknowledge that another icon has fallen. They have not, on the whole, left themselves a lot of room for deniability on this.

So really, the post is just an excuse to mention Jonathan Wells’s new book again? Great. You had us going there for a while, David.

Some anti-ID bloggers have attacked the first paragraph of the post with vigor as being ridiculous: I mean, Obama really tried to do that? Really? Of course, well, it is a joke. It’s a bad joke, to be sure, but a joke nonetheless. David’s not being serious.

A lot of people in the anti-ID community see ID proponents as being unintelligent pot-stirrers, but this is rarely the case, at least for the upper levels of the Discovery Institute. No, they know what they’re doing, they’re not stupid. They might be misguided, biased and uninformed, but they don’t lack a savvy sense of self-awareness. If anything, public relations is the Discovery Institute’s strongest suit, even given their religious/scientific image problems.

No, David’s post was just a publicity stunt to draw attention to both themselves and Wells’s new book, which they have been heavily promoting recently. Such behaviour should come as no surprise to any ID critic who knows what he/she is up against.

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The next post was written, again, by David Klinghoffer about Oxford University’s decision to advertise for a new research position in the field of evolutionary mathematics. According to David, this obviously means that the theory of evolution is shaky, because why would you want to employ researchers if your ideas were perfect?

File this one under: Mission Impossible. An Oxford college, St. John’s, is advertising to hire a pair of researchers to undertake a tough assignment: shore up the admittedly unsteady mathematical foundation of Darwinian theory, specifically in the ever distressing area of population genetics.

In a downloadable document of particulars for the two-year assignment, the college frankly concedes that ranged against them the new hires will face, well, basically the entire rest of the scholarly field that studies the subject. Biologists may accept that “natural selection leads to organisms that maximize their fitness,” the document observes.

However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is.

For half a century, mathematicians have been telling Darwinists to get stuffed. If only that would change! Maybe if we enter the figures again and push the “equals” button on our hand calculator just one more time, it will give a different answer. I’ve sometimes wished the same in seeing what the balance in our family checking account will be once those outstanding checks are cashed.

Wow. Er, there’s no easy way to back up from that…

I feel like the St. John’s document is rather overstating a non-problem, which is probably why David jumped on it in the first place. Perhaps they were referring to the inefficiency of natural selection in small populations, where neutral drift reigns supreme over fluctuating allele frequencies? Or perhaps, just perhaps, David was isolating a quote in order to make the contention of the document seem more dramatic. Here’s the quote in a larger amount of context:

The concept of fitness optimization is routinely used by field biologists, and first-year biology undergraduates are frequently taught that natural selection leads to organisms that maximize their fitness. Dawkins’ The Selfish Gene (1976) promoted a conceptual integration of modern evolutionary theory in which genes are viewed as optimising agents, which is extremely influential and widespread today and encompasses inclusive fitness theory and evolutionarily stable strategies as well as general optimality ideas. However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is. One underlying cause is that the link between natural selection and fitness optimization is much more sophisticated than the usual optimization principles associated with dynamical systems, namely Lyapunov functions and gradient functions.

Note that there is a difference between the maximisation of fitness and general increases in fitness. No mathematician would deny that natural selection cannot increase fitness, that would be absurd. (Which leads to a strange implication: does David Klinghoffer think that natural selection cannot increase fitness?) What is clearly in question is how effective is selection at increasing fitness: what are the theoretical and practical restrictions on fitness increase in various situations?

Think about this another way – if this problem was as major as David is making it out to be, why would the project be for only two researchers? Why is it not attracting major attention in the scientific community? It makes little sense to blow this up into a huge issue. Evolution is safe from mathematical falsification, and it’s only small details that need to be worked out – hence this project.

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Next up – Anika Smith wrote about an exchange between Karl Giberson and William Dembski. I mention it for a revisitation to the old idea of there being significant challenges to evolutionary theory from within the scientific community, something that ID proponents have both fantasised about and perpetrated as much as they can in popular culture:

When he finally does get around to addressing Dembski himself, Giberson objects to Dembski’s use of marketing metaphors as an ad hominem attack, which is strange considering that Dembski wrote that this is something that scientists and people with ideas generally ought do to communicate and advance them, with nothing cynical or slimy about it. Either Giberson is hypersensitive and looking for an excuse to display his lofty umbrage, or he is working to avoid the actual questions raised by Dembski’s review. Most likely it’s both.

He does, however, give us a nice quote for giggles:

The scientific literature is not filled with growing concerns about the viability of the theory; scientific meetings do not have sessions devoted to alternative explanations for origins; and leading scientists are not on record objecting to the continuous and blinkered embrace of evolution by their colleagues.

Has he never heard of Jerry FodorLynn MargulisThe Altenberg 16?

Apparently, these scientists (who are emphatically not ID proponents) and these meetings and these papers are somehow overlooked by Giberson. This may be because he’s not engaged with the science himself, trusting in others to tell him whether or not it works out, which is what he recommends we all do:

My response, which I provided at greater length a while ago on the BioLogos site, is “Of course we cannot confront the data ‘on our own’.”

It’s strange that Giberson would emphasize the need for logic and reasoning, then go right back to his appeal to authority — as long as it’s the proper, respected authority in the right community. (You know, not those evangelicals who are so intellectually impoverished.)

It’s not that evolution does not have dissenters in the ranks, so to speak – that’s the hallmark of healthy science, every theory should have its opponents so as to prevent scientific knowledge from inadvertently becoming stale – it’s just that when these dissenters’ arguments are weighed up and examined, they aren’t of much substance. Jerry Fodor seems to take issue with the very idea of natural selection itself, Lynn Margulis has some funny, mostly unsubstantiated ideas about symbiosis being the major evolutionary force, and the Altenberg 16, from what I can tell, was a conference that discussed ideas of evolution past the Modern Synthesis, something that has been coming for a while, but as more of an add-on to existing ideas, not the paradigm shift or wholesale rejection of evolution that ID proponents have been craving.

Evolutionary theory has criticism, yes, but it is neither significant criticism, in terms of numbers, nor legitimate criticism, in terms of ideas and arguments. Dissenters are at the basal level we would expect for a theory as major and as old as evolution – and ID proponents are trying to make a mountain out of that molehill.

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In a pseudonymous post, Evolution News & Views interviewed Ann Gauger about her and Douglas Axe’s latest paper in BIO-Complexity on enzyme evolution. I touched on this paper in the last TWiID and hopefully explained why the results don’t have much impact on evolution, but this interview has an extremely interesting section near the end – it appears that they’re at least aware of the specific problem with their paper, but they don’t seem to be acknowledging it as a major one:

AG: [...] Alternatively, what if what we see now is the fortuitous product of one-way evolution? Ancestral proteins diverged into modern enzymes in a contingent fashion, following the paths natural selection and random mutation laid down, but epistatic interactions acquired over time now prevent any simple adaptive path between modern forms. That might be why it is so difficult to convert modern enzymes from one function to the other.

This pretty much cuts their paper in half, in terms of its implications for evolution, so why aren’t they saying so?

To refresh your memory from three weeks ago, Gauger and Axe took a modern protein, Kbl, and attempted to evolve a protein with equivalent function to BioF, another modern protein in the same enzyme superfamily as Kbl, but with a different enzymatic function. They found that it took seven mutations to switch between functions, something they claim is beyond the reach of stepwise evolution, as the intermediate stages were not functional (or were very weakly functional). My (and a lot of other ID critics’) criticism of the paper is that they weren’t testing an evolutionary hypothesis – they were transitioning from one modern protein to another, not from an ancestral protein to one of either Kbl or BioF1, which is not what would have happened in the evolutionary history of this particular enzyme family.

Of course, this is what Gauger is talking about in the above quote – history constrains the evolutionary process to only what paths are available to the enzyme at the time. Downstream, two rivers might have to jump their banks to join, but upstream their ancestral river split into two without any problems. The same is true of proteins: two modern enzymatic functions are hard to transition between, but earlier in time (“upstream” of the phylogenetic tree) the progression would have been easier. Note that it’s not necessarily a “transition” at all when it happens in nature – as with the rivers, each potential modern protein could have been contained in one common ancestral protein, which then had its gene sequence duplicated, allowing for multiple paralogs to evolve separate functionalities from the same starting point.

Unfortunately, instead of seeing this major flaw in their paper, Ann Gauger (presumably sharing the same thoughts as Douglas Axe) wrote it off as another confirmation of intelligent design:

But if protein evolution is so highly constrained, either ancestral proteins would have had to be remarkably designed indeed, or we must have been extremely lucky that just the right variants appeared whenever needed to provide new functions. More studies that examine the constraints on adaptive evolution of proteins are needed.

Any work on enzyme evolution (or any evolution, for that matter), to the ID proponent, can be boiled down to that statement in order to defend ID. “How lucky it is that mutation just happened to create protein variants that were functional!”, implying that any pathway to a new protein, however well-demonstrated, is still implausible because it involved chance event, which may not have actually happened historically. And with that you can see the ID movement’s logic at its most raw: anything less than 100% certainty of specific evolutionary pathways for all of life’s diversity is not good enough, lending plausibility to intelligent design as the best explanation for that diversity by default.

Isn’t it strange that most scientists don’t take them seriously?

———

The last post this week is by, for the third time, David Klinghoffer, who seems to be overtaking Casey Luskin in the highly recent posting frequency stakes (a highly important competition over at Evolution News & Views). David wrote about junk DNA, as, of course, it was once again time to plug Jonathan Wells’ new book, The Myth of Junk DNA:

Over the weekend, Jonathan Wells’s The Myth of Junk DNA broke into the top five on Amazon’s list of books dealing with genetics — a list normally dominated at its pinnacle by various editions of Richard Dawkins’ The Selfish Gene. Not bad, Jonathan.

The juxtaposition with Dawkins’ Selfish Gene is appropriate, notwithstanding the demurrals of biochemist Larry Moran et al. Dawkins and other Darwinists, such as Jerry Coyne, have indeed posited that neo-Darwinian theory predicts that swaths of the genome will turn out to be functionless junk. The Junk DNA argument has been a pillar of the Darwin Lobby’s efforts to seduce public opinion and influence public policy. Professor Moran wants to imagine that Dawkins never held that neo-Darwinism predicts junk DNA. But that’s not how other Darwinists see it. (Compare, for example, Dennett’s Darwin’s Dangerous Idea, page 316.)

First off, nice job, Jonathan. The Amazon Genetics Top Five is a lofty goal, and now that you’ve achieved it, don’t let it get to your head. Okay, I don’t mean to be snarky, but Stephen C. Meyer’s Signature in the Cell got onto the Amazon Top 10 Science books for 2010 list, so you’ve got a bit to live up to, especially when the Discovery Institute’s famous PR team is involved.

Secondly, Larry Moran, over at Sandwalkresponded to this post by David, and raised some extremely good, if unlikely-to-persuade-an-ID-proponent-of-their-truth, arguments:

The IDiots have a bit of a problem. In order to make this book look important they have to first establish that the concept of abundant junk DNA in our genome was a “pillar” of support for evolution. That’s hard to do when their understanding of evolution is so flawed that they don’t see the difference between “Darwinism” and evolution by random genetic drift.

Their claim that evolutionary theory PREDICTED the presence of huge amounts of junk DNA in our genome is just plain false. They been told this but they keep repeating their error. There’s a word for that kind of behavior. 

It’s easy to see how they got confused. It’s because they’re IDiots. It’s partly because they don’t understand that an argument for inheritance of a few pseudogenes is not the same as an argument that more than 50% of our genome is junk. There are plenty of scientists who will use the pseudogene argument to challenge Intelligent Design Creationism but who don’t believe that MOST of our genome is junk.

Well put2. Larry then goes on to explain the difference between Dawkins’ concept of “selfish DNA” and “junk DNA”, and discusses some further points. Make sure you read it, especially if you don’t know much about what junk DNA actually is.

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Rapid fire ID news!

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  1. An ancestral protein could be reconstructed using paleoenzymological techniques, involving phylogenetic analysis and statistical modelling.
  2. Even though I would never use the term “IDiot” myself, but that’s just my preference for keeping these sorts of discussions at a certain personally-respectful tone.

53 thoughts on “These Weeks in Intelligent Design – 18/05/11

  1. "if this problem was as major as David is making it out to be, why would the project be for only two researchers? Why is it not attracting major attention in the scientific community?"

    Because it's clearly all a ruse. Quite unlike the ID community, biologists are too busy lobbying congress and quote mining the vast libraries of ID research for anything attackable. Hiring two mathematicians is part of their PR campaign to convince people that they're actually doing something instead of just waving their hands.

    No wait. It's biologists that do that, right? I'm pretty sure I heard that somewhere.

  2. It's somewhat disturbing that the DI has the time and resources to monitor the job postings from St. John's College of Oxford University for a faculty position that might have some nugget of propaganda value buried within a downloadable "document of particulars." Makes you wonder if all that effort couldn't be put to better use somehow…

  3. "No mathematician would deny that natural selection cannot increase fitness, that would be absurd." How about backing that statement up with evidence. Show me a time when a mathematician actually did prove that NS increased the fitness of an organism.

    • Bob, I’m no mathematician mate, but from quite simple observation we can see how artificial selection works – Animal breeders use it to develop new breeds all the time. How do you suppose the same principle applies in the natural world? As is obvious to those of us who condemn ID the answer is natural selection: environmental factors play the same role as human interference does. Can you provide an alternate account of why artificial selection works but natural selection doesn’t?

    • Bob, are you familiar with the field of population genetics? Honest question.

      (Also, try to click "Reply" under the comment you're responding to, it makes it easier to track the conversation. Cheers.)

    • Either you have not done any research or you're purposefully ignoring the entire field of population genetics, but either way, see R.A. Fisher's "The genetical theory of natural selection" (ISBN 978-0198504405) or any other peer-reviewed paper or book among the 10,000+ publications in this field.

      The observation that natural selection increases fitness follows trivially from the mathematical definition of population genetics, and this has been confirmed empirically from experimentation in many, many studies (check Google Scholar). This is a pretty ridiculous claim to make.

    • I'm a mathematician, and I just made up a mathematical model and proved that natural selection increased fitness in the model. I'm too lazy to type up the details for someone who couldn't understand them anyway.

      I'm pretty convinced that you're thoroughly stupid and wilfully ignorant. Nevertheless, if I'm wrong, you can prove it easily by spotting the glaring error in your challenge, explaining what went wrong and presenting a corrected version.

  4. You're not answering the question. The point is there is no mathematical support for Darwinism. If there is not math support for it, then there is no reason to believe it. A scientific theory cannot be true if math denies it.

    As for AI – AI proves that you can't change one species into another. Human breeders have been breeding dogs for centuries and the same basic body plan remains unchanged. Moreover, AI requires intelligence, something nature doesn't have.

    • Sure, if you can show that mathematicians have even attempted the question, and come to the conclusion that it is mathematically impossible. Your request is on the level of someone who insists (prior to Newton and Leibnitz) that one cannot prove that the surface of a circle is a constant multiple of the radius square. While a detailed mathematical understanding might be useful, its absence isn't going to make basic facts disappear. So show us where the math 'denies' (i.e. contradicts – absence is not sufficient) natural selection (or whatever you mean by Darwinism). My own understanding of probability suggests that you are off to lunch.

      • Saskydic,

        Basically your shifting the burden of proof. The burden of proof is on the person that has a theory to prove his theory. What you're saying is prove to be that mathematics disproves Darwinism. The burden is on you to come up with the math to buttress your theory. You can't do that, so I have no reason to believe in Darwinism.

        In any case, let me try to outline why there is no hope in the world for Darwinism to be proved by math.

        The human body has 100 trillion cells divided into about 200 cell types and about 25 genes which serve as instructions for which proteins need to be built in those 200 cell types and when. That requires planning. Random mutation cannot plan.

        Let's now look at an attempt to actually prove that Darwinism can build an organ through stepwise mutation.
        http://www.pnas.org/content/104/17/7116.abstract

        FlgF and FlgG are of similar size (251 aa vs. 260 aa in E. coli) and show 31% amino acid identity over their entire lengths. In contrast, the flgE gene is much longer and appears to have evolved iromflgG through an intragenic duplication that added a 160-aa domain to the N terminus of its encoded protein. PSI-BLAST searches reveal two significant alignments between FlgE and FlgG in E. coli: one with 24% identity between whole length of FlgG and the C terminus of FlgE (156-401 aa), and the other with 29% identity between the N terminus of two proteins («460 aa). … The most striking finding from our analysis is that these core genes originated from one another through a series of duplications, an inference based on the fact that they still retain significant sequence homology.

        Here is the article's basic logic:
        1. The flagellum is composed of about 50 genes.
        2. There are many different flagellum.
        3. All flagella share a core set of 25 genes about 160 – 400 amino acids long.
        4. This core set are about 25% identical to each other.
        5. Therefore, all 25 of these genes arose from the same gene, to say nothing of the other 25.

        To account for the rise of 25 genes is to explain how about 5000 mutations or amino acids sequences arose due to NS acting on RM. The authors did not even provide one explanation for any mutation. Moreover, they didn't even try to explain the rise of the other 25 genes.  

        The odds of forming just one protein at random, provided

        • Quoting, "The burden of proof is on the person that has a theory to prove his theory." Nope, and we've been over this repeatedly in the last week alone. In mathematics, one can prove something based on certain axioms, but in science, you take a hypothesis, and hit it with data until the hypothesis breaks, and/or you can show the hypothesis to be incoherent (e.g. mathematically). The burden is on you (and scientists generally) to show that either the hypothesis fails to explain data or is incoherent – but you actually realise this, as you attempt to attack the paper you cite. Perhaps you could post the rest of your argument as replies, considering that you ended mid-sentence.

          That said, I believe random mutation is well understood – copying errors, duplications, and the like, so the authors didn't need to explain any mutation, unless one can show that the mutations were impossible.

        • Another comment. You wrote, "That requires planning. Random mutation cannot plan. "

          Why? When one builds a structure (e.g. a wooden enclosure, such as a shed) without a plan, one is frequently confined (and given opportunity) by previous decisions in the building of the structure. Likewise with computer programming, or any other creative yet practical project. In human relations, the same goes – when you burn bridges, you are severely constrained in some matters, and liberated in others. After the fact, someone could claim planning, but often it is random misunderstandings, and taking opportunities. If a certain random path of action was successful, one can try to systematize it, and justify each step. Then one can check what the program's success-rate is, and modify individual steps to optimize the program. I take it that you don't have a programming background, so I'll suggest that you learn some BASIC or Pascal and write two dozen programs of your own after mastering the language, or alternatively, if you prefer physical activity, that you try building a shed without a plan, but using just a saw, drill, screws, planks and paint.

        • "Basically your shifting the burden of proof. The burden of proof is on the person that has a theory to prove his theory"

          Indeed it is, and the empirical observations that evolution occurs have unerringly been shown to be explained elegantly and accurately by the theory of natural selection. Along with other mechanisms such as sexual selection and random genetic drift, this is the current best-fitting theoretical framework for explaining the diversity of both extant as well as extinct life on Earth, and is supported by empirical research in many fields (population genetics, biogeography, molecular biology, geology, paleontology, to name a few).

          "The human body has 100 trillion cells divided into about 200 cell types and about 25 genes which serve as instructions for which proteins need to be built in those 200 cell types and when. That requires planning. Random mutation cannot plan."

          You assert that this requires planning (implying a supernatural plan I would assume), but you provide no justification for this assertion. Why does this require planning? Are you unaware of the field of developmental biology and embryology? The mechanism for cell and tissue differentiation is extremely well understood. You also assert that we require only 20 genes to control this differentiation — you're going to need to provide a citation for that.

          "To account for the rise of 25 genes is to explain how about 5000 mutations or amino acids sequences arose due to NS acting on RM. The authors did not even provide one explanation for any mutation. Moreover, they didn't even try to explain the rise of the other 25 genes. The odds of forming just one protein at random, provided"

          This is an elementary (and unfortunately common) misunderstanding of evolution. We only have the benefit of studying the genetics of extant organisms, which means when we compare a gene or protein in two organisms we observe the result of many millions of generations of evolutionary divergence. At no point in evolution is it the case that one organism gains dozens, hundreds or thousands of mutations that immediately gives rise to a novel function of a gene. Evolution happens when small changes occur that give a selective advantage to an organism. The 5000 mutations to which you refer are the result of many millions of generations of natural selection, and it is unreasonable to claim that we somehow need a step-by-step breakdown of these mutations.

          Let me ask an analogous question: can you prove that you exist, going off your geneology and by providing a location for the remains of your ancestors? How many generations can you go back? I would be surprised if it's more than 2, and astounded if it's more than 5. If you can't provide evidence of the mechanism of your existence, how would you expect molecular biologists would be able to go back in time and perform genomic analysis on long-extinct bacteria? We can only investigate the evidence for evolution that is found in extant organisms, and this evidence clearly and succinctly points to the common descent of all life on Earth.

          All this aside, there have been some fascinating long-term experiments done on the evolution of novel function (citrate metabolism) in bacteria. Twelve populations of bacteria were founded, and they were grown in glucose-deficient medium for tens of thousands of generations. Samples were taken regularly and frozen, and after about 30,000 generations a mutant was observed that had evolved the ability to metabolize citrate. They went back to the freezer and did genetic analysis of the population that derived this functionality, and have shown a virtual step-by-step mechanism for this. See Blount & Lanski (2008): http://myxo.css.msu.edu/lenski/pdf/2008,%20PNAS,%… and later publications on this subject by these authors.

        • flawedprefect

          "Basically your shifting the burden of proof." Uh – no. If you claim an intelligence did it, burden of proof is on you to prove how.

          "To account for the rise of 25 genes is to explain how about 5000 mutations or amino acids sequences arose due to NS acting on RM. The authors did not even provide one explanation for any mutation. Moreover, they didn't even try to explain the rise of the other 25 genes."

          I don't even NEED to read the paper to figure out this is an argument from ignorance. You're basically claiming "I can't figure out how NS acting on RM can explain this, therefore: an intelligence MUST have done it."

          I'm a lay person, enjoying the information presented by those arguing against you here, Bob. They really know their stuff. I'll admit I don't know nearly as much as they do, but I do know enough to see how random mutation can provide a basis from which natural selection can work from in selecting the most adaptable forms. No intelligence is required to send evolution one way or another to a pre-determined purpose. If you claim ONLY an intelligence can account for a mutation being successful, you have to show HOW. You cannot just throw your hands up and say "I don't understand how these mechanisms work in an evolutionary framework, therefore in MUST be intelligence by default". Sorry, Bob, but your argument is bunk.

          But hey, Saskydisc and Justin have you p0wned. JUst commenting from the sidelines here. Carry on! :)

          • The irony is that I'm actually also a lay person – I hated biology in high school, and it was only much later that I got interested – what he's trying to do is claim that mutation isn't random, by claiming that the odds of successful mutation are much smaller than what random variation could achieve. To make this argument, he must grossly underestimate (or avoid discussing) the relevant rates of mutation (note that gene duplication is so frequent in humans that it apparently contributes substantially to breast cancer, yet is so rarely useful that it took on average (until relatively recently, maybe 15k years ago) about a thousand years for any gene duplication to become established in the human population – google scholar is my friend :) – I never even took biology after grade ten. Certainly, it boggles my mind that something that probably occurs at least in one in every hundred persons in their germ lines, yet is generally so pathological that it takes a thousand years to find a useful mutation, would be evidence of the hand of god. Think of it! God only bothers to make a useful gene duplication in the germ-line every 6000th time, or less, but does it all the time to cause cancers and the like? (With apologies to Mark Twain…)

  5. "I believe random mutation is well understood – copying errors, duplications, and the like, so the authors didn't need to explain any mutation, unless one can show that the mutations were impossible."

    You're just watching DNA get shuffled around and are assuming that it's not intentional. If that shuffling around of DNA is random then there is a mathematics that can prove it because randomness has a mathematical definition. The shuffling of genes is not random because math tells us that it is not random.

    In order for NS + RM to be the only agent of design, then every mutation, or almost every mutation must serve a definite survival advantage to the organism. It takes about 10,000 mutations to change one gene into a full-fledged bacterial flagellum and Liu did not provide even one explanation how any of those mutations provided any selective advantage to the organism.

    • Natural selection and random mutation are not the only agents of 'design'. Natural selection is just one way that evolution can occur (cf random drift) and random mutation is just one way of introducing genetic variation (cf gene duplication, horizontal gene transfer) on which natural selection can work. The important line from the paper you cite (which I haven't read) is that the genes arose through duplication. That is, because of mistakes in meiosis one or more additional copies of a gene occur in the genome. An additional copy of the gene initially produces the same protein, but can acquire mutations that lead, through evolution, to new function.

      You have not provided your workings to show how you came to the figure of 5,000/ 10,000 (you state to figures in different places) mutations, but if it is as I suspect a multiplication of the number of genes by the number of amino acids then your calculations are totally wrong. They're wrong for two reasons that are immediately obvious. Firstly, the genes arose through duplication not random mutation. Secondly, the amino acids are in the proteins coded for by the genes and not in the genes themselves. The base pairs in the genes would be a little over 3 times the number of amino acids in the protein. It is very difficult to go from amino acid sequence similarity to base pair similarity because single mutations, such as additions and deletions, can have huge effects on amino acid sequences.

      Evolutionary biology is backed up by mathematics. Much of it was worked out during the modern synthesis. The field is called quantitative genetics (also population genetics or evolutionary genetics). This has already been pointed out to you. You should read up on it. You could start with Fisher's "The Genetical Theory Of Natural Selection". If you look you can probably download the whole book for free. Although, "Evolutionary Genetics" by John Maynard Smith may be more your level as it's an introductory text.

    • "You're just watching DNA get shuffled around and are assuming that it's not intentional. If that shuffling around of DNA is random then there is a mathematics that can prove it because randomness has a mathematical definition. The shuffling of genes is not random because math tells us that it is not random."

      If you are claiming that every time your DNA gets "shuffled" it is performed purposefully by a supernatural designer, does this mean every time a gamete forms God gets out his cosmic scissors to perform the synapsis and crossing over? In other words, for every male human alone he performs this 200 million times per day. How exactly does this hypothesis make more sense than the hypothesis that these are random unguided processes? (a hypothesis supported by actual research) This is yet another unsupported claim on your part — either provide references or drop it.

      "It takes about 10,000 mutations to change one gene into a full-fledged bacterial flagellum and Liu did not provide even one explanation how any of those mutations provided any selective advantage to the organism."

      Take for example the claim that you walked from your house to a town 5 miles away. It takes about 10,000 steps to walk from your house to a town 5 miles away, and you cannot provide even one explanation how any one of those steps provided any positional advantage to yourself. After all, after each step you took you were approximately the same distance to the destination as after the one preceding it, so how could you have walked to this town? That you must have been teleported by an intelligent transporter in a single step is the only conclusion I can reach.

      Do you see the analogy? Evolution is a slow, unguided process resulting from nonrandom selection from a pool of random variation. At any point it appears that the progeny of a given organism is identical to its parent, yet when viewed on a deep enough time scale evolution can and does occur. This has even been verified experimentally — evolution occurs, it is a simple fact just like the fact that the sun rises in the East every morning, and like heliocentric theory is to the rising sun, natural selection is our best explanation for the mechanism of this evolution.

  6. "Natural selection and random mutation are not the only agents of 'design'. Natural selection is just one way that evolution can occur (cf random drift)" — genetic drift is a random process, so it is basically the same as random mutation.

    [and random mutation is just one way of introducing genetic variation (cf gene duplication, horizontal gene transfer) on which natural selection can work.]

    No one is suggesting that HGT and gene duplication does not happen, what I'm suggesting is that those acts are the result of intelligence.

    [An additional copy of the gene initially produces the same protein, but can acquire mutations that lead, through evolution, to new function.]

    Of course this is true, what is not true is that the mutations are random. The mutations are the result of intelligence.

    [You have not provided your workings to show how you came to the figure of 5,000/ 10,000 (you state to figures in different places) mutations, but if it is as I suspect a multiplication of the number of genes by the number of amino acids then your calculations are totally wrong. They're wrong for two reasons that are immediately obvious. Firstly, the genes arose through duplication not random mutation. Secondly, the amino acids are in the proteins coded for by the genes and not in the genes themselves. The base pairs in the genes would be a little over 3 times the number of amino acids in the protein. It is very difficult to go from amino acid sequence similarity to base pair similarity because single mutations, such as additions and deletions, can have huge effects on amino acid sequences.]

    The only mutation that matters are mutations that result in a different amino acid. So when I say 10,000 mutations, I'm talking about mutations of an amino acid. The authors asserted that the flagellum arose from a single gene and that all the other 49 genes arose from it. Most of the genes that they discussed had about 250 aa, so I just rounded down to 200 aa to be nice to the Darwinists. Well, to get from 1 gene of 200 to 50 genes of 200, that's 50 * 200 which equals 10,000. In order for NS + RM to be true, about half of those mutations have to serve a definite selective advantage, moreover, each of those mutations has to be functional.

    [Evolutionary biology is backed up by mathematics.]

    Prove it. Saying X started the field of population genetics is not proof.
    The why is Oxford university seeking mathematicians to shore up Darwinism? Why does Oxford university claim that mathematics denies Darwinism?

    [ Much of it was worked out during the modern synthesis. The field is called quantitative genetics (also population genetics or evolutionary genetics). This has already been pointed out to you. You should read up on it. You could start with Fisher's "The Genetical Theory Of Natural Selection".]
    Fisher came up with his ideas in the 30s when it wasn't even known how large the genome actually is.

    • Where does Oxford university claim that mathematics denies (natural selection or) Darwinism? Justify your ex cathedra claim that intelligence is involved. Random input with a shaping filter is no longer all that random – deleterious mutations are tested and rejected, not avoided initially. And if you continue to post new comments, instead of replying to existing comments, you delay responses.

      Why should the 200 mutations be specifically advantageous, rather than not overly disadvantageous?

      You wrote, "Saying X started the field of population genetics is not proof. " And saying that god wrote the bible isn't either. The issue is whether population genetics is coherent, not who founded it, so you are playing red herrings. If you take issue with population genetics, argue against it.

      • Saskydisc,

        As for Oxford university claiming that math denies Darwinism:

        The concept of fitness optimization is routinely used by field biologists,
        and first-year biology undergraduates are frequently taught that natural selection leads to
        organisms that maximize their fitness. Dawkins’ The Selfish Gene (1976) promoted a
        conceptual integration of modern evolutionary theory in which genes are viewed as
        optimising agents, which is extremely influential and widespread today and encompasses
        inclusive fitness theory and evolutionarily stable strategies as well as general optimality
        ideas. However, mathematical population geneticists mainly deny that natural selection leads
        to optimization of any useful kind. This fifty-year old schism is intellectually damaging in
        itself, and has prevented improvements in our concept of what fitness is. http://www.sjc.ox.ac.uk/3498/RA%20in%20Mathematics_FPs.p...

        [Justify your ex cathedra claim that intelligence is involved]

        Randomness = one event has no bearing on the following event
        intelligence = one event does have a bearing on the following event (provided no natural law is involved)

        There is no natural law that governs the order of DNA nucleotides because all nucleotide sequences are equally stable.

        [Random input with a shaping filter is no longer all that random - deleterious mutations are tested and rejected, not avoided initially.]
        If I have 10K airplane parts and 10K non-airplane parts and pass all those parts through a filter that filters out all the non airplane parts, then those parts are not going to form an airplane.

        [Why should the 200 mutations be specifically advantageous, rather than not overly disadvantageous? ]

        Because if there not then you're just relying on mere luck to form an organ and you need a lot more mutations than 200 to form an organ. Just to build an organ you need anywhere from 50 to 1000 genes, moreover, not only do you need the genes, you need the non-coding regions of the genome to instruct when those genes get turned on and off. If you rely on randomness to come up with the right sequence for even just one 120 aa protein, then the odds of that are easily higher than 1 in 10^150. (there are only 10^80 particles in our universe).

        [The issue is whether population genetics is coherent, not who founded it, so you are playing red herrings. If you take issue with population genetics, argue against it.]

        It's not coherent which is why Oxford university is looking for someone to shore it up.

        • Where to start? The airplane analogy is ludicrous – to wit, in a genetically stable population, the analogue to your airplane, the organism, does organise its own development – the 'airplane parts' are amino acids, sugars, proteins, etc., or ultimately, generally, the lighter elements. A great many mutations exist that don't make the organism dysfunctional. But the problems with your analogy become worse – nature constantly cannibalises itself.

          Take an organic population of billions, that is relatively stable (for micro-organisms, this is a puny population), that reproduces rather quickly, e.g. every four hours. So now we can calculate some probabilities. Let's assume that one in every ten thousand members of a generation undergo some substantial mutation – for a population of one billion, that gives one hundred thousand mutations per generation (every four hours in this example). Let's make the probability of a useful mutation one in a billion – 4 hours x 10^4 = 4.5 years – under hugely unfavourable assumptions. Let's make the assumptions more unfavourable – only one in ten survive, which increases the time to 45 years – the genetic inventions must arise before they become subject to selective pressures.

          But your argument is ultimately about macro-fauna, especially their organs. Inherent in your argument is an implicit claim that each organ is perfect, or at least optimal (genetically), in that mutations that are likely to occur are likely to be suboptimal – "nearest neighbour" (single) mutations generally result in inferior organs, i.e. an organ must become worse before it can become better, which appears to contradict natural selection. (I'll note in passing that this actually contradicts your reliance on your interpretation of the Oxford U advertisement – you need natural selection for species stability – intelligence could create new species much faster than nature could.) This comes back to Gould's arguments about break-away populations, and is why a formal mathematical statement is useful (more on later) – one can then mathematically check whether natural selection can allow species genesis, what the probability of that is, under which situations natural selection is sufficiently weakened to allow for intermediate (semi-pathological) mutants, before a population can naturally select toward a new advantageous state.

          Do you have a basic background in vector calculus? If you do, think of fitness as a multi-dimensionally (different mutations being 'distances' along different axes) dependent scalar quantity, with stable species occupying local maxima, and the gradients arising from natural selection at small deviations pointing back to the stable species, and making the probability of new species arising very small – a large 'space' must be overcome before a population can select toward a different local maxima. We then extend this by assuming that natural selection must converge immediately (or very quickly) back to the stable species, thus making speciation a rarity.

          The issue boils down to two issues imao – whether a mutation can arise, that isn't pathological in itself, that can lead to further mutations which are advantageous – to extend the multi-dimensional analogy, whether a new set of 'dimensions' can arise which suddenly make the local maxima a saddle point (think of duplications, which fit the bill nicely), and what determines the rate of natural selection. I'm not aware of the current state of the mathematical understanding (if others chip in with references, I'll be very happy) of what determines the rate of elimination in natural selection, but if it can be shown to be variable – and it probably can be: natural selection most likely arises when resources are sufficiently abundant to allow more 'reproductively fit' to reproduce faster than less 'reproductively fit' – then we can find situations where sufficient initial genetic diversity can arise to 'move' toward a different new optimal.

          Other comments:
          As to your abuse of the term random, I'll assume that it is out of ignorance. Try Papoulis and Pillai's basic text on random variables – it is a graduate level text that assumes basic familiarity with integral calculus (including multivariable calculus), and in the later chapters, with Fourier transforms.

          As to your probability calculation, you are assuming that intermediates (in time) between two species are sufficiently dysfunctional as to be non-reproductive.

          • "I'm not aware of the current state of the mathematical understanding (if others chip in with references, I'll be very happy) of what determines the rate of elimination in natural selection, but if it can be shown to be variable – and it probably can be: natural selection most likely arises when resources are sufficiently abundant to allow more 'reproductively fit' to reproduce faster than less 'reproductively fit' – then we can find situations where sufficient initial genetic diversity can arise to 'move' toward a different new optimal."

            The "puncutated equilibrium" hypothesis is consistent with this. Basically, it is hypothesized that species in given ecosystem are relatively stable until new ecological niches arise due to extinction, drastic environmental changes, etc. When this occurs, the natural variation present in the individual organisms of the surviving species allows for relatively rapid adaptation and eventual reproductive isolation and speciation. This explains the observed evolution of the cichlid fishes of the Great Lakes in Africa, the evolutionary convergence in the existence of the many marsupial species in Australia that are analogous to placental species elsewhere, and (perhaps more significantly) the dramatic appearance of new species following the mass extinctions that define the major geological time divisions.

            Basically, the species in a stable ecological equilibrium are successful in exploiting their niche and exist at a local maximum on the fitness landscape. Since most genotypic changes are relatively small and natural selection is undirected, the vast majority of individuals that deviate from this equilibrium (by mutation and other variation) are not as successful as their wild-type parents and cannot easily reach a greater (but nonlocal) maximum. This results in species that are relatively stable, and do not change much phenotypically. For example, consider the coelocanth fishes: they were thought to be extinct for at least 80 million years until the early 20th century when one turned up in a fisherman's net off the coast of South Africa. While it is not identical to fossil coelocanths it is startlingly similar, suggesting that its ecological niche has remained relatively unchanged during this period.

            After a mass extinction or other drastic change, the topography of the fitness landscape can shift dramatically. This results in new maxima near the old point of equilibrium providing an opportunity for natural selection to test the existing variation against this fitness landscape. It's a fascinating model, and explains the data quite well.

            As an aside, I am curious how many creationists are aware that we found coelocanth fossils fully 100 years before we found live coelocanths. If something like this can go unnoticed for so long, why is it surprising that we have not found fossils of all organisms, living or extinct?

          • I didn't see this post before.

            [Let's assume that one in every ten thousand members of a generation undergo some substantial mutation - for a population of one billion, that gives one hundred thousand mutations per generation (every four hours in this example). Let's make the probability of a useful mutation one in a billion - 4 hours x 10^4 = 4.5 years - under hugely unfavourable assumptions. Let's make the assumptions more unfavourable - only one in ten survive, which increases the time to 45 years - the genetic inventions must arise before they become subject to selective pressures]

            Your math is deeply flawed. First, I'd like to see you justify why you think the probability of a useful mutation is one in a billion. Second, the odds of successful mutation are not one in 10^9, it's much closer to one in 10^20,000. Just one mutation by itself has never shown to substantially increase fitness, except for those mutations which break genes that are currently being used by parasites to invade the organism and kill it, or some variation on that theme. In order to build a whole new organ or a whole new pathway, you need about 10 proteins to work in a team, and that's just for pathways. If you want to build a sense such as vision or hearing you need about 200 genes, and not only do you need those genes you need the noncoding DNA to instruct those genes how to work together. If you build 200 proteins, you've done nothing to make them work together. Proteins range in size from 100 to 1000. Just for a protein of size 100 is 10^130 possible combinations.

            [Do you have a basic background in vector calculus? If you do, think of fitness as a multi-dimensionally (different mutations being 'distances' along different axes) dependent scalar quantity, with stable species occupying local maxima, and the gradients arising from natural selection at small deviations pointing back to the stable species, and making the probability of new species arising very small - a large 'space' must be overcome before a population can select toward a different local maxima. We then extend this by assuming that natural selection must converge immediately (or very quickly) back to the stable species, thus making speciation a rarity.]
            This is just trying to hide behind words such as: scalar, maxima, gradients, axes – if you're not talking numbers, then you have no argument and no evidence.

            [As to your probability calculation, you are assuming that intermediates (in time) between two species are sufficiently dysfunctional as to be non-reproductive.]

            This is just an assertion, or an assumption on your part. I need evidence.

            • Out of order:
              [This is just trying to hide behind words such as: scalar, maxima, gradients, axes - if you're not talking numbers, then you have no argument and no evidence. ]
              No, it was an argument that attempted to explain using vector calculus. I take it then that you don't have the relevant background, and I will try to explain without resort to calculus.

              A useful mutation need not build an organ – a mere improvement in function will do. Why should it be 10^-20 000? Just looking at human genetic variability – as an example, look at the variation in the Cohen marker, between the Venda, Yemenis, and Askhenazi Cohens – the accumulated variations aren't so great as to suggest, to my knowledge, substantial selective advantage, but death didn't occur – more random changes are necessary before they become selectively (dis-)advantageous.

              But let's go further – do you agree that there are genes (or at least large sections of DNA) that can be duplicated without pathology? Recall that the reason why point mutations are often fatal is that vital proteins don't get made. If you have two copies of the instructions, and one copy gets fudged (mutated), the other copy can still make the vital protein, and mutation can continue to a much greater extent without pathology. In this situation, frankly, I don't see why the probability of a mutation on a copy of the gene being useful should be less than 1% – perhaps you could explain* – then the question is what the probability is of a mutation occurring on the copy of the gene. Considering that the genes for smell in mice are the length you gave (400 codons out of a genomic length of 830 Mcodons = 1 / 1 million x 1% – and this is ignoring the actual sequence, which would be more informative – and the obvious evidence of genetic drift, which shows that non-harmful mutations occur all the time). Then there is non–coding DNA – huge sections of which can be modified with no ill-effect, until they are modified to become coding, and thus become harmful or helpful.

              *Hint: absence is not evidence of pathology – nature can only select against it if it by chance arises – and the argument to pathology of the mutation without gene duplication fails

              But your argument has a deeper problem, as pointed out before – you are assuming an organ in one step, with prior forms being non-functional – where the evidence exists, often the coding for organs/proteins etc. start on one level of complexity, become more complex (e.g. gene duplication), then become less complex.

              [This is just an assertion, or an assumption on your part. I need evidence. ]
              You are exactly assuming that in (random + NS) evolution, intermediates between two species are sufficiently dysfunctional as to be non-reproductive – you even tried to justify it by arguing that individual mutations would be fatal!

        • As to the Oxford U advertisement, I notice that you quote rather selectively – you omit such (juicy, against your perspective) quotes as,
          "The core argument is that the mechanical processes of inheritance and reproduction, today represented by equations of motion of gene frequency change, can give rise through natural selection to the appearance of design, today represented by the mathematics of optimisation. The formal approach is therefore to construct links between equations of motion and optimisation programs. The project has been substantially begun, and most of the ingredients identified. But the main work requires to be done of constructing a single over- arching model of the optimising tendency of natural selection, and that is the work proposed in this project."

          "Of course, there are many mathematical models that show natural selection at work, but they are all examples. None claims to capture Darwin's central argument in its entirety. In its grandest conception, this project aims to do just that, and even to include all the valid additions to the theory, namely sexual selection, the merging of Darwinism and Mendelism, inclusive fitness and evolutionary game theory.
          "

          And best of all, To extend the formal links between equations of motion and the mathematics of optimisation begun by Grafen (1999, 2002, 2006a, 2006b), as a formal representation of what biologists have meant by ‘fitness optimisation’, and so clear up a misunderstanding with mathematical population geneticists.

          Notice that they substantially contradict your position – the mathematics doesn't 'deny' natural selection, but rather, there is no general mathematical theory of natural selection, only ad hoc models, and (in the opinion of the writers of the advertisement – feel free to disagree) the mathematicians have misunderstood the arguments made by the biologists.

        • You wrote, "There is no natural law that governs the order of DNA nucleotides because all nucleotide sequences are equally stable.
          Is that a statement about their chemical stability, the stability of populations having members that have the different orders, or what kind of stability are you trying to describe?

        • "There is no natural law that governs the order of DNA nucleotides because all nucleotide sequences are equally stable. "

          Other than this being a non sequitur argument, it is patently false that all nucleotide sequences are equally stable. A 5 second search came up with this: http://hmg.oxfordjournals.org/content/1/7/467.sho

          It is very much known that there are DNA sequences that are inherently unstable, especially those with short repeating sequences.

          "Because if there not then you're just relying on mere luck to form an organ and you need a lot more mutations than 200 to form an organ. Just to build an organ you need anywhere from 50 to 1000 genes, moreover, not only do you need the genes, you need the non-coding regions of the genome to instruct when those genes get turned on and off. If you rely on randomness to come up with the right sequence for even just one 120 aa protein, then the odds of that are easily higher than 1 in 10^150. (there are only 10^80 particles in our universe)."

          Argument from personal incredulity. Come on, I can tell you possess intelligence, why not apply it rigorously? A fallacious argument is self-refuting. People in this thread have been providing researched, reasonable arguments in response to you, and all you've given in return is more fallacies.

  7. You wrote, "The very definition of random means one event has no bearing on a future event." Nope, the definition you supplied just means statistical independence – it is not at all the definition of randomness – two random events can be variously correlated and one event can greatly modify the probability of a subsequent event – you are sneaking in bizarre premises. As to intelligence, that is merely feedback into a neural network – feedback generally constrains random variations, which you would know if you had a basic background in control systems – or maybe you do, and are playing the troll. Anyhow, in natural selection, reproductive fitness is the feedback mechanism. As to human development, it is rather haphazard, and many developmental disorders can arise from variations in growth, and far more functional possibilities exist.

    With your strange accusation of me changing the subject (I recall it was you above who raised the issue of the burden of proof), and your refusal to actually read up on population genetics (what with your weird conflation of the mathematics of population genetics and who initiated the field and denying that the mathematics of population genetics exists), I take it you are another troll who is bored. Well, ok, we can play along, but doesn't it get even more boring playing the troll? I mean, doesn't playing the troll increase ennui?

    • Saskydisc,

      [Nope, the definition you supplied just means statistical independence - it is not at all the definition of randomness - two random events can be variously correlated and one event can greatly modify the probability of a subsequent event]

      Evolutionary theory is very clear that evolution is blind, non-teleological and has no plan or purpose. It's not for nothing that Dawkin's book is called the BLIND watchmaker. Let me quote the Oxford dictionary as to what random means:

      Having no definite aim or purpose; not sent or guided in a particular direction; made, done, occurring, etc., without method or conscious choice; haphazard.

      [Anyhow, in natural selection, reproductive fitness is the feedback mechanism.]

      That doesn't prove that mutations are random. No one is arguing that those beings which cannot reproduce will not reproduce. That's a tautology. Natural Selection is nothing more than a tautology, it just says that those who are too weak to reproduce will not reproduce. It doesn't follow that mutations are random. To say:

      1. the strong survive
      2. therefore mutations are random

      Is a complete non sequitar.

      [As to human development, it is rather haphazard, and many developmental disorders can arise from variations in growth, and far more functional possibilities exist.]
      Prove it.

      [With your strange accusation of me changing the subject (I recall it was you above who raised the issue of the burden of proof), and your refusal to actually read up on population genetics (what with your weird conflation of the mathematics of population genetics and who initiated the field and denying that the mathematics of population genetics exists), I take it you are another troll who is bored. Well, ok, we can play along, but doesn't it get even more boring playing the troll? I mean, doesn't playing the troll increase ennui? ]

      Now, you're just using Ad Hominem attacks. You've basically given up on science and now have resulted to name calling. Let me quote Christopher Hitchens: once you move on to ad hominem attacks I've won the debate.

      Basically, you're whole argument comes down to:

      1. population genetics exists
      2. therefore, mutations are random

      You're not even bothering to discuss the scientific literature.

      Since you've moved over to ad hominem attacks, I've concluded that you do you lack the sufficient respect for reason necessary to make dialogue a useful.

      • I see I've hit a nerve. Anyhow, you quote the relevant parts, so I reckon any reasoning person can see who's doing what, and whether I've been unreasonable in my conclusions – thanks, actually. Well, if you aren't a troll, you must be very confused – and self-unaware, considering what you've quoted. Oh well…

        Your quote of a dictionary for the meaning of the word 'random' is strange – it might have made sense if you were trying to understand common speech, but in a scientific context, one generally refers to standard works in the field. Below, I referred you to Papoulis and Pillai – simpler texts are available, but if you limit yourself to chapters 1-4, it shouldn't be too hard – assuming that you have a basic background in calculus. PARAGRAPH EDIT: Papoulis and Pillai are overkill. You are denying the concept of conditional probability.

        As to the non-sequitur that you give, it is yours alone, as I never made it. The closest that I got to the non-sequitur in my own thought can be described as follows:
        If random mutations with natural selection is insufficient to produce the species, then intelligence is required. (This seems to be your implicit premise – which is plausible – which you might use with your now explicit premise that random mutations with natural selection is insufficient to produce the species – with which I take issue.)

        Then you get into another non-sequitur that you ascribe to me – my argument is rather,
        1. Mutations are random,
        2. population genetics describes evolution (whether completely or not is a side matter, but in principle it could completely),
        3. therefore intelligent design is superfluous.

        You wish to attack my first premise – fine – so you do so with a dubious calculation, smuggling of premises, etc. So I'll restate my other request – give me the background rate of gene duplication – if it is different for different species, give me one species for which such a rate/frequency has been measured.

        Once you give me that rate, we'll need the rate of mutations, and at least an estimate of the rate of elimination of pathological variants from a given population, at three different population sizes, in order to do useful calculations.

        As to the scientific literature, if you feel that there are good papers that support your position, cite them to bolster your argument, as appropriate – otherwise you are asking me not only to prove a negative, but to prove an unstated negative.

      • "That doesn't prove that mutations are random. No one is arguing that those beings which cannot reproduce will not reproduce. That's a tautology. Natural Selection is nothing more than a tautology, it just says that those who are too weak to reproduce will not reproduce. It doesn't follow that mutations are random. To say:"

        Are you seriously asserting that mutation is non-random? You'll need to provide a citation on this. This is a very odd claim to make.

        Mutation is one source of random variation on which natural selection and other evolutionary mechanisms act. These mechanisms are precisely the opposite of random (other than genetic drift), and this nonrandom selection is how evolution is able to occur.

        "To say:
        1. the strong survive
        2. therefore mutations are random "

        This is a strawman argument. The only person claiming that the randomness of mutation is the result of natural selection is yourself. This is a nonsensical and ridiculous non sequitur.

        "Natural Selection is nothing more than a tautology"

        This, again, shows your complete ignorance of evolutionary theory. See http://www.talkorigins.org/faqs/evolphil/tautolog… for a consise refutation of this misunderstanding.

        "Now, you're just using Ad Hominem attacks"

        Saskydisc responded to your post with a reasoned argument, and instead of addressing his argument directly you accused him of an ad hominem attack. I find it ironic that you don't recognize this as an ad hominem argument on your part.

        (http://en.wikipedia.org/wiki/Ad_hominem)

  8. "The only mutation that matters are mutations that result in a different amino acid."
    – But 1 mutation in base pairs (in the gene) does not necessarily equal 1 change in an amino acid sequence (in the protein), making your calculations totally wrong. An addition or a deletion of a base pair can cause a change in most, sometimes all, of the amino acids downstream of the mutation because it causes a 'frame-shift' in the way the base pairs are translated to amino acids. What's more, you can get duplication of parts of a gene that are added to increase the length of the gene and consequently the protein. This is probably what accounts for the differences in the amino acid lengths of the various proteins in the study.

    "Why does Oxford university claim that mathematics denies Darwinism?"
    – They don't. Not anywhere. Also I think this argument lacks the strength that you give it. Mathematics is an abstraction of reality that must be built around assumptions. Where empirical evidence and mathematics are not in agreement it is always the assumptions that the mathematics are based on that are wrong. Look at your own simple calculations. They are based on the incorrect assumption that 1 mutation equals 1 amino acid change. Even though you can correctly calculate the number 10,000 from your equations the number is meaningless because basic assumption from which you get your parameter values is false. Your equations also do not account for the similarity between amino acid sequences which are a result of duplicate genes not mutating. Thus, even if your assumptions were correct you overestimate the number of mutations required.

    • I should add…

      "Prove it. Saying X started the field of population genetics is not proof."
      – The mathematics of population genetics (it's linear algebra) is consistent with evolution by natural selection. Thus proving that there is mathematical support for evolution by natural selection. You've been supplied with many references to get you started. Or do you seriously want someone to regurgitate the formulae and logic because you are too lazy to go and read it for yourself? If you bother to look there are even examples of population genetic models that explicitly include our modern understanding of genomes.

  9. [But 1 mutation in base pairs (in the gene) does not necessarily equal 1 change in an amino acid sequence (in the protein), making your calculations totally wrong. An addition or a deletion of a base pair can cause a change in most, sometimes all, of the amino acids downstream.]
    I never said that this wasn't true. The only thing that matters are those DNA substitutions that result in an aa substitution. You keep misunderstanding what I write. When I say 10,000 mutations, I mean 10,000 aa mutations, not DNA mutations.

    [you can get duplication of parts of a gene that are added to increase the length of the gene and consequently the protein]
    Of course, but these gene duplications are not random. They are the work of intelligence. It continually amazes me how often Darwinists make this mistake:

    1. Gene duplication happens
    2. therefore it's random

    ["Why does Oxford university claim that mathematics denies Darwinism?"
    - They don't. Not anywhere.]

    See quote above. I can't wait to watch you move the goal post when you find out that Oxford is claiming that math denies Darwinism.

    One does not prove the other.

    [Where empirical evidence and mathematics are not in agreement it is always the assumptions that the mathematics are based on that are wrong]

    Right, and in this case, the assumption is that mutations are random.

    [They are based on the incorrect assumption that 1 mutation equals 1 amino acid change.]
    I never said that. You're misunderstanding that. I said that 1 amino acid mutation equals 1 amino acid mutation. I was never talking about DNA mutations I was talking about aa mutations from the beginning. You just assumed that I was talking about DNA mutations.

    [Even though you can correctly calculate the number 10,000 from your equations the number is meaningless because basic assumption from which you get your parameter values is false. Your equations also do not account for the similarity between amino acid sequences which are a result of duplicate genes not mutating. Thus, even if your assumptions were correct you overestimate the number of mutations required.]

    Face it, you're never going to point to math that supports Darwinism. This whole post began when the blogger claimed that no mathematician would ever deny that NS increases fitness. I said show me that the math establishment says that NS supports fitness. You've never done that. Instead you've just succeeded in changing the topic.

    Let me spell out the math for you very clear.

    The amount of events in our universe's history are 10^150. That's 10^80 particles, 10^26 seconds and 10^43 divisions of a second. Therefore, any event whose odds are way above 1 in 10^150 randomness cannot accomplish it.

    The amount of AA you need to form the bacterial flaggellum are about 10,000. Studies of the genome reveal that on average proteins with the same function are usually anywhere from 60 to 100% identical. Moreover, there are more ways to form a flaggellum than one, it's probably around 3,000 but let's be generous and say that there are a trillion ways to form a flaggellum, or 10^12. Ok, what's 20^10,000? It's about 10^1300 – far beyond the 10^150 that randomness requires. Moreover, we have not even calculated the odds for putting those proteins together, we've only calculated the odds for creating all those proteins independently at the same time.

    • Show that gene duplication is not random. You are attempting it, but you are making very basic mistakes. Your argument that gene duplication is not random relies on a dubious calculation of the probability of a given structure arising in one step. So let's go through this step (reply) by step (reply). What is the probability of a gene duplication occurring randomly? If you have a problem with the question as stated, I can rephrase: what is the frequency of gene duplication?

      • Saskydisc,

        You've already proven yourself to be someone not interested in reason with the use of your ad hominem attack. Now you've proven yourself to be someone who does not read your opponents arguments. I'm not going to debate with someone who can't understand that Ad Hom attacks are not legitimate. I've got better things to do with my time. I will answer your question what are the odds of gene duplication.

        [Your argument that gene duplication is not random relies on a dubious calculation of the probability of a given structure arising in one step.]
        Just read the article I referred to on the stepwise formation of the flagellum. Those authors provided no evidence that any mutation provides any stepwise selective advantage to the organism.

        [What is the probability of a gene duplication occurring randomly]
        Did you even read my post?

        The amount of events in our universe's history are 10^150. That's 10^80 particles, 10^26 seconds and 10^43 divisions of a second. Therefore, any event whose odds are way above 1 in 10^150 randomness cannot accomplish it.

        The amount of AA you need to form the bacterial flaggellum are about 10,000. Studies of the genome reveal that on average proteins with the same function are usually anywhere from 60 to 100% identical. Moreover, there are more ways to form a flaggellum than one, it's probably around 3,000 but let's be generous and say that there are a trillion ways to form a flaggellum, or 10^12. Ok, what's 20^10,000? It's about 10^1300 – far beyond the 10^150 that randomness requires. Moreover, we have not even calculated the odds for putting those proteins together, we've only calculated the odds for creating all those proteins independently at the same time.

        • You abused burden of proof, and started accusing me of ad hominem attacks when I pointed it out, asked whether you are a troll and asked questions on that hypothesis.

          [Just read the article I referred to on the stepwise formation of the flagellum. Those authors provided no evidence that any mutation provides any stepwise selective advantage to the organism. ]

          Nice dodge. As to the argument you make in your dodge, you are requesting huge calculations, or huge experimentation – worthwhile perhaps in themselves, but until (and only if) such calculations and experiments disprove the hypothesis, we keep the hypothesis around – especially considering its explanatory power. And you are requesting rather strong guesses as to the initial state – we do not have the initial state, i.e. the ancestral bacteria, and we cannot really guess too well at it, as we do not have its exact environment.

          That said, given that proteins that have similar function generally have similar structure, and given that that generally occurs due to gene duplication, with one or both genes losing and changing function, it seems entirely plausible that more or less functional changes can arise in one step (e.g. after a gene duplication), each of which can be an improvement – it is not that there are e.g. 3000 ways to make a flagellum, but probably 3000 locally optimum ways, with less good flagella arising initially, steadily improving by other random mutations with selection.

          [Did you even read my post? ]
          Show your calculation of your probability (10^-1300), with your assumptions – your assumptions seem to be that one needs an average of one codon change to achieve one AA change in a protein, that the evolution is (semi-)ergodic, i.e. that it will have exhaustively examined the possibilities and have chosen the best in one step, that proteins with the same function develop independently, rather than by gene duplication and subsequent NS, and probably some others that you can supply.

          As to the first assumption, namely that one codon change in the DNA (or RNA, as appropriate to the organism) would cause a change in one AA in a resulting protein, justify, or show how else you make your probability estimate – a change in a few codons can radically change outcome – you do realise that any calculation must rely on probabilities of DNA changes, right?

          As to the second assumption, again, justify or supply an alternative – it seems blindingly obvious that this is your assumption – why shouldn't gene duplication allow for a step-by-step improvement? In humans the rate at which gene duplications became established in the population was about 1e-3 per year – note that the actual rate of gene or DNA portion duplication was much higher – are your perhaps under the assumptions that gene duplication can copy only one codon at a time, and that gene duplication requires randomly happening to copy the next codon adjacently, etc., as opposed to randomly copying an entire segment (number of adjacent codons) at once? This also applies to your third apparent assumption.

    • "I never said that. You're misunderstanding that. I said that 1 amino acid mutation equals 1 amino acid mutation. I was never talking about DNA mutations I was talking about aa mutations from the beginning. You just assumed that I was talking about DNA mutations."
      – Amino acid sequences don't mutate, ever. Amino acid sequences only change when the DNA that codes for them mutates. Thus, the assumptions underlying your calculations are wrong and 10,000 is a meaningless answer.

      "Face it, you're never going to point to math that supports Darwinism."
      – I have pointed to math that supports evolution by natural selection. I gave you several references that outline it. Others have given you further references.

      "…we've only calculated the odds for creating all those proteins independently at the same time."
      – Indeed. Which is why the calculations are wrong. The proteins are not created independently. They have evolved through natural selection from a common ancestor. You seem to know that the 'selection' part on natural selection means the process is not random, but you fail to grasp the implications of that for your calculations.

      Another flaw in these calculations is that you assume sequential trials rather than many simultaneous trials. That essentially means that you are only allowing for mutation in a single individual. Evolution occurs in populations of individuals that are all mutating at the same time, which dramatically shortens the time to achieve a particular outcome. For instance, if a mutation occurs in 1 individual every minute and the odds of achieving a specific mutation are 1 in a trillion, then in a population of 1 trillion that mutation occurs once a minute on average.

    • "I can't wait to watch you move the goal post when you find out that Oxford is claiming that math denies Darwinism."
      – The goal is simply for you to show me which bit of the quote says anything about mathematics disproving evolution. I have read the whole document, not just the quote, and at no point do they say that mathematics is inconsistent with evolutionary theory. The project is simply to turn verbal arguments into formal mathematical ones and, in doing so, produce a precise definition of fitness. The schism is between the mathematical population geneticists and people who use other mathematical approaches (e.g. inclusive fitness and game theory) because of the different operational definitions of fitness that are used.

      I just reread your post and I laughed when I read this bit:

      "Of course, but these gene duplications are not random. They are the work of intelligence. It continually amazes me how often Darwinists make this mistake:

      1. Gene duplication happens
      2. therefore it's random"

      Priceless. It makes me wonder if this back and forth is an example of Poe's Law (i.e. Without a winking smiley or other blatant display of humor, it is utterly impossible to parody a Creationist in such a way that someone won't mistake it for the genuine article).

  10. [Priceless. It makes me wonder if this back and forth is an example of Poe's Law (i.e. Without a winking smiley or other blatant display of humor, it is utterly impossible to parody a Creationist in such a way that someone won't mistake it for the genuine article).
    This is just an argument from ridicule:
    1. You're argument makes me laugh
    2. Therefore, it's wrong.

    [I have read the whole document, not just the quote, and at no point do they say that mathematics is inconsistent with evolutionary theory.]
    So you think Oxford is hiring mathematicians so that they can have a good time? When they hire mathematicians to underpin Darwinian theory, you can bet that Darwinism is in need of mathematical support that it does not have.

    [Another flaw in these calculations is that you assume sequential trials rather than many simultaneous trials. That essentially means that you are only allowing for mutation in a single individual. Evolution occurs in populations of individuals that are all mutating at the same time, which dramatically shortens the time to achieve a particular outcome. For instance, if a mutation occurs in 1 individual every minute and the odds of achieving a specific mutation are 1 in a trillion, then in a population of 1 trillion that mutation occurs once a minute on average.]

    Sure, mutations happen all the time, but the odds of a set of mutations forming a functioning organ are on the order of 1 in 10^30,000 at the lowest. The amount of particles that exist in our universe is 10^80, so there is not enough time in our universe's history to overcome such odds.

    Also when you say sequential trial you're assuming that far too many mutations benefit the organism than happens in reality. Just reread the Liu paper that I referred to. They did not mention one mutation in the flagellum that benefited its survival advantage. To be honest, I'm skeptical that one mutation exists at all which by itself which can provide the organism with a clear advantage over its peers, with the exception of mutations that destroy genes and thus make it impossible for parasite to lodge in the organism as is the case with sickle cell anemia. There are roughly 20,000 genes (even though there really is no such thing as a gene) and the genome is simply so huge that the change of one letter, is immediately drowned out by all the other changes in the genome happening simultaneously. The whole modern synthesis was made not knowing how big the genome is.

    [Amino acid sequences don't mutate, ever. Amino acid sequences only change when the DNA that codes for them mutates.]
    I know that. When I said it takes 10,000 mutations, I thought you would know what I mean because no one cares about a DNA mutation that does not result in a change in the aa sequence.

    [I have pointed to math that supports evolution by natural selection. I gave you several references that outline it. Others have given you further references.]
    No you haven't. If you have show me again. The only math I see from you is what you just provided above.

    • I think, when evaluating any argument, contrary to your own view or not, it is important for every rational person to fully understand the position of their opponent. Can you honestly say that you understand the basics of natural selection, population genetics, mathematics and general biology, enough that you can honestly say that you have the contextual knowledge to critically analyze these papers you are citing?

      "Of course, but these gene duplications are not random. They are the work of intelligence. It continually amazes me how often Darwinists make this mistake:

      1. Gene duplication happens
      2. therefore it's random "

      This is a straw-man argument. No scientist concludes that gene duplication is random a priori, they conclude it is random because it appears randomly in the genome. If you disagree, provide me with a study that has shown that gene duplication is nonrandom. If you don't, I will assume you have conceded this point. Further, what justification do you provide for your conclusion that gene duplication is the result of an intelligent designer? For a claim this big you will need a significant amount of evidence that unequivocably points to a designer.

      "When they hire mathematicians to underpin Darwinian theory, you can bet that Darwinism is in need of mathematical support that it does not have. "

      First, the entire field of population genetics has mathematics as its foundation. Does this count? Why or why not? Do you have any specific criticisms or questions about the work of R.A. Fisher or any other population geneticist? Have you read any of their work? Second, where in that paper does it state that they are hiring mathematicians to "underpin Darwinian theory"? From my reading, they are seeking mathematicians to formalize natural selection mathematically. I see no implication that they are trying to prove that natural selection is impossible, and even if they were, so what? What does that have to do with your argument? This sounds a lot like the "more and more" argument. [1]

      "Sure, mutations happen all the time, but the odds of a set of mutations forming a functioning organ are on the order of 1 in 10^30,000 at the lowest"

      We've already established that you do not know what a random variable is, and this statement shows that you are ignorant about the concept of probability as well. When someone says some random event has a probability of "1 in x", this means that there are x equally likely, independent events, and the event in question is 1 of those. What are the other 10^30,000 – 1 equally likely, independent events in your calculation? This type of calculation of probability does not make one iota of sense in the context of natural selection. No scientist would claim that functional organs spontaneously arise, and this claim in your argument is indicative that you do not understand evolution, at all. Furthermore, where did the 10^30,000 come from? You can't just make up numbers like that arbitrarily and expect anyone to take your argument seriously.

      "there really is no such thing as a gene"

      Umm, ok. Since I can't find anything in a cursory literature search that concludes this, I take it it's yet unpublished and your Nobel prize is pending?

      "the genome is simply so huge that the change of one letter, is immediately drowned out by all the other changes in the genome happening simultaneously"

      This makes no sense whatsoever. There are significant portions of the genome that are not under selection — that is, mutations in these regions do not confer a selectional advantage nor disadvantage — and most of the DNA sequence of functional genes can change with apparently no phenotypic effect, but to say that these changes are "drowned out" by all the other DNA in the genome is ludicrous. Either a mutation happens in a conserved region of the genome or it doesn't. If the former, most mutations would result in a selective disadvantage, and if the latter, they would not likely affect the fitness of the organism. Motoo Kimura's Neutral Theory explores the latter possibility in great detail.

      "I know that. When I said it takes 10,000 mutations, I thought you would know what I mean because no one cares about a DNA mutation that does not result in a change in the aa sequence. "

      What about DNA mutations in rRNA genes? Or tRNA? Those most definitely do not result in a change of a.a. sequence. For that matter, when you say it will take 10,000 mutations, how are you calculating this? Do you mean that the Hamming distance between the amino acid sequences of this protein in the two extant organisms in the study is 10,000?

      "No you haven't. If you have show me again. The only math I see from you is what you just provided above. "

      If you have seen no math in evolutionary research then you have not read a single population genetics paper. I think this speaks for itself.

      [1] http://home.entouch.net/dmd/moreandmore.htm

  11. "Why you think randomness plus a filter can arrange 100 trillion cells into a human being employing a code of 3.2 billion letters, moreover, grow it from a fetus to an adult in 25 years is completely out of line with common sense."

    Indeed it is against common sense, just as quantum mechanics is against common sense, heliocentricity is against common sense, the mechanism of volcanic eruption is against common sense, plate tectonics is against common sense, atomic theory is against common sense, etc.

    It's a good thing we have this thing called "the scientific method" which helps us test these explanations by formulating testable hypotheses and performing empirical experimentation. Prior to Darwin, few scientists would have agreed that natural processes could have possibly resulted in the diversity of life we observe today.

    After Darwin published The Origin of Species, most scientists were skeptical (as well they should be). In the 150 years since then, experiments, mathematical models, observations from the fossil record, etc. have shown to be completely consistent with, and elegantly explained by, natural and sexual selection and genetic drift. The hypotheses tested by these experiments were falsifiable — meaning the data gathered from the experiment could have disproved the hypothesis. The data failed to falsify them, and collectively they have shown that natural selection and the previously mentioned mechanisms are our best framework for understanding the diversity of life that we observe.

    For example, imagine a set S, composed of all species of all extant organisms on Earth, and construct an interconnected graph [1] structure based on the relatedness of each organism s in S. There are an astronomically large number of feasible graphs that can be constructed in this way. Hillis et al. (2008) [2] compared the similarity of thousands of organisms by studying the similarity of their ribosomal RNA (rRNA) sequences. The graph structure they obtained from this study was a special subset of graphs called a tree [3]. Note that a tree was not necessarily the resulting graph structure — they could have gotten a circular graph, or any number of non-tree graph structures. The tree that Hillis et al obtained from this study matched perfectly with similar trees constructed from paleontology and classical cladistics. [4] (full PDF of the tree they obtained)

    Assuming any arbitrary tree was equally likely, What are the chances that these trees exhibit this sort of confluence? Why would this study have resulted in this tree, or any tree for that matter, given that all these organisms were created at the same time by a single creator? We have known examples of the end products of intelligent design, and the pattern of inheritance observed in these is not a tree but a cyclical graph [5]. Innovations made in later designs are copied into plans for earlier designs, resulting in this cyclical structure. Why is it that we do not see this pattern in real-world analyses of biogeography and molecular biology, and instead see a strict tree structure as would be expected given common descent?

    The only explanation consistent with a creator that I can see for this and all the other paleontological, biogeographical and molecular biological evidence consistent with evolution is that the creator made all these organisms in such a way that it appears they evolved from a common ancestor. I will leave the question-begging justification for this to the theologians, but I will apply Occam's razor and conclude that all life on Earth descended from common ancestor.

    I gather that you are a supporter of intelligent design creationism. Please state a single falsifiable hypothesis that would provide positive evidence of design. I hope you are not relying on the false dichotomy of "it's either evolution or intelligent design" — criticisms of evolutionary theory are not evidence for intelligent design, just as criticisms about our very real lack of understanding of many phenomena in cosmology and astrophysics is not evidence for astrology. That's not how science works.

    References:

    [1] http://en.wikipedia.org/wiki/Graph_%28data_struct
    [2] http://www.sciencemag.org/content/300/5626/1692.s
    [3] http://en.wikipedia.org/wiki/Tree_%28data_structu
    [4] http://www.zo.utexas.edu/faculty/antisense/tree.p
    [5] http://www.blc.arizona.edu/courses/schaffer/449/T

  12. Justin,

    [I think, when evaluating any argument, contrary to your own view or not, it is important for every rational person to fully understand the position of their opponent. Can you honestly say that you understand the basics of natural selection, population genetics, mathematics and general biology, enough that you can honestly say that you have the contextual knowledge to critically analyze these papers you are citing?]
    Yes.

    [If you disagree, provide me with a study that has shown that gene duplication is nonrandom. If you don't, I will assume you have conceded this point.]

    Natural Selection does act as a filter, for example, genes that do not work do not get used. Life is mostly made up of hydrogen, carbon, oxygen and nitrogen and a few others, even if you were to pass all 100 or so elements through a filter and only select the above elements, you still wouldn't get a living organism because you need to arrange those elements into a specific pattern. Random objects acting in accord with natural law are still random. Random means one event has no bearing on the next event, or no planning, no intention. All random objects act according to natural law, so even if you add the law: that which does not work, will not get used, (which is nothing more than a tautology), you still get randomness, or absence of intention. It's not for nothing that NS + RM is called the BLIND watchmaker.

    [Further, what justification do you provide for your conclusion that gene duplication is the result of an intelligent designer? For a claim this big you will need a significant amount of evidence that unequivocably points to a designer.]

    Simple mathematics. If you see a sequence of DNA and if you do the math and you conclude that randomness cannot have accomplished it given the finiteness of time in our universe, then the only other possibility is intelligence.

    randomness: movement without planning
    intelligence: movement with planning

    Just take a look at the human body. You've 100 trillion cells, divided into 200 cell types, with about 25,000 polypeptide chains (though I wouldn't be surprised if there are a lot more than 25K) and a genome of 3.2 billion letters. You've got to use that genome to instruct which of the 25K polypeptide chains get used in which of the 200 different cell types for the 100 trillion cells. This is not something randomness can do. NS + RM cannot plan. You need planning in order to get those 100 trillion cells to coordinate.

    [First, the entire field of population genetics has mathematics as its foundation. Does this count? Why or why not?]

    First, population genetics was concerned with the frequency of alleles in populations. They didn't even start to try to figure out if NS could build genes until 2001 with the Stone, J. R., and G. A. Wray, 2001 article.(Rapid evolution of cis-regulatory sequences via local point mutations. Mol. Biol. Evol. 18: 1764–1770.)

    Second, right in Darwin's Dangerous Idea by D. Dennett, a work essentially dedicated to proving Darwinism, you have Dennett quoting Francis Crick as calling the whole field of population genetics a fraud.

    Third, no, I have not read Fisher, but I plan to. Have you read Douglas Axe?

    Fourth,
    1. You have not read a book by X
    2. Therefore, Darwinism is true

    Is not a logical argument.

    If you want to accept that as an argument then I can do it too:
    1. You have not read D Axe
    2. Therefore, Darwinism isn't true

    • [1. You have not read a book by X
      2. Therefore, Darwinism is true]
      Seriously? More like,
      1. The argument is standard and is well supported – see reference by X.
      2. If you wish to attack the argument, attack the evidence and arguments in reference above.

    • "Yes"

      I hypothesize that you do not. Let's investigate your arguments as a test of this hypothesis:

      "Random means one event has no bearing on the next event, or no planning, no intention"

      As has been already pointed out to you, that is not the definition of randomness. That is a definition of statistical independence. How exactly is it that you can understand the basics of population genetics without knowing this?

      "Simple mathematics. If you see a sequence of DNA and if you do the math and you conclude that randomness cannot have accomplished it given the finiteness of time in our universe, then the only other possibility is intelligence."

      This is both an argument from incredulity and a false dichotomy. Since you've "done the math", show it.

      "This is not something randomness can do"

      Correct. But it is something that evolutionary processes such as natural and sexual selection can do. How do you not know the difference, what with your basic understanding of biology? This is something that would be covered in the first week of any biology course.

      "First, population genetics was concerned with the frequency of alleles in populations"

      Evolution is defined as a change in allele frequencies in a population. What is your point? Again, how is it that you do not know this, given your claimed basic knowledge of biology and natural selection?

      You've claimed that you have a basic understanding of the fields mentioned above. Your posts in this thread indicate that this is not the case. Please give a list of any introductory peer-reviewed textbooks that you have read, even partially, in any of the fields of general biology, evolutionary biology, population genetics or mathematics. If you do not respond, I will assume you are lying.

      "Fourth,
      1. You have not read a book by X
      2. Therefore, Darwinism is true
      Is not a logical argument. "

      Correct. The problem is that nobody in this thread has made this argument, so this is another straw-man argument on your part. I have an idea. How about you pick any single argument given to you in this thread and attack it directly. Make a reasoned argument of your own, and back it up with references or at least a plausible hypothesis. As I've already stated, fallacious arguments are self-refuting.

  13. [Second, where in that paper does it state that they are hiring mathematicians to "underpin Darwinian theory"? From my reading, they are seeking mathematicians to formalize natural selection mathematically. I see no implication that they are trying to prove that natural selection is impossible, and even if they were, so what? What does that have to do with your argument? This sounds a lot like the "more and more" argument.]

    Let me quote the article again: The mainstream of mathematical population geneticists since about 1964 has emphatically rejected the claim that fitness is maximised. Ewens (2004) discusses an optimisation principle that is a generalisation of a Lyapunov function, but that optimisation is an analogy to help understand the dynamical system and where it will go next, and not about whether individuals in the population are maximising their fitness subject to physical, physiological and informational constraints. The early denial of optimisation has matured into a later acceptance, but of a kind of optimisation that is quite different from the one needed in behavioural ecology. There has been essentially no formal consideration of the kind of optimisation that emerges so naturally from verbal arguments such as those of Darwin (1859) and Dawkins (1976).

    It doesn't get more explicit than that.

    It also says: The successful applicants will work with Professors Alan Grafen and Charles Batty on an abstract mathematical project that underpins and develops modern Darwinian theory.

    It also uses the word damaging, let me give you a clue, damaging is not a positive word: mathematical population geneticists mainly deny that natural selection leads
    to optimization of any useful kind. This fifty-year old schism is intellectually damaging in
    itself, and has prevented improvements in our concept of what fitness is

    [We've already established that you do not know what a random variable is, and this statement shows that you are ignorant about the concept of probability as well. When someone says some random event has a probability of "1 in x", this means that there are x equally likely, independent events, and the event in question is 1 of those. What are the other 10^30,000 - 1 equally likely, independent events in your calculation?]

    The other equally likely events result in death.

    [Furthermore, where did the 10^30,000 come from? You can't just make up numbers like that arbitrarily and expect anyone to take your argument seriously.]

    Let's take the sense of smell in mice. That requires about 1200 genes. A typical gene in a mammal is about 400 aa long. How many aa is that? (1200* 400 = 480,000). Now, all of those aa have to be left-handed. So what are the odds of 480,000 all being left-handed? The odds of one aa being left-handed is about 50%. Well, just 2^1000 equal 10^301, to say nothing of 2^480,000. My computer won't calculate any higher than that, but I'm sure it's higher than 10^30,000. Then you have to factor the odds of forming a peptude bond, which is also 50%. You also have to calculate the odds the DNA in the non-coding region will successfully instruct when the proteins are to be turned on and off and we can't even do that part yet.

    ["there really is no such thing as a gene"

    Umm, ok. Since I can't find anything in a cursory literature search that concludes this, I take it it's yet unpublished and your Nobel prize is pending?]

    Have you ever heard of alternative splicing? It's not that there's one gene of 400 letters on the genome. The splicesome will cut up the introns and the exons of the DNA code and rearrange it to build new proteins. This is very important with the immune systems when the body has to produce about 10 billion different proteins so that one of them locks on to the foreign invader. Have you every tried to build 10 billion proteins with a genome of 3.2 billion letters? It's pretty hard.

    • The paragraph you cite demolishes your argument. Perhaps you hope that we are somehow functionally illiterate?

      And your arguments from incredulity get more laughable by the moment – where is the organism supposed to find right-handed amino acids? The probability of them being all left-handed, given that evolution is occurring on earth, is one, i.e. 100%. Moreover, there is no reason to assume up front that early variants of the genes in mice (or their ancestors) weren't functional, in their less developed form – death prior to reproduction (and complete lack of smell) are hardly guaranteed. How about a reference for those strong claims?

  14. ["the genome is simply so huge that the change of one letter, is immediately drowned out by all the other changes in the genome happening simultaneously"

    This makes no sense whatsoever. There are significant portions of the genome that are not under selection -- that is, mutations in these regions do not confer a selectional advantage nor disadvantage -- and most of the DNA sequence of functional genes can change with apparently no phenotypic effect, but to say that these changes are "drowned out" by all the other DNA in the genome is ludicrous. Either a mutation happens in a conserved region of the genome or it doesn't. If the former, most mutations would result in a selective disadvantage, and if the latter, they would not likely affect the fitness of the organism]

    " Either a mutation happens in a conserved region of the genome or it doesn't," you act as if one mutation builds an organ. You need a whole suite of aa to build an organ, not to mention you need instructions about when the genes need to be turned on and off. Just look at the bacterial flaggellum, it requires about 50 different proteins, each around 250 aa long.

    " What about DNA mutations in rRNA genes? Or tRNA? Those most definitely do not result in a change of a.a. sequence. For that matter, when you say it will take 10,000 mutations, how are you calculating this? Do you mean that the Hamming distance between the amino acid sequences of this protein in the two extant organisms in the study is 10,000?"

    50 genes, each with about 200 aa, 50 * 200 = 10,000. Those aa didn't just appear out of nowhere. They had to be duplicated from other genes or placed in there by viruses, then the genes had to be turned off, then it required an intelligence to mutate those genes until you have a working suite of genes that can form an organ. When the entire sequence is set up, that's when the genes get turned on.

    ["No you haven't. If you have show me again. The only math I see from you is what you just provided above. "

    If you have seen no math in evolutionary research then you have not read a single population genetics paper. I think this speaks for itself.]
    My whole post began when I quoted the Ryan Liu paper. You can't even read the posts of the people you're debating with.

    [There is no natural law that governs the order of DNA nucleotides because all nucleotide sequences are equally stable. "

    Other than this being a non sequitur argument, it is patently false that all nucleotide sequences are equally stable. A 5 second search came up with this: http://hmg.oxfordjournals.org/content/1/7/467.sho.... ]

    What I mean is that you can put any of the 4 DNA letters in any order and the laws of chemistry will allow them to remain there. Of course if you put them in the wrong order you won't get a functioning organism.

    ["Because if there not then you're just relying on mere luck to form an organ and you need a lot more mutations than 200 to form an organ. Just to build an organ you need anywhere from 50 to 1000 genes, moreover, not only do you need the genes, you need the non-coding regions of the genome to instruct when those genes get turned on and off. If you rely on randomness to come up with the right sequence for even just one 120 aa protein, then the odds of that are easily higher than 1 in 10^150. (there are only 10^80 particles in our universe)."

    Argument from personal incredulity. Come on, I can tell you possess intelligence, why not apply it rigorously? A fallacious argument is self-refuting. People in this thread have been providing researched, reasonable arguments in response to you, and all you've given in return is more fallacies.]

    You have misused the fallacy from incredulity. Those who commit the fallacy of incredulity do so when they posit no evidence for their incredulity. I have reason for my incredulity, namely there is not enough events in the history of our universe to overcome the odds. You're the one who is committing a fallacy not me.

    What you're saying is:

    1. It's possible
    2. Therefore, it happened

    Rational humans always base their reason on what they think is probable, no one makes life and death decisions based on what is merely possible. You're believing that Darwinian evolution can overcome such amazing odds not because you think it's probable, but only because it's possible. In other words, you don't believe the more probable explanation for no reason other than that you do not want to.

    • Your calculations of odds assume that all the proteins spontaneously popped into existence all at the same time and all in the same individual. You completely exclude any evolutionary mechanisms from your calculations and therefore you can't draw any conclusions about the probability that these structures could have evolved. If you want to draw conclusions about evolution, you need to include evolutionary mechanisms in your calculations. If you account for evolutionary mechanisms (i.e. gene frequencies changing within populations over time) then your calculated odds will shorten dramatically as I have already shown.

      Your calculations of changes in amino acid sequences are also spurious because you cannot infer mutation number, favourable or otherwise, from changes in amino acid sequences. In your calculations you do not account for mutations (or other genetic changes) that cause changes in more than one amino acid at a time. A single addition or deletion mutation, for example, can change one amino acid in a sequence or it can change tens to hundreds or more at a time. You also make no allowance for gene duplication which doubles amino acid number in a single change. You also make no allowance for intra-gene duplication which changes amino acid number and can change identity. In the study you cited on the bacterial flagella, mutation, gene duplication and intra-gene duplication were all operating to change amino acid identity and number. You must take these into account in your calculations or whatever number you calculate is meaningless.

      It is wrong to assert that only one set of all possible mutations will result in a viable organism. Mutations have a spectrum of effects on fitness from death through negligible to strongly enhancing. Remember that natural selection works on variation in fitness. One reason variation in fitness arises is because there is variation among individuals in the heritable genetic information passed to them from their parents. Remember also that to be selected for an individual does not need to be perfectly adapted, it just needs to have high fitness relative to other individuals in the population. Thus a poorly functioning flagellum can be favoured if it functions better than most others.

      If you want to look at some mathematics that includes evolutionary mechanisms in its calculations then you should look to the the literature on population genetics. You can look at the Wikipedia page on the Price Equation as a place to start.

  15. flawedprefect

    @bobbyllew smith – it baffles me that you have so much to write, yet choose to argue with a handful of commenters, than go and write a paper, submit it to a journal and see if your arguments hold any merit among peer review. Who are you trying to convince? What do you hope to achieve reaching (with all respect to Jack) such a small audience who’s only aim is to argue with you, and (me included) won’t be convinced and/or moved to do anything about it without evidence, or being shown work you’ve gone out and done to collect evidence to support your claim?

    It seems an awful waste of time, IMO, but hey: it’s your life. Wish I believed in an afterlife, but sadly I don’t, so every day is precious. Gonna go take a crap, now. And enjoy it.

  16. [...] while 3 is from one of Thomas’ own articles, which is surprising as it seems to be related to Junk DNA, a common subject in the ID community at the moment, for some reason. There are therefore plenty of [...]

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