Uncommon Descent Serving The Intelligent Design Community

When I’m wrong

Share
Facebook
Twitter
LinkedIn
Flipboard
Print
Email

In a recent post in which I questioned the claim that over 100 mutations get fixed in the human population in every generation, I remarked, “I’m happy to be proved wrong.” Guess what? I meant it. After weighing the evidence presented on both sides, I’ve decided that there are no good mathematical arguments showing that 130 mutations couldn’t have been fixed in each generation of the human lineage, over the past five million years. Although the equations of population genetics are based on assumptions, these assumptions have been tested – and validated – for bacteria. And while the mutation rate per individual per generation is five orders of magnitude greater for human beings than for bacteria, the fact that the human genome is about 1,000 times larger than that of a bacterium, coupled with the fact that there are multiple cell divisions per generation in animals, explains why humans would have a much higher mutation rate. Of course, arguments from extrapolation aren’t always valid, and for all I know, there might be any number of reasons why fixation rates of 100 per generation for human beings (as predicted by the equations of population genetics) are biologically implausible. But the onus is clearly on the skeptic to explain why we shouldn’t believe the claim that 100 mutations are fixed in the human population in every generation. Dr. Kozulic (who is a well-published biochemist) is a prominent skeptic; and in my last post, Branko Kozulic responds to Professor Moran, I gave him the opportunity to state his case. Since Dr. Kozulic is from Croatia, I also assisted him in presenting his argument as clearly as possible, in English. After sifting through the replies by wd400 and Nick Matzke, I have come to the conclusion that the arguments that Dr. Kozulic and I presented in our post failed to establish that a fixation rate of 100 per generation for human beings, even during the Paleolithic era, would be infeasible. To uninitiated laypeople like myself, such a high rate of fixation for a very thinly scattered Stone Age population sounds highly counter-intuitive at first sight, but that does not make it untrue. After weighing the arguments, I now think that the neutral theory of evolution can account for the number of mutations fixed in the human population over the last five million years (roughly 22.4 million).

My concession on this point does not mean that I think the neutral theory of evolution can account for the pattern of fixation events observed in the human lineage, let alone the existence of orphan genes. Those are separate issues, and should be addressed as such.

After reading Professor Moran’s recent post, On being “outed” as a closet Darwinist, I would like to make it clear that I am fully aware that Moran publicly disagrees with many of Darwin’s ideas. In our previous post, Dr. Kozulic and I characterized Professor Moran as a “Darwinist” in one important respect only, as we expressly stated. To illustrate what I mean, I’d like to quote from his 2006 essay, Macroevolution:

The Creationists would have us believe there is some magical barrier separating selection and drift within a species from the evolution of new species and new characteristics. Not only is this imagined barrier invisible to most scientists but, in addition, there is abundant evidence that no such barrier exists. We have numerous examples that show how diverse species are connected by a long series of genetic changes.

If Professor Moran can think of a handy label to describe someone who holds such a view, then I shall gladly use it in future, when referring to him. “Gradualist” is a term that comes to mind, but I don’t think Professor Moran would appreciate that label, either. Moran also rejects the view that microevolution is sufficient to account for macroevolution, as his essay makes clear.

Professor Moran and I disagree on many things, and I’m sure we’ll have many lively exchanges in the future, but it would be downright churlish of me not to acknowledge that my attempts to show that the neutral theory could not account for 22.4 million mutations arising in the human lineage over the last five million years have failed. I also wish to state that I had no intention of giving any offense to Professor Moran in our exchange of views, and that I have always striven to remain as polite as possible, while publicly disagreeing with him. The next time I’m dining out, I shall order a glass of red wine and silently toast him.

Before I finish this post, I’d like to quote a passage from Dr. Kozulic’s 2011 paper, Proteins and Genes, Singletons and Species – a paper which I have cited on numerous occasions, on Uncommon Descent:

If just 200 unique proteins are present in each species, the probability of their simultaneous appearance is one against at least 104,000. [The] Probabilistic resources of our universe are much, much smaller; they allow for a maximum of 10149 events [158] and thus could account for a one-time simultaneous appearance of at most 7 unique proteins. The alternative, a sequential appearance of singletons, would require that the descendants of one family live through hundreds of “macromolecular miracles” to become a new species – again a scenario of exceedingly low probability. Therefore, now one can say that each species is a result of a Biological Big Bang; to reserve that term just for the first living organism [21] is not justified anymore.

The fallacy in the logic here should now be apparent. There is no reason to suppose that one singleton has to be fixed in the population before another one can be. The paper has therefore failed to demonstrate that speciation is an event that lies beyond the reach of chance.

An excellent case can be made that not only the emergence of life, but also key events in the history of life such as the Cambrian explosion, in which 30 novel body types emerged over a relatively short span of 20 million years, were events whose occurrence lies far beyond the reach of chance. Intelligent Design is on very strong ground here. However, I now believe that the argument that speciation itself is equivalent to a Biological Big Bang is a much weaker one. The origin of orphan genes remains an ongoing scientific mystery, but we should be wary of making a mountain out of a molehill. The imputation of design in this case would require much stronger supporting calculations than we have seen to date, and the mathematics contained in these calculations also needs to be very carefully scrutinized. During this time of scrutiny, we must be our own harshest critics. In a 2013 post on Uncommon Descent, I suggested that the “edge of evolution” may lie at the species level, using the definition of “species” employed in Dr. Kozulic’s paper. It appears that I spoke too soon. I think it is fair to say that the question of where the edge of evolution lies has now been thrown open again.

Comments
Paul: I am very glad too :) Sometimes I feel real compassion for our "adversaries". It must be really bad to have to defend something which cannot be defended. I say that seriously, I am not joking.gpuccio
April 18, 2014
April
04
Apr
18
18
2014
03:17 PM
3
03
17
PM
PDT
There is an important philosophical point here. Remember that the function of natural selection is to explain the appearance of design in living organisms. That appearance of design is strong enough to inspire Richard Dawkins to say, "Biology is the study of complicated things that give the appearance of having been designed for a purpose." So any system that does not invoke a designer has to explain away that appearance of design. Neutral mutations cannot do that, as is commonly recognized. So we have to have positive selection if the BW thesis is to be supported. But as P. Z. Meyers points out, the scientific evidence strongly supports the idea that evolution is overwhelmingly neutral (And Sanford points out that it is actually slightly deleterious). So there is no good explanation for the appearance of design. The only way to make a case for evolution is to say that we have the mutations necessary because of neutral mutations, and that they are also selected so as to design new ORFan genes, or to deny that such genes exist. I'm glad I don't have to argue on that side. :)Paul Giem
April 18, 2014
April
04
Apr
18
18
2014
03:58 AM
3
03
58
AM
PDT
VJ: Let's say that mammals originated about 300 million years ago. Let's say that in humans there are 130 mutations per genome per replication. Let's take that number for all mammals, just as an approximation. I have no idea what the mean generation time for mammals could be. Let's take 1 year. I am not sure how many mammals there could be on the earth. From some internet gross evaluations, let's say 10^12. So, let's compute the higher threshold for new states reach since mammals appeared on earth: 3*10^8 (number of years) * 1 (mean generation time) * 130 (mutations per generation per genome) * 10^12 (population size) = 3.9e22 That is about 20 orders of magnitude smaller than the states tested in my bacterial model. So, if the appearance of one new functional protein of average functional complexity was utterly unlikely in the bacterial model (10e-66), here, in the whole span of mamal evolution, we are at about 10e-89 for one protein. Does this give some idea of "how to apply these calculations to the human case"? Regarding the paper, it is just another example in favor of my scenario: a) New genes appear at a greater rate than suspected, even in humans. b) Many of them are both transcribed and translated c) Many of them are probably functional, and their function could be very refined (see preferential expression of some of them in the testis and in the brain) d) Many of them seem to derive from non coding DNA in precursor species, where they are not translated and almost certainly they are not functional. e) Nothing of that can be explained by a traditional darwinian scenario, neither by neutral mutations nor by NS. f) These are clear examples of design. The design starts in advance, and is completed if and when the desired effector is necessary. However, I still believe that new protein coding genes, even if relatively abundant, cannot explain the huge phenotypic differences between chimps and humans. The explanation must certainly reside in the elusive regulatory components.gpuccio
April 15, 2014
April
04
Apr
15
15
2014
01:55 PM
1
01
55
PM
PDT
Hi gpuccio, Thanks very much for the clarifications. I think we can agree that the de novo appearance of new proteins in bacteria would have been an event beyond the reach of chance, and thus achievable only as a result of Intelligent Design. The question I'm currently wrestling with is how to apply these calculations to the human case. I'd be interested to hear your opinions of the following paper: http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1002379#pgen-1002379-g002 "De Novo Origin of Human Protein-Coding Genes" by Dong-Dong Wu, David M. Irwin, Ya-Ping Zhang, in PLoS Genetics. Published: November 10, 2011. DOI: 10.1371/journal.pgen.1002379. Thoughts?vjtorley
April 15, 2014
April
04
Apr
15
15
2014
10:37 AM
10
10
37
AM
PDT
VJ: Please, look also at this post of mine (#56) in the thread: https://uncommondescent.com/news/1177-human-orphan-genes-removed-by-evolutionists-from-databases/#comment-496408 And please, consider the important article I mention there: http://genome.cshlp.org/content/19/10/1752.full.pdfgpuccio
April 14, 2014
April
04
Apr
14
14
2014
10:33 PM
10
10
33
PM
PDT
VJ: I have to make a correction in the computations I gave. That's because I considered the higher tail, but I made a mistake in introducing the data in the program. The probability for 3 proteins is 6.550667e-198, and not 5.568067e-264 as I had given. That's the probability for 4 proteins. The probability for one protein is 3.4e-66, and not 5.78e-132, which is the probability for 2 proteins. The consclusions do not change at all, but I apologize for the error.gpuccio
April 14, 2014
April
04
Apr
14
14
2014
04:45 PM
4
04
45
PM
PDT
VJ: Here are the answers: We must start with the functional units that are completely and certainly unrelated, at all levels, sequence, structure and function. The best option for that is to consider protein superfamilies, and that is the model I have always defended here. Now, I am not particularly interested in how many new basic protein domains (superfamilies) a particular species exhibits. I usually refer to the appearance of a new superfamily as a moment of certain design intervention. At present, there are a little more than 2000 superfamilies listed in SCOP. The existing literature tells us that about half of them were already present in LUCA. All the others appeared at various times, in various phyla and species, at a slowing rate, up to mammals (included). I refer to superfamilies to be sure, completely sure, that the whole functional complexity has to be explained, and that no related precursor is known at the time of first appearance of a new superfamily. The evolution of proteins inside a superfamily or a family is less extreme, because some homology to similar precursors can be found. I am sure that in most cases design can be inferred even in those cases, but why should we start with the more difficult scenario, when even one new protein superfamily is completely unexplainable in darwinian terms? You mentioned 200 proteins in a new species. I reduced that to 3 unrelated new proteins. If the new proteins can be matched to some homologue already existing in the precursor, then we have to compute the functional information of the transition from one protein to the new one. Durston's method can do that. However, it is more simple to reason in terms of even one new superfamily, and relate to the list of 35 protein families for which Durston has already computed functional complexity, as an example. The second argument you give is very popular among darwinists. It's what I call the argument of "any possible function". It goes more or less this way: Evolution is not looking for a specific target. Indeed, any possible function that emerges from a random walk can be used. That is completely wrong, for many reasons: a) In a complex system, like a prokaryote, new functions can be useful only if well integrated with what already exists. The more complex a system, the less likely it is that generic functions can have a role in it. Indeed, I believe that it is extremely unlikely that one single new functional protein may be of any help even in a prokaryote, except in very selected cases. In the general case, a certain number of new proteins will be needed, and adjustements will be necessary to what is already there. IOWs, the concept of irreducible complexity comes in. So, when I compute only the functional complexity of one or a few isolated proteins, I am really being generous with the enemy. b) The new function, however complex it is, must not only do something in the cell. It must give a reproductive advantage to the cell. Otherwise, it has no hope to be fixed. You will say: but your model was about neutral evolution, not about NS. That's true. My model is about neutral evolution of a new function, but it assumes that the new function, however unlikely it is, will be recognized, expanded and fixed by ND once it has been achieved by neutral mutations. Otherwise, it will be only a transitory state like any other, designed to remain confined to the cellular clone where it originated, and to be quickly degraded by new mutations. IOWs, even if neutral mutations were able to generate a new functional protein (and they are not), that protein should be functional enough to give a reproductive advantage to the existing cell, otherwise it could never emerge. OK, it could be fixed by drift, but that would add huge new improbabilities to the original computation of how likely it is to simply reach that sequence. Now, can you imagine how many new proteins, however functional, can give a reproductive advantage to an existing cell? IOWs, if we introduced in an existing bacterium, one at a time, one gene for one protein of the 2000 existing superfamilies, in how many cases would that immediately confer a reproductive advantage to the cell? c) Finally, even we we ignored the two above objections, and if we admitted that any of the existing 2000 superfamilies could give a reproductive advantage, if found, that would not really change much the computation. Our global target space would just be the sum of the functional spaces of the existing 2000 superfamilies. That would give an advantage of a few orders of magnitude. Do you think that would count? No. We are talking about improbabilities of hundreds of orders of magnitude here, just for 3 medium proteins. Of course, it would be a little bit easier to find those superfamilies which are simpler, let's say with domains definitely shorter than 100 AAs, but even for them the improbabilities are huge. And what about the others? What about proteins of 300, 500 or 1000 AAs? All unrelated? Let's talk a minute of the edge of evolution. IOWs, about how much functional variation RV + NS can really do in the real world. Behe has put it above two AAs, in his very good book, and considering very good arguments from observable scenarios. Axe, with different experimental consideration, puts it at about 5 AAs. I believe that is probably very true. Dembski, with very general considerations, proposes 500 bits (about 116 AAs) as universal probability bound. I have proposed 150 bits (about 35 AAs) starting from a model like the one I posted here. You mention 1:10^70 as the number of folding proteins, from Axe again, I believe. That is probably true. But remember, folding is not all. A protein must not only fold to be visible to NS. It must confer a reproductive advantage in a definite environment. I often quote the following paper: "Experimental Rugged Fitness Landscape in Protein Sequence Space" http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0000096 which experiments with a mutated protein in a phage, trying to find the original wild type sequence which confers full infectivity. Well, here RV and NS are acting at their most, starting from a random library of peptide sequences, in a very favorable context (the function is maintained, even if at low levels, so NS can act just from the beginning). I always quote the final conclusion of the authors: "The question remains regarding how large a population is required to reach the fitness of the wild-type phage. The relative fitness of the wild-type phage, or rather the native D2 domain, is almost equivalent to the global peak of the fitness landscape. By extrapolation, we estimated that adaptive walking requires a library size of 10^70 with 35 substitutions to reach comparable fitness." Well, 10^70 is the order of magnitude proposed by Axe for folding proteins, and 35 AAs is my "universal biological bound". Coincidences? Probably, but what it means is that we are on the right way, and that our intuitions about the functional space of proteins are quite right. Durston has computed functional information for 35 different protein families. Only six of them have functional complexity below 150 bits (my biological bound). All of them are very short peptides (33 -55 AAs). Insulin (65 AAs) already has a functional complexity of 156 bits. The biggest protein in the list, Paramyx RNA Pol, has a functional complexity of 1886 bits. In my simple model, even if only one new unrelated protein of the median functional complexity of 357 bits, were to be found to confer some definite advantage to a new species, the probability of that single event in 4 billion years, in the whole planet, would still be 5.78e-132. IOWs, not a single new protein superfamily of median complexity could ever be generated on our planet by neutral mutations alone. And no functional precursors to superfamilies have ever been shown to exist, so the role of NS in that scenario is nil.gpuccio
April 14, 2014
April
04
Apr
14
14
2014
03:31 PM
3
03
31
PM
PDT
Hi gpuccio, I'd just like to ask a couple of questions about your model. I note that your bacterial mutation rate of 0.003 mutations per genome per generation agrees with the figure given in Wikipedia and in Nature magazine (see http://www.nature.com/nrmicro/journal/v11/n5/box/nrmicro3003_BX1.html ). So far so good. Your next critical assumption is that the new species of bacterium is characterized by three new proteins which are completely unrelated to existing proteins, chemically speaking. That might be a bit strong. What if we relaxed the assumption a little, and assumed that the three new proteins each had a 50% similarity to some existing protein? Finally, your proof correctly calculates the odds of Nature hitting upon three particular proteins within the time available. But it doesn't have to be those three particular proteins, if we want to get a new species of bacterium. It can be any three new proteins, so long as they're biologically compatible with the existing ones. (Not being a biologist, I'd have no idea how you'd calculate the proportion of new proteins that are biologically compatible with the existing set. Kirk Durston might have some good ideas on that point.) What does your model look like if you incorporate these more relaxed assumptions?vjtorley
April 14, 2014
April
04
Apr
14
14
2014
02:08 PM
2
02
08
PM
PDT
Salvador:
Mung makes an innuendo that I never mentioned Rupe and Sanford to VJTorley.
Liar. Repent.Mung
April 14, 2014
April
04
Apr
14
14
2014
12:30 AM
12
12
30
AM
PDT
Upright BiPed, Salvador refuses to argue with me.Mung
April 14, 2014
April
04
Apr
14
14
2014
12:15 AM
12
12
15
AM
PDT
Sal, Refrain from invoking my name in your arguments with Mung.Upright BiPed
April 13, 2014
April
04
Apr
13
13
2014
08:55 PM
8
08
55
PM
PDT
Salvador, you can't debate either myself or Upright Biped. You delete my posts from your threads. Pat yourself your backs.Mung
April 13, 2014
April
04
Apr
13
13
2014
07:37 PM
7
07
37
PM
PDT
Salvador Cardoza:
What I would have done different over the course of these discussions when I provided a link my essay on Rupe and Sanford, was to have specifically highlighted this discovery of the Mendel team:
In this thread where did you provided a link to that essay? I can’t find it.
ROTFL! That's not the only thread involved in this discussion. My mention of NEUTRAL theory to Dr. Torley in a comment on March 4, 2014 probably had some influence, and it was in that comment that I linked to Rupe and Sanford's work. Of course you didn't find mention of it, you're looking in the wrong thread (the one dated March 30, 2014). Mung makes an innuendo that I never mentioned Rupe and Sanford to VJTorley. This whole discussion began possibly because of a comment that mentioned Rupe and Sanford Haldane's Dilemma comment
March 4, 2014 at 4:04 pm VJTorley, Something very important, Larry Moran isn’t using natural selection as the mechanism of the fixation rate for evolution, he is using NEUTRAL EVOLUTION. See: IF not rupe or Sanford would you believe Wiki Compare what I said with what Moran said
says the rate of new mutations is the rate at which new mutations become features of every member of the population (a process called fixation).
and that agrees with Moran
This corresponds to a substitution rate (fixation) of 121 mutations per generation and that’s very close to the mutation rate as predicted by evolutionary theory.
Mung fails yet again to discredit me despite his creepy stalking vendetta behaviors. What's the matter Mung, having to grasp at straws since you have nothing substantive? :-) You're right down there with Upright Biped, casting insults as if I had orchestrated something against my friend VJ Torley. Baloney on both you guys. Find something better to do Mung than pursuing your vendetta against me. It makes you say stupid things.scordova
April 13, 2014
April
04
Apr
13
13
2014
11:45 AM
11
11
45
AM
PDT
Barb, if you are interested, Johanan Raatz has just loaded a new video in response to an atheistic physicist who challenged him: Martymer81, Quantum Non-Realism, AND Magic Powers!! :D - video https://www.youtube.com/watch?v=cpw8PieSSg8bornagain77
April 13, 2014
April
04
Apr
13
13
2014
05:10 AM
5
05
10
AM
PDT
Hi gpuccio, I greatly appreciate the work you've put into your model. I'm a little busy at the moment, but I'll get back to you with some comments in a few hours. Thanks again.vjtorley
April 12, 2014
April
04
Apr
12
12
2014
10:28 PM
10
10
28
PM
PDT
Hi Sal, Much appreciated. Thank you.vjtorley
April 12, 2014
April
04
Apr
12
12
2014
10:26 PM
10
10
26
PM
PDT
Here you go VJ, especially for you: Neutral theory and non-Darwinian for newbies, Part 1.scordova
April 12, 2014
April
04
Apr
12
12
2014
10:18 PM
10
10
18
PM
PDT
IMHO, the mathematics of fixation includes a significant flaw. It assumes that everyone on Earth is equally likely to produce offspring from anyone else on Earth. This is demonstrably false. Isolation of populations is one requirement for speciation. Even imperfect isolation will protect variations and mutations from fixation over time. -QQuerius
April 12, 2014
April
04
Apr
12
12
2014
08:11 PM
8
08
11
PM
PDT
Is it the same foreign-language school you've been going to as Cornelius Hunter, GP and BA77? They don't look like Cyrillic script to me, so I'd take a stab at Croation. Bit puzzled by the occasional monosyllabic, Anglo-Saxon word somebody's mischievously interpolated, though. The penalty of understanding zilch about the nitty-gritty of the empirical nub of science, I suppose. Still, it tickles the heck out of me when I see such densely esoteric disquisitions. Keep up the good work, both of you (and CH). Just the sight of it, I find beautiful to look at.Axel
April 12, 2014
April
04
Apr
12
12
2014
03:37 PM
3
03
37
PM
PDT
Barb, here is his response:
What exists prior to space-time, even if describable by physics, is not what the materialists assume it to be: And the Spirit of God was hovering over the waters/wavefunctions (of chaos/probability)." :) They don't realize the implications of Hempel's Dilemma here on the blurring of the line between physics and metaphysics. "The question is: does the Wheeler-DeWitt equation allow this? “We prove that once a small true vacuum bubble is created, it has the chance to expand exponentially,” say Dongshan and co." Hempel's dilemma is very much relevant here! The Wheeler-DeWitt equation specifies a wave-function of the universe, BUT on a materialist paradigm there is something they do not know about the wave-function of the universe that becomes apparent on an idealist understanding: https://www.youtube.com/watch?v=sTnnZNNbrUc This applies Orch-OR to the WDW Equ, which I think needs upgrading, but the same metaphysical implications are valid on digital physics.
bornagain77
April 12, 2014
April
04
Apr
12
12
2014
02:16 PM
2
02
16
PM
PDT
VJ at #47: There is no problem about the simultaneous or sequential appearance of new proteins. Just follow me a little bit. a) "Simultaneous" obviously does not mean "in one attempt". What we have to consider is the whole system, which is made of: a1) a population size (a number of replicators) a2) a mean replication time a3) a time span (the time available for the new "species", or whatever, to appear), IOWs for the transition from A (the precursor) to B (the new thing) a4) a mutation rate a5) the number of new proteins that characterizes the new state (B) versus A a6) the probability for each new protein to arise in a random system, in one attempt b) Given those numbers, we can make a few easy computations c) I will assume an extremely generous model. c1) Out population is the whole prokaryotic population on our planet. I will estimate it at 5*10^30 individuals (I have found that on the internet) c2) I assume a mean replication time of one division every 30 minutes c3) I assume a time span of 4 billion years (2.1*10^15 minutes) c4) I assume a mutation rate of 0.003 mutations per genome per generation (from internet, again) c5) I assume that B is characterized, versus A, by 3 new proteins, completely unrelated at sequence level with all the proteins in A, and unrelated one with the others c6) I assume the same functional complexity for each of the 3 proteins, of 357 bits (Fits), which is the median value for the 35 protein families evaluated in Durston's paper. Multiplying c1 by c2 by c3 by c4, we get the total number of possible mutations in our system in the time span of 4 billion years. The result, with those numbers, is 1.0512*10^42. That is a higher threshold for the total number of individual new states that can be reached in our system in the time span (if each mutation gives a new state). OK? Now, each of our 3 functional proteins has a probability of 1:2^357 of being found in one attempt (one new state tested). That is 1:(3.4*10^108). Now, using the binomial distribution, it is easy to compute the probability of having 3 successful results in 1.0512*10^42 attempts, when the probability of success in one attempt is 1:(3.4*10^108). The result is: 5.568067e-264 That is the probability of finding our 3 new functional proteins in our system, in all the time span, with all the reproductions and mutations possible in that system. Obviously, I am considering the system as random, with uniform probability distribution. I am not considering any intervention of NS, in any sense, so this is a computation for the powers of neutral variation. As already said, genetic drift is irrelevant in that reasoning, because we are already considering all the possible states that can be reached in the system. I am fully available to discuss any aspect of this model.gpuccio
April 12, 2014
April
04
Apr
12
12
2014
12:10 PM
12
12
10
PM
PDT
Timeus (42) . I have noticed that myself with JLAFAN1 He has said on numerous occasions that he won't accept something unless it is with a certain brand of Christian belief. You hit the nail, right on the head . He ignores all the great evidences for God's existence and when a tiny breadcrumb is brought up by atheists against Christianity , no matter how bad the odds for it being true automatically registers in his mind as all Christianity not being true . We have discussed the shroud of turin for many months and despite the massive evidence for authenticity one article comes out by an amateur scientist claiming that he can replicate the shroud and JLAFAN automatically blows up and enters the "this proves Christianity wrong " Despite the fact that this scientist has been challenged to do it and chickens out saying he doesn't feel like it lolololololololo. JLAFAN's mind has been conditioned as you said to get clear black and white answers. This also flies against the face of what Christ tells us in the bible , that there has to be some faith involved here in order for anyone to follow him. He didn't tell us to through our brains out the window, but he also didn't tell us to throigh our faith out the window like Jlafan has done. What he doesn't understand is that the fundamentalism he used to practice Was never true Christianity in the first place.wallstreeter43
April 12, 2014
April
04
Apr
12
12
2014
12:00 PM
12
12
00
PM
PDT
Hi Sal, Thank you for your posts. I’m very interested in your models of the neutral theory.
And thank you again. I'd have been in the doghouse with other IDists again if it weren't for you posting this discussion and supporting some of my claims.
I can’t claim to be able to comment on them in any detail, as I haven’t studied the theory in the same depth as you have, but the overall approach you’re taking, of showing that too may harmful mutations would eventually build up over the course of time, sounds very promising. By the way, what do you recommend in the way of good online resources for studying the neutral theory, for laypeople like myself?
Actually there are no really good resources for the layman, and my posts at UD have been an attempt to help develop such material for consumption in the public domain for free. Nick, WD400, Gordon Davisson, Joe Felsenstein, Larry Moran, Allen MacNeill and so many others have helped me get some of my educational ideas "peer reviewed" over the net. I'm now at the point of writing the ideas up, and you'll get to see them publicly peer reviewed, and if there are errors we all can work at cleaning them up. For example, I just threw out a trial balloon here to see if any one would pounce on it:
Kimura’s second result was that if the mutation is slightly deleterious according to S less than 4ne Then 50% of these deleterious mutations would fix in the population.
Our "peers" didn't object, so I suppose the claim is good enough to move forward with for now. They know of course if they complain, I'll simply ask, "then what proportion of bad will get fixed, tell me the percentage?" Of course, I think they realize there isn't much way of getting out of it, it's like me asking, "so how badly did Darwin beat the puppy?" Whatever figure they give won't be a figure that is supportive of mindless evolution. I'll post some of the discussions at UD and CEU. The CEU forum is a more formal forum for scholarly discussion rather than advocacy (which blogs tend to be). So to answer your question, I'll be writing some posts with you as the primary audience in mind and maybe college level students as well. I hope we can dialogue in the comment section so as to help me articulate the case with as much clarity and simplicity as possible.scordova
April 12, 2014
April
04
Apr
12
12
2014
11:03 AM
11
11
03
AM
PDT
Nick,
after several days of epic confusion, aspersions being cast at the evolutionists trying to point out the errors, and even at Sal Cordova!
No kidding! If VJ didn't step in, I'd be in the dog house again as the ID turncoat. Now I know what it's like to be as "loved" as Nick at UD. :-) Much as I hated taking on your side of the question, Nick, and being against the claims of one of my own beloved associates here at UD, I felt I would be doing VJ a disservice by not saying something. Well, we're all on the same page now pretty much at least about the rate of fixation relative to the rate of mutation, at least in terms of an abstract mathematical theory. However, I take VJ's side that Kimura's theory fails as functional theory for the evolution of complexity. To the rest of the readers: Perhaps to alleviate confusion, I'll use Kimura/Nei to emphasize the mindless variety of neutral theory that attempts to explain the deep past vs. ReMine/Sanford neutral theory that merely asserts the general absence of selection in the wild. ReMine/Sanford agrees with Kimura/Nei that selection is generally not working on most of the genome, but it would be wrong to say ReMine/Sanford are really neutral evolutionists since they are clearly creationists. The fact that neutral and nearly neutrals get fixed at a high rate is devastating to anti-teleological versions of evolutionary theory. It shows the opposite of what Darwin claimed. Real evolution keeps losing the good, and adding up the bad. It is as simple as this: if the ratio of dysfunctional to functional mutations is 10 to 1 (or whatever, just as long as dysfunctional is higher), and most fixation (what is made permanent) has little to do with selection but just random chance, where does this lead? Not to more coordinated and integrated IC systems. There is abundant evidence evolution destroys IC in the wild. A consequence of Kimura/Nei is we should all be dead 100 times over (to quote Kondrashov), but we obviously are not dead, so I don't think whatever "fixed" our genes was due to random mutations getting fixed by random events. Kimura's claim, though mathematically feasible as affirmed also by Mendel's accountant, utterly fails in terms of being functionally feasible. Mendel's accountant affirmed Kimura's results, but connected the dots in ways Kimura himself didn't see coming. Kimura's "2nd result" pretty much demolished the implicit hypothesis of increasing complexity claimed by Darwin and Dawkins. The complexity of organisms today indicates the mode of evolution that created complexity was not according to chance mechanisms of Kimura/Nei neutral theory. And we know if something is not by law and chance, it likely to be designed.scordova
April 12, 2014
April
04
Apr
12
12
2014
10:42 AM
10
10
42
AM
PDT
I don’t think anyone could credibly describe Dr. Douglas Axe as an incompetent biologist. You mean Douglas "protein corc-oduck" Axe - i think it's probably possible. As to credit where it's due - given these posts, Kozulic wouldn't be due credits for an undergrad genetics course. He might be good at what he does, but he's demonstrated himself to be all at sea (and extraordinarily arrogant) when it comes to pop. gen.wd400
April 12, 2014
April
04
Apr
12
12
2014
10:09 AM
10
10
09
AM
PDT
Hi Nick, I have previously thanked you for making the effort to educate people on this thread about population genetics. That is commendable. I do feel, however, that you're over-generalizing when you complain about "the general incompetence of the biology arguments of IDists." I don't think anyone could credibly describe Dr. Douglas Axe as an incompetent biologist. If you'd care to debate him, go ahead. Personally, I think you'd come off second best. Dr. Kozulic can speak for himself, and I'm quite sure he'd be very happy to debate you in a public forum on the topic of fixation. May I remind you also that whatever the merits of his views on population genetics, he is a well-published biochemist. Give credit where credit's due, I say.vjtorley
April 12, 2014
April
04
Apr
12
12
2014
09:20 AM
9
09
20
AM
PDT
Hi Sal, Thank you for your posts. I'm very interested in your models of the neutral theory. I can't claim to be able to comment on them in any detail, as I haven't studied the theory in the same depth as you have, but the overall approach you're taking, of showing that too may harmful mutations would eventually build up over the course of time, sounds very promising. By the way, what do you recommend in the way of good online resources for studying the neutral theory, for laypeople like myself?vjtorley
April 12, 2014
April
04
Apr
12
12
2014
09:09 AM
9
09
09
AM
PDT
NickMatzke_UD, I find it strange that you would think it a victory for Darwinian thought when no empirical evidence whatsoever was presented to prove unguided material processes can produce functional information. In fact the only admission on Dr. Torley's part that I can see is that he finds Darwinian conjectures for the generation of functional information to be somewhat less impossible than he thought so before. But an argument for a theory based on the premise of 'you have not proved my theory absolutely impossible therefore it must be true' is not a scientific argument in the first place! If fact such an argument is an completely absurd form of argument as far as science is concerned:
Darwinism Not Proved (Absolutely) Impossible Therefore Its True - Alvin Plantinga http://www.metacafe.com/watch/10285716/
Of related note, Matzke has been shown to use the dishonest practice of 'literature bluffing' here:
Calling Nick Matzke's literature bluff on molecular machines - DonaldM UD blogger - April 2013 Excerpt: So now, 10 years later in 2006 Matzke and Pallen come along with this review article. The interesting thing about this article is that, despite all the hand waving claims about all these dozens if not hundreds of peer reviewed research studies showing how evolution built a flagellum, Matzke and Pallen didn’t have a single such reference in their bibliography. Nor did they reference any such study in the article. Rather, the article went into great lengths to explain how a researcher might go about conducting a study to show how evolution could have produced the system. Well, if all those articles and studies were already there, why not just point them all out? In shorty, the entire article was a tacit admission that Behe had been right all along. Fast forward to now and Andre’s question directed to Matzke. We’re now some 17 years after Behe’s book came out where he made that famous claim. And, no surprise, there still is not a single peer reviewed research study that provides the Darwinian explanation for a bacterial flagellum (or any of the other irreducibly complex biological systems Behe mentioned in the book). We’re almost 7 years after the Matzke & Pallen article. So where are all these research studies? There’s been ample time for someone to do something in this regard. Matzke will not answer the question because there is no answer he can give…no peer reviewed research study he can reference, other than the usual literature bluffing he’s done in the past. https://uncommondescent.com/irreducible-complexity/andre-asks-an-excellent-question-regarding-dna-as-a-part-of-an-in-cell-irreducibly-complex-communication-system/#comment-453291
And he was also exposed here:
Hopeless Matzke -David Berlinski & Tyler Hampton August 18, 2013 http://www.evolutionnews.org/2013/08/hopeless_matzke075631.html
Matzke was also heavily involved in the theatrical literature bluff(s) at the Dover Trail as well he was recently involved in a concerted effort to censor publication of ID friendly material (details upon request). Thus Matzke, IMHO, (from what little I know of the man) has repeatedly shown himself to be a dogmatist who is willing to distort anything and everything in order to keep his preferred Darwinian worldview from being threatened. i.e. He could could care less about investigating whether Darwinian evolution is actually true or not.bornagain77
April 12, 2014
April
04
Apr
12
12
2014
08:53 AM
8
08
53
AM
PDT
The main problem scientists have with ID isn’t about atheism/theism or whatever. It’s about the general incompetence of the biology arguments of IDists.
This is a rather stupid comment. Apparently some people here have wrestled with one aspect of evolution, originally came to a wrong conclusion, and then retracted. This sounds like honest debate. Also it is not reflective of ID in general since most of the major players in ID rarely if ever comment here. Also the topic itself has not been shown to amount to much by anyone. Maybe you could address why the neutral theory explains a large percentage of the evolution debate. From what I gather it is just a minor side issue. But I would like to be proven otherwise. That would be very helpful.jerry
April 12, 2014
April
04
Apr
12
12
2014
08:39 AM
8
08
39
AM
PDT
I hold that JLAfan's preferred Nihilistic worldview is false because it is unable to be lived out in any realistic sense:
Atheism and Nihilism - Dr. Craig - video https://www.youtube.com/watch?v=2cWLvp_6wq0 Existential Argument against Atheism - November 1, 2013 by Jason Petersen 1. If a worldview is true then you should be able to live consistently with that worldview. 2. Atheists are unable to live consistently with their worldview. 3. If you can’t live consistently with an atheist worldview then the worldview does not reflect reality. 4. If a worldview does not reflect reality then that worldview is a delusion. 5. If atheism is a delusion then atheism cannot be true. Conclusion: Atheism is false. http://answersforhope.com/existential-argument-atheism/ The Heretic - Who is Thomas Nagel and why are so many of his fellow academics condemning him? - March 25, 2013 Excerpt: Nobody thinks his daughter is just molecules in motion and nothing but; nobody thinks the Holocaust was evil, but only in a relative, provisional sense. A materialist who lived his life according to his professed convictions—understanding himself to have no moral agency at all, seeing his friends and enemies and family as genetically determined robots—wouldn’t just be a materialist: He’d be a psychopath. http://www.weeklystandard.com/articles/heretic_707692.html?page=3
Moreover, this psychopathic characteristic inherent to the atheistic philosophy is born out empirically, in that people who do not believe in a soul tend to be more psychopathic than the majority of normal people in America who do believe in a soul. You can pick that psychopathic study of atheists around the 14:30 minute mark of this following video:
Anthony Jack, Why Don’t Psychopaths Believe in Dualism? – video http://www.youtube.com/watch?list=UUmmObUi8Fq9g1Zcuzqbt0_g&feature=player_detailpage&v=XRGWe-61zOk#t=862s
Of related interest:
Does the Causal Principle Apply to the Universe? - Dr. Craig - video https://www.youtube.com/watch?v=dxU4ND8HdYg
bornagain77
April 12, 2014
April
04
Apr
12
12
2014
08:28 AM
8
08
28
AM
PDT
1 2 3

Leave a Reply