Mark Frank wants to know what all of the fuss is about regarding the recent empirical verification of Michael Behe’s prediction in Edge of Evolution.
In response to the News post Evolutionary biologist Larry Moran tries calculating with big numbers re evolution Mark asks:
I must be missing something important. As far as I can see everyone seems to agree that the mutations required for chloroquine resistance are extremely improbable and this is born out by the rarity of such resistance in the wild. So what?
Fair question, to which gpuccio aptly responds:
Mark:
The point is simple. The malaria parasite under the extremely strong selection of chloroquine is a model extremely favourable to the neo darwinian algorithm: huge populations, very high reproduction rate, very strong and precise selective pressure, and a rather simple advantageous variation thta can be attained (just two AA variation to confer resistance to a lethal drug).
We can say that this the perfect scenario for the neo darwinian model, and a good way to measure its powers.
Now, in such a favourable scenario, how does the model work? It works (in the end, chloroquine resistance arises), but it definitely requires a lot of time and huge population numbers. IOWs, it happens with some difficulty.
That’s all. That difficulty is exactly what is needed to infer how much more “difficult” (indeed, impossible) it would be for the same neo darwinian model to explain the emergence of a new complex protein when the necessary transition is, say, of 300 AAs, and the population number, reproduction rate and selective pressure are much less favourable to the model. For example, to evolve just one new useful protein in vertebrates or mammals.
That is, and always has been, Behe’s point. And the point of ID.
Can you really say “so what” to that argument?
I would add to gpuccio’ response an issue that BA77 brought up earlier in the thread:
It is interesting to note that Chloroquine Resistance, as hard as it is for Darwinian processes to account for, (whether in the 1 in 10^14 calculation or in the 1 in 10^20 observation), it is not even a gain in functional complexity for the malaria parasite in the first place but is a loss of functional complexity for the parasite. . . . Thus the resistance, as crushing as it is, number-wise, for Darwinists to explain the origin of, is doubly crushing for Darwinists, since the adaptation, as hard as it was for Darwinian processes to acquire, was still ‘downhill’ evolution anyway and adds nothing as to explaining microbes to man evolution is remotely possible in a Darwinian scenario!
Conclusion. So what Mark? The “what” is that it has been mathematically demonstrated that Darwinian processes are real and they can account for small scale changes — which everyone concedes — but the same math demonstrates convincingly that they are not up to the larger task assigned to them by the theory — i.e., large scale changes requiring dozens if not hundreds of mutations.
“I must be missing something important.”
Mark, if you believe Darwinian Evolution works at any level, you aren’t just missing something but rather everything!! 😉
In larger animals, like humans. After 100 million years or so waiting for this mutation, I wonder in the rest of the genome what genetic degeneration had occurred. LOL. One step sorta (i.e. sorta, since it’s a degenerative benefit) forward, how many steps back?
Must truly suck to be a Darwinian. Then again, maintaining that view amidst the math would require a certain level of dimness that further insulates one from the raw mathematical embarassments.
Reminds me of this Sternberg talk…
https://www.youtube.com/watch?v=KbAzZEu13_w
ID in the evolution debate is mainly about the origin of new alleles. Mark Frank has been here longer than I have and I that is over 8 years. If he doesn’t understand this by now, it is either pathetic or willful insertion of obstructive comments just for the hell of it.
Gpuccio’s response is excellent.
It takes a tiny bit of conceptual comprehension to “get it.” It is not as simple as a pig tail photoshopped onto a baby picture or a National Geographic artist rendering of a Neandertal.
I’m inclined to think the one in 10^14 calculation is wrong. Take a look at the bottom of the comment:
If you take a doubling series: 1, 2, 4, 8, 16…, it’s sum is twice the last number minus 1. So after 30 generations the cumulative population would have been 2.14 billion cells. The mutation rate is 2.5 x 10^-9. Times 2.14 billion is 5.35, not 53.7. But somehow diogenes has malaria finding the first mutation 10 times faster than it’s possible to look for it. That can’t be right.
It would be good if someone could check my work.
Ding! I think you got it.
JoeCoder,
You are both wrong 🙂
It’s not the sum of the number of cells that have existed that matter, so we don’t need to sum the series. Instead, we want to know how many cell divisions have occured.
Diogenes has calculated the population size presuming the infection starts form two sporozites, which is indeed 2^30 or about a billion. Seems like he created a complex way of tracking the mutations, but we can’t instead use basic probability.
We are looking for cells that have acquired exactly one mutation in 30 generations. If we call the mutation rate u the probability this happens is
p = 30 * u *(1-u)^29
and the expected number of these from n trials is n.p so
E = 2^30 * (30 * (2.5e-9) * (1-2.5e-9)^29)
~ 80.5
Diogenes then multiplies that by 2/3 to get ~53.7.
But diogenes has assumed that the infection starts from two sporozites, which is not necessarily the case, and that the malaria paraise it diploid (in fact it’s haploid).
If an infection started from 10 sporozites, factor in the haploidy and say only one of 3 possible mutations is the right one you’d end up with
(10 * 2^30) * (30 * (2.5e-9) * (1-2.5e-9)^29) * 1/3
~268 single mutants.
(the above should say the malaria parasite is haploid in humans, it’s diploid in other stages. THere are many other subtlties these back of the envelope calculations ignore too)
#3 Jerry
I total agree this is true but I am afraid I don’t see the relevance of this remark. It is not a case of wilful insertion of obstructive comments so I guess it must be pathetic. So help this poor pathetic person understand the relevance of the point.
wd4000, thank you for the friendly feedback, but I think you are wrong :). Specifically here:
I’m not sure where this formula comes from but I tried plugging some different numbers into it:
That would mean that a single mutant arises once once the population reaches 2^24=16.7 million in size. Times two would be a total cumulative population of 33 million.
Those 33 million cells times u=2.5e-9 times a 23 million base genome size = 1.9 million mutations that would have occurred.
1.9 million / 23 million is 8.2%.
That would mean that on average they find the first single-point mutation after only exploring 8.2% of their genome. But that can’t be right because you can’t find it faster than you can look for it. So I think that must be a wrong result. Are your formulas the correct ones to use in this exercise?
Please check my work to see if I’m wrong 🙂
Above you can remove the steps of multiplying and then dividing by 23 million to simplify the calculation. But the result it the same.
We all agree that some genotypes, like chloroquine resistance in Plasmodium, are extremely rare. That’s not an issue. We also agree that such combinations of mutation will be beyond the reach of some species.
What we’re contesting is the claim that Behe’s predictions were recently confirmed. They were not. Behe predicted that only two mutations were required and that the probability of this happening is 10^-20. We said his calculation was wrong. Behe challenged us to come up with our own numbers. We did – to the best of our ability.
Turns out that that the probability of two mutations is much higher than Behe claimed but that there’s more to the issue than just the occurrence of a mutation. Behe didn’t take fixation/detection into account. He also doesn’t admit that you probably need FOUR mutations in order to get effective chloroquine resistance.
Some of us are still waiting to see if Michael Behe can meet his own challenge.
The rest of Behe’s argument is as bogus as his calculation of the probability of chloroquine resistance.
Am i reading this right? Larry Moran says it is even more complicated than what Behe suggests so therefor he is wrong?
LOL!!!! thank you for proving Behe’s point Larry….. This post is a keeper!
This just shows even if the IDIOT is more right than materialists they will cook up a scheme to say….. “You’re wrong because its even worse than you claimed”
Did a professor just say that?
Hahahaha!!!!!
Just admit it Larry Behe busted you lot…..
wd400 I think I see the problem in your math now, the error (30) is in bold:
You’re calculating the odds for 30 generations with each generation having 2^30. Not a population that’s growing up from a small number to 2^30 in size.
So your result of 268 single mutants is after a cumulative population of 30 x 2^30 = 32 billion cells.
Or one mutant arising every 32 billion / 80.5 = 397 million cells. Which is the inverse of the mutation rate we started with, as it should be.
Sorry the above should say “So your result of 80.5 single mutants…”
Strange that Dr Behe flat out states that more than 2 mutations are required. As for fixation, well when has that ever been observed in wild populations of the malaria parasite?
With stochastic processes, such as natural selection and drift, specific combinations of mutations are beyond the reach of all species.
JoeCoder,
Ha, seems Diogenes and I made the same mistake by different routes.
p = 30 * u *(1-u)^29 is from the biomial distribution, which would apply if each cell went through 30 cell divisions all by itself, but doesn’t count here since all cells share some history with each other.
You approach is right (though I’d stress the number of cell divisions, not the number of cells that have existed, ,which is slipery with daughter cells anyyway). Ignoring the starting population you end up with 2^(N+1)-2 trials so 5 single mutants after 30 gens.
Andre I don’t think that’s what Dr. Moran is saying. It looks like it takes less than 10^20 for the mutation to appear, and probably pretty close to 10^18 — which itself is close to the inverse square of the mutation rate.
But because it’s only very weakly beneficial, it must appear multiple times before selection will cause it to spread. And it must spread at least to a population in the millions before the third and fourth single-step mutations have a good probability of arising.
So IMHO, while it takes less than 10^20 to appear (as Behe said), it still likely takes around 10^20 to appear and be headed toward fixation. Which at the end of the day is all that matters in studying chloroquine resistance. But if there’s a two-step mutation that is strongly beneficial, it will take less than 10^20 to fix in the population.
We cross posted JoeCoder,
So just to clarify I wan’t assuming the population didn’t grow. The 30 is the is the number of ways you can get one success and 29 failures in 30 trials (“30 choose 1”), It would work if each cell was one experiment to itself, but doesn’t here because they share some of the divisions.
wd400 I’m sure I’ve made some mistakes in my comments here too! Thanks for all of your past contributions to UD. Even though I’m an ID person I generally look forward to seeing your comments on a thread.
Dr Behe got his numbers from peer-review. The numbers are not as Behe said, they are as Behe cites.
When your numbers appear in peer-review Behe will consider them- or even if you send him an email once you hammer it all out.
Joe @22
I’m on Behe’s side, Edge of Evolution was actually one of my favorite books, and I think Behe was right on many his points.
But because two mutations confer only very weak chloroquine resistance, those two mutations would have to occur hundreds of times before they spread far enough to be detected. So it’s probably closer to 10^18 than to 10^20. I think that’s close enough and if you swap that number into Edge, the rest of Behe’s arguments aren’t significantly affected. And it still means the reviewers were wrong in their bickering that a simultaneous mutation was significantly less likely than a stepwise one through neutral space, or saying that selection at each step.
I thought his point about mutations was to show how difficult they were to get specific combinations of, let alone be able to get beyond the Edge of two new protein-protein binding sites.
Joe:
All the time Joe, all the time.
But it’s the allele that does not confer chloroquine resistance that gets fixed!
🙂
True and humans have a fixation with the malaria parasite in the wild. So that’s something. 😉
JoeCoder
It is true that Larry Moran’s calculations take him to 10^18 and I guess in a mathematical sense he could say “the probability is much higher” but that is not what I’m alluding to…….
Larry said;
Larry makes Behe’s point here about the difficulty and then tells us that he’s wrong!!!!!
Dies 4 instead of 2 not lower the odds considerably? Want to some math around that?
The odds of the first two mutations are about one in 10^18, since you need both before selection can start to act on them. Mutations 3 and 4 have odds of about one in 10^9 because selection can act at each step.
In order for naturalistic evolution to take place, new alleles have to arise naturally. These calculations show that just simple modifications of current alleles to reach a new function seem out of reach of naturalistic processes. Let alone of de novo functional alleles. Thus, it is impossible for naturalistic evolution to take place and one must look for an alternative explanation.
If you do not understand this then you should go to lurker status till you understand the basic issue. But, you have been here longer than I have and I first came here over 8 years ago. How could you not understand what it is all about. Thus, my two alternatives. You do not have to agree but you have to know. If you know, willful obstruction is the diagnosis. If you do not know this, then the word “pathetic” is appropriate.
Isn’t it amazing that thousands of evolutionary biologists over the past one hundred years don’t understand this simple explanation? We must be really, really, stupid.
Or is there another possibility?
We must be really, really, stupid.
LOL, surely you don’t think you are going to get disagreement on UD do you?
But don’t feel too bad Moran, we are ALL really, really, stupid when it comes to trying to understand the unfathomed complexity of even the simplest of cells!
“Although the tiniest living things known to science, bacterial cells, are incredibly small (10^-12 grams), each is a veritable micro-miniaturized factory containing thousands of elegantly designed pieces of intricate molecular machinery, made up altogether of one hundred thousand million atoms, far more complicated than any machine built by man and absolutely without parallel in the non-living world”. Michael Denton, “Evolution: A Theory in Crisis,” 1986, p. 250.
The Cell as a Collection of Protein Machines
“We have always underestimated cells. Undoubtedly we still do today,,, Indeed, the entire cell can be viewed as a factory that contains an elaborate network of interlocking assembly lines, each which is composed of a set of large protein machines.”
Bruce Alberts: Former President, National Academy of Sciences;
“To grasp the reality of life as it has been revealed by molecular biology, we must first magnify a cell a thousand million times until it is 20 kilometers in diameter and resembles a giant airship large enough to cover a great city like London or New York. What we would see then would be an object of unparalleled complexity,…we would find ourselves in a world of supreme technology and bewildering complexity.”
Michael Denton PhD., Evolution: A Theory In Crisis, pg.328
“Each cell with genetic information, from bacteria to man, consists of artificial languages and their decoding systems, memory banks for information storage and retrieval, elegant control systems regulating the automated assembly of parts and components, error fail-safe and proof-reading devices utilized for quality control, assembly processes involving the principle of prefabrication and modular construction and a capacity not equaled in any of our most advanced machines, for it would be capable of replicating its entire structure within a matter of a few hours”
Michael Denton PhD. Evolution: A Theory In Crisis pg. 329
“a one-celled bacterium, e. coli, is estimated to contain the equivalent of 100 million pages of Encyclopedia Britannica. Expressed in information in science jargon, this would be the same as 10^12 bits of information. In comparison, the total writings from classical Greek Civilization is only 10^9 bits, and the largest libraries in the world – The British Museum, Oxford Bodleian Library, New York Public Library, Harvard Widenier Library, and the Moscow Lenin Library – have about 10 million volumes or 10^12 bits.” – R. C. Wysong
‘The information content of a simple cell has been estimated as around 10^12 bits, comparable to about a hundred million pages of the Encyclopedia Britannica.”
Carl Sagan, “Life” in Encyclopedia Britannica: Macropaedia (1974 ed.), pp. 893-894
HISTORY OF EVOLUTIONARY THEORY – WISTAR DESTROYS EVOLUTION
Excerpt: A number of mathematicians, familiar with the biological problems, spoke at that 1966 Wistar Institute,, For example, Murray Eden showed that it would be impossible for even a single ordered pair of genes to be produced by DNA mutations in the bacteria, E. coli,—with 5 billion years in which to produce it! His estimate was based on 5 trillion tons of the bacteria covering the planet to a depth of nearly an inch during that 5 billion years. He then explained that,, E. coli contain(s) over a trillion (10^12) bits of data. That is the number 10 followed by 12 zeros. *Eden then showed the mathematical impossibility of protein forming by chance.
“It has become clear in the past ten years that the concept of design is not merely an add-on meta-description of biological systems, of no scientific consequence, but is in fact a driver of science. A whole cohort of young scientists is being trained to “think like engineers” when looking at biological systems, using terms explicitly related to engineering design concepts: design, purpose, optimal tradeoffs for multiple goals, information, control, decision making, etc. This approach is widely seen as a successful, predictive, quantitative theory of biology.”
David Snoke*, Systems Biology as a Research Program for Intelligent Design
OT: podcast: “David Snoke: Systems Biology and Intelligent Design, pt. 1”
http://intelligentdesign.podom.....9_09-07_00
podcast: David Snoke: Systems Biology and Intelligent Design, pt. 2
http://intelligentdesign.podom.....0_01-07_00
Larry Moran 30
Stupid, not in the least.
Blinkered by a priori materialist assumptions, yes. Just as many brilliant minds believed in the Ptolemaic system of epicycles because of an a priori commitment to circular orbits.
Yes, there is another possibility- some hybrid of naturalistic evolution, ID, and creation is true.
Let us take advantage of every opportunity to advance knowledge and understanding, with sincere and honest dialogue, and brotherly love.
Amen?
#29 Jerry
I think there is a misunderstanding between us. Of course I know that new alleles have to arise naturally. I also understand that in this particular case it took a lot of generations to get to a fairly simple change. But it doesn’t follow that a more complex change such as new allele should take proportionally more generations. There are so many other factors to take into account. That is why I wrote:
On the original thread I had a brief but interesting discussion with the polite and intelligent Gpuccio about the factors that might make a difference (of course he did not agree with me but I don’t think he found my position either wilfully obstructive or pathetic). I expect you were not aware of that – (which is quite understandable – no one can read everything that is posted) – and that may account for the misunderstanding.
BA77
The more I try to understand the mechanisms behind the cell fate determination, intrinsic asymmetric mitosis, timely centrosome segregation, precise spindle checkpoints, cell polarization, extrinsic or intrinsic factors, signaling pathways, the whole nine yards, mind-boggling, overwhelming, I feel more and more stupid, completely ignorant. In my many years working on engineering design software development I never ever felt this way. Looking back at those years, now it seems like my work was so easy and simple. Now for every outstanding question that gets answered, new questions are raised. Unending revelation of the ultimate reality.
Then when I talk to friends biologists and ask them to help me with understanding all that, everyone and their cousins look at me with wide open eyes and confess they don’t understand that either.
We are approaching a major ‘told you so’ moment in science. Someone said, long ago, that He will make us feel this way, realizing our limitations to comprehend everything, and swallowing our ridiculous pride.
It’s not too late to humbly admit we are studying and trying to understand an amazing creation.
But we are free to continue in our foolishness going back to our vomit too.
It’s up to each of us to decide.
Larry Moran,
It is an empirical observation by Nicholas White that chloroquine resistance arises in 1 in 10^20 parasites. As to the question of how many mutations this takes, you are prevaricating. From the abstract of the Summers paper:
It is amazing that Miller, Coyne, Dawkins, Matzke, and Carroll all went on record stating that each mutation could provide cumulative resistance. Behe said no, a minimum of two is required. Now here comes Moran ex post facto saying, “No it’s not one, it’s not two, it’s four!”
Moving. Goalposts.
Larry Moran
For one thing, nobody new about DNA 100 years ago. And it is only relatively recently that DNA could be sequenced and empirical observations made about the fidelity of the sequence information and how many/few changes were required to make a selective difference.
Larry Moran
Really? I am not sure what you mean by “effective chloroquine resistance” from an evolutionary perspective. But are you willing to bet against the fact that two mutations sufficient for a selective advantage? From the Summer’s paper:
Funny that before the Summer’s paper the Darwinists argued in favor of cumulative selection. Now after the Summer’s paper Moran goes the other way and tries to argue against cumulative selection. Moving. Goalposts.
I went back and looked at Moran’s comments about Behe’s Edge prior to the Summer paper, and he didn’t throw in with the rest of the crowd and argue for cumulative resistance at each mutation. So I can’t claim that Moran has moved goal posts.
Larry Moran,
Here is what you said in 2010:
No. No there are not. From the Summer’s paper:
It is funny that Darwinists would be so up in arms about the math whilst Behe’s focus is on the 1 in 10^20 empirical observation.
No amount of mathematical theorizing by Darwinists is going to get them past that empirical observation of 1 in 10^20 ! Because in science, (at least in how science is practiced apart from Darwinism), empirical observation trumps theory all the time,,,
Moreover, If Darwinists were genuinely concerned with the math of Darwinian evolution, instead of trying to make ‘mathematical excuses’, they should focus all their attention on figuring out why Darwinism has no rigid mathematical basis in the first place as other overarching theories of science do:
Berlinski is not whistling Dixie.
No less than Gregory Chaitin thinks it is a ‘scandal’ that evolution has no mathematical proof that it works:
Wolfgang Pauli, certainly no slouch in math himself, finds Darwinian biologist to be ‘irrational’ because of their treatment of math:
MIT’s Murray Eden echos Pauli’s concern:
Of supplemental note: It is interesting to point out, in all the trouble Darwinists have in defining their mathematical basis, that, whilst Darwinists in general adamantly deny the existence of the soul, man’s ability to do mathematics in the first place is solid evidence that man has a mind/soul. No less than the co-discoverer of Natural Selection, Alfred Wallace, held as such:
Or if you think Alfred Wallace not qualified to make the judgment as to whether man has a soul because of his ability to do mathematics, then how about Gödel’s, who proved the ‘incompleteness’ of mathematics, opinion on the matter:
Verse and Music:
Follow-up to # 36
What amazes me is not so much the still unknown, but that what has been discovered already, which is so elaborate and finely orchestrated. There are many missing pieces in the puzzle, hence I look forward with much anticipation to read newer reports about discoveries that could fill the remaining gaps, because I believe the new information will shed more light on the complex mechanisms, thus allowing us to enjoy their awesomeness. As professor Lennox said, our God is not a god of the gaps, but the God of the whole show. True wisdom only comes from Him. The wisdom of this world is ridiculously inadequate. If we delight in the Lord, He will provide the good desires of our hearts. Some of those desires could be to pursue scientific research studies and enjoy what He will reveal to us about His amazing creation.
Larry Moran:
Have you ever heard of cognitive bias?
Consensus is no guarantee of truth.
gpuccio
“Larry Moran:
Have you ever heard of cognitive bias?
Consensus is no guarantee of truth.”
Below here is an etched in stone proof example of how successful consensus has been in history. In other words, if you have consensus on your side, you win:
http://i.imgur.com/VQDwlC8.jpg
Problem is, people like Larry will invoke Godwin’s Law as their lame default answer and in their minds all is still well in EvoLand
Jehu:
“Moving. Goalposts.”
Larry has no problem with moving any goalposts which favor evolution. After all, evolution is a fact, Goalpost movement is merely an evolutionary adaptation for proving that evolution is true despite the reality of how the natural world actually works. Besides, if evolution is true, there exist no moral authority which emphatically states that lying is wrong.
gpuccio
Excellent point. History shows examples of that.
OT: Dionisio, I think you will be both pleased and frustrated by the following paper:
It’s Optimal. It Must Have Evolved! – August 16, 2014
Excerpt: “Cell-surface signaling receptors are organized into different architectures that have been arrived at multiple times in diverse contexts. To understand the trade-offs that lead to these architectures, we pose the generic information-processing problem of identifying the optimal strategy for distributed mobile noisy sensors to faithfully “read” an incoming signal that varies in space-time. This involves balancing two opposing requirements: clustering noisy sensors to reduce statistical error and spreading sensors to enhance spatial coverage, resulting in a phase transition that explains the frequent reemergence of a set of architectures. Our results extend to a variety of engineering and communication applications that involve mobile and distributed sensing, and suggest that biology might offer solutions to hard optimization problems that arise in these applications.”
These solutions “have been arrived at” — by design? No; read the last sentence in the paper: “It is appealing that one might look to biology for insights into solutions of hard optimization problems, arrived at as a result of evolution within an information niche.” Evolution did it. Give evolution the engineering design award.
http://www.evolutionnews.org/2.....89031.html
DavidD
A picture is worth a thousand words. Sadly in that gathering were probably many people who claimed to be followers of ‘VIA VERITAS VITA’ but disobeyed an important commandment ‘VIA VERITAS VITA’ Himself told us to observe: to love our neighbors as ourselves. By ignoring that important commandment, one automatically ignores the main one: to love our Creator with all our strengths. There were some exceptions, whose vision were not blurred by the loud screaming around them, stood firm by their beliefs and did not submit to the consensus. One of them was Wilhelm Busch, who resisted enormous pressures to join the consensus. Few years later pastor Wilhelm’s firm resistance was proven right. Eventually history was on his side. The consensus crowd was proven wrong. Maybe there are few things we could learn from these stories and apply them to our current situation?
In the first part above it seems Larry Moran is agreeing with my comment and with ID’s assessment of the situation. In the second part of the comment he says there is another possibility. Has he elaborated on what this possibility is?
Allen MacNeill has appeared her occasionally saying that there is a process that explains the origin of new alleles. It his 47+ engines of variation. According to Allen, these variation processes will produce the alleles that then can be chosen by environmental pressures and reproductive success to account for the changes in life forms over the eons.
However, anyone espousing this has to be able to show the progress in genomes that actually happened that led to novel complex capabilities. In many cases this evidence should be present in current genomes. With current technology this thesis should be able to be supported or falsified. My guess is that it will be mainly falsified. There will be a couple successes but that is all.
BA77
OT
Thank you for the interesting link and for the warning about it.
Perhaps unexpectedly, after being exposed to the ‘misconception’ and the ‘deceiving’ viruses for so long, apparently my ‘reading’ immune system has been substantially strengthened out and now I skip over all that ‘hogwash’ embedded in the text of some articles I read, and I can focus in on the real stuff, which by itself is quite difficult for me to understand. Perhaps other folks in this blog have gone through a similar experience? It’s a blessing after all, isn’t it? 🙂
Again, thank you for bringing this article up to my attention now. I have used some of the links you provide in your comments in other threads within this site. 🙂
It has been shown that for this particular change, it will take an extremely large number of generations or reproductive events to get to a simple change. You seem to agree on that but suggest that in different circumstances this might not be true.
There are literally thousands of incredibly complicated changes that have taken place in organisms over the past 500 million years. Showing genetically how some of these may have taken place would be a start to supporting your alternative thesis. Till that time, one has to acknowledge that it may be an essentially impossible process. One can not just say it may have happened. One has to provide examples and reasonable pathways that new alleles have arisen.
ID has shown the near impossibility of such a process happening naturally just once and by extrapolation this implies it could not happen the tens of thousands of times naturally it apparently happened. To counter ID’s conclusion, it is indicative on evolutionary biologist to provide a mechanism where new alleles are not only possible but likely.
bornagain77 @ 49
OT: I return you the favor
Here’s another example of bad design in nature 😉
Bats Bolster Brain Hypothesis, Maybe Technology, Too
http://www.biosciencetechnolog.....cation=top
Hi Larry,
Can you recommend a good book on macroevolution?
I’m not sure what Larry will come up with, perhaps Evolution is a Fact and a Theory, but why not go to the source:
The Origin of Species by Means of Natural Selection or the Preservation of Favoured Races in the Struggle for Life by Charles Darwin, M.A., F.R.S., &c., First Edition 1859
-Q
DavidD@46 observed
Excellent example!
Just look at all those scientists lining up behind the recognition that since we have the ability to control our evolution, we also have the moral obligation to do so.
-Q
I posted this elsewhere regarding the evolution of chloroquine resistance in malaria. Are any of you familiar with this 2010 paper?
http://www.malariajournal.com/content/9/1/217
Here’s an excerpt:
-Q
My favorites are:
Genetics, Paleontology, and Macroevolution 2nd ed. (2001) by Jeffrey S. Levinton, Cambridge University Press
Macroevolution: Diversity, Disparity, Contingency (2005) Essays in honor of Stephen Jay Gould, E.S. Vrba and N. Eldredge eds., The Paleontological Society
I’ve written a little essay on Macroevolution to help you understand the concept.
Dr. Moran, in the recent vindication of Dr. Behe, this following quote is even more relevant now than when it was first written decades ago:
That’s a good paper. It illustrates the point that many biologists are trying to make—a point that Michael Behe always ignores.
The point is that there’s a big difference between the mutation rate to a chloroquine resistant strain and the successful appearance of such a strain in a particular locality. The right combination of mutations is going to arise much more often than our ability to detect it so it’s quite wrong to equate mutation rate and appearance.
Think of it this way. What if there was only one in a million chance of a chloroquine resistant strain becoming well-enough established to be detectable in a local population? That would mean that the mutations arise once in every 10^14 parasites and the combined probability of detecting it is one in 10^20.
Other combinations of mutations might arise at the same frequency but 100% of them could spread in the population. That would mean that a CCC only applies to chloroquine resistance but not to, say, protein-protein interactions.
Behe’s failure to take this into account is a major weakness in his book. However, his error is compounded by a flawed calculation of the probability of mutation and the two errors pretty much cancel out. They are still errors. His reasoning is still wrong even though he accidentally stumbled on an answer that makes a bit of sense.
10^14 parasites???
wow, no big deal huh Larry???
So we only have to wait for 100 trillion (1 in 10^14) tries in humans to get a similar trait in humans???
A degenerative trait that is not even a demonstration of ‘uphill’ evolution???
It is interesting to note that Chloroquine Resistance, as hard as it is for darwinian processes to account for, is not even a gain in functional complexity for the malaria parasite in the first place but is a loss of functional complexity for the parasite.
Metabolic QTL Analysis Links Chloroquine Resistance in Plasmodium falciparum to Impaired Hemoglobin Catabolism – January, 2014
Summary: Chloroquine was formerly a front line drug in the treatment of malaria. However, drug resistant strains of the malaria parasite have made this drug ineffective in many malaria endemic regions. Surprisingly, the discontinuation of chloroquine therapy has led to the reappearance of drug-sensitive parasites. In this study, we use metabolite quantitative trait locus analysis, parasite genetics, and peptidomics to demonstrate that chloroquine resistance is inherently linked to a defect in the parasite’s ability to digest hemoglobin, which is an essential metabolic activity for malaria parasites. This metabolic impairment makes it harder for the drug-resistant parasites to reproduce than genetically-equivalent drug-sensitive parasites, and thus favors selection for drug-sensitive lines when parasites are in direct competition. Given these results, we attribute the re-emergence of chloroquine sensitive parasites in the wild to more efficient hemoglobin digestion.
http://www.plosgenetics.org/ar.....en.1004085
Obviously probabilistic barriers are not a problem for evolution, otherwise, life would not have continued to thrive for the past 4-Billion years. Why?
A-Life evolved to evolve?
B-Life was designed to evolve?
C-Both of the above
D-None of the above
Dr. Moran, if I skimmed your macro-evolution article correctly, it seems that you believe that macro-evolution can be accounted for by mutations to DNA. i.e. through the neo-Darwinian mechanisms of Random Mutation/Variation and Natural Selection? Please correct me if you do not believe in Neo-Darwinism.
(and Dr. Moran if you believe in Neo-Darwinism),,, There are two HUGE problems, among many problems, with your belief in neo-Darwinism. One HUGE problem is that body plan information is NOT reducible to the information on DNA.
This is not a minor problem for neo-Darwinism Dr. Moran!
Another HUGE problem with Neo-Darwinism Dr. Moran, that compounds the previous problem exponentially, is what is termed ‘ontogenetic depth’
Moreover, these regulatory regions are found to be ‘orders of magnitude’ different even between chimps and humans:
Thus where Darwinian theory most needs plasticity in order to be viable as a hypothesis, i.e. in developmental gene regulatory networks, is the place where it is found to be least flexible. Yet, it is in these developmental gene regulatory networks where the greatest differences are found!
,,, If neo-Darwinism were a normal science, instead of being primarily a cornerstone of the atheistic religion that is basically impervious to empirical falsification, this finding, along with many other lines of evidence (J. Shapiro etc,,) would be enough to overturn neo-Darwinism as a hypothesis of serious consideration in science.
Thanks Larry,
I have the Vrba book, not really what I was looking for, though it does contain some interesting papers and worthwhile reading.
I’ll check out the Levinton text and your essay.
The Vrba book is sometimes hard to digest. The first article is the essence of macro evolution thinking. It is by Jurgen Brosius and is the crucial thinking supporting naturalistic evolution.
Allen MacNeill first brought it up about six years ago. I have mentioned it several times but no one here pays attention to it. Brosius acts like macro evolution is a done deal. He is a very prolific author on this topic.
My guess is that this too will pass here. If one has access to a college library over the internet, all the articles were published in a journal and are available as PDFs.