About twenty years ago the television show Dallas was in trouble. The writers had eliminated a popular character named Bobby and the show was losing popularity. The writers began thinking up ways to solve the problem. They finally decided that the previous year of programming would become nothing more than a dream in the mind of another character named Pam. It was a ridiculous solution, but it was all they had. A new show would begin with Pam restlessly awakening, only to discover Bobby was not dead, but alive and well. Everything was back to normal as Bobby announced to the loyal viewers at the 2:10 mark that “It’s over—none of that happened.” Dallas needed a do-over, and it got one.
Evolution also needs a do-over. In fact evolution routinely needs do-overs as the scientific evidence continually refutes the theory. And so evolutionists are constantly rewriting their script. For instance, evolutionists expected that proteins arose relatively quickly in the early stages of evolutionary history and new, de novo, proteins would not appear thereafter. Here is how evolutionist François Jacob explained it in an influential article which appeared in Science, one of the world’s leading journals:
Obviously, for life to emerge, a number of new molecular types had first to be formed. During chemical evolution in prebiotic times and at the beginning of biological evolution, all those molecules of which every living being is built had to appear. But once life had started in the form of some primitive self-reproducing organism, further evolution had to proceed mainly through alterations of already existing compounds. New functions developed as new proteins appeared. But these were merely variations on previous themes. A sequence of a thousand nucleotides codes for a medium-sized protein. The probability that a functional protein would appear de novo by random association of amino acids is practically zero. In organisms as complex and integrated as those that were already living a long time ago, creation of entirely new nucleotide sequences could not be of any importance in the production of new information.
Of course we now know this is false. Plenty of de novo proteins have been discovered in single species and evolutionists are now walking it back with up all kinds of speculation. For instance, they say that these de novo proteins aren’t very good proteins. They really don’t do much, and aren’t comparable to the well-studied proteins that appear in many species. And when, in the future, a de novo protein is shown to be a real protein, evolutionists will simply walk it back some more.
In addition to predicting that no de novo proteins would be found, evolutionists also predicted that the well-studied proteins evolved rather rapidly. They have to say this because these proteins are found in many different species which, for evolutionists, means that such a protein must have evolved from an early version present in an ancient, common ancestor, such as ancient single-celled bacteria. But if the protein was present so early in history, then it must have evolved quickly. As Jacob explained:
During chemical evolution in prebiotic times and at the beginning of biological evolution, all those molecules of which every living being is built had to appear.
This means evolution had only a few tens of millions of years to evolve these proteins. Call it 100 million years to be conservative. The problem here is that science tells us this doesn’t make sense.
Several different studies indicate that, at a minimum, about 10^70 (a one followed by 70 zeros) evolutionary experiments would be needed to get close enough to a workable protein design before evolutionary mechanisms could take over and establish the protein in a population.
For instance, one study concluded that 10^63 attempts would be required for a relatively short protein. And a similar result (10^65 attempts required) was obtained by comparing protein sequences.
Another study found that 10^64 to 10^77 attempts are required, and another study concluded that 10^70 attempts would be required.
This requirement for 10^70 evolutionary experiments is far greater than what evolution could accomplish. Even evolutionists have had to admit that evolution could only have a maximum of 10^43 such experiments. It is important to understand how tiny this number is compared to 10^70. 10^43 is not more than half of 10^70. It is not even close to half. 10^43 is an astronomically tiny sliver of 10^70.
Furthermore, the estimate of 10^43 is, itself, entirely unrealistic. For instance, it assume the entire history of the Earth is available, rather than the limited time window that evolution actually would have had. Even more importantly, it assumes the pre existence of bacteria and, yes, proteins. In fact, the evolutionists assumed the earth was covered with bacteria, and each bacteria was full of proteins. That of course is not an appropriate assumption for the question of how proteins could have evolved in the first place.
And so evolutionists are having to continue to rewrite the script. What they told us before—forget it. “It’s over—none of that happened,” they now tell us.
Actual lab studies find functions in screens of random libraries of size 10^10-10^12. But it would require having knowledge, competency, and honesty all at once to mention those results to your readers.
ReplyDeleteActual lab studies find functions in screens of random libraries of size 10^10-10^12. But it would require having knowledge, competency, and honesty all at once to mention those results to your readers.
DeleteDid you just wake up?
"Actual lab studies find functions in screens of random libraries of size 10^10-10^12. But it would require having knowledge, competency, and honesty all at once to mention those results to your readers."
DeleteSpeaking of "knowledge, competency, and honesty all at once" how about we also include some reality that would also be required to be calculated and added to the possibility of the origination of a functioning cellular protein.
Let's say that your references are correct that "studies find functions in screens of random libraries of size 10^10-10^12" ok? now what happens with a new protein that has a function when it is formed within the controlled closed system of the cell? Do you suppose that the new funtional protein can actually begin to function at the spatial location it originates at within the cell? If such a functional protein occurred whose function was only possible at a specific spatial location within the cell what are the odds that it would actualy arrive at that place? Do you suppose the cell just keeps producing the new protein until by chance they end up in the one place that they can function? To calculate that chance you would need to define the number of possible spatial locations it can be positioned at within the cell and that is a huge number all by itself. Just to give you an idea here, a liver cell has around 7.9 × 10 to the 9th power of individual protein molecules and each of these occupies a posible spatial location within the cell.
If you really think this through you should come to the conclusion that simply coming into existence with a possible function is only one small part of the odds calculation that would be 'required' to provide a fitness increase to the cell. Some of the other additional odds that must be added to that initial calculation would be the odds of correct generation time and correct quantities and correct interactions with other existing proteins to name but a few.
NickM, of all people, states:
ReplyDelete'But it would require having knowledge, competency, and honesty all at once to mention those results to your readers.'
Yet we find, in the 10^10 to 10^12 results that NickM only alluded to but did not specifically cite:
How Proteins Evolved - Cornelius Hunter - December 2010
Excerpt: Comparing ATP binding with the incredible feats of hemoglobin, for example, is like comparing a tricycle with a jet airplane. And even the one in 10^12 shot, though it pales in comparison to the odds of constructing a more useful protein machine, is no small barrier. If that is what is required to even achieve simple ATP binding, then evolution would need to be incessantly running unsuccessful trials. The machinery to construct, use and benefit from a
potential protein product would have to be in place, while failure after failure results. Evolution would make Thomas Edison appear lazy, running millions of trials after millions of trials before finding even the tiniest of function.
http://darwins-god.blogspot.com/2010/12/how-proteins-evolved.html
This following paper 'put the nail in the coffin' for Szostak's work:
A Man-Made ATP-Binding Protein Evolved Independent of Nature Causes Abnormal Growth in Bacterial Cells
Excerpt: "Recent advances in de novo protein evolution have made it possible to create synthetic proteins from unbiased libraries that fold into stable tertiary structures with predefined functions. However, it is not known whether such proteins will be functional when expressed inside living cells or how a host organism would respond to an encounter with a non-biological protein. Here, we examine the physiology and morphology of Escherichia coli cells engineered to express a synthetic ATP-binding protein evolved entirely from non-biological origins. We show that this man-made protein disrupts the normal energetic balance of the cell by altering the levels of intracellular ATP. This disruption cascades into a series of events that ultimately limit reproductive competency by inhibiting cell division."
http://www.plosone.org/article/info:doi%2F10.1371%2Fjournal.pone.0007385
Here is a very interesting comment by Jack Szostak himself:
The Origin of Life on Earth
Excerpt: Every living cell, even the simplest bacterium, teems with molecular contraptions that would be the envy of any nanotechnologist. As they incessantly shake or spin or crawl around the cell, these machines cut, paste and copy genetic molecules, shuttle nutrients around or turn them into energy, build and repair cellular membranes, relay mechanical, chemical or electrical messages—the list goes on and on, and new discoveries add to it all the time.
It is virtually impossible to imagine how a cell’s machines, which are mostly protein-based catalysts called enzymes, could have formed spontaneously as life first arose from nonliving matter around 3.7 billion years ago.
Dr. Jack Szostak - Nobel Laureate and leading Origin of Life researcher who, despite the evidence he sees first hand, and even readily admits to, still believes 'life' simply 'emerged' from molecules
http://www.scientificamerican.com/article.cfm?id=origin-of-life-on-earth
But Nick I guess I can see why you only alluded to this evidence and failed to mention any of this evidence specifically. It would have required having knowledge, competency, and honesty all at once to mention those results to your readers.
By the way Nick why don't you demonstrate a little integrity yourself and address the following honestly:
DeleteOn top of the fact that Origin of Life researcher Jack Szostak, and others, failed to generate any biologically relevant proteins, from a library of trillions of randomly generated proteins, proteins have now been shown to have a ‘Cruise Control’ mechanism, which works to ‘self-correct’ the integrity of the protein structure from any random mutations imposed on them.
Proteins with cruise control provide new perspective:
"A mathematical analysis of the experiments showed that the proteins themselves acted to correct any imbalance imposed on them through artificial mutations and restored the chain to working order."
http://www.princeton.edu/main/news/archive/S22/60/95O56/
Cruise Control permeating the whole of the protein structure??? This is an absolutely fascinating discovery. The equations of calculus involved in achieving even a simple process control loop, such as a dynamic cruise control loop, are very complex. In fact it seems readily apparent to me that highly advanced mathematical information must reside 'transcendentally' along the entirety of the protein structure, in order to achieve such control of the overall protein structure. This fact gives us clear evidence that there is far more functional information residing in proteins than meets the eye. Moreover this ‘oneness’ of cruise control, within the protein structure, can only be achieved through quantum computation/entanglement principles, and is inexplicable to the reductive materialistic approach of neo-Darwinism!
Ho hum. CH mails another one in.
ReplyDeleteHow many times have you used the same dishonest misrepresentation of those particular probability numbers now CH? Seven? Ten?
I guess when the DI is paying you on a per lie basis it doesn't matter if you repeat yourself. They're going for quantity, not quality.
dishonest misrepresentation of those particular probability numbers
DeleteHow so?
Cornelius Hunter
DeleteT: dishonest misrepresentation of those particular probability numbers
How so?
The numbers don't support your claimed "Several different studies indicate that, at a minimum, about 10^70 (a one followed by 70 zeros) evolutionary experiments would be needed to get close enough to a workable protein design before evolutionary mechanisms could take over and establish the protein in a population."
Take the 10^63 number from this paper. The authors were investigating how much mutational change a particular protein could tolerate and still function. The 1 in 10^63 represents the probability of working out of the total possible 92-residue sequences. It says nothing about taking 10^63 tries or having to sample all possible sequences to get the working protein in the first place. Your use of the number would only be valid in the case all 92 residues self assembled all at once.
And there's the 10^70 number you pulled from here. The authors were studying how quickly the proteins in a bacteriophage could advance up the fitness landscape through 'adaptive walks' of one mutational substitution at a time. What they found was that their laboratory specimens would rapidly increase in fitness but tended to get stuck in local maxima instead of finding the absolute fitness peak exhibited by a wild type phage. The researchers estimate that to find the absolute fitness peak would take 10^70 tries if the evolution was limited to single random substitution mutations. But in the very next sentence they point out that real evolution incorporates many other mechanisms for genetic variation that greatly shorten the time, such as homologous recombination. So your use of the 10^70 number is pure bull.
I really don't get you CH. Half the time you seem like a decent enough guy, cracking jokes, running this blog with minimal censorship. Then you turn around and post the most egregious misrepresentations and lies about actual scientific work. These aren't simple differences in interpretations either. They're deliberate dishonesty on your part.
How you look at yourself in the mirror is beyond me.
Thorton, you state:
Delete'But in the very next sentence they point out that real evolution incorporates many other mechanisms for genetic variation that greatly shorten the time, such as homologous recombination.'
Revisiting the Central Dogma in the 21st Century - James A. Shapiro - 2009
Excerpt (Page 12): Underlying the central dogma and conventional views of genome evolution was the idea that the genome is a stable structure that changes rarely and accidentally by chemical fluctuations (106) or replication errors. This view has had to change with the realization that maintenance of genome stability is an active cellular function and the discovery of numerous dedicated biochemical systems for restructuring DNA molecules.(107–110) Genetic change is almost always the result of cellular action on the genome. These natural processes are analogous to human genetic engineering,,, Homology-dependent and -independent recombination. For many years, geneticists spoke of legitimate and “illegitimate” recombination. The former was used in genetic mapping studies and exchanged segments in DNA molecules that had extensive homologous sequences. The latter produced rearrangements involving exchanges between DNA molecules with little or no sequence homology. We now know that living cells contain multiple biochemical systems for joining together DNA molecules in ways that are either homology-dependent or -independent.110 ,,,(Page 15) Genome change arises as a consequence of natural genetic engineering, not from accidents. Replication errors and DNA damage are subject to cell surveillance and correction. When DNA damage correction does produce novel genetic structures, natural genetic engineering functions, such as mutator polymerases and nonhomologous end-joining complexes, are involved. Realizing that DNA change is a biochemical process means that it is subject to regulation like other cellular activities. Thus, we expect to see genome change occurring in response to different stimuli (Table 1) and operating nonrandomly throughout the genome, guided by various types of intermolecular contacts (Table 1 of Ref. 112).
http://shapiro.bsd.uchicago.edu/Shapiro2009.AnnNYAcadSciMS.RevisitingCentral%20Dogma.pdf
Thus your appeal to 'non-random' evolutionary processes to explain 'real evolution' smacks of 'deliberate dishonesty on your part'. Why should you appeal to the elegant 'non-random' design that is already present in the cell to cover up the failure of random evolutionary processes to generate biologically relevant proteins? How you look at yourself in the mirror is beyond me.
Thorton:
DeleteTake the 10^63 number from this paper. The authors were investigating how much mutational change a particular protein could tolerate and still function. The 1 in 10^63 represents the probability of working out of the total possible 92-residue sequences.
No, that is not what the number represents. Or perhaps your explanation is just not very clear. Just to be clear, the number, 1 in 10^63, equals the estimated fraction of sequences which would adopt the N-terminal domain of lambda repressor.
It says nothing about taking 10^63 tries or having to sample all possible sequences to get the working protein in the first place. Your use of the number would only be valid in the case all 92 residues self assembled all at once.
You must not know much about proteins. What you are discussing here is precisely the problem. These fitness landscapes away from the native protein are rugged. That’s not controversial. Likewise, the fitness drops off rapidly as you move away from the native sequence. Everything science is telling us indicates you do not have smooth, gradual fitness landscapes sloping up to the native protein.
The researchers estimate that to find the absolute fitness peak would take 10^70 tries if the evolution was limited to single random substitution mutations. But in the very next sentence they point out that real evolution incorporates many other mechanisms for genetic variation that greatly shorten the time, such as homologous recombination. So your use of the 10^70 number is pure bull.
No, they did not demonstrate a faster way. They pointed out that gradualism wouldn’t work, and so some other mechanisms must have been at play. In other words, as usual the evolutionists assumed evolution from the outset. Negative results can do no harm to evolution, they merely indicate another sub hypothesis must be employed. The authors had nothing but speculation about recombination, and they admitted that recombination wouldn’t alter the landscape itself, but speculated that it “may affect the speed of search in sequence space.” Of course they’re going to speculate, they’re assuming evolution from the outset. They didn’t provide any details of how that could happen, because there are no details, merely speculation. There is no evidence of theory that recombination could solve this problem. Jumping from one sequence in a rugged landscape to some other location isn’t going to solve a 27+ orders of magnitude shortfall. All you are getting is a non local move. And it is a random move. It is not moving up some mythical fitness slope.
I really don't get you CH. Half the time you seem like a decent enough guy, cracking jokes, running this blog with minimal censorship. Then you turn around and post the most egregious misrepresentations and lies about actual scientific work. These aren't simple differences in interpretations either. They're deliberate dishonesty on your part. How you look at yourself in the mirror is beyond me.
Well you are certainly correct that “These aren't simple differences in interpretations.” What I am reporting is what the science is telling us. This is not particularly controversial. Evolutionists aren’t going to say “Gee, the science indicates evolution probably didn’t occur.” It isn’t going to happen as that simply is not one of the choices. It is not an option. They’ll always present another just-so story to explain the findings. But setting those aside and just looking at the evidence, there really isn’t a lot of room for different interpretations, as you say. And this is pretty easy to see when you study the science, and set aside the speculation and just-so stories.
There’s no question that the evidence is substantially against evolution, even as reported by the evolutionists. Could this change? Sure. Does it mean evolution is necessarily false? No. But the scientific evidence does give pretty strong indications.
Cornelius Hunter
DeleteNo, that is not what the number represents. Or perhaps your explanation is just not very clear. Just to be clear, the number, 1 in 10^63, equals the estimated fraction of sequences which would adopt the N-terminal domain of lambda repressor.
LOL! So now you're admitting that the number doesn't represent the "number of evolutionary experiments that would be needed to get close enough to a workable protein design."
That's the problem with lying about the actual contents of a scientific paper CH. You end up perjuring yourself.
No, they did not demonstrate a faster way. They pointed out that gradualism wouldn’t work, and so some other mechanisms must have been at play.
LOL! You mean all the other mechanisms of genetic variations besides single point mutations, mechanisms that have been well known and well documented for decades.
There’s no question that the evidence is substantially against evolution, even as reported by the evolutionists.
Oh dear, there goes the dishonest propagandist in you again. You must really need the DI's money something awful. I bet you wear out the door of the confessional asking forgivness for all the lies.
LOL! So now you're admitting that the number doesn't represent the "number of evolutionary experiments that would be needed to get close enough to a workable protein design."
DeleteThat's the problem with lying about the actual contents of a scientific paper CH. You end up perjuring yourself.
No, the 1 in 10^63, 1 in 10^70, 1 in 10^77, etc., do represent the number of evolutionary experiments that would be needed to get close enough to a workable protein design. Obviously you don’t understand the science here and this getting embarrassing. Again, the fitness landscape falls off rapidly as you move away from the native sequence and if a rugged landscape after that. You can’t just play rhetorical games with these numbers. They’ve been arrived at by different investigators, using different methods. This is what science is indicating.
LOL! You mean all the other mechanisms of genetic variations besides single point mutations, mechanisms that have been well known and well documented for decades.
Yes, precisely. You obviously don’t understand optimization and search either, or the curse of dimensionality. You don’t just magically move toward native sequences with non local moves. Sorry, but evolution doesn’t just happen. That’s why the evolutionists didn’t give any details, but instead hmmed and hawed for a few sentences and dropped it like a hot potato. It’s just astronomically unlikely to make a non local move that takes you even in the right direction in hyperspace. If you want to demonstrate it for us and explain how this happens, then be my guest. And while you’re doing it we’ll be contacting the Nobel prize people so they can get you your medal. This should be interesting.
Cornelius Hunter
DeleteNo, the 1 in 10^63, 1 in 10^70, 1 in 10^77, etc., do represent the number of evolutionary experiments that would be needed to get close enough to a workable protein design.
LOL! Of course they don't. The phages that rapidly found the local fitness maxima were perfectly good and workable. They just weren't as optimized as the wild phages. In the real world an organism doesn't have to be perfect, it just has to be better than its neighbors. Differential reproductive success, remember? Pretending to not understand the basics doesn't make you look very good at all.
That’s why the evolutionists didn’t give any details, but instead hmmed and hawed for a few sentences and dropped it like a hot potato.
Double LOL! That study wasn't done in a vacuum CH. There are tens of thousands of others that show how the mechanisms of genetic variation work. Are you going to go with the stupid Creationist demand that every genetics paper produced must replicate the decades of work that came before it?
I know you're getting paid to write this hooey, but you must think everyone is as clueless as the Creationists you pander to.
The phages that rapidly found the local fitness maxima were perfectly good and workable. They just weren't as optimized as the wild phages.
DeleteNo, you’ll need to learn more about biology in order to overcome your “evolution is a fact” dogma. The phages did not find any “local fitness maxima.” Nor did even a single protein “find” such a maxima. The researchers randomized merely a segment of a single protein.
Double LOL! That study wasn't done in a vacuum CH. There are tens of thousands of others that show how the mechanisms of genetic variation work.
Well then you should make sure to tell the authors about these “tens of thousands” of papers. That sounds very important, for the authors certainly should have cited some of those “tens of thousands” of papers. I’m sure they’ll be delighted to hear from you. One paper you can scratch off the list, though, is the one paper the authors actually did cite as “suggesting” the importance of recombination or DNA shuffling, since it doesn’t solve the problem like those other “tens of thousands” of papers do.
Are you going to go with the stupid Creationist demand that every genetics paper produced must replicate the decades of work that came before it?
You’ve argued strenuously that evolution must be a fact. Unfortunately the science just doesn’t back that up, creationism or no creationism.
Cornelius Hunter
DeleteThe phages that rapidly found the local fitness maxima were perfectly good and workable. They just weren't as optimized as the wild phages.
No, you’ll need to learn more about biology in order to overcome your “evolution is a fact” dogma. The phages did not find any “local fitness maxima.” Nor did even a single protein “find” such a maxima. The researchers randomized merely a segment of a single protein.
Maybe you should try actually reading the paper instead of butchering it
"On a rugged landscape, the adaptive walk can become trapped by local fitness optima. To find the global peak on the rugged landscape, the adaptive walk requires enormous sequence diversity."
"Although adaptive walking in our experiment must have encountered local optima with basin sizes of 1, 2, and probably 3, the observed stagnations are likely due only to the mutation-selection-drift balance."
Falsehoods on top of falsehoods just make you look worse every day CH.
Well then you should make sure to tell the authors about these “tens of thousands” of papers.
No authors cite every last paper done in the last 50 years which support the underlying principles behind biology. That work has already been demonstrated and accepted. The papers are there for everyone to read, and for certain Creationist to lie about.
T: Are you going to go with the stupid Creationist demand that every genetics paper produced must replicate the decades of work that came before it?
You’ve argued strenuously that evolution must be a fact. Unfortunately the science just doesn’t back that up, creationism or no creationism.
So I guess the answer is yes, you really are going that stupid Creationist route.
Maybe you should try actually reading the paper instead of butchering it
Delete"On a rugged landscape, the adaptive walk can become trapped by local fitness optima. To find the global peak on the rugged landscape, the adaptive walk requires enormous sequence diversity."
"Although adaptive walking in our experiment must have encountered local optima with basin sizes of 1, 2, and probably 3, the observed stagnations are likely due only to the mutation-selection-drift balance."
Well you got the right part of the paper. Now you just need to understand it. They only randomized one part of one protein. The majority of the phage was fixed at the extant design. The search was not over the entire phage design space, only that of the segment of one protein. But that doesn’t sound as good.
No authors cite every last paper done in the last 50 years which support the underlying principles behind biology. That work has already been demonstrated and accepted. The papers are there for everyone to read, and for certain Creationist to lie about.
Ah yes, “the papers are there, trust us.” There’s no need to look behind the curtain, it has all been proven (to our satisfaction). We know the truth, so move along, nothing to see here. Strange that the authors didn’t cite a single one of this mysterious massive database of “tens of thousands” of papers, while they did cite one meager paper that grasped for straws and “suggested” a solution. Just trying to fool us I guess.
Monod said that in what, 1977? It is incredible that you think progress since then in our understanding is a net negative for evolutionary theory. The fact that hydro-plate theory, creation science, and intelligent design haven't advanced since their definition is also not a net positive for them.
ReplyDeleteApplication of religious heuristics like "older sources are better" doesn't work in science. Get used to it.
It is incredible that you think progress since then in our understanding is a net negative for evolutionary theory.
DeleteHow is it that a 27 order of magnitude shortfall fails to be a "net negative" for evolution? What progress are you thinking of that negates such a shortfall?
Application of religious heuristics like "older sources are better" doesn't work in science. Get used to it.
Where did I say that?
It is one thing to mess with biology or the Catholic Church or even the Constitution of the United States but it is quite another to change the historical record of "Dallas" with your conspiracy theories. The writers were not responsible for the Bobby Ewing's absence from Dallas. Patrick Duffy chose to leave the show. Second,it was the producers of Dallas who realized their mistake in letting Duffy leave the show when the ratings dropped. Hagman convinced Duffy to return. The writers made no mistake,in fact they created one of the classic moments in TV history.
DeleteAh, hah. Thank you for that correction. As you can see there are some holes in my classical training.
DeleteAlso, apparently Patrick's career did not take off as much as he had anticipated, which made him more willing to rejoin the cast.
DeleteFascinating stuff! ;)
Apology accepted, we will pretend it was a dream. Old enough to remember "Man From Atlantis" ?
DeleteAh, that's funny. I never heard of that show.
DeleteWhat's the matter batspit77, not enough people paying attention to your idiotic C&Ped word salads over at UncommonlyDense anymore?
ReplyDeleteBully Arrington sure killed that place deader than dead with all the bannings, didn't he?
But Dr Hunter, evolutionists have great FAITH that it can happen - praise be to darwin! ;-)
ReplyDeleteHere is a article, by Dr. Hunter, that clearly illustrate that the protein evidence, no matter how crushing to Darwinism, is always crammed into the Darwinian framework by Evolutionists:
ReplyDeleteThe Hierarchy of Evolutionary Apologetics: Protein Evolution Case Study - Cornelius Hunter - January 2011
http://darwins-god.blogspot.com/2011/01/hierarchy-of-evolutionary-apologetics.html
To question neo-Darwinism is simply not allowed no matter how crushing the evidence is against it!
During chemical evolution in prebiotic times and at the beginning of biological evolution, all those molecules of which every living being is built had to appear.
ReplyDeleteHow does prebiotic evolution occur without a selection mechanism, pray tell? How can a selection mechanism decide which random sequence will be needed for an eventual life form that will not appear for millions of years after? And how can a sequence last millions of years without being destroyed by natural destructive forces?
The problem with evolution is not that it has a very low probability of occurring. The problem is that it has a ZERO probability of occurring. Both evolutionists and critics of evolution are overlooking an aspect of random organization (an oxymoron in any other context) that renders evolution not just improbable but impossible. Both camps assume that the extremely complex combination sequences responsible for life can happen given enough time but this is simply not true.
The truth is that nature maintains a chaotic equilibrium that can only be broken if the random constructive forces are greater than the random destructive forces. Life can appear only if there is a major imbalance between the probability of the two forces. However, this will not happen because the two forces have equal probability. In other words, the random appearance of any initial sequence that can partially and potentially lead to life forms will be destroyed by random destructive forces long before that happens. The probability of that happening is 100%.
Conclusion: Evolution is a religion of cretins for cretins.
Louis the fruit loop
ReplyDeleteThe problem with evolution is not that it has a very low probability of occurring. The problem is that it has a ZERO probability of occurring.
You forgot to show your probability calculations.
The probability of life appearing at random is equal to the probability of a star evolving a rectangular shape. That is to say, the probability is zero.
ReplyDeleteConclusion: Evolution is a religion of morons for morons.
Louis the fruit loop
ReplyDeleteThe probability of life appearing at random is equal to the probability of a star evolving a rectangular shape. That is to say, the probability is zero.
Hey fruit loop, you forgot to show your probability calculations again.
And please, leave your Mom out of this.
I was not talking to you, moron. Kiss, kiss, kiss my you know what.
DeleteLouie the fruit loop
ReplyDeleteI was not talking to you, moron. Kiss, kiss, kiss my you know what.
Kiss your Mom? Again??
Sorry, but I hate standing in line.
At least we know how much we despise each other. That's one bright spot.
DeleteYankees and Red Sox
DeleteLouis the fruit loop
ReplyDeleteAt least we know how much we despise each other. That's one bright spot.
I don't despise you at all Louis. I pity those like you with mental and emotional problems.
Yeah, right. Nothing you say is the truth, Thornton. You pontificate about your alleged intellectual superiority but you are in fact stupid. Answer the questions I posed, goddammit, or admit your stupidity.
Delete1. How does prebiotic evolution occur without a selection mechanism?
2. How can a selection mechanism decide which random sequence will be needed for an eventual life form that will not appear for millions of years afterwards?
3. How can a sequence last millions of years without being destroyed by natural destructive forces?
You cannot answer these questions because you are a bozo masquerading as a scientist. Nobody is fooled.
I apologize to the Red Sox for comparing them to Louis
DeleteLouis the fruit loop:
ReplyDelete1. There are selection mechanisms.
Multilevel Selection in Models of Prebiotic Evolution II: A Direct Comparison of Compartmentalization and Spatial Self-Organization
2. They don't.
3. If a sequence is beneficial it keeps being replicated as it. There are many know highly conserved sequences.
At least you didn't drool as much as normal on this one.
This comment has been removed by a blog administrator.
DeleteLOL!
DeleteGood job Louis. You made up for the last one by drooling twice as much on this one.
This comment has been removed by a blog administrator.
DeleteTake your meds Louis, before the drool shorts out your keyboard.
ReplyDeleteThis comment has been removed by a blog administrator.
DeleteThorton: "1. There are selection mechanisms."
ReplyDeleteIf your computer model only has 2 entities, why can't they get it to work in the lab? Maybe they made too many assumptions?
Thorton: "2. They don't."
They do - http://tolweb.org/Bilateria/2459
Hox genes for mice and fruitfly eyes are nearly identical. Aren't mice lucky they also independently developed eyes so they could take advantage of the same Hox gene? Isn't that just another example of painting the target before the shot (in this case literally :D )?
Thorton: "If a sequence is beneficial it keeps being replicated as it. There are many know highly conserved sequences."
From the RNA world? Really? Which?
If your computer model only has 2 entities, why can't they get it to work in the lab? Maybe they made too many assumptions?
ReplyDeleteBecause you're assuming we should simply be able to use induction to mechanically extrapolate what the first replicators were, the conditions under which they appeared, etc.
However, as Karl Popper pointed out, induction is a myth.
We create theories using conjecture, then test those theories using observations, not vice versa.
Scott: "Because you're assuming we should simply be able to use induction to mechanically extrapolate what the first replicators were, the conditions under which they appeared, etc"
ReplyDeleteThe reason they could not get it to work in the lab certainly has nothing to do with my assumptions. Besides their computer program did not model the replicators by their structure anyway, and it assumed the ability to replicate from the get go.
Scott: "We create theories using conjecture, then test those theories using observations, not vice versa."
Did you learn that via the principle of induction?
John: The reason they could not get it to work in the lab certainly has nothing to do with my assumptions. Besides their computer program did not model the replicators by their structure anyway, and it assumed the ability to replicate from the get go.
ReplyDeleteYour expectation that it should be simple to duplicate in the lab has nothing to do with your assumptions about how knowledge is created?
John: Did you learn that via the principle of induction?
Are we unable to criticize our explanations for how we make progress, find errors in these explanations and discard them?
Scott: "Your expectation that it should be simple to duplicate in the lab has nothing to do with your assumptions about how knowledge is created?"
ReplyDeleteTo be clear, I think it is impossible to reproduce in the lab because of this; "Secondly, we design vesicle-level processes such that they do not introduce an extra burden for survival that is independent of the replicator dynamics itself; e.g., we neglect the problem of substrate uptake through membranes". When replicator studies are done in the lab, this is what limits 'growth' and therefore the ability of nature to select.
Scott: "Are we unable to criticize our explanations for how we make progress, find errors in these explanations and discard them?"
Not without using language, and that is based on inductive reasoning.