Posted on 11/01/2007 5:53:26 PM PDT by truthfinder9
This will be interesting, a documentary movie by Ben Stein on the new wave of thought police and academic suppression in academia and science:
Ben Stein, in the new film EXPELLED: No Intelligence Allowed
His heroic and, at times, shocking journey confronting the world’s top scientists, educators and philosophers, regarding the persecution of the many by an elite few.
In theatres near you, starting February 2008
Ben travels the world on his quest, and learns an awe-inspiring truth…that bewilders him, then angers him…and then spurs him to action!
Ben realizes that he has been “Expelled,” and that educators and scientists are being ridiculed, denied tenure and even fired – for the “crime” of merely believing that there might be evidence of “design” in nature, and that perhaps life is not just the result of accidental, random chance.
To which Ben Says: "Enough!" And then gets busy. NOBODY messes with Ben.
***
At Big Science Academy we take our motto seriously: “No Intelligence Allowed.” And this year, we are proud to report that in every subject but Science, students and faculty are free to challenge ideas, and seek truth wherever it may lead.
But Science is different. In Science, there is no room for dissent, for dissent is dangerous. That is why we at Big Science simply refuse to allow it. Like dancing, “dissent” can lead to other things.
As Class President Richard Dawkins put it so well: “Shut up!”
As you know…last year we had the misfortune of “presupposition of design” rearing its ugly head, with several students challenging Neo-Darwinian materialism, and arguing incessantly for the right to examine Intelligent Design.
They were all Expelled, of course – but still: it just goes to show where academic freedom can lead, if not shut down immediately!
Sincerely,
Charles Darwin Principal, President, Admissions and Diversity Affairs Officer, Big Science Academy “No Intelligence Allowed”
The simplest known living cell is extraordinarily complex. You say that the first cell could have been simpler. I agree, it could have been simpler. However, we have no evidence of such a simpler cell.
Furthermore, various analysts have shown that any cell capable of replicating must have a certain minimum level of complexity, and that is still too complex to have come about randomly.
So your argument is rather weak.
I also think you have a fundamental misunderstanding about the “burden of proof.” You seem to think that proponents of ID are obligated to *prove* that the first living cell could not have fallen into existence at random. But as I have tried to explain before, that is impossible. That would be like trying to prove that the entire text of Macbeth never appeared on the sands of the Sahara Desert due to random winds. It cannot be proven. But that means it is “unfalsifiable,” hence unscientific.
Until the first cell can be explained by purely naturalistic, random mechanisms, ID is the default reality that must be accepted. Whether you like that or not is irrelevant. And if it violates your naturalistic premises, then you need to rethink your premises based on the actual evidence — as opposed to some imaginary simpler cell that has never been found.
Very good. The details of biological design are explained by descent with modication and natural selection.
If you have an alternate agent for biological design, and have evidence for how, when and where it operates, whip it out.
[[Very good. The details of biological design are explained by descent with modication and natural selection.]]
no I’m afraid that is not true- it is biologically and mathematically impossible for the trillions of changes between disimilar species makes it impossible for design to be constructed through random mutations as required by descent with modification.
Show us your math.
Who needs science to “prove” there is a God? I can tell you for a fact He’s far more real to me (and billions like me) than you are.
Are you questioning the age or the birthday? The leap year person will have indeed aged another year, birthday or no.
The details could be understood as you propose, but I do not consider assumptions regarding the connection between morphology and history to be reliable when stretched into periods of unobserved history. To say such things have been “explained” is to overstretch credibility.
I’m sorry- I did list Creationsafari by accident- they track more the biological blunders of science and point out the fallicies perpetrated on society in the name of science. The site I was thinking to list was Darwinisdead.com or somethign liek that- I can’t recall the name now- but Behe’s site, Demski’s site etc are all full of bioligical importance of hte study of Design. As mentioend before, when science is stuck searchign for cures based on their beleif that everythign is mutated and random, then they obviously can not look for hte links in design and the conenctions between the designs. They are stuck beleiving species share common mutational experiences, and can’t conceive of the possibility that we are all uniquely created, and thus the biologcal research is stunted to common descent only- there are several articles on tyhis site that discuss how TOE has hampered the search for cures.
I don’t really care if Behe is mistakenly bound to descent with modification- he has NO evidences to back that particular belief up- however, I am very much interested in the evidences he gives for intelligent design and specified irreducible complexity, and hte implications it has in our scientific investigations- Besides, you seem to be under the illusion that ONLY ID has to be specifically advancing medicine to be concidered a valid science? First- good news, it is advancing understanding in that department, secondly, it is advancing knoweldge in several other areas as well as laid out on Behe’s site, Demski’s and many others that specifically deal with the science of ID.
[[I asked for “how”. Please explain HOW to falsify it.]]
Behe explained HOW to falsify ID i nthe famous sham of a trial called the dover trial- and the site Darwinisdead has given several examples of how it can be falsified. Behe however is under the delusion that if an instance of ID can be falsified that that would then render the whole system wrong- however, it would not- it would render that one particular instance wrong and would indicate another approach is needed.
Here are several links to the falsifiability of ID, not that this is even the gold standard of science, but for your edification, here they are:
http://www.evolutionnews.org/2006/01/intelligent_design_is_empirica.html
http://www.discovery.org/scripts/viewDB/index.php?command=view&id=584
http://www.idthefuture.com/2007/08/what_is_falsifiability_and_can.html
Exposing hte sham and lies that were presented for evolution in the dover tiral and hsowing ID is falsifiable:
http://www.evolutionnews.org/2005/09/title_43.html
If Evolution by common descent with modification can be proven, then you’ve falsified Intelligent design- so far, Macroevolution has not been proven and is nothign but an assumption.
as Well, I’d liek you to take a look at just what consititutes science and what doesn’t- Karl Popper introduced an unscientific criteria for science inthat somethign must be falsifiable to be concidered science- Evolutionists opposed to any opposing hypothesis have taken this unscientific criteria and shoved it in the faces of ID and Creationsism as though it has some kind of scientific weight when infact it doesn’t- A theory is simply:
theo·ry n. a formulation of apparent relationships or underlying principles of certain observed phenomena which have been verified to some degree.
science is:
sci·ence n. 1 the state or fact of knowledge 2 systematized knowledge derived from observation, study and experimentation carried on in order to determine the nature or principles of what is being studied
While it is an interesting proposal to see if somethign can be falsified, falsifiability are MOT what constitute TRUE science
http://www.trueorigin.org/creatheory.asp
You look it up- They held a whole huge meeting presenting hte math by top scientists and mathemeticians in the world- I’ve presented links time and time again- and time and time again whenever a new thread talking about the issue crops up folks like you come in stomping hter foot and demanding the evidence which onlyy be ignored and will be shoved aside when hte next thread on the issue crops up and you come in demanding the math- this time you do your own work- the meeting was the Wistar meeting- As well there is plenty on the net showing that there simply is not enough time to accumulate ‘positive mutations’ in the numbers needed for descent with modification to be a reality. Google “Mathemtatical impoosibility of Macroevolution” and you’ll have more links than you can shake a stick at, yet, I’m predicting they will be ignored, dismissed, and the demand will crop up again hte next thread on the viability of evolution
and don’t worry- Google will correct the spelling of “Mathemtatical impoosibility of Macroevolution” when you type it in lol
Fixed it for you.
Although I am a layman, the two articles I read relied, entirely it appears, on Behe's irreducable complexity arguments. Is this correct?
Oh, I see. So you don’t need no stinkin’ evidence of that imaginary simpler cell. If you can imagine it, that’s proof enough.
You guys with your double standards never cease to amaze me. I’m starting to realize that you guys are beyond the reach of reason.
By the way, the British astronomer Fred Hoyle was an atheist who was absolutely convinced of intelligent design and wrote books about it. So much for the canard that we need to find the “designer.”
I want you to prove to me that you understand the math and the consequences of the calculations. Without that understanding you are not in a position to discern accuracy from propaganda.
Show me the numbers. Not a link, nor a group of links. I want you to explain it to me in your own words.
Do the same for information.
I suspect you haven’t a clue about either abiogenesis or information. I also suspect you haven’t a clue about probability.
Prove me wrong.
One more thing about this notion that design cannot be detected without finding and identifying the “designer.”
Frankly, I am amazed that some people cannot see beyond this little ruse. If it were true, you could not determine that a car is designed until you find the designer.
OK, you say, we know about car designers. Fine. Suppose we travel someday to another galaxy and find the remnants of a lost civilization. Suppose we find evidence of advanced technology, but no sign of life because perhaps it was all vaporized in a massive nuclear war. According to your “logic,” we cannot determine that their technology was “designed” until we find the designers.
The whole notion that science cannot detect design without also identifying and studying the designer is patent nonsense. If you cannot see past this ruse, you cannot think their way out of a wet paper bag. I’d be downright embarrassed if I were that unintelligent. (Pun intended.)
Better yet, suppose we find an advanced electronic gadget on the Moon or Mars someday that we know was not left behind by a human. Could we not determine that it was intelligently designed until we find the designer? Of course not.
Suppose SETI detects an apparently intelligent signal from space. Can they not determine that the source of the signal was intelligent until they identify the source? Of course not.
Suppose forensic scientists detect evidence of a murder. Can they not conclude that a murder occurred until the identify and find the murderer? Of course not.
I’m sorry, but the whole notion that design cannot be detected without identifying the designer is just incredibly stupid. No way around it.
Q. And let me just ask you a few questions, and you tell me if I’m fairly summarizing the results of your computer simulation. What you’re asking is, how long will it take to get — and please follow with me, I’m trying to do this slowly and methodically — two or more specific mutations, in specific locations, in a specific gene, in a specific population, if the function is not able to be acted on by natural selection until all the mutations are in place, if the only form of mutation is point mutation, and the population of organisms is asexual?
A. I would have to look at that statement closely because there are so many different aspects to it that I don’t trust myself to sit here and listen to you say that and form a correct judgment.
Q. Anything I said about that sound incorrect?
A. If you repeat it again, I’ll try.
Q. I’d be happy to. Two or more specific mutations?
A. Actually, this dealt with one or more.
Q. One or more mutations?
A. Yes. If you notice, in figure — if you notice in figure 3, you look at the x axis, you notice that there are data points there that start at one. So we considered models where there were one, two, and more mutations.
Q. Fair enough. In specific locations?
A. No, that’s not correct. We assumed that there were several locations in the gene that could undergo these selectable mutations, but we did not designate where they were.
Q. In the specific gene?
A. We were considering one gene, yes.
Q. In a specific population?
A. Yes.
Q. Okay. If the function is not able to be acted on by natural selection until all mutations are in place?
A. Yes, that’s what’s meant by multiple amino acid residue, multi-residue feature, yes.
Q. If the only form of mutation is point mutation?
A. Yes, that’s a very common type of mutation, which is probably half or more of the mutations that occur in an organism.
Q. And if the population of organisms is asexual?
A. Yes, we did not — actually, we did not confine it just to asexuals, but we did not consider recombination.
Q. Are prokaryotes an example of the kind of organism that you were studying there?
A. Again, we weren’t studying organisms, but, yeah, they’re a good example of what such a model has in mind.
Q. And to say this very colloquially, you conclude that it will take a large population a long time to evolve a particular function at disulfide bond, right?
A. A multi-residue feature. That’s correct, that’s correct.
Q. And specifically —
A. I’m sorry.
Q. Go ahead.
A. Let me just finish. Depending on — as we emphasize in the paper, it depends on the population size. And, of course, prokaryotes can oftentimes grow to very large population sizes.
Q. And here the conclusion, the calculations you concluded was that, if you had a population of 10 to the 9th power, that’s a population of 1 billion?
A. That’s correct.
Q. To produce a novel protein feature through the kind of multiple point mutations you’re talking about, it would take 10 to the 8th generations, that’s what it says in the abstract, correct?
A. If, in fact, it was — if, in fact, the intermediate states were not selectable.
Q. Okay.
A. And if this is by gene duplication as well.
Q. Okay. So 10 to the 8th generation, that’s 100 million generations?
A. That’s correct.
Q. And yesterday, you explained about bacteria, that 10,000 generations would take about two years in the laboratory, correct?
A. Yes.
Q. So 100 million generations, that would take about 20,000 years?
A. I’m sorry?
Q. 100 million generations, which is what you calculated here, that would take about 20,000 years?
A. Okay, yes.
Q. And those are numbers based on your probability calculations in this model, correct?
A. Yes.
Q. Now it would be true that, if you waited a little longer, say, instead of 10 to 9th generations, 10 to the 10th generations, then it would mean that you wouldn’t need as big a population to get the function that you are studying?
A. That’s right. The more chances you have, the more likely you are to develop a feature. And the chances are affected by the number of organisms. So if you have a smaller population time, and more generations, that could be essentially equal to a larger population size and fewer generations.
Q. So, as you said, so if we get more time, we need less population to get to the same point, and if we had more population, less time?
A. That’s correct, yes.
Q. Now would you agree that this model has some limitations?
A. Sure.
Q. And you, in fact, were quite candid in indicating that in the paper?
A. That’s correct.
Q. And if we could turn to, what I believe is, page 8 of the document. And if you look in the paragraph that’s actually continued from the previous page that says, we strongly emphasize. And if you could —
A. I’m sorry. What page number is that?
Q. It’s page 8 in the document. And it’s up on the screen as well.
A. Yes, okay. I’ve got it.
Q. Could you read into the record the text to the end of the paragraph beginning with, we strongly emphasize?
A. We strongly emphasize that results bearing on the efficiency of this one pathway as a conduit for Darwinian evolution say little or nothing about the efficiency of other possible pathways. Thus, for example, the present study that examines the evolution of MR protein features by point mutation in duplicate genes does not indicate whether evolution of such features by other processes, such as recombination or insertion/deletion mutations, would be more or less efficient.
Q. So it doesn’t include recombination, it doesn’t include insertion/deletion of the mutations?
A. That’s correct.
Q. And those are understood as pathways for Darwinian evolution?
A. They are potential pathways, yes.
Q. This study didn’t involve transposition?
A. No, this focuses on a single gene.
Q. And transpositions are, they are a kind of mutation, is that right?
A. Yes. They can be, yes.
Q. And so that means, this simulation didn’t examine a number of the mechanisms by which evolution actually operates?
A. That is correct, yes.
Q. And this paper, let’s be clear here, doesn’t say anything about intelligent design?
A. Yes, that’s correct. It does imply irreducible complexity but not intelligent design.
Q. But it doesn’t say it?
A. That’s correct.
Q. And one last other question on your paper. You concluded, it would take a population size of 10 to the 9th, I think we said that was a billion, 10 to the 8th generations to evolve this new disulfide bond, that was your conclusion?
A. That was the calculation based on the assumptions in the paper, yes.
MR. ROTHSCHILD: May I approach the witness, Your Honor?
THE COURT: You may.
BY MR. ROTHSCHILD:
Q. What I’ve marked as Exhibit P-756 is an article in the journal Science called Exploring Micro—
A. Microbial.
Q. Thank you — Diversity, A Vast Below by T.P. Curtis and W.T. Sloan?
A. Yes, that seems to be it.
Q. In that first paragraph, he says, There are more than 10 to the 16 prokaryotes in a ton of soil. Is that correct, in that first paragraph?
A. Yes, that’s right.
Q. In one ton of soil?
A. That’s correct.
Q. And we have a lot more than one ton of soil on Earth, correct?
A. Yes, we do.
Q. And have for some time, correct?
A. That’s correct, yes.
Q. And, in fact, he gives us a good way of comparing it. It says, as compared to a mere 10 to the 11th stars in our galaxy?
A. Yes, that’s what he writes, uh-huh.
Q. And 10 to the 16th prokaryotes is 7 orders of magnitude higher than the population you included in your calculations, correct?
A. No. We considered a wide range of populations, and we considered a wide range of number of substitutions that would be — or point mutations that would be necessary. You’re focusing on two, but perhaps I can direct your attention again to that figure from the paper — excuse me. Let me find it.
The best place I think to look is figure 6, which is on page 10 of the document. Up in the upper right-hand corner, that figure there.
Q. Sure.
A. If you look on the bottom, the x axis there, the bottom of the figure that’s labeled lambda, it has the numbers 2, 4, 6, 8, 10, and so on, those are the number of point mutations that we consider perhaps some multi-residue feature might entail. As we said in the paper, forming a new disulfide bond might require as few as two point mutations.
But forming other multi-residue features such as protein, protein binding sites might require more. And so the number on the X axis lambda 2, 4, 6, 8, those are the number of point mutations that we entertained or we calculated numbers for to see how long such things would be expected to take under our model.
And if you look up at the top axis, the top x axis labeled N, at the top of the figure. N stands for population size. Okay. So if you look at the figures there on the left, it’s slanted, and it’s not enlarged yet, so it’s hard to see. It says, 10 to the 6th. That’s a million. And then skip a line. These are in every 10 to the 3rd increments of population size. That would be 10 to the 9th.
The next label is 10 to the 12th, which is a trillion. The next label is 10 to the 18th, which is much more. The next label is 10 to the 24th, which is much, much, much more. The next label, 10 to the 30th, which, again, is very much more.
So, in fact, we considered population sizes from 1000 all the way up to 10 to the 30th, and multi-residue features from 2, which might involve disulfide bonds, up to many more, which might be involved in protein, protein binding sites.
Q. 10 to the 30th, that is quite a lot, right?
A. Yes. That’s roughly what is calculated to be the bacterial population of the Earth in any one year. And so over the course of the billion year, 4 billion year history of the Earth, there would probably be a total of roughly 10 to the 40th.
Q. And so in the case of prokaryotes, which you said was a good example of what you were studying, 10 to the 16th in one ton of soil?
A. Yes.
Q. So a few tons of soil, and we’ve gone past that 10 to the 30th?
A. Well, no. In the 10 to the 14th tons of soil. 10 to the 30th is the number that’s in the entire world, according to the best estimates, including the ocean as well as soil. So — but I agree with your point, that there’s a lot of bacteria around and certainly more than 10 to the 9th.
Q. So just with the prokaryotes, 10 to the 16th, 7 orders of magnitude higher than what you were calculating here?
A. That’s certainly true, but in our paper, we had our eye not only on prokaryotes, but also on eukaryotes as well, which, if you leave out recombination, one can — they certainly undergo point mutations. They certainly have genes and so on. So much of this is also applicable to eukaryotes.
And the populations of eukaryotes and certainly larger plants and animals are much, much smaller than populations of bacteria. So we view our results not just as supplying that, but to giving us some feel for what can happen in more complex organisms as well.
Q. Well, you’re not talking about more complex organisms here, are you?
A. I think we do. I think at the end, if I’m not mistaken, if I remember correctly — okay, yes. On page 11, the second full paragraph, on page 11. It begins on the right-hand column, the second full paragraph. It says, The lack of recombination in our model means it is most directly applicable to haploid, asexual organisms. Nonetheless, the results also impinge on the evolution of diploid sexual organisms.
The fact that very large population sizes, 10 to 9th or greater, are required to build even a minimal MR feature requiring two nucleotide alterations within 10 to the 8th generations by the processes described in our model, and that enormous population sizes are required for more complex features or shorter times, seems to indicate that the mechanism of gene duplication and point mutation alone would be ineffective, at least for multicellular diploid species, because few multicellular species reach the required population sizes.
Thus, mechanisms in addition to gene duplication and point mutation may be necessary to explain the development of MR features in multicellular organisms.
So here we were trying to point out that, because of the results of the calculation, it seems that, when we’re trying to explain MR features in multicelled organisms, then we’re going to have to look to other processes for that.
Q. Okay. So if we exclude some of the processes by which we understand evolution to occur, it’s hard to get there for multicellular organisms?
A. I’m sorry.
Q. If we exclude some of the mechanisms by which we understand evolution to occur, like recombination, it’s hard to get there?
A. Yes.
Q. And bringing it back to the prokaryotes. We’re in agreement here, the number of prokaryotes in 1 ton of soil are 7 orders of magnitude higher than the population, you said it would take 10 to the 8th generations to produce the disulfide bond?
A. Yeah, certainly. Yeah, the bacteria are — can grow to very large population sizes.
Q. So the time would be?
A. Much shorter.
Q. Much shorter?
A. Absolutely.
Try dissenting against CO2 driven global warming. You will find the computer models supporting this *theory* will trump evidence from the real world every time.
For example in reaction to learning the ice core records show that temperature change has consistently proceeded CO2 change by 200 to 800 years, climate *scientists* claimed that this only strengthened their theory.
Decades ago, Karl Popper wisely opined that theories that don't risk falsification should not be considered scientific. I find myself one of many very impressed at his insight in the matter.
Not necessarily.
Max Planck was right. Science proceeds one funeral at a time.
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