Evolutionists have a wide range of explanatory mechanisms from which to draw when trying to figure out how the species evolved. But sometimes these supposed mechanisms look more like a cover-up than an explanation. For instance, the differences between the human and chimp DNA instructions are not sprinkled, more or less at random, throughout our genome. Rather, these differences are found in clusters. Even more interesting, at these locations the chimp's genome is quite similar to other primates--it is the human that differs from the rest, not the chimp. Evolutionists refer to these clusters as human accelerated regions (HARs) because they believe the human genome evolved from a human-chimp common ancestor. These HARs cause several problems for evolution. For instance, we must believe that evolution magically caused rapid changes to occur right where needed to improve function and eventually create a human. As one evolutionist wrote:The way to evolve a human from a chimp-human ancestor is not to speed the ticking of the molecular clock as a whole. Rather the secret is to have rapid change occur in sites where those changes make an important difference in an organism’s functioning. HAR1 is certainly such a place. So, too, is the FOXP2 gene, which contains another of the fast-changing sequences I identified and is known to be involved in speech.
This is truly a whopper of a just-so story and you can read more here and here.
Now, evolutionists are again appealing to this accelerated evolution "mechanism" to explain the origin of a toxic protein found in the saliva of a North American shrew. The protein chops up other proteins using a novel mechanism, and evolutionists are saying that it "evolved adaptively via acquisition of small insertions and subsequent accelerated sequence evolution."
There you have it--evolution happens. But that's not all. Evolution implemented the same clever design in a Mexican lizard. Amazing.
This is yet another example of a striking design repeat in biology, but this time it is via accelerated evolution. Evolutionists have not calculated the probability of blind mutations doing this not once but twice, probably because it doesn't matter. After all, evolution is a fact.
Cornelius -
ReplyDelete"the differences between the human and chimp DNA instructions are not sprinkled, more or less at random, throughout our genome. Rather, these differences are found in clusters."
Why exactly should this be suspicious? I know I'm not a professor of biology or anything, but why exactly should we predict mutations to be scattered randomly throughout the genome if evolution is correct, rather than clustered?
"the secret is to have rapid change occur in sites where those changes make an important difference in an organism’s functioning...
truly a whopper of a just-so story"
Again, why should this be so? If a selection pressure favours, say, mice to have longer legs (just to make up a random example), surely that would necessitate a number of changes in the mouse genes which go to making legs.
"Evolution implemented the same clever design in a Mexican lizard."
Isn't that just parrallel evolution?
"Evolutionists have not calculated the probability of blind mutations doing this not once but twice,"
They're far, far, far better than the chances of a supernatural being existing which can create such features on a divine whim, I can tell you that for free!
Ritchie writes:
ReplyDelete"Again, why should this be so? If a selection pressure favours, say, mice to have longer legs (just to make up a random example), surely that would necessitate a number of changes in the mouse genes which go to making legs."
Selection pressure would necessitate a number of genetic changes...?
Surely, you don't mean what you seem to imply here. Your wording seems to have cause and effect backwards. This is how I would interpret what you said:
There is a force in nature that would require the legs of the mouse to become longer. This force then causes those exact genetic changes that would elongate the legs to occur.
The fact that one can speculate that natural selection would favor a particular change does not mean that those changes are somehow going to occur if they are truly random.
And I'm not so sure that science could determine before the fact what natural selection would prefer. Science can only observe after the fact that whatever change did occur was due to natural selection. How convenient!
There are more interesting conclusions if what you say is true. If the differing genes are found in clusters, then what does that say about the supposed common ancestor?
ReplyDeleteCan the common ancestor be said to have aspects of both chimps and humans from which to diverge? If so, then it looks like the chimp in its decent had to loose whatever clusters the common ancestor might of had.
Or if the common ancestor had none of these clusters partialy developed, then either the common ancestor is the chimp itself with all its same genomic locations similar to other primates, or the human diverging branch would have to have developed at least some of those same patterns it shares with primates independantly.
This seems to muddy any just-sos that could come up.
Cornelious,
ReplyDeleteAbout the article "Convergent Evolution of Novel Protein Function in Shrew and Lizard Venom", it's a nice example of the acquisition of a new function (toxicity: cleavage of other species proteins) using already available genes with a different function (in this case, housekeeping: the cleavage of their own proteins). The mutations identified do not chop up proteins using a novel mechanism: "[...] the molecular changes required for toxicity have probably occurred along the BLTX lineage and are associated with an increase in enzyme activity".
It seems that the use of proteases in venom is rather common. The authors pointed out that 2 different organisms used different variations of the same gene (or a duplicated version) in order to get a similar result. What would be interesting to know if both the shrew and mexican lizard use the same mechanism(s) to protect themselves from their venom.
I could not find the expression "accelerated sequence evolution" in the article except in the part of the abstract cited so I guess they simply meant positive selection since I can't find any data that could mean that they observed enhanced mutation rate.
About HARs...
From Pollard et al 2006: An RNA gene expressed during cortical development evolved rapidly in humans
"Here we scan these ancestrally conserved genomic regions to find those that show a significantly accelerated rate of substitution in the human lineage since divergence from our common ancestor with the chimpanzee."
What they call human accelerated regions (HARs) are regions which were previously under strong purifying selection in our ancestor but that were subject to strong selection in the human lineage (ie: genes modifications that could explain how/why we are different from chimps). The acceleration in this case mean a switch from strong negative selection (changes that get fixed less frequently than neutral changes) to strong positive selection (changes that get fixed faster than neutral changes).
About FOXP2...
From Zhang et al 2002: Accelerated Protein Evolution and Origins of Human-Specific Features: FOXP2 as an Example
"Driving forces behind the accelerated evolution of human FOXP2:
It would be interesting to identify the driving force behind the two amino acid substitutions and the accelerated evolution of human FOXP2. There are three possibilities: enhanced mutation rate, relaxed purifying selection, and positive selection. Because synonymous nucleotide changes are usually immune to selection, the rate of synonymous substitutions can be used to measure the mutation rate (NEI and KUMAR 2000). Using parsimony, we determined the number of synonymous substitutions in each branch of the FOXP2 gene tree of five hominoids and mouse (Fig 4). It can be seen that the number of synonymous substitutions in the human lineage (two) is smaller than that in the two chimpanzee lineages (three and four, respectively). The number of synonymous substitutions per MY is also smaller in the human lineage (2/5.5 MY = 0.36) than in the lineage before the human-chimpanzee separation ([2.5 + 4.5 + 127.5]/[90 MY x 2 - 5.5 MY] = 0.77 for the branches linking node A and mouse; see Fig 4). Thus, there is no indication of enhanced mutation rate at FOXP2 in the human lineage."
Hope this help!
Charles.
Cornelius,
ReplyDeleteI'm sure you believe you are being clever when you refer to magic, but surely this is disingenuous of you.
You must be aware that it is not the occurrence of mutations that is "magically" accelerated in important regions, rather the population-genetic processes that fix them, based on straightforward , decades-old, statistical inferences. This is simply the interplay between population size and natural selection and is a basic prediction of evolutionary theory.
Humans have experienced a population explosion relative to the primates. Larger population = more effective positive selection. It is hardly suprising genes implicated in the differences between humans and chimps are under positive selection here.
If you have some information that challenges these established principles of population genetics, please share them.
abimer:
ReplyDelete==========
I'm sure you believe you are being clever when you refer to magic, but surely this is disingenuous of you.
You must be aware that it is not the occurrence of mutations that is "magically" accelerated in important regions, rather the population-genetic processes that fix them, based on straightforward , decades-old, statistical inferences. This is simply the interplay between population size and natural selection and is a basic prediction of evolutionary theory.
Humans have experienced a population explosion relative to the primates. Larger population = more effective positive selection. It is hardly suprising genes implicated in the differences between humans and chimps are under positive selection here.
If you have some information that challenges these established principles of population genetics, please share them.
==========
Why is it that evolutionists never tell anyone about how they have rigged the game?
To explain molecular evolution, such as these HARs, they make at least two optimistic assumptions: No order dependence and no functional dependence. If I'm mixing paints there is no order dependence but if I'm building a house then I better lay down the foundation first. A mixture of paints is a pretty simple system. More complex system usually have order dependence. But not so for changing a primate into a human (and all the rest of evolutionary history by the way) according to evolutionists.
Second, evolutionists assume that the mutations have no functional dependence. If I'm adding a color to a vision system then adding a new opsin gene, appropriately mutated to sense the new light frequency, doesn't do the job. I also have to change some wiring, post processing and brain functions at the same time. There is much functional dependence between the different mutations needed to add a new color. In fact, just changing the opsin gene alone will probably screw things up and degrade fitness.
But evolutionists assume, not only no order dependence, but no functional dependence. The mutations can occur in any order, and one at a time. Each one adds its own contribution to fitness, making for a relatively smooth fitness landscape no matter how you climb the mountain.
And from where did these rosy assumptions come? Did evolutionists construct a cell from an organic soup, or an insect or amphibian or reptile from lower species? Did they observe smooth fitness landscapes and successful evolution of these lab organisms? No, the assumptions came from the belief that evolution is true, and so all of biology is, by definition, more like a mixture of paint than a machine.
Ritchie: "They're far, far, far better than the chances of a supernatural being existing which can create such features on a divine whim, I can tell you that for free!"
ReplyDeleteFor petes sake Ritch do you ever think before posting?
Show me the math you have that demonstrates this gratuitous and ridiculous statement - or stop dropping crud into the comments all the time here.
Cornelius Hunter: "If I'm adding color to a vision system then adding a new opsin gene, appropriately mutated to sense the new light frequency, doesn't do the job."
ReplyDeleteThis is a curious example you raise. Female mice supplied with the human L-opsin gene in addition to their normal complement of pigment genes could immediately discriminate colors that cannot be discerned by dichromats. (Science 315: 1723)
The biggest problem I see, however, with this line of argument you introduce is naive teleology.
"we must believe that evolution magically caused rapid changes to occur right where needed to improve function and eventually create a human."
Like everyone else, I am the product of one particular sperm that melded with one particular egg, an exceedingly low probability event. Am I a miracle baby? Should I call the press? Only if I am extremely naive and infused with an undeserved sense of self-importance. The same is true for Homo sapiens. Like every other species alive today, our ancestors drew some good cards and we caught some lucky breaks, leaving dozens of fellow hominin species in our wake. Had we not accrued the mutations that allowed us to emerge, then life and its evolution would have gone on without us.
Cornelius,
ReplyDeletewhat you state is neither a response to my comment, nor accurate. Instead of making a case, you just give us some unhelpful analogies about mixing paint and building houses.
How can you make the unsupported assertion that "evolutionists" assume neither functional nor order dependence in adaptive evolution?
Even when Darwin hypothesised a theoretical pathway for the eye, he was concerned with mutation order. Ironically, when you give the opsin example, you state there is no order dependence: all changes must happen at once, so says Cornelius. Or else there will be a loss of fitness. Sounds like one of those unsubstantiated assumptions that are so mockably unscientific. I mean, have you ever duplicated an opsin gene in an organism, induced mutations in the new gene, and evaluated the new genotypes fitness? It's less than what you ask of "evolutionists" who you believe must construct a cell from an organic soup to have any right to model adaptive evolution.
abimer:
ReplyDeleteYou asked for information that that would challenge your use of the established principles of population genetics. I explained that as you are applying these principles (ie, to explain how easy it is to explain the HARs), there are two, unsupported, unfounded and dubious assumptions.
Your reply was that my answer "is neither a response to my comment, nor accurate." After all, you pointed out, Darwin himself "was concerned with mutation order." So apparently my answer is accurate. After all, Darwin shared the concern, right?
As for not being a response, that is false. Of course it is a response. You asked why I think your reasoning fails, and I gave a straight answer.
You say my analogies were unhelpful, but you don't explain why. Why is it unhelpful to provide examples where the assumption works, and where it doesn't work, to illustrate the point? Or is this just the usual evolutionary defense of criticizing without substance?
=========
How can you make the unsupported assertion that "evolutionists" assume neither functional nor order dependence in adaptive evolution?
=========
Because that is common, and it is necessary to make evolution look plausible. I thought it was clear that, in typical fashion, that is what you were doing. Was I wrong, and did I mis interpret your comment? If so, all you need do is provide the details. How do you model order and functional dependencies for the HARs? And how is the story plausible? No need to keep secrets here. I will gladly admit my error, and that I incorrectly and unfairly interpreted your point. You're in a great position to enlighten me here, and I will recant.
Instead you alluded to Darwin. But my point was not that evolutionists never have considered these problems. Of course they consider order and functional dependencies when they are trying to explain how a complex structure could have evolved via intermediates which may have served different functions along the way.
My point was that in their claim that there is no problem with events such as the evolution of the HARs, as you are making here, they make these optimistic assumptions. Darwin was deep into one of his dubious thought experiments, but here we actually have some biological details. So instead of recounting Darwin's absurd thought experiment, you can simply set the record straight regarding the HARs (or any similar such example which you might have handy). You can explain to us how evolution remains plausible if there are order and functional dependencies.
And then next comes the usual strawman:
========
Ironically, when you give the opsin example, you state there is no order dependence: all changes must happen at once, so says Cornelius. Or else there will be a loss of fitness. Sounds like one of those unsubstantiated assumptions that are so mockably unscientific.
========
No, I did not say "or else there will be a loss of fitness." I suggested that it seems likely. I wrote: "In fact, just changing the opsin gene alone will probably screw things up and degrade fitness." I have no certainty here.
Nor did I say there is no order dependence to evolve the new color. My point merely was that to add a new color to a vision system, multiple changes need to happen. In any order you like, but having only one won't do the job by itself. My point was not about order dependence, rather it was about functional dependence. I said you need them all to achieve the function.
(continued)
abimer:
ReplyDeleteIt seems to me that in order to make the evolution of the HARs plausible, you need (i) order and functional independence so there is a relatively smooth fitness landscape leading up the the current design, or you need (ii) some other functions that the intermediates sequences provide, so that when the first mutation occurs, for instance, you get some other function which serves to keep the mutation.
To forestall the coming strawman, I am *not* saying either of these is impossible. Obviously neither of these are well supported by science at this point, but that doesn't mean they are not possible. In any case, the point merely is that you need some type of assumption such as these, in order to make the HARs evolution plausible.
But instead of acknowledging these issues, in typical evolutionary fashion you write:
=======
You must be aware that it is not the occurrence of mutations that is "magically" accelerated in important regions, rather the population-genetic processes that fix them, based on straightforward , decades-old, statistical inferences. This is simply the interplay between population size and natural selection and is a basic prediction of evolutionary theory.
=======
No, this is not merely "population-genetic processes ... based on straightforward, decades-old, statistical inferences." That's the point. In claiming that this all is just so reasonable and plausible you are glossing over substantial and unstated assumptions, implicit in your calculation.
But I must be misinterpreting your point. Please disabuse us of our ignorance and explain how this all makes sense, and how the HARs evolution is so plausible.
John:
ReplyDelete=================
The biggest problem I see, however, with this line of argument you introduce is naive teleology.
"we must believe that evolution magically caused rapid changes to occur right where needed to improve function and eventually create a human."
Like everyone else, I am the product of one particular sperm that melded with one particular egg, an exceedingly low probability event. Am I a miracle baby? Should I call the press? Only if I am extremely naive and infused with an undeserved sense of self-importance. The same is true for Homo sapiens. Like every other species alive today, our ancestors drew some good cards and we caught some lucky breaks, leaving dozens of fellow hominin species in our wake. Had we not accrued the mutations that allowed us to emerge, then life and its evolution would have gone on without us.
=================
Good point, I'll add that to the list of explanations. So the assumption here is that, in spite of order and functional dependencies and the fact that such dependencies make the observed HARs a low probability evolutionary outcome, there are a large number of such HAR sequences that would do the job. When you account for that large number you obtain a plausible result.
Of course the key question here is: How many sequences are there that do the job? Do you agree that it is quite possible the answer might be too low to make for a plausible result?
Cornelius:
ReplyDelete"Of course the key question here is: How many sequences are there that do the job?"
The only answer I can think to this question is: exactly the right number of sequences.
Unless you can provide an alternative mechanism to DNA being responsible for our development, the explanation for our differences with our ancestors has to be in the genetic differences.
Whether or not you think evolution was a driving force, you have to admit that our differences have to be explained at the genetic level.
It does not have to be only HARs though, any other kind of genetic changes could do.
Charles.
Doublee -
ReplyDeleteA fair point. Perhaps I wasn't clear there. It does seem I spoke carelessly.
When I said 'necessitate' I did not mean 'cause'. I meant something along the lines of 'allow' or 'necessitate if the mice are to survive'.
Consider this - most mutations are disadvantageous, that it, selection pressures will punish most mutations. I mutation on the gene sequence which goes towards making eyes will probably render the eyes functionless, since all the parts need to be just so in order for the eyes to form properly and work 'correctly'. Most mutations will impair the sight its individual host, rendering it at a distinct disadvantage to its fellows.
However, in rare cases, small mutations may actually improve the eyesight of the individual, giving it a survival advantage over its fellows. We can thus talk about selection pressures favouring better eyesight - that simply means they don't punish improved eyesight.
Selection pressures do not 'cause' mutations to happen, but by not punishing certain mutations, they allow those mutations to prosper.
Hitch -
ReplyDelete"Show me the math you have that demonstrates this gratuitous and ridiculous statement - or stop dropping crud into the comments all the time here."
Ah, Hitch. Always delightful to see you on here.
You want my calculations? Okay...
The thing abut supernatural beings is that they are hugely unlikely. Their existence relies on the universe working in certain ways we have no reason to belive is true.
Consider a being great enough to create the universe. Such a being must be more complex than the universe, and all things being equal, would therefore be more unlikely than the universe.
Not only that, but if such a being created natural laws, then it must be more complex than natural laws, and therefore more improbable than natural laws. So absolutely ANY explanation you can come up with for anything at all using merely natural laws must, by definition, be more likely than the intervention of such a supernatural being.
Follow that? I hope so. Now the universe is at a further advantage - we know it exists (as much as we can know anything). We're in it. Which hugely increases the odds of the universe existing. Something similar applies to natural laws - we have reason to believe they exist. So they gain probability points too.
Now let's take this calculation method and apply it to the case in hand - Cornelius implied the odds for the same mechanism for toxins in saliva occurring through random chance were very long. Perhaps so long as to dismiss the idea as a plausible explanation.
But random chance is at least, a real, natural mechanism. We can be fairly sure random chance actually exists. Which makes it a much more likely explanation than the intervention of a being whose existence is more unlikely than that which it is used to explain.
No matter what the problem, explanating it through natural means (including 'it's just a coincidence') is ALWAYS going to be more likely than explaning it as the work of supernatural agents/forces, because the existence of such agents/forces are so gob-smackingly tiny.
Ritch:
ReplyDeleteI asked for math, you give speculations and assumptions.
You say, "The thing abut supernatural beings is that they are hugely unlikely."
According to whom? You've already gone wrong.
"Their existence relies on the universe working in certain ways.."
You're clearly making assumptions that you're not stating.
"Consider a being great enough to create the universe. ... more unlikely than the universe."
"Who designed the designer?" comes to mind ;-)
Here you have your foot in your mouth again - for the P that the universe exists is 1, thus, based on your own reasoning, the probability of God is just something less than 1 - but anything over P=0.6 is a high P indeed.
You don't understand probabilities.
"..but if such a being created natural laws, then it must be more complex than natural laws, and therefore more improbable than natural laws."
Again, natural laws have a P=1 so you just destroyed your argument against God and gave one for God!
"So absolutely ANY explanation ...using merely natural laws must,..be more likely than the intervention of such..."
Irrelevant. Its just methodological naturalism in a nutshell -but MN itself is based on the teleological, and indeed theological, assumptions that nature is all there is!
This is called - now look it up please - "begging the question".
No supernatural entity can be dependant on natural law.
"Now the universe ...- we know it exists ... We're in it. Which hugely increases the odds of the universe existing."
Actually no, the probability that something that exists exists is always 1.
You actually gave a good argument for the existence of God and the rest of your drool fairs no better.
"Now let's take this calculation method and apply it to the case in hand" "
This is not a calculation method at all! It is merely a very faulty & poorly structured thought experiment you picked up off the web somewhere.
"- Cornelius implied the odds ...Perhaps so long as to dismiss the idea as a plausible explanation."
Indeed, and we have hard numbers for such probabilities that intrinsically exclude the possibility of natural law doing it all w/o plan or direction.
Go read my "Reasons" blog - there's math there.
"...Which makes it a much more likely explanation than ...whose existence is more unlikely than that which it is used to explain."
You already demolished this argument yourself!
"No matter what the problem, explanating it through natural means ..more likely than ..because the existence of such agents/forces are so gob-smackingly tiny."
Well you proved, based on your own reasoning - that P(God) is almost = to 1 above so...
You really, *desparately* need to read Stephen Unwin's "The Probability of God" - all math based.
"Only in Atheism does the spring rise higher than the source, the effect exist without the cause, life come from a stone, blood from a turnip, a silk purse from a sow's ear, a Beethoven Symphony or a Bach Fugue from a kitten walking across the keys....." - James M. Gillis
This is where you all fail so miserably as Voltaire stated, "The atheists are for the most part imprudent and misguided scholars who reason badly who, not being able to understand the Creation, the origin of evil, and other difficulties, have recourse to the hypothesis the eternity of things and of inevitability..."
Sad you deem yourself unworthy by joining them.
Hitch -
ReplyDeleteWhat? I don't follow you at all.
Say I have a puzzle - perhaps apples fell from a tree to make a pattern and I want to know how this happened. Perhaps it was a coincidence. Perhaps someone placed them there. Perhaps a supernatural force/agent caused it. The supernatural explanation will ALWAYS be the least likely because it relies on the premise that such a supernatural force/agent exists - which is an assumption. An assumption we have no reason to believe is even possible.
Any explanation which uses nothing but natural forces is always going to be more likely. Always. That is not begging the question, because the supernatural explanation MIGHT nevertheless still be true. I am not saying it is impossible. But if we're counting the odds, the supernatural loses every time.
The traditional depiction of God has him as creator of the universe. Therefore he must be greater than the universe, more complex than the universe, and thus, his existence is less likely than the universe. That's just plain, simple logic.
Any explanation for my apples which hypothesises such a God will have to take into account how phenominally unlikely such a being is.
Saying 'it must have been done intentionally - the odds of it being a coincidence are terribly small' is one thing. But if you then need to postulate a SUPERNATURAL agent to do it, you are smuggling in the supernatural agent's existence. You should take into account the very existence of the agent in the first place (a calculation which is unnecessary for 'random chance' or 'human intervention').
How can this be turned into an argument FOR the existence of God? The mind boggles...
Cornelius,
ReplyDeleteHAR1, especially, is indeed an impressive distance from its chimpanzee homolog, but the HARs were cherry picked from the genome specifically with regard to this criterion. You can't just put a probability on it without viewing it from the context that you cherry picked it from 3 billion bases as being the most extreme case. Based on my sampling of height measurements among American males, I might decide that maximum height might peak at about 7'2". It might seem implausible that any U.S. male would ever reach 9 feet tall (ok, 8'11"), but indeed it happened.
Furthermore, functional and order dependence is something you presumed rather than something you demonstrated. In the absence of evidence for any particular case, there is no reason to assume either functional or order dependence.
Your argument for functional dependence concerning the opsin genes falls with a thud. You shouldn't feel bad, there were some evolutionary biologists who were sweating that one out. They shouldn't have. A change in opsin protein changes its absorption profile, which yields a distinct firing pattern with respect to the old version. Color differences that were not detectable before will be now that a third opsin is in place. For the first trichromat catarrhine, the difference between "red" and "green" may not have been the blazing one I see; that may indeed be influenced by functional brain changes that came later. But just being able to discriminate more shades is a big advantage in a world of ripening fruits and hardening leaves. Dichromatic primates in the Paleotropics are today relegated to the refugia of darkness or Madagascar as they are not competitive with the catarrhines.
As evidence of order dependence, you offer up an analogy between proteins and buildings. If I was having a house built and it look nearly as haphazard as a protein, I would definitely sue to get out of the contract. Proteins look like crumpled masses of yarn, springs, and party favors. I don't think you would find a pair of spectacles in the lost and found of the Discovery Institute that would be rosy enough to see God's hand in a protein structure.
Ritch: Forget your pattern puzzle for a sec.
ReplyDelete"The traditional depiction of God has him as creator of the universe. Therefore he must be greater than the universe, more complex than the universe, and thus, his existence is less likely than the universe. That's just plain, simple logic."
You miss the point - and it's a very obvious one.
Point by point:
1) The universe exists. That means its likelihood of existing is 100%.
In math terms - say P(G) = the probability that God exists;
P(U) is the probability that the universe and its laws exist;
P(G|U) is the probability of G given U;
Therefore, by your own logic P(G|U) ˜ 1
(˜ is the approximation symbol - just in case you didn't know)
i.e. P(G|U) is just slightly less than one
But to be sure you understand I continue ...
2) You based you whole argument for the probability that God exists on the probability that the universe and its laws exist.
3) The universe DOES exist! The universe and its laws DO exist therefore P(U) = 1 = 100%
4) Therefore P(G|U) is necessairly almost as certain as the P(U)
i.e. The prob that God exists is extremely high!!
See?
(I sure hope so cause if you can't understand the error and consequences of your own proposition I have little hope you'll understand anything else)
You add, "Any explanation for my apples which hypothesises such a God will have to take into account how phenominally unlikely such a being is."
Yes, and that is exactly what I just did by showing that P(U) = 1.
Thus your proposition AGAINST God actually turns out to be major support FOR God.
"...But if you then need to postulate a SUPERNATURAL agent to do it, you are smuggling in the supernatural agent's existence."
If I were to claim a supernatural agent did it I would not be smuggling in anything at all - I would be declaring it outright!
You don't appear to know the difference between a subtly "smuggled in" argument and an outright one. A "smuggled in" argument is one that is not declared nor obvious outright but is found by logical scrutiny.
"You should take into account the very existence of the agent in the first place (a calculation which is unnecessary for 'random chance' or 'human intervention')."
No. You're wrong - but that's what I just did anyway just to help you!
As I said, atheists ALWAYS reason badly as Voltaire stated.
1) There is no need to take that into account because ID isn't even postulating a supernatural being!!!
- only a vast and powerful intelligent agent or agents! If "God" fits the role so be it. If not so be it.
Darwinists never get this point which is why they're ALWAYS arguing against a straw man!
Nevertheless, you have several serious misunderstandings or errors in your whole position!!
ID is not looking to prove the existence of God at all!
ID proposes that intelligent agency is the far more likely cause for the design we see in life forms. And with good LOGICAL, SCIENTIFIC reason!
ID, contrary to all you've been miserably trying to prove, looks at the evidence and says "the ONLY source of functionally organized, prescriptive information known to us is intelligence. There are NO OTHER KNOWN SOURCES! Therefore, if we find functionally specified prescriptive information within living things (we do!) it MUST HAVE come from the ONLY KNOWN SOURCE!!"
Can you at aleast see that ??!
"How can this be turned into an argument FOR the existence of God? The mind boggles..."
If you don't get the simple logic I used above then I am forced to conclude that thus far the only boggled mind here is yours.
And I don't mean that as an insult at all!
John:
ReplyDelete"As evidence of order dependence, you offer up an analogy between proteins and buildings. If I was having a house built and it look nearly as haphazard as a protein, I would definitely sue to get out of the contract. Proteins look like crumpled masses of yarn, springs, and party favors. I don't think you would find a pair of spectacles in the lost and found of the Discovery Institute that would be rosy enough to see God's hand in a protein structure."
I appreciate the fact that you have strong religious beliefs, and that they bias your science. It's the reason for this blog. Religion drives science, and it matters.
"A change in opsin protein changes its absorption profile, which yields a distinct firing pattern with respect to the old version."
I want to blog on this, so I'll hold off on commenting for now.
John:
ReplyDelete=========
Furthermore, functional and order dependence is something you presumed rather than something you demonstrated. In the absence of evidence for any particular case, there is no reason to assume either functional or order dependence.
=========
No, I'm not the one who is presuming here. My point was not that functional and order dependence are known to exist. This strawman argument of yours is so common I anticipated it: "To forestall the coming strawman, I am *not* saying [order and functional independence] is impossible."
The point is that it is evolutionists who are presuming. They're making the claim that the origin of HARs merely follow the "straightforward , decades-old, statistical inferences" of population genetics, and functional and order independence are standard assumptions in those methods.
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HAR1, especially, is indeed an impressive distance from its chimpanzee homolog, but the HARs were cherry picked from the genome specifically with regard to this criterion. You can't just put a probability on it without viewing it from the context that you cherry picked it from 3 billion bases as being the most extreme case.
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Yes, you made that point and I agreed. The key question is: How many sequences are there that do the job? How many other possible sequences are there that would have helped turn a chimp-human ancestor into a human? If there is order and functional dependence, then it likely would swamp this effect.
Hitch -
ReplyDeleteOkay, lets do this one more time in baby steps...
"The universe exists. That means its likelihood of existing is 100%."
Yes, fine by me. I mean we may come across philosophers with a Matrix fixation who want to challenge this, but as reasonable scientists who want to learn something about the world around us, yes lets take it as 100% certain the universe exists.
So, in the terms you have outlined, P(U)=1
However P(G) is a totally different calculation.
I don't follow where P(G/U) comes from. What do you mean 'the probability of G given U'? What do you mean by 'GIVEN'? Is G more likely bearing in mind U exists? Surely not. This seems to me to be a mistake. Why should the existence of U affect the probability of G?
It seems you are trying to imply that given the universe, God is likely. But doing it in mathematical language. This is a heavily flawed argument for God, and stating it in mathematical terms does not improve it.
The universe does not imply the existence of a God. There is nothing about the universe which demonstrates the existence of such a being - unless you can FIRST show otherwise of course. So P(U) does not affect P(G).
In other words, P(G/U) seems to me to be a bogus calculation. The universe is an extremely complex thing. Therefore it is an extremely mathematically unlikely thing. God is (supposedly) even more complex. And therefore even more unlikely. But the universe has another advantage in that we know it's real, which puts P(U) up to 1. P(G) remains extremely low.
Or to highlight your fallacy further, consider your calculation as an alleged proof for the existence of Zeus - P(Z). The ancient Greek myths account for the existence of the universe. So if P(U) is 1 and your calculations are sound, surely P(Z) is "1 as well?
I suspect you would say not. Why? Because the existence of U does not affect the probability of Z!
"There is no need to take that into account because ID isn't even postulating a supernatural being!!!
- only a vast and powerful intelligent agent or agents! If "God" fits the role so be it. If not so be it."
ID may OFFICIALLY claim not to be imposing a God, but it certainly is postulating a supernatural being. I claim this because ID never proposes any NATURAL mechanisms (or, frankly, any mechanisms at all) for phenomena we find. It just looks at the evidence and concludes nothing less than a miracle. If you do not propose natural mechanisms for this apparent design or biological tinkering, then the agent must be supernatural.
Whether this supernatual entity is the Christian God is a point ID proponents are generally very coy on. Suffice to say that though I know of many ID proponents who happily consider it as evidence for the Christian God, I know few who as readily admit it is equally sound evidence for Zeus or the Flying Spaghetti Monster, or the Magic Dancing Pixie who brought forth the whole of creation with her magic knickers. Because if ID really did not identify the cretor, all of these really would be equally probable candidates.
Cornelius,
ReplyDeleteYou wrote:
"Yes, you made that point and I agreed. The key question is: How many sequences are there that do the job? How many other possible sequences are there that would have helped turn a chimp-human ancestor into a human? If there is order and functional dependence, then it likely would swamp this effect."
If you go back and read my first post, there's nothing about cherry picking in it. The point you ceded to me was about the low probability of my birth. You interpreted that to mean there are many pathways to adaptation. While that's generally true, what I really meant was this: Obscenely low probability events take place all the time in the wake of numerous other scenarios that go unfulfilled. Babies get born; people win huge lotteries. "Chuman" ancestors didn't have to become what we are today. They could have, under different selection pressures, become better brachiators, like chimps did. We could have become more herbivorous, like Paranthropus. Or we could have just gone extinct, and there are many, many other possibilities that just didn't happen. There is only one sequence that was actually taken and made us precisely the kind of meta-ape that we are. That would have been true no matter what the specific route and end result were. Low probability arguments lack much bite after the fact. If you were commenting during the Pliocene and predicted that one population would leave descendants that would one day construct an internet, that would have been something.
Contingency! Chuman ancestors would have already been as brainy (or almost as brainy) as living apes. We are just starting to learn just how intelligent our fellow hominids are. Starting with an animal that is already bright as a result of social behavior, varied diet, vocal and nonvocal communication and simple tool use, the new setting of more open woodland to savanna could select for further intelligence. This is not a just-so story; braincase volume and tool sophistication both increase more or less monotonically through the Pleistocene in the lineage leading to H. sapiens.
Question: According to your worldview, when exactly did we become human?
Homo sapiens sapiens you would probably accept as human. How about Homo sapiens idaltu? heidelbergensis and neanderthalensis? erectus and ergaster? habilis? rudolfensis? Australopithcus garhi? africanus? afarensis? or is Mesopotamia, 4004 B.C.E. the starting point for humanity in your view? Creationists always say the fossils are either all ape or all human, but they can't all agree on where to draw the line. Neither can anthropologists - exactly the kind of problem we should be having if common descent is correct and if we have a substantial (not complete by any means but substantial) fossil record.
Any way, cherry picking is now at least a second point, 2 more than I ever thought I'd see. Given the reality of cherry picking (by the researchers, not by you), don't you need to fix this sentence from the original post:
"Even more interesting, at these locations the chimp's genome is quite similar to other primates--it is the human that differs from the rest, not the chimp."
This is not interesting or unexpected at all! It's exactly what the researchers were scanning for.