Recombination and mutation, just like the mechanisms that generate de novo information in all of biology.
I don’t observe anything of the sort.
Would you please stop making false statements with this ridiculous “we observe” construction? It’s perfectly clear that you don’t observe most of the biology we know. I mean, a good example of one of your “observations” is that bigger proteins require more specificity to bind, when everyone who has studied it knows that the opposite is true.
Please speak only for yourself.
Not in terms of FI generated per day; it’s a lot more.
But hey, since you went there, how does your design hypothesis explain the 1:500 incidence of inherited hypertrophic cardiomyopathy? Most is caused at very low penetrance by variants of genes encoding muscle proteins.
Which is the “ID theory” as I described it. You just wrote the exact same nonsense I said you did. As I stated, the sentence “A mind can make X” is not a scientific theory Bill. And yet despite your protestation, you go an confirm that your “theory” is exactly like this.
Let’s see:
What I wrote that the ID “theory” is like: “A mind can make X”.
Break it up like this:
[“A mind”] [“can make”] [“X”].
What you wrote that the ID “theory” is like can be broken up into the same three parts: [“A mind”] [“as a mechanistic explanation for”] [“functional information and other cellular artifacts”].
That’s essentially the same thing.
[“A mind”] = [“A mind”]
[“can make”] = [“as a mechanistic explanation for”]
[“X”] = [“functional information and other cellular artifacts”]
It’s completely vacuous(you lack the “mechanistic explanation”) and doesn’t rise to the level of a testable hypothesis.
The fact that there is no predictive model due to a minds non deterministic qualities is true but does not pose a problem as we can test the hypothesis without a model.
No, you can’t. That’s exactly why you can not test the model. If the model does not predict anything, then it is not testable. A model can only be testable if it says that something should be a certain way, and reciprocally that it should not be some other way.
Because only then, when the model says “it should be like this, and not like that” can it become possible for observation or experiment to contradict the model.
How is it possible you have still not wrapped your head around this elementary concept after over half of a decade having had this explained to you over and over again?
All of the evidence that you ignore, Bill, your false claim about larger proteins requiring more specific binding sites being a perfect example of the same.
No, you’re fabricating evidence again, very few cases are caused by de novo mutations. Try again. Engage that powerful mind.
Your straw man perhaps but the design hypothesis does.
Because your claim is false. The model is based on the mechanism. You can test either. If the mechanism is deterministic then it can be modeled and be predictive. If it is not you can test the mechanism directly as we are with these exchanges.
So there is a mutant variant of this disease. You already stated the other cause so why are you asking this question. I also believe you misrepresented by claim about large protein binding. In addition you did not support your claim that mutation and recombination can explain complex adaptions but other than that your having a pretty good day.
There is no straw man. I reproduced your words faithfully, and explained how they were wrong by showing how they were saying exactly the same thing I did.
No, there is no mechanism in the not-even-a-model gibberish you wrote. “As an explanation for” is not a mechanism.
False, you have not created any functional biological molecules, much less life. We are not “testing” any ID model about life’s origin by typing into this window.
That’s an absurd response. It’s word salad, as there is no such thing as a “mutant variant” of any disease. “Mutant variant” doesn’t even make any sense.
You didn’t explain the majority, inherited ones. Why is it so frequent, Bill?
You might want to look it up before falsely presenting your assumption as fact.
Here’s another assumption of yours from last year, falsely presented as fact–doubling the falsehood by falsely portraying direct scientific observations as a mere assumption: “This is based on the faulty assumption that binding to substrate A has anything to do with binding to substrate B. When mutating to substrate B the sequence is still facing the large void of non functional space.”
Did you ever retract that objectively, doubly false claim, Bill?
No he’s exactly correct. You have stated numerous times that you think that increasing the size of sequence space, hence increasing sequence length, negatively correlates with the frequency of finding functions.
So he’s exactly right when he states that in fact larger proteins are more likely to be able to bind things, than shorter ones, constitutes an observation in diametrical opposition to your mistaken hunch about the scaling relationship between frequency of function and sequence length.
It’s interesting that Bill routinely and falsely presents his assumptions as everyone’s observations, while falsely portraying scientists’ detailed, direct, routine observations as assumptions.
You mean it’s a great mystery to Bill Cole. Everyone else with the slightest bit of training the the evolutionary sciences knows how it happens. Science has known for 70-some years.
Bill, are you ever going to explain how your ID “Theory” gets past Step 1 of this diagram? Where are the ID testable hypotheses and why isn’t anyone testing them?
Are you going to admit ID doesn’t have anything to do with the scientific method? Or will you keep on being Bill?
Which ones? Point out the exact words you are claiming aren’t yours.
False. I never changed your argument. I simply explained how your sentence contains essentially the same three elements. That X did Y.
Let me copy past it again here:
What I wrote that the ID “theory” is like: “A mind can make X”.
Break it up like this:
[“A mind”] [“can make”] [“X”].
What you wrote that the ID “theory” is like can be broken up into the same three parts: [“A mind”] [“as a mechanistic explanation for”] [“functional information and other cellular artifacts”].
That’s essentially the same thing.
[“A mind”] = [“A mind”]
[“can make”] = [“as a mechanistic explanation for”]
[“X”] = [“functional information and other cellular artifacts”]
It’s completely vacuous(you lack the “mechanistic explanation”) and doesn’t rise to the level of a testable hypothesis.
No straw man, no changing of your argument.
Perhaps I do understand it, and you are just making bad excuses out of some sense of pride.
I have not made any misrepresentations.
Actually we are not at all showing how “minds” can generate information, at most we are showing that Human organismscan generate it. Not how they are doing that.
But we can’t appeal to Human organisms as an explanation for the functional biological polymers of life, because humans were not around to design them. So your explanation is a failure right out of the gate.
Even if humans could in principle design living organisms, that still doesn’t mean they did it for any currently known life.
It may be a mystery how the very first information bearing polymers of life originated(we still don’t know that), but once there was life capable of evolving, getting new information is simple as you have been shown numerous times before. It’s evolution!
Okay, that is fair enough Bill. I just want to make sure I understand now. Are you saying that you were in error when you insisted that the size of sequence space inversely correlates with the frequency of finding functions in that space? You no longer believe that?