Re: Richard says Howard Hershey is wrong

On Dec 26, 2:19 pm, Seanpit <seanpitnos...@naturalselection.
0catch.com> wrote:
On Dec 26, 10:41 am, hersheyh <hershe...@xxxxxxxxx> wrote:



Still think its "nonsense"?

Yes, I do! Howard Hershey is wrong. He is making the same mistake as
you persist in doing, which is assuming characteristics of unknown
natural processes.

Actually I am assuming 1) relatively complete knowledge about what can
occur in the *absence* of an intelligent actor. And 2) knowledge of
how the products of an [known] intelligent actor can go beyond the
limits of what can occur in nature [in the absence of such an actor].

That's not what Richard Forrest says. You directly disagree with him
here. You actually agree with me on this one. Knowledge of the
limits of natural processes is in fact important when it comes to the
recognition of artifacts.

Yes it is. But it is not sufficient by itself. Finding something
that 'seems' to be beyond the capacity of any known natural process
would be the first step in determining that that object was made by an
intelligent agent, not the last. A beautiful calcium carbonate shell
is as intricate and symmetrical as any solid cube. Yet it is
demonstrably created by a dumb mollusk, not an intelligent designer.

< snip >

But, as the below commentaries note, none
of this tells us squat about biological organisms and their evolution
because 1) the relatively complete knowledge about what can occur in
the *absence* of an intelligent actor over geological time frames says
that evolution can explain the features of biological organisms

Not remotely close when it comes to systems having a minimum
structural threshold requirement of more than 1000 fairly specified
residues.

And that is nothing but a bull*** assertion. You have not cited a
single 1000 aa *function* where the 1000 aa is 1) the "minimum
threshold level" and 2) the "sequence specificity" is the same as
cytochrome c's. But, of course, "average gap size", even for
cytochrome c, the only sequence you have presented actual data for, is
still bull*** numerology. It is neither an "average" nor is it "gap
size". It is, quite clearly, the equivalent of randomly synthesizing,
from scratch, a peptide with a length equivalent to the number of
invariant aa residues if one only had invariant and fully variant aa
residues. IOW, it is NOT an average. And it is not a "gap size"
unless you mean a gap which is the equivalent of randomly synthesizing
an entire 100 aa long protein that has a single *specified* function
in which there is, effectively, 31 invariant aa sites. It is not even
*all* such proteins. It is certainly NOT all proteins 100 aa long
that have "potential benefit" to the organism. Change your wording so
that you are at least HONEST about that.

and 2)
there is no [known] intelligent actor who has ever been observed to go
beyond the limits of what nature itself can do.

It happens all the time in real time by ID at high levels of
functional complexity. Ever hear of designer genes?

Yes. Where is the evidence of genetics labs in the Precambrian?

Sean, obviously disagrees with both statements and does NOT agree with
me.

That's right . . .

BFD. It is a demonstrable fact that his "proof" that evolution
is impossible is merely bogus GIGO numerology that is not based on
evidence, but on a bogus strawman model of evolution where proteins
are randomly assembled from scratch and don't have any possible
function until the *specified* (aka teleological) function is
reached.

Rather, my position is based on a great deal of evidence that suggests
that your notion of the minimum possible gap size (i.e., 1) always
being the most likely gap size is utter nonsense.

Actually it is not nonsense at all. In fact, if you assume that the
"island" with your *specified* function represents coherently similar
sequences, it must *necessarily* be surrounded by similar sequences
that do not have the SINGLE *function* you specified but would have
many or most of the necessary subfunctions needed to generate the
*specified function* by rather short gap sizes. And the difference
between "subfunction" and "beneficial function" can be nothing.

Likewise, your
notion of the maintenance of the same degree of target clustering
regardless of level is demonstrably false. You yourself recognize
that there is a linear increase in the average and minimum gap
distances with increasing minimum structural threshold requirements.

Actually I was wrong. Under the bogus assumptions you make, the
increase in gap size is indeed exponential, meaning it increases as a
constant percentage rather than constant amount for an increase in
"minimum threshold size". But, of course, that doesn't mean ***
because all your assumptions are bogus and the number you generate
isn't "average gap size" at all. The number you generate and falsely
call "average gap size" is exactly what you would generate if you
simply increased the 30.7 number for the single *specified* function
of cytochrome c proportionately to molecules of larger "minimum
threshold size". This *requires*, of course, that the un-named
specified *function* of this larger protein have the same level of
"sequence specificity" as cytochrome c.

Your "average gap size" is *still* nothing but the 20th root of the
ratio of the number of sequences that lack the *specified* function
(which you misleadingly claim are *all* non-functional for any
function) for each sequence that has the *specified* function. It is,
thus, the equivalent of the effective number of invariant aa residues
predicted for a protein of that level of sequence specificity.

Increasing the size of the "minimum threshold size" 10-fold (and
assuming no change in sequence specificity) means that the length of
the effective number of invariant sites will increase 10-fold. But
neither number is "average gap size" between *functional* proteins.
The number is simply the strawman idea that all the "functional
sequences" for the *specified function* are randomly distributed in
total sequence space and that each is constructed by random assembly
from a starting sequence that has NOT a single invariant site being
the terminal single functional aa. That is *maximal*, not *average*.
And it is not "gap size", for which one needs both a starting sequence
and ending sequence.

It is just that after you made this statement, you realized the
exponential implications of this linear relationship when it comes to
random searches of sequence/structure space and have since snipped any
reference to this comment of yours.

Actually, I decided to focus on the fact that your "average gap size"
is not what you claim it is. And your math is bogus.

The only contribution he makes to this bogus math is that,
in a confused and rather ignorant way, he does deal with the problem
that the "747 in a tornado) strawman has with the existence of
multiple sequences that have the *specified* (aka teleological)
function. He confuses the idea of total number of effectively
"invariant aa residues" for some modern protein with its modern
function and the idea of "average gap size".

The effective number of invariant residue positions does indeed affect
the average gap size - and the minimum likely gap size.

But, of course, the fraction of a protein composed of invariant
residue positions is completely a function of "sequence specificity".
And cytochrome c is not an "average" protein. Why not use "fibrinogen
peptide"? More importantly, the level of sequence specificity (and
hence your bogus 'gap size') is only valid for the single *specified*
function. But all protein 'functions' are a combination of
subfunctions performed by different parts of the sequence. Thus a
protein can still bind heme (a "potential beneficial function" in its
own right) and have a sequence that differs from 'cytochrome c' by a
single aa, yet not function as a "cytochrome c". When you divide the
number of single *specified* function sequences to get the ratio of
"potential beneficial vs non-beneficial" sequences, you are not
dividing by the number of "totally functionless proteins" of that
size. You are dividing by the total number of sequences of that
size. It is quite likely that almost all 100 aa sequences interact
with *some* biological material or potential biologic material. Any
protein that folds into a specific structure at least part of the time
likely can interact with *some* biological material. And that is the
only measure of "potential benefit" that I can think of.

At least you admit when you disagree with those who are usually on
your side in this forum. That's at least something. What is
interesting here though is that nobody in this forum of any
consequence is comming to your side on this particular issue. In
fact, most who frequent this forum seem to disagree with you here.
http://groups.google.com/group/talk.origins/msg/bc341bd3804df2f8?hl=e...

http://groups.google.com/group/talk.origins/msg/ea437e08aa7745ee

http://groups.google.com/group/talk.origins/msg/72c3f0dcb141f89c?hl=en&;

http://groups.google.com/group/talk.origins/msg/c9bc1d7877d8a69e

RF

None of the above are coming to *your* defense. They all are saying
that Sean's argument is bull***.

Not when it comes to what it takes to detect artifacts. Your past
comments actually agree with me on this particular issue.

Howard also wrote the following:

He has also written a lot in which he makes mincemeat of your fatuous
and mathematically incompetent assertions about gap size.

I see that you have modified your math on your web site by referring
people to the discussion. That is insufficient. You have to CORRECT
your disingenuous wording. The ratio you present is NOT what you
claim it is. The number you call "average gap size" is NOT average
nor gap size. It is insufficient to refer your readers to the
discussion. You have to CORRECT what your math really is saying.
Failure to do so will bring upon you the accurate claim that you are a
"liar" and not just "wrong" or "deluded".

You evidently still don't understand the concept of the average gap
size or the difference between the average gap size and the minimum
likely gap size.

I understand the *concept* of average gap size. I also understand
that you are unable to calculate that number. The problem is that it
is a useless concept because evolution does not work by randomly
assembling proteins from scratch via a "747 in a tornado" strawman
mechanism. That would be the only model in which the "average gap
size", even if you could actually calculate it, would be useful.

The only useful numbers are *actual* gap sizes between an ancestral
sequence and a modern one that performs a modified or different
function. That number is always relatively small *when* evolution has
occurred.

For those who may want to see your own arguments to
correct my position, I've included a link for them to read. If your
counter arguments are so convincing, you should have no worries. You
have to admit that providing a link to your arguments is about as good
as I can do to present a balanced perspective on this topic . . .
wouldn't you say?

No. You can correct the dishonest presentation in your appendix that
claims that what the 'ratio' of cytochrome c single specified
sequences to total sequence space at that level of "minimum threshold
size" is "potential beneficial vs. non-beneficial sequences". It is
NOT. And you can accurately present that what you have calculated is
NOT "average gap size" but rather the number of invariant aa residues
(i.e. a measure of sequence specificity) in cyt c estimated from the
ratio of Yockey. And it would be nice if you would point out that
cytochrome c is not an "average" protein wrt sequence specificity, but
rather one with a much higher than average specificity.

That would be presenting an honest argument. I don't care a fig about
'balance' when one argument is as bogus and disrespectful of the truth
as yours.

I know your training is in medicine and the surgeon's creed is "Not
always right, but always certain." But this is science. It is quite
acceptable to be wrong. I have been.

I've been wrong too. But, I don't see that I'm wrong on this issue.
You know, it is possible that you could be wrong here as well . . .

You are wrong. Your calculation of "average gap size" is bogus
numerology.

I'm only refering to Howard's arguments here because you seem to think
so much of them whenever he tries to counter me with his nonsense.
Interestingly, you also seem to think his arguments are nonsense, but
only when he directly counters your position.

I think you are mislabelling which arguments are "nonsense". Both
Harshman and I agree that your arguments are "nonsense" and bold
"pseudoscience" at best.

Not when it comes to what it takes to adequately detect artifacts.

And I suspect that we basically agree about
what is involved in declaring some *specified* object similar to those
that humans produce but nature doesn't as being "more likely" to have
been produced by some "intelligent agency" when and if any such thing
is found. You are probably taking some things out of context.

What am I taking out of context Howard? You just can't stand it that
you've actually agreed with me on any point?

I have no doubt that whenever one meets those criteria, one has a
reasonable probability (but not a certainty) of correctly determining
that an object was manufactured by an agent capable of manipulating
objects in ways that would not occur in nature.

Same goes for SETI. Any test that would be specific for SETI would
also involve a tremendous amount of prior knowledge about what can
happen in the absence of a designer *and* what known designers can or
potentially could do that would be different.

And indeed it would. But SFW?

The SFW is that this statement is in direct opposition to Richard's
position.

< snip repetitive >

I can't and don't really care to
change the notions of others regarding this issue. That's not my
purpose for being here.

Your purpose is to teach idiots that 2+2 = a trillion.

Rather, part of my purpose is to see how you could possibly think that
winning the lottery is a piece of cake regardless of if the averages
are 1 in 1 or 1 in trillions upon trillions.

You mean that no one ever wins the lottery? But, of course, a
lottery, unlike evolution is a completely random process.

Sean Pitmanwww.DetectingDesign.com

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