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The strange case of John Sanford, creationist

shunyadragon

shunyadragon
Premium Member
Again given the definition of “falsifiable” that you quoted a claim can be falsifiable independently of weather if there is verifiable evidence supporting this claim or not…. All you need is an observation that is logically possible that would refute that claim,

If you are using a different definition of “falsifiable” then provide your new definition.

Read the definition again. Objective verifiable evidence is necessary for the falsification of hypothesis by the definition provided. By definition being logically possible requires observation. Please note the highlight in bold and underlined.


Falsifiability - Wikipedia

In the philosophy of science, a theory is falsifiable (or refutable) if it is contradicted by an observation that is logically possible—i.e., expressible in the language of the theory, which must have a conventional empirical interpretation.[A] Thus the theory must be about scientific evidence and it must prohibit some (but not all) logically possible observations. For example, the statement "All swans are white" is falsifiable because "Here is a black swan" contradicts it, whereas "All men are mortal" is not, because, unlike a swan being black, a man being immortal is not an inter-subjective property—there is no shared procedure to systematically conclude to immortality.[1][2]

Falsifiability was introduced by the philosopher of science Karl Popper in his book Logik der Forschung (1934), revised and translated into English in 1959 as The Logic of Scientific Discovery. He proposed it as the cornerstone of a solution to both the problem of induction and the problem of demarcation.

The role of falsifiability in Popper's philosophy is to make a rational critic or a deductive testing of the theory possible. This logical side is complemented by a methodological side that is hardly rigorous, because it involves irrational creative processes and, as pointed out by Duhem and others, definitive experimental falsifications are impossible. In this context, Popper argued for falsifiability and opposed this to the intuitively similar concept of verifiability. Verifying the claim "All swans are white" would require assessment of all swans, which is not possible in any theory that has a reasonable empirical interpretation. In contrast, the single observation of a black swan is sufficient to falsify it. Moreover, even if a black swan was in principle impossible due to a fundamental law of biology, it would still be a potential falsifier—i.e., an observation that is logically possible and in contradiction with the claim, which is enough to show that the latter is falsifiable.[C]

As a key notion in the separation of science from non-science and pseudo-science, falsifiability has featured prominently in many scientific controversies and applications, even being used as legal precedent.
 
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tas8831

Well-Known Member
No I never said, nor implied that transposons get fixed and dominant in all the population and even if I did use the “wrong words” I have clarified this multiple times and you still repeat the same comment..
You absolutely implied it - otherwise, what would be the point of hammering on this over and over:

"If transposons (or similar mechanisms) played a mayor role you can have more genetic changes in less time (this would help to explain the 60M differences between chimps and humans)"

"This mechanism can produce new proteins in just 1 generation so yes under that basis the mechanism is “fast enough “

That is true by definition, directed mutations by definition are more likely to be positive, that is part of the definition of “directed mutations”

First, a quick comment - when I asked for "evidence", I did not actually mean that I wanted you to just write an unsupported claim again.

Definitions are irrelevant if you cannot provide actual evidence that "directed mutations" even occur.

Directed mutations occur, and that they cause “fast” evolutionary changes at least at the “micro evolution scale”

My evidence
Those are Shapiro's assertions, extrapolations and wishful thinking are not evidence.
So from this source we get that:

There are nonrandom mechanisms that have been observed
False.
and that can cause evolution at a much faster rate than would have been possible with random mutations.
Also false. Those are Shapiro's claims, but he provides no actual evidence. He has been at this for some time, eagerly seeking name-recognition and fame. The evidence for this includes his many essays written for social media sites in which he argues - much as creationists do - that he is being marginalized, etc. His claims have been debunked repeatedly. Here, for example:
James Shapiro goes after natural selection again (twice) on HuffPo
James Shapiro, in his attempts to forge a new evolutionary paradigm, is reduced to going after my commenters
Should there be a “Third Way” of evolution? I think not.

The evidence for fast evolution in humans and mammals is already available in the source that you provided, from your sources we get that there is difference of 33M site differences between humans and chimps and that they diverge 5-7M years ago. So using your sources and your numbers, can you show that 5-7M years is enough time to account for the 33M site differences using the mechanism that you are suggesting?
I have done this 2 times for you already. You merely assert 'too fast.'
I am already providing a mechanism that can alter many sites at the same time, so why isn’t this mechanism a good candidate to explain such differences.
Because you are just parroting charlatans that write things that you want to hear.
I told you why your questions are irrelevant,
Because you cannot answer them.
you don’t have to explain the “physical traits” that make use humans, you have to explain the 33M nucleotide differences that we know exists between humans and chimps. Weather if this defferences can explain “the traits” or not, is irrelevant
It is a shame that your amazing scientific paper searching capabilities only seem capable of finding what you think are creation-friendly (e.g., Shapiro) nonsense as opposed to relevant scientific papers.
For you could have easily found this paper:

Initial sequence of the chimpanzee genome and comparison with the human genome
The Chimpanzee Sequencing and Analysis Consortium
Nature volume 437, pages69–87 (2005)

"On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ∼90 Mb. This difference corresponds to ∼3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies. Of course, the number of indel events is far fewer than the number of substitution events (∼5 million compared with ∼35 million, respectively)."​

Indels are, of course, one-time (i.e., single-mutation) events, as I'm sure you must know. You've been debunked all along, even when I used your own erroneous numbers, the numbers were not in your favor.
No magic un-evidenced transposons, 'natural genetic engineering', etc., needed. But this will not discourage you from reiterating your long-ago debunked claims for... ever.

Well I already provided evidence for directed mutations, what else are you expecting, what does it take to convince you that such mutations do occure?
Actual evidence. Shapiro's paper that you linked was not a research paper, for one thing. For another, none of the papers HE cited provided the evidence you pretend he presented. His reference, for example, to Ty retrotransposons is outdated (1993, though since he wrote what you quoted in 1999, I guess we can forgive him) and newer papers reveal a nucleosomal structural site that favors its integration (as opposed to 'direction'):
"Two integration hotspots per nucleosomal DNA separated by about 70 bp and located near the H2A/H2B interface were identified (Figure 10B). The unexpected asymmetry in the Ty1 insertion sites relative to the nucleosome dyad axis suggests that a dynamic process of nucleosome remodeling exposes a specific H2A/H2B surface permissive to Ty1 integration. "
... but I'm guessing Shapiro has moved on from those 20 year old claims.
Ok “too fast” is a subjective term, but we can agree on the fact that 33/2 M nucleotide differences evolved in the human line in 5M years….. weather if you arbitrary what to call this “fast” or not is irrelevant, the point is that you have to show that your model of “almost only random mutations” can account for such differences.
Done - see above.
 

tas8831

Well-Known Member
Still haven't explained how transposons are non-random, nor how they can produce rapid evolution.
that is expalined with detail in this article which you have ignored for months
DNA Transposons and the Evolution of Eukaryotic Genomes
OK, let's see - so I'll be looking for how transposons are non-random (as in the way creationists and mystics like to claim - 'directed' by magic to a specific area for insertions) and how they produce "rapid evolution", like 1 generation-style as LeRoy likes to claim...

Read it all.
Did not see any references to "nonrandom" (as in directed)... No references to "rapid evolution."
The only context in which 'rapid' was mentioned was in the rapid diversification of alleles produced by excision/expansion of copy numbers.
But what Leroy does still not seem to understand is that a 'new' allele produced by transposition STILL has to be selectable and spread throughout a population in order for any actual evolution to occur. I am unsure why this is so difficult for you to grasp.
 

shunyadragon

shunyadragon
Premium Member
You are moving the goal post.

You are supposed to define the concept of “falsifiable”

No just citing the definition as referenced. I presented again the definition of falsifiability as referenced requiring scientific evidence.
 

tas8831

Well-Known Member
Yes, they evolved too fast to be explained by RM and NS that is what I would claim, is there any academic source that concludes otherwise?
If yes, can you present that source?

If not, then why are so affirming with a seemingly high level of certainty that RM and NS are fast enough?
"On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ∼90 Mb. This difference corresponds to ∼3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies63,64,65,66,67. Of course, the number of indel events is far fewer than the number of substitution events (∼5 million compared with ∼35 million, respectively)."
 

leroy

Well-Known Member
OK,
But what Leroy does still not seem to understand is that a 'new' allele produced by transposition STILL has to be selectable and spread throughout a population in order for any actual evolution to occur. I am unsure why this is so difficult for you to grasp.
It’s not difficult to grasp, I completely agree and I haven’t made any comment that suggest otherwise. The sad thing is that you’ve been told multiple times that I am not making such a claim, and you keep repeating your straw man.

If I ever said something that confused you in to thinking that I am making such a claim then I apologize for that (I take the blame)….

Just to be clear, no I don’t think that transposons magically change the traits of a population in 1 generation.

So with that said, is there anything related to transposons that I claimed and that you disagree with?
 

leroy

Well-Known Member
"On the basis of this analysis, we estimate that the human and chimpanzee genomes each contain 40–45 Mb of species-specific euchromatic sequence, and the indel differences between the genomes thus total ∼90 Mb. This difference corresponds to ∼3% of both genomes and dwarfs the 1.23% difference resulting from nucleotide substitutions; this confirms and extends several recent studies63,64,65,66,67. Of course, the number of indel events is far fewer than the number of substitution events (∼5 million compared with ∼35 million, respectively)."
Once again an irrelevant quote that doesn’t answer the question.
 

tas8831

Well-Known Member
It’s not difficult to grasp, I completely agree and I haven’t made any comment that suggest otherwise.
Sure you have. You have mentioned many times that transposons can make "new proteins" in 1 generation.

What else, exactly, can that imply?
The sad thing is that you’ve been told multiple times that I am not making such a claim, and you keep repeating your straw man.
I am just going by what you write. Why do you keep writing strawmen of your own position?
If I ever said something that confused you in to thinking that I am making such a claim then I apologize for that (I take the blame)….
OK, great.
Just to be clear, no I don’t think that transposons magically change the traits of a population in 1 generation.
And yet you have written that the changes do occur in 1 generation. So what, exactly, is your point?
So with that said, is there anything related to transposons that I claimed and that you disagree with?
Yes - that the paper you linked to claiming vindication does NOT provide what you claim it does.
 

tas8831

Well-Known Member
Once again an irrelevant quote that doesn’t answer the question.
LOL!
Yes, right - a quote showing that the bulk of the mutational difference between humans and chimps is produced by larger-scale indels and such thus rendering you continued harping on 33 million mutations/not enough time- slogan moot.
Totally irrelevant.
 

tas8831

Well-Known Member
2nd try
Whats so hallarious about that?
LOL!
That you cannot see tells me all I need to know (and already knew).

Here is a hint for you, Johnny Science - estimates vary, but the average mammalian gene contains ~1500 exonic nucleotides.

If a 'new' gene requires "thousands" of point mutations... Well, I hope even you can see how bogus your position is.

Also:

1. These (your) arguments seem to imply that any particular trait is brand new and thus must be accounted for by some large number of mutations. This exposes the multi-level ignorance of those making them.

Look at the generic mammal body type - what specific trait does a human have that, say, a lemur or a dog does not? All human traits are essentially variations on a theme, not brand new. Developmental tweaks are all that is actually needed, not some suite of new beneficial mutations to get, say, the human shoulder joint from an ancestral primate shoulder joint.
There is the case of familial achondroplasia (dwarfism) - a single point mutation causes alterations in limb proportion (to include all muscle/nerve/soft tissue/etc. changes), joints, facial features, etc. All from a single point mutation. I am not saying that this is beneficial or adaptive, I am merely explaining that some huge number of mutations is NOT needed to produce relatively large-scale phenotypic changes. THIS is what your Haldane's dilemma-spewing creationist sources can't or won't understand or mention - usually because THEY don't know this, or because they don't want their target audience to know about it.

2. These arguments imply that some huge number of beneficial mutations MUST HAVE BEEN required for this transition to take place. Given that we know that single point mutations can affect multiple body systems and overall morphology, other than a desire for it to be so, what do these Haldane's dilemma types present that actually supports their position?

I've read ReMine's book - he offers nothing in that regard. I've read more recent treatments of it - more of the same.

I mentioned that a creationist once claimed that just to get the changes in the pelvis for bipedal locomotion a million mutations would have been required. Do you think he provided a million 'changes' that had to have been made? Nope. He could not provide A SINGLE example, but as is is the way of the creationist, he merely insisted that he was correct.


My argument against such claims are 1. that there is no argument (see the Ewen's quote); 2. that the arguments are based on ignorance of developmental biology; 3. that they are premised on the argument from awe (big numbers).
 

leroy

Well-Known Member
Also false. Those are Shapiro's claims, but he provides no actual evidence. He has been at this for some time, eagerly seeking name-recognition and fame. The evidence for this includes his many essays written for social media sites in which he argues - much as creationists do - that he is being marginalized, etc. His claims have been debunked repeatedly. Here, for example:
James Shapiro goes after natural selection again (twice) on HuffPo
James Shapiro, in his attempts to forge a new evolutionary paradigm, is reduced to going after my commenters
Should there be a “Third Way” of evolution? I think not.
https://whyevolutionistrue.com/2015/01/30/a-third-way-of-evolution-i-think-not/

The claims made by Shapiro are reported in multiple peer review articles.

Your supposed refutations are presented in a blogpost

So until you present a peer reviewed article that debunks Shapiro I would argue that he deserves the benefit of the doubt.


HONESLTY what else do you want? What else do you expect from me? I am supporting my claims with peer reviewed articles if this is not enough to convince you then I don’t know what else to do
 

leroy

Well-Known Member
LOL!
Yes, right - a quote showing that the bulk of the mutational difference between humans and chimps is produced by larger-scale indels and such thus rendering you continued harping on 33 million mutations/not enough time- slogan moot.
Totally irrelevant.
Irrelevant, you still have to explain the 30M single nucleotide mutations that I mentioned + the larger scale mutations , for the sake of simplicity I am just focusing on the 30M mutations , but feel free to provide an explanation for all the differences between chimps and humans
 

leroy

Well-Known Member
2nd try
LOL!
That you cannot see tells me all I need to know (and already knew).

Here is a hint for you, Johnny Science - estimates vary, but the average mammalian gene contains ~1500 exonic nucleotides.

If a 'new' gene requires "thousands" of point mutations... Well, I hope even you can see how bogus your position is.
.
No I don’t see it, please justify your assertion.
 

leroy

Well-Known Member
2

1. These (your) arguments seem to imply that any particular trait is brand new and thus must be accounted for by some large number of mutations. This exposes the multi-level ignorance of those making them.

NO I am not making that statement, I don’t believe that the statement is true and I haven’t said such a thing….. I f I ever said something that confused you in to believing that I believe such a thing I apologize for that.


Look at the generic mammal body type - what specific trait does a human have that, say, a lemur or a dog does not? All human traits are essentially variations on a theme, not brand new.

agree

2. These arguments imply that some huge number of beneficial mutations MUST HAVE BEEN required for this transition to take place.

Again you´ve been told multiple times, headlines dilemma is only a problem for those who affirm that evolution is caused mainly by random mutations (beneficial mutations) and natural selection.

If this doesn’t represent your view, then you don’t have to worry about this dilemma
 

tas8831

Well-Known Member
Ok my evidence that random mutations and natural selection by themselves are not good enough to explain evolution.

1 there are zero peer reviewed papers that conclude that random mutations and natural selection is enough
Where are the peer reviewed papers that offer EVIDENCE that it is not?
2 there are multiple papers that conclude that random mutations and natural selection is not enough to explain evolution. (Some of these articles are here Is Darwinism proven/accepted by official Science? )
From your list:

As the result of studies of bacterial variation, it is now widely believed that mutations arise continuously and without any consideration for their utility. In this paper, we briefly review the source of this idea and then describe some experiments suggesting that cells may have mechanisms for choosing which mutations will occur The origin of mutants

This is Cairns' 1988 paper hawking 'directed mutations.'

Here is a 2004 paper by one of his collaborators:

"Fairly early on in our studies, Cairns and I eliminated the hypothesis that mutations were “directed” toward a useful goal. The first negative evidence was obtained not with FC40, but with SM195. SM195 has an amber mutation in lacZ and so reverts both by intragenic mutations and by the creation of tRNA suppressors (11). The continued appearance of extragenic suppressors during lactose selection allowed us to dismiss the hypothesis that the selective conditions “instructed” the cell to make appropriate mutations—in the case of extragenic suppressors, there is no direct path from the phenotype (Lac+) to the mutated gene (encoding a tRNA) (23). Later it was shown that about two-thirds of the late-appearing Lac+ revertants of SM195 were due to slow-growing ochre suppressors that probably arose during growth prior to lactose selection (57). Nonetheless, the continued appearance of fast-growing amber suppressors in addition to the true revertants demonstrated that mutations appear elsewhere than in the gene directly under selection (24)."


But you go on citing that 1988 paper...
 

tas8831

Well-Known Member
No I don’t see it, please justify your assertion.
Wow, OK -

Typical exonic portion of a gene is ~1500 bp.
YOU claim that there would need to be "thousands" of mutations to make it a 'new gene'.

Just as absurd as Sanford's nonsense.

You can search for scientific papers (or do you just copy-paste your refs from some creationist site?), look up 'gene families' and 'exon shuffling' and so on.
 

tas8831

Well-Known Member
The point mutation differences is about 1.2% (LINK)
1.2% of 3 billion is 36 million.
The point mutation rate per generation is about 60. (Revising the human mutation rate: implications for understanding human evolution | Nature Reviews Genetics).
Humans and chimps diverged at least 8 million years ago (based on more recent molecular clock as well as fossils like Sahelanthropus). LINK
Human generation time is 30 years. Chimpanzee generation time is 20 years.
So the Number of point mutations that can accumulate in humans in 8 million years is 16 million.
And the Number of point mutations that can accumulate in chimpanzees in 8 million years is 24 million.
So total possible point mutations is 40 million and the total that is present is 36 million.
So...what is the problem?
It is even more than that. But he doesn't accept what he doesn't want to hear.
 

tas8831

Well-Known Member
The problem with your math is that it assumes that all 60 mutations will become dominant and fixed in the population.

No, you have the problem.

You cannot seem to grasp that fact that the mutational differences we see are NOT all fixed.
I have tried to explain this to you several times over a few years, but you cannot grasp it (or purposefully refuse to) - from the first time you referred to Haldane's model and totally misrepresented it.

My gosh, do you really think you can hang with the big boys when you - for YEARS - keep making the same dopy erroneous claims???
 
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