Why are We Disagreeing with ID?

[lee_merrill]

@lee_merrill

@Faizal_Ali

There is very good reason to believe our thoughts can be completely accounted for by the physical processes of our brains. Unless you’d care to provide scientific evidence that conclusively shows otherwise.

Out-of-body experiences are one evidence, where people reported for example, a shoe that was outside on a ledge while they were flatlined.

But this was verified, as have the descriptions people gave of the attempts to resuscitate them while they were out. Not all scientific evidence is taken with a thermometer.

[CrisprCAS9]

@lee_merrill

But this was verified, as have the descriptions people gave of the attempts to resuscitate them while they were out.

It hasn’t been scientifically verified. What are you even talking about?

[John_Harshman]

@lee_merrill

Because I believe I have experience in being a soul, and controlling my thoughts.

Perhaps your belief is a misinterpretation of your experience.

@lee_merrill

Do you believe that none of your choices are due to a person choosing, that mindless atoms do control you? Tell that to the judge.

I would prefer not to argue about the incoherence of libertarian free will. Perhaps someone else would like to take it up with you, but I think it would be futile.

[Faizal_Ali]

@lee_merrill

No, I’m saying that mindlessness does not produce mind.

Like I say, fallacy of composition.

Hydrogen is waterless.

Oxygen is waterless.

Waterlessness cannot produce water.

Therefore, hydrogen and oxygen cannot produce water.

Agree?

@lee_merrill

But this was verified

Where?

@lee_merrill

as have the descriptions people gave of the attempts to resuscitate them while they were out.

Which only means they made lucky guesses (We all know what is likely to happen during a resuscitation by watching ER and other medical TV shows) or they were still able to perceive things while apparently unconscious. Your use of the term “flat line” is deceptive. Everyone who was resuscitated had brain activity throughout the procedure, because if someone has no brain activity, they are permanently dead and cannot be resuscitated.

[RonSewell (RonS)]

@lee_merrill

Premise1: I am in control of my thoughts
Premise2: My reasoning can be trustworthy
Premise3: Mindless atoms cannot be trusted to produce reliable reasoning
Conclusion: My thoughts cannot be controlled by mindless atoms

Premise 1: I think your sense of identity and control is an artifact of your thoughts.
Premise 2: You think that I am wrong, and it is my thoughts that are untrustworthy.
Premise 3: Mindless atoms produce can produce all sorts of conflicting reasoning.
Conclusion: Whatever controls thoughts, it cannot be very reliable.

[colewd (Bill Cole)]

@Paul_King

I disagree. Lynch’s model can easily be adjusted to deal with more slowly evolving genes, while Behe’s model would need to be made more like Lynch’s.

What we are observing is proteins that are not evolving in the classic sense as the variation over long time periods is very small. They are essentially held the same form for 50 million generations.

@Paul_King

And of course, you cannot determine the speed of evolution by only looking at the genes which are evolving at the slowest rates. The fact that Behe’s model does not apply to all genes is sufficient to destroy his argument.

We need to ask the question if evolutionary theory explains the origin of genes that are not changing over long periods of time. These genes appear to have very high levels of functional information. Many also first appeared in vertebrates.

How does Lynch change his model and still avoid prohibitively long waiting times for a 2 AA adaption?

[Paul_King]

@colewd

What we are observing is proteins that are not evolving in the classic sense as the variation over long time periods is very small. They are essentially held the same form for 50 million generations.

So you’re looking at highly-conserved genes. That really doesn’t seem relevant. They certainly can’t be used to set a limit on the rate of evolution.

@colewd

How does Lynch change his model and still avoid prohibitively long waiting times for a 2 AA adaption?

This question makes no sense. If you are talking about highly conserved genes where a “2AA” change would not be adaptive then why would Lynch need to avoid “prohibitively long waiting times”?

[Faizal_Ali]

@colewd

What we are observing is proteins that are not evolving in the classic sense as the variation over long time periods is very small. They are essentially held the same form for 50 million generations.

That’s right, folks. Bill still does not understand the concept of conservation.

But keep trying!

[Rumraket (Mikkel R.)]

@lee_merrill

Let’s try:

Premise1: I am in control of my thoughts
Premise2: My reasoning can be trustworthy
Premise3: Mindless atoms cannot be trusted to produce reliable reasoning
Conclusion: My thoughts cannot be controlled by mindless atoms

Thanks. Now the problem is premise3. Why can’t atoms be trusted to produce reliable reasoning? It seems to me that in fact certain material structures made of mindless atoms are incredibly reliable. So reliable in fact that we use them to aid or even correct our own reasoning. My calculator never misbehaves, gets tired, or drunk, or angry, or exhausted. Contrary to people, fed the exact same huge calculation it will reliably produce the exact same result every time.
So, what is it about mindless atoms that means they can’t be trusted to produce reliable reasoning?

[colewd (Bill Cole)]

@Paul_King

So you’re looking at highly-conserved genes. That really doesn’t seem relevant. They certainly can’t be used to set a limit on the rate of evolution.

How do you show new proteins are the product of evolution is the evidence shows so little variance?

@Paul_King

This question makes no sense. If you are talking about highly conserved genes where a “2AA” change would not be adaptive then why would Lynch need to avoid “prohibitively long waiting times”?

If genes are this mutation sensitive then you need a gene duplication prior to the gene exploring different sequences. The waiting differences depend on this issue. This is Behe’s thesis and the data supports it for vertebrates. Lynch’s hypothesis of neutral mutations or equal substitutability of amino acids is not viable.

[Faizal_Ali]

@colewd

If genes are this mutation sensitive then you need a gene duplication prior to the gene exploring different sequences. The waiting differences depend on this issue. This is Behe’s thesis

Incorrect.

Behe’s thesis is that it is possible to make up a completely imaginary model that, if it were true, evolution would not be possible.

He supported his thesis by making up a completely imaginary model that, if true, would make evolution impossible.

Good for him.

[Faizal_Ali]

@Rumraket

Why can’t atoms be trusted to produce reliable reasoning? It seems to me that in fact certain material structures made of mindless atoms are incredibly reliable. So reliable in fact that we use them to aid or even correct our own reasoning.

An answer to that question might be that the calculator is only reliable because its atoms were deliberately arranged by a human being. And the brain of a human being is only able to create a calculator because its atoms were deliberately arranged by God.

Which is all well and good, but it still does not address the question of why atoms arranged by the evolutionary process could not also result in a brain that could produce a reliable calculator.

[Mercer (John Mercer)]

@colewd

@Paul_King

So you’re looking at highly-conserved genes. That really doesn’t seem relevant. They certainly can’t be used to set a limit on the rate of evolution.

How do you show new proteins are the product of evolution is the evidence shows so little variance?

Looking at newer proteins would be a good start.

[Paul_King]

@colewd

How do you show new proteins are the product of evolution is the evidence shows so little variance?

If the evidence showed very little variance then that little variance is all you’d have to account for. It’s question begging to look at examples where change hasn’t occurred and then dismiss examples where more change exes to have occurred.

@colewd

If genes are this mutation sensitive then you need a gene duplication prior to the gene exploring different sequences

But they aren’t all that sensitive, are they? And you’d only need gene duplication if the advantageous variations were inaccessible to other paths. What’s the evidence that there are beneficial variations to these highly conserved genes that can be reached only through duplication? Isn’t the conservation evidence suggesting that the gene is at or very near to an adaptive peak? And if that’s the case, then the argument is useless.
The more so since duplication and variation is more associated with new functions than improving the existing function anyway.

[T_aquaticus]

@colewd

If genes are this mutation sensitive then you need a gene duplication prior to the gene exploring different sequences.

If genes are this sensitive, then how is it that species are so different from each other while sharing the same genes?

@colewd

The waiting differences depend on this issue.

Multiple adaptations can be evolving in parallel.

@colewd

This is Behe’s thesis and the data supports it for vertebrates.

What data?

[Rumraket (Mikkel R.)]

@colewd

How do you show new proteins are the product of evolution is the evidence shows so little variance?

You do what they did here:

A Molecular Portrait of De Novo Genes in Yeasts

Which I also expounded on at length here and which you never responded to:

Criticism of Both Flavors of Creationism

There are some things in biology that only make sense in the light of evolution, and the gradual and de novo gain of novel protein coding genes is one such thing. I mean just take a look at this section in this paper: De Novo Genes Have Unique Sequence Characteristics as Compared with Conserved Genes The de novo candidates share a number of structural properties that differentiate them from the genes conserved outside the two genera. They are significantly shorter, have a lower codon adaptation index and a higher aggregation propensity compared to conserved genes (supplementary fig. S5, Supplementary Material online). Their biosynthetic cost is also lower than those of noncoding sequences, in agreement with an intermediate stage from a noncoding to a coding state (supplementary fig. S5, Supplementary Material online). When recent, de novo genes are not enriched in intrinsically disordered regions compared to conserved genes. The low propensity of recent genes to disorder was previou…

And your crap about duplications and more about that yeast de novo gene paper and how to show they evolved here:

Criticism of Both Flavors of Creationism

Those are fixed gene-duplicates in yeast, not the rate of occurrence of duplication mutations “in vertebrates” that you asked for. I quote that paper for you again like I did a month ago: Note that by “gene duplication rate we” mean the rate at which a duplicated gene is created by mutation and becomes fixed in the population. The fixation probability of duplicated genes should be largely affected by natural selection (14). I could of course just refer to that offshoot of the Lenski experiment in which the total genome size for E coli increased by over 20% from hundreds of duplications in less than 3000 generations to show what happens when a locus prone to duplication suddenly has a positive fitness effect when amplified. Incidentally the method used in the paper you link is phylogenetic, that is they’re using common ancestry to calculate a rate of fixed duplicates over deep time by counting differences between species thought to share common ancestry. A method you explicitly r…

Your endlessly recycling questions and arguments have been answered by pretty much everyone around here probably a hundred times by now.

[colewd (Bill Cole)]

@Paul_King

If the evidence showed very little variance then that little variance is all you’d have to account for. It’s question begging to look at examples where change hasn’t occurred and then dismiss examples where more change exes to have occurred.

Here is uniprot and you just need to look at proteins between mouse and rats and you can try and find examples where there are more then a few mutations. I have yet to find more then a few.

https://www.uniprot.org/align/A202205275BF3C56A578D7D6DFD1FC81EE5DA7730020699P

@Paul_King

But they aren’t all that sensitive, are they?

The evidence says they are and this is why Behe has the right model for vertebrates.

[T_aquaticus]

@colewd

Here is uniprot and you just need to look at proteins between mouse and rats and you can try and find examples where there are more then a few mutations. I have yet to find more then a few.

At Ensembl, I am counting 416 missense mutations (i.e. changes in amino acid sequence) for the MMP3 gene within the human population.

https://uswest.ensembl.org/Homo_sapiens/Gene/Variation_Gene/Table?db=core;g=ENSG00000149968;r=11:102835801-102843609

@colewd

The evidence says they are

What evidence?

[Paul_King]

@colewd

Here is uniprot and you just need to look at proteins between mouse and rats and you can try and find examples where there are more then a few mutations. I have yet to find more then a few.

Ther are more than 86,000 mouse proteins, so I suspect that your sampling is inadequate to come to a strong conclusion.

@colewd

The evidence says they are and this is why Behe has the right model for vertebrates.

Well, no even if that was correct it wouldn’t say anything about the accuracy of Behe’s model. You need to look at the genes that are evolving not those that aren’t.

[Mercer (John Mercer)]

@colewd

Here is uniprot and you just need to look at proteins between mouse and rats

Why would you only look at consensus sequences? Why wouldn’t you look at variation within species?

Why do you think I keep bringing up MYH7?