Remdial Education: Jack and the Mendelian Beanstalk

[Ophiolite]

Resumption from a locked thread of a potentially interesting point.

Recent acceleration of human adaptive evolution

http://www.anthro.utah.edu/PDFs/accel.pnas.smallpdf.pdf

You folks will now need to use genetics and natural selection to explain this acceleration of human evolution.

How do you explain acceleration in TOE? I want to see the math.

”
You don't seem to understand the research you are presenting. The authors of this study provide the answers to the questions you pose.

"Larger populations generate more new selected mutations, and we show the consistency of the observed data with the historical pattern of human population growth."

In support of this contention they cite Fisher [Fisher, R. A. (1930) The Genetical Theory of Natural Selection (Clarendon, Oxford).] and Otto et al Otto, S. P. & Whitlock, M. C. (1997) Genetics 146, 723–733..

I have never before heard anyone complain about lack of maths in Fisher's work. What do you find unsatisfactory about the authors' own explanation? And, if you are doubting Fisher, could you also specify what you find questionable in the works of Haldane, Dhobzansky, Simpson and Mayr.

Darn, it seems I am over my head.

What do you mean?

Which reference of the posts are you using?

:shrug:
What do I mean? You think the referenced paper requires we provide an explanation for accelerated human evolution. I observe that the referenced paper supplies an explanation for accelerated human evolution. Consequently I am forced, reluctantly, to conclude that you didn't understand the paper.

You ask for the math and I point out that the authors of the paper justify their explanation by referencing Fisher. You must know who Fisher is, so I am bemused that in an argument supported by a reference to Fisher you would even raise a question of the math.

However, since you seem - implicitly - to be questioning Fisher I wonder if you also question others involved in the development of the Modern synthesis. Hence my interest in which of their views, specifically, you also question.

I shall be happy to do anything practical to help you towards a better understanding of material that you seem to find difficult.

 

[Jack_]

Resumption from a locked thread of a potentially interesting point.


”
You don't seem to understand the research you are presenting. The authors of this study provide the answers to the questions you pose.

"Larger populations generate more new selected mutations, and we show the consistency of the observed data with the historical pattern of human population growth."

In support of this contention they cite Fisher [Fisher, R. A. (1930) The Genetical Theory of Natural Selection (Clarendon, Oxford).] and Otto et al Otto, S. P. & Whitlock, M. C. (1997) Genetics 146, 723–733..

I have never before heard anyone complain about lack of maths in Fisher's work. What do you find unsatisfactory about the authors' own explanation? And, if you are doubting Fisher, could you also specify what you find questionable in the works of Haldane, Dhobzansky, Simpson and Mayr.

:shrug:
What do I mean? You think the referenced paper requires we provide an explanation for accelerated human evolution. I observe that the referenced paper supplies an explanation for accelerated human evolution. Consequently I am forced, reluctantly, to conclude that you didn't understand the paper.

You ask for the math and I point out that the authors of the paper justify their explanation by referencing Fisher. You must know who Fisher is, so I am bemused that in an argument supported by a reference to Fisher you would even raise a question of the math.

However, since you seem - implicitly - to be questioning Fisher I wonder if you also question others involved in the development of the Modern synthesis. Hence my interest in which of their views, specifically, you also question.

I shall be happy to do anything practical to help you towards a better understanding of material that you seem to find difficult.

I did not see this.

In humans, this effect may have
been augmented by vast changes in cultures and ecology during the
Late Pleistocene and Holocene, creating newopportunities for adaptation.
Such acceleration does not require any change in the per-genome
rate of adaptive mutations; it is a simple effect of changing demography,
possibly increased by changing ecology. The best analogy may
be the rapid recent evolution of domesticates such as maize [3, 4].


The above is from the paper.

What page of your bible can I find may have been as an explanation of science?

Your thesis failed.

Let me know if I can help you further.

 

[Ophiolite]

In what way does the hypothetical nature of the postulated explanation render your interpretation, which seeks to overthrow the theory of evolution, more viable and plausible?

Aside:
If we are going to have a proper discussion please avoid introducing strawman arguments or other logical fallacies. The third and second last sentences fall into such a category.

Your last sentence is also unhelpful. You may feel it is mirroring my last sentence "I shall be happy to do anything practical to help you towards a better understanding of material that you seem to find difficult." However mine was in response to your declaration that "Darn, it seems I am over my head."

 

[Jack_]

In what way does the hypothetical nature of the postulated explanation render your interpretation, which seeks to overthrow the theory of evolution, more viable and plausible?

Aside:
If we are going to have a proper discussion please avoid introducing strawman arguments or other logical fallacies. The third and second last sentences fall into such a category.

Your last sentence is also unhelpful. You may feel it is mirroring my last sentence "I shall be happy to do anything practical to help you towards a better understanding of material that you seem to find difficult." However mine was in response to your declaration that "Darn, it seems I am over my head."

You do not get it and neither does anyone here.

I am not trying to overthrow TOE like I am SR.

I said specifically TOE is not sufficient.

I did not say TOE is wrong in what it provides.

It just does not provide complete answers.

If it does, them we are automatons only capable of executing our DNA instruction sets.

Those in genetics should be forced to take courses in recursion theory.

In this way, they would understand the implications that of suggesting human life no more than a sequence of chemical operations as proposed by TOE.

 

[James R]

Jack_:

If it does, them we are automatons only capable of executing our DNA instruction sets.

I have a brain. Do you?

My DNA doesn't determine what I think about. It isn't involved in any day-to-day decisions I make. It doesn't know about the internet (among many other things).

In short, I'm obviously not an automaton controlled by my DNA. How about you?

 

[AlphaNumeric]

If it does, them we are automatons only capable of executing our DNA instruction sets.

Those in genetics should be forced to take courses in recursion theory.

In this way, they would understand the implications that of suggesting human life no more than a sequence of chemical operations as proposed by TOE.

No one suggests that because it has the obvious and immediate implication of two twins behaving exactly the same, which is not the case and so is immediately falsified.

Clearly you do with biology what you do with physics, assume your interpretation is precisely what scientists say and then you attack your interpretation, not the science. And thus your epic failing is not restricted to physics.

 

[GeoffP]

What page of your bible can I find may have been as an explanation of science?

This is ridiculous.

The modern synthesis of genetics was as much a welding of biostatistics as Mendelian theory. Jack has not thie slightest understanding of, or interest in, statistics as a descriptive system of biology. He thinks - or pretends that he does - that biological systems should follow direct mathematical rules as in physics. They don't. I think the discussion is done: Jack is unwilling or unable to grasp the science of biology and genetics. Herc had the right idea from the start.

 

[Crunchy Cat]

I think the discussion is done: Jack is unwilling or unable to grasp the science of biology and genetics. Herc had the right idea from the start.

Correct.

 

[Jack_]

Jack_:



I have a brain. Do you?

My DNA doesn't determine what I think about. It isn't involved in any day-to-day decisions I make. It doesn't know about the internet (among many other things).

In short, I'm obviously not an automaton controlled by my DNA. How about you?

If this is true, you are greater than the sum of your components.

How does this work under TOE?

 

[Jack_]

No one suggests that because it has the obvious and immediate implication of two twins behaving exactly the same, which is not the case and so is immediately falsified.

Clearly you do with biology what you do with physics, assume your interpretation is precisely what scientists say and then you attack your interpretation, not the science. And thus your epic failing is not restricted to physics.

Yea, well, we have TOE and then we have adaptive mutation.

Explain which is in control.

Explain a math equation that describes which will win over which.

TOE is supposed to be a correct theory.

This should not take you long.

 

[Jack_]

This is ridiculous.

The modern synthesis of genetics was as much a welding of biostatistics as Mendelian theory. Jack has not thie slightest understanding of, or interest in, statistics as a descriptive system of biology. He thinks - or pretends that he does - that biological systems should follow direct mathematical rules as in physics. They don't. I think the discussion is done: Jack is unwilling or unable to grasp the science of biology and genetics. Herc had the right idea from the start.

You continue to make these kinds of statements, but you fail to correctly explain the demarcation of random mutation and adaptive mutation.

You fail to explain why adaptive mutation is not more viable compared to random mutation.

These are simple subjects and demand simple answers.

 

[GeoffP]

If this is true, you are greater than the sum of your components.

How does this work under TOE?

Look up pleiotropy and epistasis, Jack.

You continue to make these kinds of statements, but you fail to correctly explain the demarcation of random mutation and adaptive mutation.

?? You have not inquired as to such demarcation, nor provided solid evidence of the latter in the first place while excluding any of the classical systems I mentioned. Why not?

You fail to explain why adaptive mutation is not more viable compared to random mutation.

Exactly why would I present your argument for you, Jack? This is becoming absurd.

These are simple subjects and demand simple answers.

Your simple answers might serve for simpletons, but they would hardly be accurate, as I've tried to illustrate to you. I could go through the laundry list of things you haven't covered again, but what would be the point?

 

[Jack_]

Look up pleiotropy and epistasis, Jack.



?? You have not inquired as to such demarcation, nor provided solid evidence of the latter in the first place while excluding any of the classical systems I mentioned. Why not?



Exactly why would I present your argument for you, Jack? This is becoming absurd.



Your simple answers might serve for simpletons, but they would hardly be accurate, as I've tried to illustrate to you. I could go through the laundry list of things you haven't covered again, but what would be the point?

Yea, we have experiments demonstrating adaptive mutation.

They have not been refuted.

You answered with things like may have and might have been.

So, I asked for specifics.

You have not given them.

That is what this is all about and you are evading the issue.

 

[Trippy]

You continue to make these kinds of statements, but you fail to correctly explain the demarcation of random mutation and adaptive mutation.

You fail to explain why adaptive mutation is not more viable compared to random mutation.

These are simple subjects and demand simple answers.

Seriously.

WTF?

Do you think bacterial Penicilin resistance is random or adaptive?

Personaly I think the only place the demarcation exits is in your head.

 

[Jack_]

Seriously.

WTF?

Do you think bacterial Penicilin resistance is random or adaptive?

Personaly I think the only place the demarcation exits is in your head.

That is the whole point of my posts.

This is not logically decidable.

Since you attack me, prove it is one way or the other.

 

[Trippy]

That is the whole point of my posts.

This is not logically decidable.

Since you attack me, prove it is one way or the other.

I attacked you?

That's funny.

I asked you if a specific mutation was random or adaptive (a question you avoided asking) and then suggested that the distinction was a purely artificial one that existed mostly in your mind.

In other words - I have simply asked you to clarify your stance on a specific example.

For what it's worth, from what I recall of the biological chemistry here's my understanding of things.

It was a random mutation, it is now an adaptive mutation.

My recollection is that penicilin, and penicilin derivatives (eg amoxicilin) act on a specific enzyme that is involved in the repair of the cell walls of bacteria. The specific enzyme site bonds with a specific 'kind' of site through a functional group, catalyzes a specific reaction, and then the bond to the functional group is hydrolyzed (my recollection of some of the specific details is a little hazy, and my notes on the matter are in the basement). Penicilin works (IIRC) by 'tricking' the enzyme into hydrolyzing the wrong location. The wrong bond gets broken, the penicilin fragments, one fragment gets stuck in the enzyme, deactivating it. However, in x% of cases, due to a mutation in the enzyme, which is confered to it by a mutation in the DNA/RNA that controls the enzymes structure (again, I have mor eprecise details elsewhere, but I feel disinclined to go hunting for them)results in the enzyme having a more open structure than it ordinarily would, this more open structure allows the correct linkage/site to be hydrolyzed, and confers the bacterium with resistance to penicilin - it's a random mutation that provides adaptive (and improved) survival value.

Sickle cell anemia, another random mutation, but it grants a degree of immunity to malaria, has value for adaptation and survival, and this can/has been tested (I have a link somewhere here) those countries that have the highest rates of malaria, also have the highest rates of sickle cell anemia.

Random mutations become adaptations when they confer some new or useful survival trait.

 

[Jack_]

I attacked you?

That's funny.

I asked you if a specific mutation was random or adaptive (a question you avoided asking) and then suggested that the distinction was a purely artificial one that existed mostly in your mind.

In other words - I have simply asked you to clarify your stance on a specific example.

For what it's worth, from what I recall of the biological chemistry here's my understanding of things.

It was a random mutation, it is now an adaptive mutation.

My recollection is that penicilin, and penicilin derivatives (eg amoxicilin) act on a specific enzyme that is involved in the repair of the cell walls of bacteria. The specific enzyme site bonds with a specific 'kind' of site through a functional group, catalyzes a specific reaction, and then the bond to the functional group is hydrolyzed (my recollection of some of the specific details is a little hazy, and my notes on the matter are in the basement). Penicilin works (IIRC) by 'tricking' the enzyme into hydrolyzing the wrong location. The wrong bond gets broken, the penicilin fragments, one fragment gets stuck in the enzyme, deactivating it. However, in x% of cases, due to a mutation in the enzyme, which is confered to it by a mutation in the DNA/RNA that controls the enzymes structure (again, I have mor eprecise details elsewhere, but I feel disinclined to go hunting for them)results in the enzyme having a more open structure than it ordinarily would, this more open structure allows the correct linkage/site to be hydrolyzed, and confers the bacterium with resistance to penicilin - it's a random mutation that provides adaptive (and improved) survival value.

Sickle cell anemia, another random mutation, but it grants a degree of immunity to malaria, has value for adaptation and survival, and this can/has been tested (I have a link somewhere here) those countries that have the highest rates of malaria, also have the highest rates of sickle cell anemia.

Random mutations become adaptations when they confer some new or useful survival trait.

Oh, I see.

I will need to post the experiment for you.

Next time you post, make sure you inherit all the logic of the experiment.


In 1988, John Cairns at the Radcliffe Infirmary in Oxford, England, and a group of other scientists renewed the Lamarckian controversy (which by then had been a dead debate for many years).[18] The group took a mutated strain of E. coli that was unable to consume the sugar lactose and placed it in an environment where lactose was the only food source. They observed over time that mutations occurred within the colony at a rate that suggested the bacteria were overcoming their handicap by altering their own genes. Cairns, among others, dubbed the process adaptive mutation.

http://en.wikipedia.org/wiki/Neo-Lamarckism

 

[Trippy]

DD Transpepsidase, and peptidoglycan crosslinks.
I don't remember the exact relationship between DD Transpepsidase and the various Beta Lactamase's off the top of my head though.

 

[Trippy]

Oh, I see.

I will need to post the experiment for you.

Next time you post, make sure you inherit all the logic of the experiment.


In 1988, John Cairns at the Radcliffe Infirmary in Oxford, England, and a group of other scientists renewed the Lamarckian controversy (which by then had been a dead debate for many years).[18] The group took a mutated strain of E. coli that was unable to consume the sugar lactose and placed it in an environment where lactose was the only food source. They observed over time that mutations occurred within the colony at a rate that suggested the bacteria were overcoming their handicap by altering their own genes. Cairns, among others, dubbed the process adaptive mutation.

http://en.wikipedia.org/wiki/Neo-Lamarckism

Yes, yes, all you've done is copy and paste the post from the TOE thread in Pseudoscience.

No, demonstrate how that contradicts anything i've said again?

 

[Jack_]

Yes, yes, all you've done is copy and paste the post from the TOE thread in Pseudoscience.

No, demonstrate how that contradicts anything i've said again?

it is my thread.

so, did you support your position yet in the light of the experiments?

How long will this take?

You claimed TOE explains it all. Are you retreating?