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Author Topic:   Explaining the pro-Evolution position
Kleinman
Member (Idle past 918 days)
Posts: 136
From: United States
Joined: 10-06-2016


Message 121 of 393 (792520)
10-10-2016 9:07 PM
Reply to: Message 119 by Dr Adequate
10-10-2016 8:16 PM


Re: It's already peer reviewed
The following post is a response to posts 119 and 120
quote:
Amplification requires improved fitness to reproduce. However, if the selection pressures don't drive the population to extinction, it is possible that a particular lineage which doesn't amplify but is still able to reproduce for enough generations will do enough replication trials that the necessary beneficial mutation can still occur. This is why the residual population of HIV in a well treated patient is still a danger. The vast majority of times 3 drug therapy works for HIV but the residual viral population requires monitoring for this possibility.
quote:
Is that a no?


Yes, but it is not a simple no. It can take thousands of generations for something like you described to happen. Evolution will have to occur at a rate of much greater than a thousand generations per beneficial mutation if scales are going to be transformed into feathers.
quote:
No, the multiplication rule applies whether the mutations occur sequentially or simultaneously. Amplification alters the value of the probabilities but the probabilities are still computed multiplicatively.
quote:
I presumed that by "the multiplication rule" you meant that P(A & B) = P(A) * P(B) if the events are independent. Hence for example we can use this rule to calculate the probability of me throwing six on two dice. If instead I keep rolling one die until I get a six, and then keep rolling a second die until I get a six, that's a whole different question, and the probability of me getting two sixes is in fact 1. I arrived at that result without using the multiplication rule, and indeed without using multiplication.


Yes. But the probability problem you must solve is the probability of a beneficial mutation occurring in a given number of replications. The analogous dice rolling problem would be for example the probability of rolling at least a single 1 in a given number of rolls.
quote:
No, what I am saying is that the creation of new alleles by rmns only works efficiently when a single gene is targeted by a single selection pressure. And that process is governed by the multiplication rule of probabilities. As soon as selection pressures target more than a single genetic locus, the process is slowed even more so because of the more complex evolutionary trajectory where the probability of each step is governed by the multiplication rule.
quote:
Well, it seems to me that you also said something about birds, and I wondered if you had any evidence for it.


What I have evidence of is real, measurable and repeatable examples of random mutation and natural selection. What I can tell you with mathematical certainty is that as you target more genes with selection pressures, the evolutionary process becomes too slow to support the theory of evolution. How quickly do you think a population can evolve to starvation selection pressure?
quote:
Do you think that starvation selection pressures can not occur simultaneously with thermal stress in nature. What do you think would happen to a population that was subjected to starvation selection pressure alone vs starvation selection pressure with thermal stress? What about diseases occurring during starvation and thermal stress, what about predation and starvation?...
quote:
Yes, many pressures are always acting on a population. Which, of course, weakens your point. A strain of bacteria evolving resistance to just one antibiotic does so in the teeth of a thousand selection pressures. Adding the antibiotic makes it a thousand and one.

And still they evolve.




The empirical evidence contradicts your claim. A common example is the rotation of herbicides to prevent the emergence of herbicide resistant weeds. Even if a variant has some resistance to one of the herbicides, the other herbicide suppresses its amplification. And populations can be subjected to many selection pressures and not go extinct but they won't evolve efficiently to any particular selection pressures. What you are describing is drift. That's what the surviving population of HIV subject to combination therapy is doing. If you want scales to be transformed into feathers, you need directional selection pressures, not drift.
quote:
What I can show you is the empirical evidence of how mutation and selection works and the underlying physics and mathematical principles which govern this phenomenon.
quote:
Well, I was already aware of that stuff. What I am unaware of is any reason why this gives us a compelling argument against the evolution of birds.


I've never said that birds can't evolve. What I am saying is that you have too many genetic loci to transform by rmns scales into feathers.
quote:
If you believe that dinosaurs can transform scales into feathers by rmns, let us know what the sequential selection pressures were and the targeted genetic loci which would do this.
quote:
I don't have a description of the sequence of mutations which produced birds, which I why I have never claimed that I did and then gone on to adduce this as a proof of the evolution of birds.

You, however, seemed to be claiming that you had a proof that no such pathway exists. If you don't, then this thread is about done.




I debated this issue with Edward Max, supervising medical doctor of the FDA who writes essays saying that rmns can account for all the complexity of life. I critiqued one of his essays and told him that if he believed that reptiles could transform scales into feathers by rmns, it would have to be one gene at a time because that was the only way that rmns works efficiently. Max didn't understand my argument and responded by sending me a link to a paper where the researchers studied the genomes of reptiles and the genomes of birds and asked which genes would have to be transformed to turn a scale into a feather. They identified at least eight different genes which would have to be transformed. My response was, "Very interesting, how can you transform eight genes at a time subject to selection when HIV, the fastest evolving replicator known can not evolve efficiently to 3 selection pressures targeting only 2 genes?"
This message is a reply to:
 Message 119 by Dr Adequate, posted 10-10-2016 8:16 PM Dr Adequate has responded

Replies to this message:
 Message 122 by Dr Adequate, posted 10-10-2016 9:47 PM Kleinman has responded
 Message 124 by AZPaul3, posted 10-10-2016 10:05 PM Kleinman has responded
 Message 144 by Taq, posted 10-11-2016 10:44 AM Kleinman has not yet responded

  
Dr Adequate
Member
Posts: 16097
Joined: 07-20-2006


(1)
Message 122 of 393 (792521)
10-10-2016 9:47 PM
Reply to: Message 121 by Kleinman
10-10-2016 9:07 PM


Birds and HIV
Yes, but it is not a simple no. It can take thousands of generations for something like you described to happen. Evolution will have to occur at a rate of much greater than a thousand generations per beneficial mutation if scales are going to be transformed into feathers.

Show your working?

Yes. But the probability problem you must solve is the probability of a beneficial mutation occurring in a given number of replications.

So, we'd need to know the number of beneficial mutations, the number of generations, and also, and this would be the really awkward bit, we'd need enough data to avoid the Sharpshooter Fallacy: what we need to know is not the probability of evolving the exact birds we have, but the probability that w'd be having this sort of conversation.

What I have evidence of is real, measurable and repeatable examples of random mutation and natural selection.

But very little about birds.

What I can tell you with mathematical certainty is that as you target more genes with selection pressures, the evolutionary process becomes too slow to support the theory of evolution.

Well, if you have mathematical certainty, you must have some actual math. Perhaps you could demonstrate it using dinosaurs and birds as an example.

I debated this issue with Edward Max, supervising medical doctor of the FDA who writes essays saying that rmns can account for all the complexity of life. I critiqued one of his essays and told him that if he believed that reptiles could transform scales into feathers by rmns, it would have to be one gene at a time because that was the only way that rmns works efficiently. Max didn't understand my argument and responded by sending me a link to a paper where the researchers studied the genomes of reptiles and the genomes of birds and asked which genes would have to be transformed to turn a scale into a feather. They identified at least eight different genes which would have to be transformed. My response was, "Very interesting, how can you transform eight genes at a time subject to selection when HIV, the fastest evolving replicator known can not evolve efficiently to 3 selection pressures targeting only 2 genes?"

To which the answer would be, "one locus at a time, over a long period".

Let's have a look again at how fast HIV adapts to combination therapy, shall we?

Reverse transcription inhibitor (RTI) mutations increased 0.5 mutations per y (STD = 0.8 mutations per y), while major protease inhibitor (PI) resistance mutations increased at a rate of 0.2 mutations per y (STD = 0.8 mutations per y) and minor PI resistance mutations increased at a rate of 0.3 mutations per y (STD = 0.7 mutations per y).

That's fast. It doesn't tell us much about dinosaurs, though, since on the one hand HIV has a higher mutation rate and population, and on the other hand the HIV is evolving to selection pressures specially designed and selected to be hard to adapt to. Still, this at least makes it look plausible that dinosaurs could evolve much more slowly than that and still produce feathers etc, since they do have an awfully long time to do it in.

Edited by Dr Adequate, : No reason given.


This message is a reply to:
 Message 121 by Kleinman, posted 10-10-2016 9:07 PM Kleinman has responded

Replies to this message:
 Message 125 by Kleinman, posted 10-10-2016 10:27 PM Dr Adequate has responded

  
Coyote
Member (Idle past 303 days)
Posts: 6117
Joined: 01-12-2008


Message 123 of 393 (792522)
10-10-2016 9:55 PM
Reply to: Message 118 by Kleinman
10-10-2016 8:02 PM


Re: Kleinman's argument
You still have not responded to my Message 47 which deals with mathematics and shows where your entire argument is flawed.

I bet you haven't even watched that on-line lecture.

Models must conform to, and hopefully explain, real world evidence or they are of little value. Or, whenever the model and the evidence disagree, it is best to reexamine the model...

My model is based on real, measurable and repeatable examples of rmns. Perhaps you should reexamine your interpretation of the fossil record.

If your model can't explain all of the real-world fossil record--that's actual data in plain English--then perhaps it needs to be reexamined.

It is a standard creationist tactic to 1) come into a website with a magic bullet that will kill off evolution right blinkin' now and 2) to have a scheme/model/hypothesis/theory that ignores a lot of the data.

We see these magic bullets several times a year here. Most of the posters who fit that description don't last long.

I remember a poster, although on another website, who assured us that the odds against evolution were 1^720. He couldn't understand why we didn't take anything he said seriously.


Religious belief does not constitute scientific evidence, nor does it convey scientific knowledge.

Belief gets in the way of learning--Robert A. Heinlein

In the name of diversity, college student demands to be kept in ignorance of the culture that made diversity a value--StultisTheFool

It's not what we don't know that hurts, it's what we know that ain't so--Will Rogers

If I am entitled to something, someone else is obliged to pay--Jerry Pournelle

If a religion's teachings are true, then it should have nothing to fear from science...--dwise1

"Multiculturalism" demands that the US be tolerant of everything except its own past, culture, traditions, and identity.


This message is a reply to:
 Message 118 by Kleinman, posted 10-10-2016 8:02 PM Kleinman has responded

Replies to this message:
 Message 126 by Kleinman, posted 10-10-2016 10:41 PM Coyote has responded

  
AZPaul3
Member
Posts: 4268
From: Phoenix
Joined: 11-06-2006
Member Rating: 3.7


(2)
Message 124 of 393 (792523)
10-10-2016 10:05 PM
Reply to: Message 121 by Kleinman
10-10-2016 9:07 PM


Re: It's already peer reviewed
They identified at least eight different genes which would have to be transformed. My response was, "Very interesting, how can you transform eight genes at a time subject to selection when HIV, the fastest evolving replicator known can not evolve efficiently to 3 selection pressures targeting only 2 genes?"

Quite easily, actually. A population of millions (+-) of dinos over a span of millions of years can easily progress from undifferentiated tubular follicle collars developed out of the old keratinocytes being pushed out, through the inner, basilar layer of the follicle collar differentiating into longitudinal barb ridges with unbranched keratin filaments, while the thin peripheral layer of the collar become the deciduous sheath, forming a tuft of unbranched barbs with a basal calamus, through the helical displacement of barb ridges arising within the collar and the barbules pairing within the peripheral barbule plates of the barb ridges, creating branched barbs with rami and barbules, then through having differentiated distal and proximal barbules producing a closed, pennaceous vane with a closed vane that develops when pennulae on the distal barbules form a hooked shape to attach to the simpler proximal barbules of the adjacent barband, and finally, developmental novelties giving rise to additional structural diversity in the closed pennaceous feather.**

With millions of dinos over millions of years nature (mutation and selection) can do such things.

Your comparison with HIV is bogus since the drug cocktails are selected specifically to kill HIV and when the virus evolves a resistance to one another is put in its place. The evolution of feathers did not have that level of artificial pressure applied and had plenty of time to experiment with incremental developments on millions of genomes over millions of years.

You do believe in millions of years, do you not?

** Thanks Wiki

Edited by AZPaul3, : No reason given.


This message is a reply to:
 Message 121 by Kleinman, posted 10-10-2016 9:07 PM Kleinman has responded

Replies to this message:
 Message 127 by Kleinman, posted 10-10-2016 10:55 PM AZPaul3 has responded

  
Kleinman
Member (Idle past 918 days)
Posts: 136
From: United States
Joined: 10-06-2016


Message 125 of 393 (792524)
10-10-2016 10:27 PM
Reply to: Message 122 by Dr Adequate
10-10-2016 9:47 PM


Re: Birds and HIV
quote:
Yes, but it is not a simple no. It can take thousands of generations for something like you described to happen. Evolution will have to occur at a rate of much greater than a thousand generations per beneficial mutation if scales are going to be transformed into feathers.
quote:
Show your working?


Study the Lenski experiment where he subjects a population of e coli to starvation selection pressure. His populations take over a thousand generations for each beneficial mutation to improve fitness against this selection pressure. His populations are not being subjected to thousands of selection pressures at the same time.
quote:
Yes. But the probability problem you must solve is the probability of a beneficial mutation occurring in a given number of replications.
quote:
So, we'd need to know the number of beneficial mutations, the number of generations, and also, and this would be the really awkward bit, we'd need enough data to avoid the Sharpshooter Fallacy: what we need to know is not the probability of evolving the exact birds we have, but the probability that w'd be having this sort of conversation.


It's not all that awkward, we have empirical examples that we can measure. Weinreich did it when he measured the number of mutations required for a bacterial population to evolve resistance to an antibiotic. He found many different lineages adapted but each of the lineages required a particular set of 5 mutations. It doesn't matter what the evolutionary trajectory is, the accumulation of mutations which allow for adaptation to a particular selection pressure will always be computed by the multiplication rule of probabilities. And if amplification doesn't occur or the lineage is able to replicate for many, many generations, that probability will remain very low of that evolutionary process occurring.
quote:
What I have evidence of is real, measurable and repeatable examples of random mutation and natural selection.
quote:
But very little about birds.


It doesn't matter what the replicator is, rmns works the same for all replicators. Perhaps you want to try and argue that recombination makes a difference?
quote:
What I can tell you with mathematical certainty is that as you target more genes with selection pressures, the evolutionary process becomes too slow to support the theory of evolution.
quote:
Well, if you have mathematical certainty, you must have some actual math. Perhaps you could demonstrate it using dinosaurs and birds as an example.


Do you think the laws of physics and mathematical principles worked differently in the past? If so, you have some explaining to do.
quote:
I debated this issue with Edward Max, supervising medical doctor of the FDA who writes essays saying that rmns can account for all the complexity of life. I critiqued one of his essays and told him that if he believed that reptiles could transform scales into feathers by rmns, it would have to be one gene at a time because that was the only way that rmns works efficiently. Max didn't understand my argument and responded by sending me a link to a paper where the researchers studied the genomes of reptiles and the genomes of birds and asked which genes would have to be transformed to turn a scale into a feather. They identified at least eight different genes which would have to be transformed. My response was, "Very interesting, how can you transform eight genes at a time subject to selection when HIV, the fastest evolving replicator known can not evolve efficiently to 3 selection pressures targeting only 2 genes?"
quote:
To which the answer would be, "one locus at a time, over a long period".


Interesting, do you want to tell us what those targeted selection pressures were and how nature applied those targeted selection pressures sequentially? We are not talking about the evolution of MRSA where we had designers designing targeted selection pressures and then applying those targeted selection pressures sequentially over a number of years.
quote:
Let's have a look again at how fast HIV adapts, shall we?

Reverse transcription inhibitor (RTI) mutations increased 0.5 mutations per y (STD = 0.8 mutations per y), while major protease inhibitor (PI) resistance mutations increased at a rate of 0.2 mutations per y (STD = 0.8 mutations per y) and minor PI resistance mutations increased at a rate of 0.3 mutations per y (STD = 0.7 mutations per y).
That's fast. It doesn't tell us much about dinosaurs, though, since on the one hand HIV has a higher mutation rate and population, and on the other hand the HIV is evolving to selection pressures specially designed and selected to be hard to adapt to. Still, this at least makes it look plausible that dinosaurs could evolve much more slowly than that and still produce feathers etc, since they do have an awfully long time to do it in.



High mutation rates and huge populations and only two genetic loci targeted. People still live for decades when combination therapy is used. And that's without driving the population to extinction. On the other hand, single drug therapy gives resistant variants in a week. There's a mathematical lesson to be learned here. Populations subject to multiple simultaneous selection pressures that are not driven to extinction don't evolve efficiently to the selection pressures, they drift.
This message is a reply to:
 Message 122 by Dr Adequate, posted 10-10-2016 9:47 PM Dr Adequate has responded

Replies to this message:
 Message 129 by Dr Adequate, posted 10-10-2016 11:24 PM Kleinman has responded

  
Kleinman
Member (Idle past 918 days)
Posts: 136
From: United States
Joined: 10-06-2016


Message 126 of 393 (792525)
10-10-2016 10:41 PM
Reply to: Message 123 by Coyote
10-10-2016 9:55 PM


Re: Kleinman's argument
quote:
You still have not responded to my Message 47 which deals with mathematics and shows where your entire argument is flawed.
I bet you haven't even watched that on-line lecture.

What's the point of your hour long video?
quote:
My model is based on real, measurable and repeatable examples of rmns. Perhaps you should reexamine your interpretation of the fossil record.
quote:
If your model can't explain all of the real-world fossil record--that's actual data in plain English--then perhaps it needs to be reexamined.

It is a standard creationist tactic to 1) come into a website with a magic bullet that will kill off evolution right blinkin' now and 2) to have a scheme/model/hypothesis/theory that ignores a lot of the data.

We see these magic bullets several times a year here. Most of the posters who fit that description don't last long.

I remember a poster, although on another website, who assured us that the odds against evolution were 1^720. He couldn't understand why we didn't take anything he said seriously.




If you want to try and draw realistic conclusions about the fossil record, you need to take into account the mechanisms of genetic transformation. If your conclusion transcends the laws of physics, you should reconsider your conclusions.
This message is a reply to:
 Message 123 by Coyote, posted 10-10-2016 9:55 PM Coyote has responded

Replies to this message:
 Message 128 by Coyote, posted 10-10-2016 10:58 PM Kleinman has responded

  
Kleinman
Member (Idle past 918 days)
Posts: 136
From: United States
Joined: 10-06-2016


Message 127 of 393 (792526)
10-10-2016 10:55 PM
Reply to: Message 124 by AZPaul3
10-10-2016 10:05 PM


Re: It's already peer reviewed
quote:
They identified at least eight different genes which would have to be transformed. My response was, "Very interesting, how can you transform eight genes at a time subject to selection when HIV, the fastest evolving replicator known can not evolve efficiently to 3 selection pressures targeting only 2 genes?"
quote:
Quite easily, actually. A population of millions (+-) of dinos over a span of millions of years can easily progress from undifferentiated tubular follicle collars developed out of the old keratinocytes being pushed out, through the inner, basilar layer of the follicle collar differentiating into longitudinal barb ridges with unbranched keratin filaments, while the thin peripheral layer of the collar become the deciduous sheath, forming a tuft of unbranched barbs with a basal calamus, through the helical displacement of barb ridges arising within the collar and the barbules pairing within the peripheral barbule plates of the barb ridges, creating branched barbs with rami and barbules, then through having differentiated distal and proximal barbules producing a closed, pennaceous vane with a closed vane that develops when pennulae on the distal barbules form a hooked shape to attach to the simpler proximal barbules of the adjacent barband, and finally, developmental novelties giving rise to additional structural diversity in the closed pennaceous feather.**

With millions of dinos over millions of years nature (mutation and selection) can do such things.

Your comparison with HIV is bogus since the drug cocktails are selected specifically to kill HIV and when the virus evolves a resistance to one another is put in its place. The evolution of feathers did not have that level of artificial pressure applied and had plenty of time to experiment with incremental developments on millions of genomes over millions of years.

You do believe in millions of years, do you not?

** Thanks Wiki




What antiviral medication kills the virus? Effective treatment of HIV still leaves populations at least in the hundreds of thousands. Isn't that enough for rmns to work to evolve resistance? Horses have keratin as well. So perhaps you want to tell us what those selection pressures were that transform keratinocytes from scale producers to feather producers?

Millions of years? Did you hear about the guy who went to the natural history museum? While on tour, the tour guide said, "This dinosaur skeleton is one million and six years old"! And the guy says to the tour guide, "What, how do you know that this dinosaur skeleton is one million and SIX years old"??? And the tour guide said, "I came to work here six years ago and the dinosaur skeleton was a million years old then"!


This message is a reply to:
 Message 124 by AZPaul3, posted 10-10-2016 10:05 PM AZPaul3 has responded

Replies to this message:
 Message 130 by Dr Adequate, posted 10-10-2016 11:30 PM Kleinman has not yet responded
 Message 136 by AZPaul3, posted 10-11-2016 5:12 AM Kleinman has responded

  
Coyote
Member (Idle past 303 days)
Posts: 6117
Joined: 01-12-2008


(1)
Message 128 of 393 (792527)
10-10-2016 10:58 PM
Reply to: Message 126 by Kleinman
10-10-2016 10:41 PM


Re: Kleinman's argument
What's the point of your hour long video?

I figured you hadn't viewed it.

You want the point? Here's the abstract:

Mathematical computer models of two ancient and famous genetic networks act early in embryos of many different species to determine the body plan. Models revealed these networks to be astonishingly robust, despite their 'unintelligent design.' This examines the use of mathematical models to shed light on how biological, pattern-forming gene networks operate and how thoughtless, haphazard, non-design produces networks whose robustness seems inspired, begging the question what else unintelligent non-design might be capable of.

In other words, your model is countered completely by this one. But of course creationists won't accept that, if they even take the time to view the on-line lecture which most won't.

If you want to try and draw realistic conclusions about the fossil record, you need to take into account the mechanisms of genetic transformation. If your conclusion transcends the laws of physics, you should reconsider your conclusions.

If you want to create realistic models about the fossil record, you need to take into account the fossil record! If your models, no matter how elegant, fail to account for the real-world evidence they are destined for the trash heap of science.


Religious belief does not constitute scientific evidence, nor does it convey scientific knowledge.

Belief gets in the way of learning--Robert A. Heinlein

In the name of diversity, college student demands to be kept in ignorance of the culture that made diversity a value--StultisTheFool

It's not what we don't know that hurts, it's what we know that ain't so--Will Rogers

If I am entitled to something, someone else is obliged to pay--Jerry Pournelle

If a religion's teachings are true, then it should have nothing to fear from science...--dwise1

"Multiculturalism" demands that the US be tolerant of everything except its own past, culture, traditions, and identity.


This message is a reply to:
 Message 126 by Kleinman, posted 10-10-2016 10:41 PM Kleinman has responded

Replies to this message:
 Message 154 by Kleinman, posted 10-11-2016 4:56 PM Coyote has responded

  
Dr Adequate
Member
Posts: 16097
Joined: 07-20-2006


(1)
Message 129 of 393 (792528)
10-10-2016 11:24 PM
Reply to: Message 125 by Kleinman
10-10-2016 10:27 PM


Re: Birds and HIV
Study the Lenski experiment where he subjects a population of e coli to starvation selection pressure. His populations take over a thousand generations for each beneficial mutation to improve fitness against this selection pressure. His populations are not being subjected to thousands of selection pressures at the same time.

Well, they are, as I pointed out; it's just that most of these are conservative. As would of course be the case with dinosaurs.

But to even start applying this to dinosaurs we'd need to know how many beneficial mutations get your from dinosaurs to birds and how long it took.

It's not all that awkward, we have empirical examples that we can measure.

But examples of something else. In order to do the working in the dinosaur-to-bird case, we'd need to know these things about dinosaurs and birds. How many beneficial mutations? How many generations? What mutation rate? What is the strength of the selection pressures? Which operated concurrently and which consecutively? How many other evolutionary pathways would have struck us as equally remarkable?

It doesn't matter what the replicator is, rmns works the same for all replicators.

Right, but in order to do the math we need the actual data.

By analogy, the formula area = width × height works the same for all rectangles, but in order to apply it to any particular rectangle we would need to know the particular width and height.

If we were to assume that birds evolved as fast as HIV does, then you, Kleinman, wouldn't have a leg to stand on. But we know that they don't. So in order for us to figure out how much water your argument holds, it's kind of important to have some actual data about birds.

Perhaps you want to try and argue that recombination makes a difference?

Well, everything that's different about the two cases makes a difference. Though I seem to remember that HIV is diploid and undergoes recombination.

Interesting, do you want to tell us what those targeted selection pressures were and how nature applied those targeted selection pressures sequentially?

Once again --- I don't go about telling people that I've found such an evolutionary pathway.

You, on the other hand, claim to have a proof that there is no such pathway. That's for you to demonstrate.

(What on earth you mean by "targeted" in this context I cannot begin to imagine, perhaps you could explain?)

High mutation rates and huge populations and only two genetic loci targeted. People still live for decades when combination therapy is used. And that's without driving the population to extinction. On the other hand, single drug therapy gives resistant variants in a week. There's a mathematical lesson to be learned here. Populations subject to multiple simultaneous selection pressures that are not driven to extinction don't evolve efficiently to the selection pressures, they drift.

And yet as I have pointed out, everything is subject to multiple simultaneous selection pressures, yet and many things do in fact evolve efficiently. This empirical observation beats your "mathematical lesson" (which does not appear to involve any mathematics).

Edited by Dr Adequate, : No reason given.

Edited by Dr Adequate, : No reason given.

Edited by Dr Adequate, : No reason given.


This message is a reply to:
 Message 125 by Kleinman, posted 10-10-2016 10:27 PM Kleinman has responded

Replies to this message:
 Message 158 by Kleinman, posted 10-11-2016 6:09 PM Dr Adequate has responded

  
Dr Adequate
Member
Posts: 16097
Joined: 07-20-2006


Message 130 of 393 (792529)
10-10-2016 11:30 PM
Reply to: Message 127 by Kleinman
10-10-2016 10:55 PM


Re: It's already peer reviewed
Effective treatment of HIV still leaves populations at least in the hundreds of thousands. Isn't that enough for rmns to work to evolve resistance?

Yes.

Millions of years? Did you hear about the guy who went to the natural history museum? While on tour, the tour guide said, "This dinosaur skeleton is one million and six years old"! And the guy says to the tour guide, "What, how do you know that this dinosaur skeleton is one million and SIX years old"??? And the tour guide said, "I came to work here six years ago and the dinosaur skeleton was a million years old then"!

If you could manage to prove that the Earth isn't old, that would be a much more effective answer to evolution than anything you've shown us so far. You would need to start a new thread so as not to annoy the moderators.


This message is a reply to:
 Message 127 by Kleinman, posted 10-10-2016 10:55 PM Kleinman has not yet responded

  
PaulK
Member
Posts: 15221
Joined: 01-10-2003
Member Rating: 3.4


(2)
Message 131 of 393 (792530)
10-11-2016 12:29 AM
Reply to: Message 100 by Kleinman
10-10-2016 5:32 PM


Re: Kleinman's argument
quote:

PaulK, the reason there is no rational way that feathers can evolve from scales by rmns is there are too many genetic loci which must be transformed simultaneously

Are there ? How do you know that ? And I note that none of the three papers you list addresses the topic.

quote:

Every evolutionary step (beneficial mutation) must amplify in order to improve the probability of another beneficial mutation occurring on some member of the lineage with that particular mutation. rmns only works efficiently when a single selection pressure targets a single gene at a time

That is really only true in cases of "hard selection". As Haldane showed, hard selection has a limit on the speed of selection, which cannot be overcome by selecting in parallel. Soft selection - and neutral drift - are not subject to this limit.

And that is why relying on antibiotic resistance as a paradigm is inadequate. You only deal with hard selection - which is not the most efficient. As I recall rapid evolution can occur from relaxing selection.

So, nothing you have said gives me any confidence that you have answered either of the concerns I raised in Message 95. Indeed, my concern that the argument relied on attempting to apply the atypical situation of antibiotic resistance to all evolution is reinforced.


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Dr Adequate
Member
Posts: 16097
Joined: 07-20-2006


(1)
Message 132 of 393 (792531)
10-11-2016 1:43 AM


Concurrent versus Consecutive Pressures
It is easy to argue that in an ideal case a population will evolve more efficiently if it is presented with a number of selection pressures concurrently than if they are presented consecutively.

Consider a set of potential adaptive mutations to n selection pressures¹, each of which (for convenience) we shall take to have a chance 1/q in each generation of arising and going on to fixation.

If the pressures are presented sequentially, then obviously the expected time (measured in generations) for the first mutation to arise is q, after which the expected time for the second to arise is also q ... and so on. The expected time at which the last mutation arises to cope with the last selection pressure is therefore nq. We may therefore say that the rate of evolution is n/nq, which is, unsurprisingly, just 1/q, the number we started with.

Now consider the case where the selection pressures are applied simultaneously. Then when we start off, the probability of any one of the mutations arising and going on to fixation is n/q, and so the time we expect to wait is q/n. Then after that any of n - 1 mutations might arise, so the probability is (n - 1)/q and the time is q/(n - 1).

Recognizing a pattern, we may say that the time until the last mutation arises will be given by qΣ(1/k), where the sum is taken from 1 to n. This sum is approximately² equal to ∫1/k·dk, the integral being taken over the same limits, and of course this integral is just equal to ln n. So we may say that the rate of evolution in this case is (1/q)n/ln n).

As we know that 1 < n/ln n) for n > 1, we can conclude that evolution goes at a faster rate when the selection pressures are encountered concurrently than when they are encountered consecutively. Indeed, at a much faster rate as n becomes large: to evolve to meet 100 selection pressures, for example, would be over 20 times faster if these pressures are encountered concurrently than if they are encountered consecutively.

BUT! WAIT!

You might think on that basis that in that case we should abandon combination therapy for pathogens for what one might call "cyclic therapy": give the patient one medicine, wait 'til the pathogen starts becoming resistant, switch to the next medicine, and so forth.

But there are a number of problems with this. I shall not list them all, but two stand out.

First, our actual objective is not to mess with the evolution of the pathogen as such, but to protect the health of the patient. Combination therapy allows us to drive the pathogen population lower, because we are poisoning the pathogens in more ways; and as the patient is therefore harboring less pathogens, the patient is (gratifyingly) less sick.

Second, lowering the population does in fact retard the evolution of the pathogen. Using Haldane's approximation³ we may say that the probability of fixation of a given advantageous allele at the point when it arises is given by π ≈ 2s for any suitably large population (where s is the fitness advantage of the mutation). But the probability of such an allele arising in any given generation is proportional to the population size. It follows that larger populations will undergo adaptive evolution faster than smaller ones. Simply by holding down the population size we retard the evolution of the pathogen.

We must therefore say that the result obtained above holds when selection just affects which of the population will survive and reproduce (soft selection), but begins to break down when the selective pressures start to affect the size of the population (hard selection), and breaks down more the more this is so. This is intuitively obvious when we consider the case in which the selective pressures are strong enough in combination, but not separately, to bring about the actual extinction of the population, which would halt evolution entirely.

It follows that (pace Kleinman), combination therapy is, after all, a special case, in that it involves the combination of selection pressures specifically designed and chosen to have the greatest possible impact on the population size of the pathogen, and so to present the hardest case of hard selection that human ingenuity can devise.

_____________________

Footnotes:

(1) Conservative selection pressures may be ignored as so much background noise for the purposes of this exercise.

(2) As n tends to infinity the difference between the sum and the integral tends toward γ, the Euler-Mascheroni constant, approximately 0.5772.

(3) J.B.S. Haldane, "The mathematical theory of natural and artificial selection", Proceedings of the Cambridge Philosophical Society 1927, 23, pp. 838–844.

Edited by Dr Adequate, : No reason given.

Edited by Dr Adequate, : No reason given.


Replies to this message:
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PaulK
Member
Posts: 15221
Joined: 01-10-2003
Member Rating: 3.4


Message 133 of 393 (792532)
10-11-2016 2:47 AM
Reply to: Message 132 by Dr Adequate
10-11-2016 1:43 AM


Speed is not efficiency
Perhaps a simpler take on the issues.

Hard selection is the fastest way to achieve fixation of a single allele. However, because it relies on a declining population - and the rate of decline is directly tied to the strength of selection - it does not work any faster in parallel, nor is it sustainable.

Soft selection is slower but it does not rely on a declining population. So it is sustainable and it can work in parallel. Soft selection, then, can be more efficient than hard selection because it can work sustainably and in parallel.


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Replies to this message:
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Rrhain
Member (Idle past 70 days)
Posts: 6349
From: San Diego, CA, USA
Joined: 05-03-2003


Message 134 of 393 (792534)
10-11-2016 3:22 AM
Reply to: Message 98 by Kleinman
10-10-2016 5:09 PM


Re: It's already peer reviewed
Kleinman responds to me:

quote:
See if you can find an error in the physics or mathematics.

Um, what do any of these papers have to do with the topic at hand? In fact, from the abstracts, you seem to accept a priori the previous work that establishes evolutionary theory. Much of it is mathematical in nature. Surely you aren't saying that because we can mathematically describe how randomness works (which is what probability in general and chaos theory in particular are about), that somehow means we have a deterministic system, are you? If you think you have something that countermands what we understand about how evolution works, it would help if you would put it here.

Use your words. Argument by footnote is not helpful.

Be specific.

I notice you didn't answer my questions. I directly stated that I wanted to hear your answers. I did not ask them for my health. I'll reduce it to the last example:

You have a trait that is in a single-gene, two-allele, dominant/recessive scenario. The recessive trait only appears when the individual is homozygous recessive. Otherwise, the dominant trait appears. Those who express the recessive trait do not reproduce.

The recessive trait currently is seen in 1 in 1,000 individuals. How many generations would need to pass in order to reduce the occurrence to 1 in 1,000,000?

What is p? What is q?


Rrhain

Thank you for your submission to Science. Your paper was reviewed by a jury of seventh graders so that they could look for balance and to allow them to make up their own minds. We are sorry to say that they found your paper "bogus," specifically describing the section on the laboratory work "boring." We regret that we will be unable to publish your work at this time.

Minds are like parachutes. Just because you've lost yours doesn't mean you can use mine.

This message is a reply to:
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vimesey
Member
Posts: 967
From: Birmingham, England
Joined: 09-21-2011
Member Rating: 6.6


Message 135 of 393 (792535)
10-11-2016 3:27 AM
Reply to: Message 115 by Kleinman
10-10-2016 7:42 PM


Re: It's already peer reviewed
No, the multiplication rule applies whether the mutations occur sequentially or simultaneously.

This is only pertinent from one perspective (the wrong perspective when it comes to evolution).

For example, what would you say if I told you that I could, right here right now, guarantee doing something that has a one in trillions upon trillions of a chance of occurring, and that I can prove it with trivial math ?


Could there be any greater conceit, than for someone to believe that the universe has to be simple enough for them to be able to understand it ?

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