Creationists: Explain your understanding of microevolution and macroevolution

[Alan Kleinman]

I have a copy on my desk- 'The Origin of Species- by Means of Natural selection'

Then as now, you can select exactly nothing into existence - it is a destructive/ filtering process that leaves you with a smaller set of options than you began with. i.e. opposite of his tree of life.

Random mutations are a diverging (entropy increasing) process. Without natural selection, over time, genomes would consist of random sequences of bases. Are you saying that in that random mutation process can't produce a mutation that might improve the reproductive fitness of the particular variant in a particular environment? How and why do drug-resistant variants appear?

After the discovery of quantum mechanics- apples still fall from trees
and genetic apples will always fall not far from theirs

That's true, but with each replication, the genetic apple can fall a little further from that tree than the previous apple, if natural selection allows it for the given environment.

The tempting mistake in both cases, is extrapolating a superficial observation into a comprehensive explanation.

Are you claiming that you can't compute the divergence of a genetic sequence based on the knowledge of the mutation rate and the number of replications?

 

[Frank Robert]

Slim 3 is nothing other than a programming environment.
Slim 3 Documentation
I had already written out the algebraic probability equations that describe biological adaptive evolution. Use whatever computer program you want to use to evaluate these equations. All it took was plugging numbers into a spreadsheet. And those results are in accurate agreement with the Kishony and Lenski experiments. Swamidass has no idea how to formulate the mathematical model of biological adaptive evolution. If I wanted some kind of online interactive model of my model, SLIM 3 might have some application. But look at what SLIM 3's intended use is in the link provided.

I then go on to say to Swamidass:

I didn't need another computer program to evaluate the math that I'd presented and I said so. If he had people experienced with that computer language, let them do the math for the Kishony and Lenski experiment. There are two ways that I know of to do the mathematics of DNA evolution. You can model the process as nested binomial probability problems or you do the mathematics as a Markov process. I've done the math both ways and you get analogous results.

What more do you want in a test case with two real, well-measured, and repeatable evolutionary experiments? I don't have a microbiology lab where I design and perform these kinds of experiments. Either Swamidass is unable to understand how the Kishony and Lenski experiments are performed or he is unwilling to consider these experiments. You don't need SLIM 3 to construct the correct model of biological evolution. Here's what SLIM 3 does:

If Swamidass wants to figure out how to formulate the mathematical behavior of these experiments so that he could plug that into SLIM 3, perhaps I should have tried to explain that to him but my papers explicitly explain how this is done.

I actually had another scientist contact me privately and he evaluated the model using MATLAB, a simulation program he has experience with. We got the same results within a small fraction of a percent as with my spreadsheet computation.

It's all straightforward, you start with a founder bacterium, how many replications does it take to give a reasonable probability of an adaptive mutation occurring on one of the descendants of that founder.

You don't need to prove anything to me. From my perspective the reality is that you had an opportunity to test your theories with experts in the field. Personally, I think you blew an excellent opportunity. If your predictions checked, out in the simulation, to have merit you would have impressed other scientists and gotten the validation that you seek.

If you got validation from another scientist great but it is different from what Dr. S was suggesting. He asked you to identify a well specified question, answerable with a simulation, where you and the experts at PS disagree on the results. If you won out the PS experts would have learned something new and that would have been something to brag about.

 

[Alan Kleinman]

You don't need to prove anything to me. From my perspective the reality is that you had an opportunity to test your theories with experts in the field. Personally, I think you blew an excellent opportunity. If your predictions checked, out in the simulation, to have merit you would have impressed other scientists and gotten the validation that you seek.

If you got validation from another scientist great but it is different from what Dr. S was suggesting. He asked you to identify a well specified question, answerable with a simulation, where you and the experts at PS disagree on the results. If you won out the PS experts would have learned something new and that would have been something to brag about.

Swamidass needs to do his validation independent of the way I did the math. If you and he can't understand how to formulate the model that describes DNA adaptive evolution, me setting up the math for him in his computer software would be like me setting up the math in MATLAB. I could also do the calculation in FORTRAN, BASIC, C, PASCAL,... but what's the point. It's the same model being evaluated using different computer software. It all comes back to the way one is trained. In the engineering school I was trained in, a lot of attention was paid to learning how to do mathematical modeling and computer simulations. If your model is correct, it shouldn't matter which computer software you use to carry out the simulation. I didn't need to explain how to do the simulation in MATLAB for the scientist I mentioned. Apparently, Swamidass couldn't do this simulation on his own despite the fact that I've given him the model. And as Hans pointed out earlier, the math is trivial, I did the calculation using a spreadsheet.

By the way, describing how a bacterial lineage can accumulate the mutations necessary to adapt to a single selection pressure is not a well-specified question, then what is?

 

[Guy Threepwood]

Random mutations are a diverging (entropy increasing) process. Without natural selection, over time, genomes would consist of random sequences of bases. Are you saying that in that random mutation process can't produce a mutation that might improve the reproductive fitness of the particular variant in a particular environment?

I agree, random action causes decay, degradation, aka entropy- and this is what we empirically observe; birds losing flight, fish losing sight, etc- it is far more difficult to verify the opposite happening through random errors.

It is not entirely impossible that randomly corrupting the characters in War & Peace will improve the story, it's just far too improbable to provide a reasonable explanation for the creation of new stories.

How and why do drug-resistant variants appear?

generally speaking these are pre-existing variants that remain when less resistant variants are killed off.

Similarly for the 'peppered moth' example. Darker moths always existed- nothing new was created.

By this rationale, if you fill a room with white cats and black cats, turn the lights down, and shoot anything you see moving- this is a demonstration of evolution in action.

That's true, but with each replication, the genetic apple can fall a little further from that tree than the previous apple, if natural selection allows it for the given environment.

That is the theory, but not the observation- like physics, scales matter, things do work differently at different scales. This is particularly apparent in hierarchical digital information systems like DNA and the one we are using right now.

I can randomly alter the 'control genes' in this forum software which describe font color style and size
Some combinations will work better than others, but most will provide viable options- because the options are already constrained within viable ranges. If you understand why I can't author a new software application by this same process- you understand, in principle at least, the problem with extrapolating superficial natural variation into macro-evolution


i.e. natural variation appears to be a necessary design feature, not necessarily a comprehensive design mechanism

Just as the 'immutable laws' of physics turned out to be features of physics, not an explanation for them.

Are you claiming that you can't compute the divergence of a genetic sequence based on the knowledge of the mutation rate and the number of replications?

To some extent we can, which is where things get even more problematic. New biological forms require new proteins which require entire new sequences of genetic information. For a modest sized chain of 100 or so amino acids- It has been calculated that multiplying the number of nanoseconds the universe has existed, by the number of individual organisms that ever existed, by the number of elementary particles in the universe- gives you a number far short of the attempts needed to randomly happen upon a new functional protein.

 

[Alan Kleinman]

I agree, random action causes decay, degradation, aka entropy- and this is what we empirically observe; birds losing flight, fish losing sight, etc- it is far more difficult to verify the opposite happening through random errors.

It is not entirely impossible that randomly corrupting the characters in War & Peace will improve the story, it's just far too improbable to provide a reasonable explanation for the creation of new stories.

I guess you have never seen the Kishony Mega-Plate experiment:

The vast majority of the mutations are neutral or detrimental but a tiny number are able to create new adaptive "words". The question you should ask is how many replications it takes to create one of these new adaptive "words".

generally speaking these are pre-existing variants that remain when less resistant variants are killed off.

Similarly for the 'peppered moth' example. Darker moths always existed- nothing new was created.

By this rationale, if you fill a room with white cats and black cats, turn the lights down, and shoot anything you see moving- this is a demonstration of evolution in action.

Take a look again at the Kishony experiment. These drug-resistant variants don't exist in the initial population he starts with but they do appear as a matter of the divergence process. Most of the mutant variants don't have any improvement in fitness for the particular environment. It is all a function of mutation rate which is acting at every site in the genome and the number of replications from the original founder of the colony. The existence of higher drug concentration regions in the experiment determines if any of the possible mutations are adaptive.

That is the theory, but not the observation- like physics, scales matter, things do work differently at different scales. This is particularly apparent in hierarchical digital information systems like DNA and the one we are using right now.

I can randomly alter the 'control' genes in this forum software which describe font color style and size
Some combinations will work better than others, but most will provide viable options- because the options are already constrained within viable ranges. If you understand why I can't author a new software application by this same process- you understand, in principle at least, the problem with extrapolating superficial natural variation into macro-evolution

There can be more than one possible adaptive mutation for a given selection condition but the mathematics for the different evolutionary trajectories is the same for each of the different lineages.

And I certainly don't extrapolate this process into macroevolution. The reason it takes a billion replications for each adaptive step in the Kishony experiment is that each of these adaptive steps is linked to the others by the multiplication rule of probabilities. You need vast population sizes to have any reasonable probability of a lineage following an adaptive evolutionary trajectory. And that's for the ideal condition of a single selection pressure environment. If the environment has 2 or more simultaneous selection pressures acting, the number of replications for each adaptive step goes up exponentially. That is the principle and reason for using 3 drug simultaneous therapy for treating HIV to give a durable treatment.

i.e. natural variation appears to be a necessary design feature, not necessarily a comprehensive design mechanism

Just as the 'immutable laws' of physics turned out to be features of physics, not an explanation for them.

Calculating the rate of natural variation is trivial. It gives the rate when the member of a lineage can occasionally get an adaptive mutation. It takes a lot of replications at each evolutionary step for that one variant to appear.

To some extent we can, which is where things get even more problematic. New proteins require entire new sequences of genetic information. For a modest sized chain of 100 or so amino acids- It has been calculated that multiplying the number of nanoseconds the universe has existed, by the number of individual organisms that ever existed, by the number of elementary particles in the universe- gives you a number far short of the attempts needed to randomly happen upon a new functional protein.

This evolutionary process cannot create new proteins, it can only slightly modify the function of existing proteins or how they are controlled. But these small changes do operate by the principles of Darwinian evolution. Most of the variants in this divergence process are neutral or detrimental for the given environment but once in a rare replication, a mutation occurs in a member that gives improved fitness for the given environment.

 

[Guy Threepwood]

I guess you have never seen the Kishony Mega-Plate experiment:

The vast majority of the mutations are neutral or detrimental but a tiny number are able to create new adaptive "words". The question you should ask is how many replications it takes to create one of these new adaptive "words".

Take a look again at the Kishony experiment. These drug-resistant variants don't exist in the initial population he starts with but they do appear as a matter of the divergence process. Most of the mutant variants don't have any improvement in fitness for the particular environment. It is all a function of mutation rate which is acting at every site in the genome and the number of replications from the original founder of the colony. The existence of higher drug concentration regions in the experiment determines if any of the possible mutations are adaptive.

There can be more than one possible adaptive mutation for a given selection condition but the mathematics for the different evolutionary trajectories is the same for each of the different lineages.

And I certainly don't extrapolate this process into macroevolution. The reason it takes a billion replications for each adaptive step in the Kishony experiment is that each of these adaptive steps is linked to the others by the multiplication rule of probabilities. You need vast population sizes to have any reasonable probability of a lineage following an adaptive evolutionary trajectory. And that's for the ideal condition of a single selection pressure environment. If the environment has 2 or more simultaneous selection pressures acting, the number of replications for each adaptive step goes up exponentially. That is the principle and reason for using 3 drug simultaneous therapy for treating HIV to give a durable treatment.

Calculating the rate of natural variation is trivial. It gives the rate when the member of a lineage can occasionally get an adaptive mutation. It takes a lot of replications at each evolutionary step for that one variant to appear.

This evolutionary process cannot create new proteins, it can only slightly modify the function of existing proteins or how they are controlled. But these small changes do operate by the principles of Darwinian evolution. Most of the variants in this divergence process are neutral or detrimental for the given environment but once in a rare replication, a mutation occurs in a member that gives improved fitness for the given environment.

I appreciate the thoughtful response

I'd say this all highlights the problem- Macroevolution claims that a single celled bacteria-like organism can, and did, through random error- evolve into a human being. Extraordinary claims require extraordinary evidence.

But the best experiments we have so far, set up with a generous helping of intelligent design to provide the best possible scenarios -take us from bacteria to- more bacteria. That's micro-evolution/ adaptation which is not disputed. As above the organism is constrained to variation within a viable range for that organism by it's biological design .

Also - I'm not sure of the specifics here -but very often what appears to be an ' advantageous mutation' in bacteria suggesting a mechanism by which evolution might keep progressing in small steps... turns out to be a very temporary advantage, achieved only by breaking some other pre-existing function.

An example of this are bacterial 'plagues' where a mutation stunts the growth of the flagellar tail which them becomes a brittle 'sword' destroying cell material- and it's devastating 'success' in spreading through medieval Europe might be presented in a similar graphic fashion to this experiment. But this mutation ultimately puts the bacteria at a disadvantage in it's reduced ability to move compared to it's competitors and so it dies out again- the original 'unmutated' bacteria ultimately prevail, and no evolution has taken place.

An analogy here- any non-mechanic can take a new car and make it faster- by throwing out the spare tire, back seats, doors, any weight you can remove without disabling the car. You can debate to what degree this is a long term advantage- but it comes back to an information problem- accounting for the car's existence still requires a vast amount of information which can never be compiled by simply corrupting previously existing information.

 

[Alan Kleinman]

I'd say this all highlights the problem- Macroevolution claims that a single celled bacteria-like organism can, and did, through random error- evolve into a human being. Extraordinary claims require extraordinary evidence.

You are being generous to believers in macroevolution.

But the best experiments we have so far, set up with a generous helping of intelligent design to provide the best possible scenarios -take us from bacteria to- more bacteria. That's micro-evolution/ adaptation which is not disputed. As above the organism is constrained to variation within a viable range for that organism by it's biological design .

The way I was trained to use antibiotics was single-drug therapy. There were only a few special circumstances when using multiple antibiotics simultaneously was called for. It turns out this is the formula for selecting for multidrug-resistant variants. When one drug fails, go on to the next drug and then the next. It squanders valuable drugs. Kishony has tried to run his experiment with 2 drugs and it won't work. I told him that the colony size necessary to have a reasonable probability for a 2 adaptation mutation variant would go to about 1 trillion. On the other hand, in his single drug experiment, there are various single drug-resistant variants to multiple different drugs appearing in his colony but only the variant resistant to the drug used in the experiment becomes apparent. Two of the drugs he has used are Ciprofloxacin and Trimethoprim. Both variants with the first adaptation mutations appear to each of the drugs occur in his colony of 1 billion, but only the variant with the mutation to the particular drug used will grow in the next higher drug concentration region. The other variant will be neutral or slightly detrimental in the given environment.

Also - I'm not sure of the specifics here -but very often what appears to be an ' advantageous mutation' in bacteria suggesting a mechanism by which evolution might keep progressing in small steps... turns out to be a very temporary advantage, achieved only by breaking some other pre-existing function.

In another interesting observation for the Lenski experiment, it was found that he had variants in his initial founders' population that had some resistance to a number of different antibiotics even though his populations had not been exposed to these antibiotics. I believe the reason for this is his founders' populations were grown in much larger colonies than his 10cc experiment populations. Those populations in the original founders' colony diverge at all sites in the genome simply as the population grew. When the drug-resistant variants were grown in the starvation selection pressure of the experiment, these variants were selected out as the experiment proceeded because these variants were slightly less fit than the drug-sensitive variants in his drug-free environment. The environment determines the fitness for the various variants.

An example of this are bacterial 'plagues' where a mutation stunts the growth of the flagellar tail which them becomes a brittle 'sword' destroying cell material- and it's devastating 'success' in spreading through medieval Europe might be presented in a similar graphic fashion to this experiment. But this mutation ultimately puts the bacteria at a disadvantage in it's reduced ability to move compared to it's competitors and so it dies out again- the original 'unmutated' bacteria ultimately prevail, and no evolution has taken place.

Sure, that's the point I'm trying to make with the different variants in the Kishony and Lenski experiment. A mutation that gives drug resistance in an environment with that drug might be neutral or even detrimental in a drug-free environment. In the case of the Lenski experiment where starvation is the selection pressure, the drug-resistant variants were selected out because of the small energy cost of that drug resistance.

An analogy here- any non-mechanic can take a new car and make it faster- by throwing out the spare tire, back seats, doors, any weight you can remove without disabling the car. You can debate to what degree this is a long term advantage- but it comes back to an information problem- accounting for the car's existence still requires a vast amount of information which can never be compiled by simply corrupting previously existing information.

Again, the Lenski experiment showed that as well. It takes energy to construct the bacterial cell wall. His bacteria are evolving into spherical forms with defective or missing cell walls. It takes less energy to replicate for these variants but this makes these variants more susceptible to osmotic pressure differences.

 

[Guy Threepwood]

You are being generous to believers in macroevolution.

The way I was trained to use antibiotics was single-drug therapy. There were only a few special circumstances when using multiple antibiotics simultaneously was called for. It turns out this is the formula for selecting for multidrug-resistant variants. When one drug fails, go on to the next drug and then the next. It squanders valuable drugs. Kishony has tried to run his experiment with 2 drugs and it won't work. I told him that the colony size necessary to have a reasonable probability for a 2 adaptation mutation variant would go to about 1 trillion. On the other hand, in his single drug experiment, there are various single drug-resistant variants to multiple different drugs appearing in his colony but only the variant resistant to the drug used in the experiment becomes apparent. Two of the drugs he has used are Ciprofloxacin and Trimethoprim. Both variants with the first adaptation mutations appear to each of the drugs occur in his colony of 1 billion, but only the variant with the mutation to the particular drug used will grow in the next higher drug concentration region. The other variant will be neutral or slightly detrimental in the given environment.

In another interesting observation for the Lenski experiment, it was found that he had variants in his initial founders' population that had some resistance to a number of different antibiotics even though his populations had not been exposed to these antibiotics. I believe the reason for this is his founders' populations were grown in much larger colonies than his 10cc experiment populations. Those populations in the original founders' colony diverge at all sites in the genome simply as the population grew. When the drug-resistant variants were grown in the starvation selection pressure of the experiment, these variants were selected out as the experiment proceeded because these variants were slightly less fit than the drug-sensitive variants in his drug-free environment. The environment determines the fitness for the various variants.

Sure, that's the point I'm trying to make with the different variants in the Kishony and Lenski experiment. A mutation that gives drug resistance in an environment with that drug might be neutral or even detrimental in a drug-free environment. In the case of the Lenski experiment where starvation is the selection pressure, the drug-resistant variants were selected out because of the small energy cost of that drug resistance.

Again, the Lenski experiment showed that as well. It takes energy to construct the bacterial cell wall. His bacteria are evolving into spherical forms with defective or missing cell walls. It takes less energy to replicate for these variants but this makes these variants more susceptible to osmotic pressure differences.

Thanks for all the detailed info!

The roots of my skepticism as a former 'devout' Darwinist- was in trying to demonstrate the power of the Darwinian algorithm to a skeptical friend via a computer program ( a Doctor I though should know better!) I've programmed everything from chess games to flight sims and felt pretty confident I could make a fairly convincing model

I'm not saying I disproved the theory- I just proved to myself that it did not play out in logical reality as it had played out in my thought experiments. It seems to me that our capacity for anticipation- which governs everything we do, is almost impossible to remove from logical thought, but a computer can.

The upshot being that without the benefit of anticipation of future payoff- the selection pressure is not nearly as great as it appears to our forward looking minds. The more real-world chaos introduced, the more readily rare advantages are discarded from the gene pool.

So the advantages must be very significant, as in this experiment- but this is very difficult to achieve without compromise and/or rigging the environment to the point of essentially specifying exactly what you want to happen- so at some point it's like pouring wax into a mold- it's not demonstrating anything about the creative power of the wax!

 

[Alan Kleinman]

Thanks for all the detailed info!

Thank you for your interest in this discussion.

The roots of my skepticism as a former 'devout' Darwinist- was in trying to demonstrate the power of the Darwinian algorithm to a skeptical friend via a computer program ( a Doctor I though should know better!) I've programmed everything from chess games to flight sims and felt pretty confident I could make a fairly convincing model

I really started learning something about the subject by studying a computer simulation of random mutation and natural selection written by a guy named Tom Schneider at the National Cancer Institute. He used to have a huge website sponsored by the NCI where you could run his model but it was taken down a few years ago. Schneider never did a thorough study with his model, he was just interested in showing that rmns could increase the system information. But he did make some really outrageous claims about what his model showed. What his model showed was that his 3 selection conditions only worked with extremely short genomes (256 bases long). If you tried to lengthen the genome in his model, the evolutionary process slowed markedly, even when you tried to evolve a virus-length genome of about 20,000 bases. You could evolve longer genomes if you set any 2 of 3 selection conditions to 0 and this was a big clue that the multiplication rule was at play. I saw the analogy between single drug and combination therapy for the treatment of HIV. I started looking at the literature and found numerous papers with empirical examples of this based on combination herbicides, pesticides, and of course, I found Edward Tatums Nobel lecture again more than 40 years after I was first told about this work in elementary school. One thing led to another and I started writing papers on the subject and they were getting published. I believe God led me on this path and revealed this to me. These atheists don't know what they are missing.

I'm not saying I disproved the theory- I just proved to myself that it did not play out in logical reality as it had played out in my thought experiments. It seems to me that our capacity for anticipation- which governs everything we do, is almost impossible to remove from logical thought, but a computer can.

I actually went in the opposite direction from you. I originally thought that Darwin was completely wrong, but when I read what he wrote, I saw his logic. Darwin just didn't have any idea how many replications it takes for there to be an adaptive improvement. DNA was unknown to him. Darwin (and most biologists) were/are not aware that competition slows adaptation. Once you understand the physics of the process, it is obvious why.

I'm not saying I disproved the theory- I just proved to myself that it did not play out in logical reality as it had played out in my thought experiments. It seems to me that our capacity for anticipation- which governs everything we do, is almost impossible to remove from logical thought, but a computer can.

The mathematics of Darwinian evolution is pretty trivial when you look at the individual components. But when you consider superimposing the different processes (competition and adaptation), at first, it is not so obvious how the processes interact. What I think you recognized was that Darwinian cannot be extrapolated to large genetic transformations. It really helps when you can "run the numbers" because something that appears should work, doesn't work when you apply the correct mathematics or run an experiment that demonstrates the process. That's why it is important to correlate one's models with the experimental data.

The upshot being that without the benefit of anticipation of future payoff- the selection pressure is not nearly as great as it appears to our forward looking minds. The more real-world chaos introduced, the more readily rare advantages are discarded from the gene pool.

Another way to look at it, if you live in an environment with disease, starvation, dehydration, predation, toxins, thermal stress,... If the disease doesn't get you, starvation might, or dehydration, or... long before you have a descendant with beneficial mutations to all these stressors.

So the advantages must be very significant, as in this experiment- but this is very difficult to achieve without compromise and/or rigging the environment to the point of essentially specifying exactly what you want to happen- so at some point it's like pouring wax into a mold- it's not demonstrating anything about the creative power of the wax!

That's the point. Antibiotics to treat infectious diseases, targeted cancer therapies, herbicides, pesticides, and insecticides are all-important selection pressures that people use in the fields of medicine and agriculture. But we are using these selection pressures on populations that are able to evolve. Understanding how this evolutionary process works is important so that we don't squander these difficult and costly to develop substances.

 

[Subduction Zone]

I have a copy on my desk- 'The Origin of Species- by Means of Natural selection'

Then as now, you can select exactly nothing into existence - it is a destructive/ filtering process that leaves you with a smaller set of options than you began with. i.e. opposite of his tree of life.

After the discovery of quantum mechanics- apples still fall from trees
and genetic apples will always fall not far from theirs

The tempting mistake in both cases, is extrapolating a superficial observation into a comprehensive explanation.

You are making one of the common creationist mistakes. It is not just natural selection. It is not just variation. It is the action of both variation and natural selection working together that makes evolution work.

Of course your strawman version of evolution is easily debunkable. But scientists never rely on the strawman versions of creationists.

 

[Subduction Zone]

Thanks for all the detailed info!

The roots of my skepticism as a former 'devout' Darwinist- was in trying to demonstrate the power of the Darwinian algorithm to a skeptical friend via a computer program ( a Doctor I though should know better!) I've programmed everything from chess games to flight sims and felt pretty confident I could make a fairly convincing model

I'm not saying I disproved the theory- I just proved to myself that it did not play out in logical reality as it had played out in my thought experiments. It seems to me that our capacity for anticipation- which governs everything we do, is almost impossible to remove from logical thought, but a computer can.

The upshot being that without the benefit of anticipation of future payoff- the selection pressure is not nearly as great as it appears to our forward looking minds. The more real-world chaos introduced, the more readily rare advantages are discarded from the gene pool.

So the advantages must be very significant, as in this experiment- but this is very difficult to achieve without compromise and/or rigging the environment to the point of essentially specifying exactly what you want to happen- so at some point it's like pouring wax into a mold- it's not demonstrating anything about the creative power of the wax!

Dude! How could you be a "devout Darwinist" when you not even know the very basics of Darwin's theory?

 

[Subduction Zone]

I agree, random action causes decay, degradation, aka entropy- and this is what we empirically observe; birds losing flight, fish losing sight, etc- it is far more difficult to verify the opposite happening through random errors.

Sorry, that is not "entropy". That is once again a strawman at best. If you want it stated simply entropy is merely the inverse of the amount of energy available for work. In a high entropy state there is very little energy available for work, In a low entropy state there is a lot of energy available for work.

With your version of "entropy" it would have been impossible for you to grow from a single cell fertilized egg to you.

 

[Hans Blaster]

The reason why I link my references with ResearchGate is that they track the number of reads of my papers. That number is now in the thousands. That may not be viral but these reads are being made by individuals who have an interest in this subject, many of the readers are faculty and researchers from major universities. This doesn't include reads by individuals that access the papers directly from the journals. Researchgate also tracks citations to these papers and besides my own, there are others occurring.

"Reads" might be the most useless stats captured in bibliometrics. (Only alt-metrics like "tweets" or media mentions might be more useless.)

People download and take a look at papers for all kinds of reasons, including from links on message boards. I'd have never looked at your papers if you hadn't linked them here. So score a couple for your "reads". Certainly you've gotten a few hundred citations from those thousands of reads.

 

[Frank Robert]

I guess you have never seen the Kishony Mega-Plate experiment:

The vast majority of the mutations are neutral or detrimental but a tiny number are able to create new adaptive "words". The question you should ask is how many replications it takes to create one of these new adaptive "words".

Take a look again at the Kishony experiment. These drug-resistant variants don't exist in the initial population he starts with but they do appear as a matter of the divergence process. Most of the mutant variants don't have any improvement in fitness for the particular environment. It is all a function of mutation rate which is acting at every site in the genome and the number of replications from the original founder of the colony. The existence of higher drug concentration regions in the experiment determines if any of the possible mutations are adaptive.

There can be more than one possible adaptive mutation for a given selection condition but the mathematics for the different evolutionary trajectories is the same for each of the different lineages.

And I certainly don't extrapolate this process into macroevolution. The reason it takes a billion replications for each adaptive step in the Kishony experiment is that each of these adaptive steps is linked to the others by the multiplication rule of probabilities. You need vast population sizes to have any reasonable probability of a lineage following an adaptive evolutionary trajectory. And that's for the ideal condition of a single selection pressure environment. If the environment has 2 or more simultaneous selection pressures acting, the number of replications for each adaptive step goes up exponentially. That is the principle and reason for using 3 drug simultaneous therapy for treating HIV to give a durable treatment.

Calculating the rate of natural variation is trivial. It gives the rate when the member of a lineage can occasionally get an adaptive mutation. It takes a lot of replications at each evolutionary step for that one variant to appear.

This evolutionary process cannot create new proteins, it can only slightly modify the function of existing proteins or how they are controlled. But these small changes do operate by the principles of Darwinian evolution. Most of the variants in this divergence process are neutral or detrimental for the given environment but once in a rare replication, a mutation occurs in a member that gives improved fitness for the given environment.

Interesting!

 

[Alan Kleinman]

You are making one of the common creationist mistakes. It is not just natural selection. It is not just variation. It is the action of both variation and natural selection working together that makes evolution work.

Of course your strawman version of evolution is easily debunkable. But scientists never rely on the strawman versions of creationists.

You know SZ, I won't use the broken clock analogy, but you are right here that it is the relationship between variation and natural selection that makes evolution work. And I am sure Guy understands this. Now, why don't you try to compute the rate at which that process occurs? Not just the rate of any evolution, but the rate of adaptive evolution. How many replications of a particular variant before there will be a reasonable probability of an adaptive mutation occurring. Why don't you start with a simple experimental example, explain why the rate of adaptive evolution in the single selection pressure environment in the Kishony experiment is 1 adaptive mutation per 1 billion replications.

Dude! How could you be a "devout Darwinist" when you not even know the very basics of Darwin's theory?

And you do?

 

[Alan Kleinman]

Sorry, that is not "entropy". That is once again a strawman at best. If you want it stated simply entropy is merely the inverse of the amount of energy available for work. In a high entropy state there is very little energy available for work, In a low entropy state there is a lot of energy available for work.

With your version of "entropy" it would have been impossible for you to grow from a single cell fertilized egg to you.

This is why biologists should take more than a couple of courses in dumbbell math and a survey course in physics.

 

[Alan Kleinman]

"Reads" might be the most useless stats captured in bibliometrics. (Only alt-metrics like "tweets" or media mentions might be more useless.)

People download and take a look at papers for all kinds of reasons, including from links on message boards. I'd have never looked at your papers if you hadn't linked them here. So score a couple for your "reads". Certainly you've gotten a few hundred citations from those thousands of reads.

Maybe so. And I do appreciate your reads. Now, why can't you see how this trivial mathematics correlates with the data from the Kishony and Lenski experiments? Why can't you recognize that these simple probability equations derived from a well-defined sample space correctly describe the random process that is DNA adaptive evolution? Did I define the random trials improperly? Did I define the possible outcomes from the random trials incorrectly? Did I apply the "at least one rule" incorrectly for computing the probability of an adaptive mutation occurring as the population grows (increasing the size of the sample space)?

You seem like a smart guy. Why can't you see that when you set the beneficial mutation rate in this probability equation to 1e-9 that it gives a probability of about 0.6 that an adaptive mutation will occur when the population size reaches about 1e9, the number Kishony uses in his video?

ResearchGate also lists citations. And you are right, my papers don't have many citations at this time. But on those rare occasions when I do get a citation, I read those papers to see whether they get it right or not. And some do, especially those who are trying to deal with the evolution of drug resistance.

I wonder how long it will take oncologists to figure out that single drug targeted therapy will rarely work. They certainly won't get the correct answer from biologists whose scientific training consists of a couple of dumbbell math courses and a survey course in physics. It takes a little more than that to understand the thermodynamics and mathematics of adaptive DNA evolution.

 

[Frank Robert]

Extraordinary claims require extraordinary evidence.

Extraordinary claims require accumulation and consilience of evidence both of which are a major fail for ID.

 

[Alan Kleinman]

Interesting!

It is! Do you see that fixation doesn't have to occur for each adaptation step to occur? Competition is minimal in this experiment because it has a large enough carrying capacity for the colony sizes to reach a population size where there is a reasonable probability of the next adaptive mutation occurring without driving the other variants to extinction.

 

[Alan Kleinman]

Extraordinary claims require accumulation and consilience of evidence both of which are a major fail for ID.

Guy was talking about the evolution of bacteria into humans. Isn't that your concept of common descent? And I'm saying you don't even have the genetic evidence to show that humans and chimpanzees came from a common ancestor let alone this ludicrous idea that somehow we are descended from bacteria.