Creationists: Explain your understanding of microevolution and macroevolution

[Alan Kleinman]

Misdirection will not get you where you want to be.

I told you several times that I have no reason to question your math. My point, for the 3rd time, your math along with your predictions does not disprove macroevolution.

You have yet to falsity even of the
29+ Evidences for Macroevolution

Your non-acceptance of evidence is not falsification of evidence.

Where's the experiment?

 

[Alan Kleinman]

Look up the book. You won't.

I edited that post and show you how to post a link and give the equation that describes the evolution of HIV to 3 simultaneous selection pressures. It's that easy. Here, I"ll do it again since you missed my edit.

Let me show you how to do it. Here's the paper that explains why combination therapy works for the treatment of HIV.
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance
Equation (9) is the correct mathematics for the evolution of HIV subject to 3 simultaneous selection pressures. A graphical representation of the equation is given in Figure (5)

It's really simple when you have the mathematics and empirical evidence which you don't have.

 

[Frank Robert]

Where's the experiment?

You believe you found a loop hole because millions of years of evolution can not be reproduced in a lab.

That you refuse to affirm the consilience of scientific evidence from numerous related fields does not disqualify it as scientific evidence. If you believe that your math is superior evidence for evolution then you should do something about it beyond bluster in a Christian forum.

 

[SelfSim]

That's why it takes so many replications to have a reasonable probability of at least one success. But when that lucky member does get that adaptational mutation, the probability of one of its descendants getting another adaptational mutation is very small unless that new variant replicates many times. If it takes two or more mutations to give an improvement in fitness, it takes exponentially more replications to have any probability of adaptation success for that circumstance.

I've lost track of the overall point you're drawing from your toy model, however, I notice a recent study, (including an evidence based quantitative math model), which appears to make the case for how evolution proceeds under the condition of two traits restricted by a trade off, along with an environment changing over long periods, (which is a much more realistic model, IMO):

Environment determines evolutionary trajectory in a constrained phenotypic space:

This study sheds new light on how evolution proceeds when performance depends on two traits that are restricted by a trade-off. Though a mathematical model suggests that the fastest migrating populations should be composed of cells that swim fast and reproduce quickly, what we found was that populations achieve faster migration through two divergent evolutionary paths that are mutually exclusive: in other words, these populations improved in either swimming speed or reproduction rate, but not both.

The phenotype evolves in the direction of breaking negative regulatory elements, because it's an easy path, statistically. This relates to the availability of useful mutations. They make the point that microevolution is dominated by changes in negative regulatory elements because it's statistically easy to find a mutation that breaks things, compared with one that builds new functions or parts.

It seems to me that what this is saying, is that the selected for beneficial mutation for any given era, can still carry other beneficial mutations forward, for use at some future time. This seems to have not been considered in your conclusions about the diminishing effects of the multiplicative probabilities?

Mutations on the regulatory elements appears to alter the simplistic assumptions you've made your model, I think(?)

(Apologies if this has already been covered, in this now huge thread).

 

[Alan Kleinman]

You believe you found a loop hole because millions of years of evolution can not be reproduced in a lab.

It's not a loophole, it's a correct explanation of the physics and mathematics of a thermodynamics process, adaptive microevolution. If you think microevolution and the laws of physics worked differently millions of years ago explain why.

Why is it that biologists don't understand that evolutionary competition is a first law of thermodynamics process?

That you refuse to affirm the consilience of scientific evidence from numerous related fields does not disqualify it as scientific evidence. If you believe that your math is superior evidence for evolution then you should do something about it beyond bluster in a Christian forum.

I do what I can, I get my papers peer-reviewed and published. I'm posting here because Pita requested a Creationist explanation of micro and macroevolution. I've had to correct you macroevolutionists of the false notion that microevolutionary steps add up. You can't even recognize that microevolutionary steps are random events and you don't compute the joint probability of random events occurring by adding their probabilities.

How do you debate with people that think they understand biological evolution yet don't understand the fundamental physical and mathematical principles of evolutionary competition and microevolutionary adaptation.

You've been listening to pseudo-scientific stories for so long, that you have immunized yourself to the physical, mathematical, and experimental facts of life.

 

[Alan Kleinman]

I've lost track of the overall point you're drawing from your toy model, however, I notice a recent study, (including an evidence based quantitative math model), which appears to make the case for how evolution proceeds under the condition of two traits restricted by a trade off, along with an environment changing over long periods, (which is a much more realistic model, IMO):

Where is your toy model that explains macroevolution. At least my model explains all the experimental and empirical evidence of microevolutionary adaption including the evolution of drug resistance and why cancer treatments fail.

Environment determines evolutionary trajectory in a constrained phenotypic space:

Do you even recognize and understand how to solve their equation (1)? I do (check out my PhD dissertation, I solved a more difficult form of this equation) and it is not the correct mathematics to describe microevolutionary adaptation. Microevolutionary adaptation is a stochastic process that is described by the mathematics of probability theory, not a conservation equation.

The phenotype evolves in the direction of breaking negative regulatory elements, because it's an easy path, statistically. This relates to the availability of useful mutations. They make the point that microevolution is dominated by changes in negative regulatory elements because it's statistically easy to find a mutation that breaks things, compared with one that builds new functions or parts.

It seems to me that what this is saying, is that the selected for beneficial mutation for any given era, can still carry other beneficial mutations forward, for use at some future time. This seems to have not been considered in your conclusions about the diminishing effects of the multiplicative probabilities?

Mutations on the regulatory elements appears to alter the simplistic assumptions you've made your model, I think(?)

(Apologies if this has already been covered, in this now huge thread).

I don't doubt that this is a microevolutionary experiment but they are not describing or measuring the rate of adaptive mutations accumulating in their lineages. What their equation (1) is modeling is the bacterial density as a function of position and time. The first term to the left of the equal sign is the change in density with respects to time, the first term to the right of the equal sign is accounts for diffusion of the bacteria, the second term to the right accounts for movement the movement of the bacteria due to a chemo-attractant, and the last term takes into account the growth of the bacteria. Equation (2) takes into account the change in concentration and diffusion of the chemo-attractant. They are not modeling mathematically microevolutionary adaptation. They are selecting for variants with different swimming speeds to a chemo-attractant from a larger population and then identifying the mutation in those variants.

This is a different experiment than the Kishony experiment where they are starting with a population that doesn't have any drug resistance, allowing the population to grow large enough so a drug-resistant variant appears with the first adaptive mutation, that variant can then grow in the next higher drug concentration region and when it's colony gets large enough a variant with the second adaptive mutation appears,... You are not comparing apples to apples, your paper is starting with variants that can already swim and are acted on by a chemo-attractant. Then they select for the fastest swimmers.

 

[Yttrium]

At least my model explains all the experimental and empirical evidence of microevolutionary adaption including the evolution of drug resistance and why cancer treatments fail.

Could you present your model in a new thread? I'm having a hard time putting what you're talking about together in this thread.

 

[Hans Blaster]

The mathematics may be trivial but you are failing to correlate the math to the physics. My model is not a model of competition, it is a model of adaptation. What you can predict with my model based on the number of replications of a particular variant and mutation rate, the probability of at least one adaptive mutation occurring.

Fixation is a possible outcome of competition between different variants in a limited carrying capacity environment. This is why I continually harp on people to study and understand the similarities and differences between the Kishony and Lenski experiments.

The Kishony experiment is carried out in a relatively large carrying capacity environment that allows sufficient population size for adaptation to occur without fixation of any variant. Look again at that experiment. Colonies of drug-adapted variants grow in the regions where drug is present while the drug-sensitive variants replicate along as long as resources are available in the drug-free region.

On the other hand, the Lenski experiment is carried out in a much lower carrying capacity environment that doesn't allow for the population size to be large enough to get that reasonable probability of an adaptive mutation occurring in a single-day growth cycle.

Understand this first and then we can discuss your Inuit example further.

You say your model is a competition model, but all I've seen is a calculation of cumulative probability of many, many chances to get at least one rare event. Where's the competition part?

 

[Hans Blaster]

Do you even recognize and understand how to solve their equation (1)? I do (check out my PhD dissertation, I solved a more difficult form of this equation) and it is not the correct mathematics to describe microevolutionary adaptation. Microevolutionary adaptation is a stochastic process that is described by the mathematics of probability theory, not a conservation equation.

I know many ways to solve the diffusion equations. Crank-Nicolson has some nice characteristics for stability. Since that paper is modeling the migration of bacteria on the medium a reaction-diffusion equation is quite appropriate.

 

[Hans Blaster]

Every site in the genome is under selection. And with every genome replication and a mutation rate of 1e-8, you should expect 30 new mutations in the genome. Care to tell us which of those mutations made your mother tell you to put your coat on when you went out in the cold?

The number I'm familiar with is 50-100 new mutations in each new human. This would put the effective rate at ~2e-8. (Which is about 20x the rate you keep quoting for bacteria and the earlier numbers you gave on how many fixable adaptive mutations in humans.)

 

[FrumiousBandersnatch]

Why couldn't you macroevolutionist predict the Kishony and Lenski experiments? Why did it take so long to figure out that the treatment of HIV requires 3 drug therapy. Why will it take so long to figure out that single drug targeted cancer therapy will only work in the very earliest stages of the cancer?

All this time touting your math around the biological community and you still don't understand how the various fields of biology and medicine work and interact? I'm shocked, I tell you, shocked!

But I suppose mostly biologists in fields where macroevolution is particularly relevant have been too busy making discoveries using a model that, in practice, works very well.

 

[Alan Kleinman]

Could you present your model in a new thread? I'm having a hard time putting what you're talking about together in this thread.

I'll think about doing that. It is no guarantee that there won't be the same extraneous noise in a new thread as on this thread. But it might be worthwhile to step back, and refresh the explanation of microevolutionary adaptation starting from the simplest cases in the simplest environments.

 

[Alan Kleinman]

You say your model is a competition model, but all I've seen is a calculation of cumulative probability of many, many chances to get at least one rare event. Where's the competition part?

Evolutionary competition and evolutionary adaptive microevolution are distinct physical phenomena with different governing physics and mathematical behaviors.

As I explained in an earlier post to Warden, evolutionary competition is a first law of thermodynamics process where different variants in a population with different relative fitnesses compete for the limited amount of energy in the environment. On the other hand, evolutionary adaptive microevolution is a second law of thermodynamics process. It is a disordering of a genome by random mutations where occasionally, one of those disordering mutations gives improved fitness to the variant that gets that mutation. In this case, the probability of that adaptation mutation occurring does not depend on the relative fitness of that variant to other variants in the population but on the absolute fitness of the variant to replicate. If that variant is able to have a sufficient number of descendants over generations, then the probability will be high that one of its descendants will get that adaptive mutation.

There are at least two ways to compute the probability of that adaptive mutation occurring. The first is with a binomial probability model, does that adaptive mutation occur or not occur on replication and you compute that probability using the "at least one rule" as I've shown in my paper. There is another way to do this probability calculation. That method is to use a random walk model, in particular the Markov Process.

The application of microevolutionary adaptive models and evolutionary competition models depends on the system you are trying to analyze. The Kishony experiment is primarily a microevolutionary adaptive experiment. The carrying capacity is large enough that multiple lineages can achieve the population size necessary for an adaptive mutation to occur. Competition is minimal and fixation does not need to occur for adaptation to occur. The Lenski experiment, on the other hand, operates with a much lower carrying capacity and much lower population size. This essentially limits the evolutionary process to a single lineage where fixation must occur before the given variant can achieve the population size necessary to give a reasonable probability for the next adaptive mutation to occur. The analysis of the Lenski experiment requires superimposing a competition model (I used a variation of the Haldane model) on the microevolutionary adaptation model.

 

[Alan Kleinman]

I know many ways to solve the diffusion equations. Crank-Nicolson has some nice characteristics for stability. Since that paper is modeling the migration of bacteria on the medium a reaction-diffusion equation is quite appropriate.

I'm familiar with the math as well but SelfSim's example isn't an experimental model of microevolutionary adaptation, as you say, it is a model of migration of bacteria model. And I have a lot of training and experience in finite-difference problems. I've got a couple of papers out there where I solved non-linear problems and that's the kind of work I did when I worked on the Space Shuttle.

 

[Alan Kleinman]

The number I'm familiar with is 50-100 new mutations in each new human. This would put the effective rate at ~2e-8. (Which is about 20x the rate you keep quoting for bacteria and the earlier numbers you gave on how many fixable adaptive mutations in humans.)

Here you are demonstrating that you haven't gotten a sense of what are the most important features of the microevolutionary adaptation problem. The mutation rate is not the primary determiner of the rate of microevolution. It is the multiplication rule of probabilities that drives this process. HIV has a mutation rate of ~1e-5, certainly much higher than the human mutation rate. However, adaptation to each additional selection pressure imposes another instance of the multiplication rule on that lineage. This means that in order for that variant to get the multiple mutations necessary to get a step improvement in fitness requires an exponentially larger population size. Even with a mutation rate of 1e-5, HIV needs a population size of about 1e15 for there to be a reasonable probability of that variant to occur for an adaptational step to 3 simultaneous selection conditions.

 

[Alan Kleinman]

All this time touting your math around the biological community and you still don't understand how the various fields of biology and medicine work and interact? I'm shocked, I tell you, shocked!

But I suppose mostly biologists in fields where macroevolution is particularly relevant have been too busy making discoveries using a model that, in practice, works very well.

Too bad none of those discoveries include the correct explanations of the evolution of drug resistance and why cancer treatments fail.

 

[FrumiousBandersnatch]

Too bad none of those discoveries include the correct explanations of the evolution of drug resistance and why cancer treatments fail.

It takes a long time for drugs to be tested for safety and efficacy, etc, particularly potentially cytotoxic drugs, and when combining them in multidrug treatments, such testing is considerably more difficult. Nevertheless, a variety of multidrug therapies are now available for cancer treatment and the benefits of multidrug treatments for bacterial and viral infections have been known for some time.

Perhaps you've missed the boat...

 

[Frank Robert]

It's not a loophole, it's a correct explanation of the physics and mathematics of a thermodynamics process, adaptive microevolution. If you think microevolution and the laws of physics worked differently millions of years ago explain why.

Macroevolution doesn't work differently. The fact that we are unable to duplicate millions to billions of years in the lab does not negate macroevolution.

Why is it that biologists don't understand that evolutionary competition is a first law of thermodynamics process?

You are not considering the fact that it is you who misunderstands macroevolution not the biologists. Why else would you need to deny the overwhelming evidence for macroevolution? Denial of evidence does not falsify the evidence.

29+ Evidences for Macroevolution

 

[Alan Kleinman]

It takes a long time for drugs to be tested for safety and efficacy, etc, particularly potentially cytotoxic drugs, and when combining them in multidrug treatments, such testing is considerably more difficult. Nevertheless, a variety of multidrug therapies are now available for cancer treatment and the benefits of multidrug treatments for bacterial and viral infections have been known for some time.

Perhaps you've missed the boat...

Sure medicine can be toxic. There's an old saying that every medicine is a little bit of poison. But that doesn't change the fact that cancers give rise to be rapidly evolving cell lines with lots of diversity in their cell lines. And because of this lots of resistant variants can appear very early. How early? Read this paper and get an idea of how to estimate that value:
Drug Resistance, An Enemy of Targeted Cancer Therapies

Well, you biologists have failed to give the mathematical explanation of why combination therapy works for the treatment of HIV. Now you will fail to explain why combination therapy is needed to treat cancer. So, what's the next microevolutionary adaptation problem we'll have to face that you will fail to correctly explain that researchers will muddle through and finally figure out that it requires combination therapy to address? How many boats have to sink before you figure this out?

 

[Alan Kleinman]

Macroevolution doesn't work differently. The fact that we are unable to duplicate millions to billions of years in the lab does not negate macroevolution.

At least it didn't take a billion years for you to figure out that I did the math correctly for Kishony and Lenski experiments. Just how many bacterial replications do you think it would take for them to evolve into a biologist?

You are not considering the fact that it is you who misunderstands macroevolution not the biologists. Why else would you need to deny the overwhelming evidence for macroevolution? Denial of evidence does not falsify the evidence.

29+ Evidences for Macroevolution

Oh? Biologists have a misconception of how macroevolution is related to microevolution. And you should understand this misconception since you now understand my explanation of the Kishony and Lenski experiments and that explanation is correct. This scientifically inaccurate way of thinking has been circulating in the field of biology for at least a century, that is, that random processes can create life but also transform life from some simple form into all the complex life forms we see today. Abiogenesis and the ToE, the dumb and dumber of the field of biology, you can choose which is which.