Darwin vs DNA

[Youwerecreated]

Non-sequitur much?

Where's the hole?

You said natural selection leans towards more beneficial mutations and I called you on it only in your imagination does it do that.

That's what natural selection means, you retard. It means that advantageous genetics are selected for, while disadvantageous genetics are selected against.

That is also the nonsense your theory teaches.

It's not "nonsense" you retard, it's verifiable fact.

While we are on it why would a nonintelligent process think to put mechanisms in the cell to prevent mutations ?

I reject your retarded superstitiously anthropomorphic premise.

Your assertion natural selection allows beneficial mutations to exist in the gene pool while eliminating harmful mutations but like I said earlier why if that is true scientists can point to more genetic disorders then benefits from mutations ?

If that is the case why are these harmful mutations not effecting the whole human gene pool ? You can't point to any beneficial mutation that has spread through the whole human population and that is what you need for evolution why is this so difficult for you to grasp ?

You can't even point to a mutant gene that has spread through the whole population whether it was a benefit or harmful to the population.

 

[Youwerecreated]

Yes, but you clearly do not.

The mutant gene must become the norm within the gene pool for evolution to take place.

Nope.

The mutated gene must become the norm within a gene pool.

Your magical notions of speciation just do not apply in the real world, and your dishonest attempts to project them upon the theory of evolution is the root of your strawman argument.

 

[Youwerecreated]

Non-sequitur much?

Where's the hole?

You said natural selection leans towards more beneficial mutations and I called you on it only in your imagination does it do that.

That's what natural selection means, you retard. It means that advantageous genetics are selected for, while disadvantageous genetics are selected against.

That is also the nonsense your theory teaches.

It's not "nonsense" you retard, it's verifiable fact.

While we are on it why would a nonintelligent process think to put mechanisms in the cell to prevent mutations ?

I reject your retarded superstitiously anthropomorphic premise.

I have already showed you why it never happened. I will not waste my time with you if you can't see how erroneous your belief is. Believe as you wish but you are wrong.

You don't even understand the argument you think natural selection only happens from survival of the fittest and traits are passed in this method. Ask yourself if this was the case why the tranitional organisms go extinct but the transitional organisms ancestors are still living ? so much for survival of the fittest.

 

[Youwerecreated]

Youwerecreated is not demonstrating "provable fact" from his thesis: absolute failure, in fact, for his conclusions.

Prove it.

 

[JakeStarkey]

It's good to see what you are doing.

I am saying that the IDers can't disprove evolution. They can't.

I am saying that the atheists can't disprove God. They can't.

I am saying that evolution is not a salvation issue, becuse it isn't.

I am saying that it takes more faith to be an atheist than a believer in deity, because it does.

Tuff beans, Loki.

I could care less, Loki, if you accept it, because your acceptance or belief/nonbelief is not relevant to the conversation.

Your strawman argument is noted, dismissed, and let's move on.

I do not accept the strawman premise of your challenge.

I also note the intellectual cowardice in your attempts to dodge the challenge I presented to you.

What strawman? I made no strawman argument. If i did, you should be able to point it out.

Do so. I dare you.

The fact of the matter is you won't. The fact of the matter is, you are stringing along all these red-herrings in order to avoid the simple and valid request I made of you:

What is this "God" thing you keep referencing. I have been exposed to literally hundreds of self-contradictory, question-begging, special-pleading appeal-to-ignorance accounts of some "God".

All I asked for was a rationally valid explanation for this "God" thing of yours. I respectfully (it's clear now, that you don't deserve it) assumed that your "God" thing did not belong to the egregiously anti-rational variety I have already been exposed to, and I generously pointed out the reasons those anti-rational accounts were invalid.

So, this "God" thing; I have no idea what you're talking about. Why won't you explain it to me? You all seem to possess such unqualified certainty. So help me out here.

 

[JakeStarkey]

Youwerecreated's arguments just got booted across the parking lot into the gutter.

 

[Hollie]

Yes you did, that was your whole point, my view on the chimp and the human according to your theory.

No, you lying retard.

You fatuously demanded that evolutionary scientists claim that humans are descended from chimps--you said evolutionary scientists regard chimps as ancestors of humans--your own retarded and intellectually dishonest posting indicted you then, just as it does now.

Your theory teaches we descended from mutual ancestors and some are saying we diverged from chimps can you explain how I am wrong ?

Retard is a term used by immature individuals.

Do you not understand the purpose of comparing chimps and human DNA by your side ?

I don't know of any science journal or science organization that has ever proposed humankind diverged from chimps. I suspect you are referencing some outlandish claim emanating from the ICR or Harun Yahya. Man was never a chimp, chimpanzee or monkey. You have issues understanding even the most basic precepts of evolutionary science.

Your appalling lack of a science vocabulary coupled with your propensity to mis-state and misrepresent science may partially account for your ignorance... but only partially.

I believe your agenda to lie about science in an effort to press your religious perspective leaves your comments subject to ridicule.

 

[Not2BSubjugated]

You said natural selection leans towards more beneficial mutations and I called you on it only in your imagination does it do that.

That's what natural selection means, you retard. It means that advantageous genetics are selected for, while disadvantageous genetics are selected against.

It's not "nonsense" you retard, it's verifiable fact.

While we are on it why would a nonintelligent process think to put mechanisms in the cell to prevent mutations ?

I reject your retarded superstitiously anthropomorphic premise.

Your assertion natural selection allows beneficial mutations to exist in the gene pool while eliminating harmful mutations but like I said earlier why if that is true scientists can point to more genetic disorders then benefits from mutations ?

If that is the case why are these harmful mutations not effecting the whole human gene pool ? You can't point to any beneficial mutation that has spread through the whole human population and that is what you need for evolution why is this so difficult for you to grasp ?

You can't even point to a mutant gene that has spread through the whole population whether it was a benefit or harmful to the population.

Your assertions here demonstrate a fundamental lack of understanding regarding the basic concept of mutations as they relate to the theory of evolution.

Nowhere does any widely accepted theory of evolution contradict the fact that most genetic mutations are harmful to the individual organism displaying said mutation. However, if that mutation makes it harder for that organism to survive, that organism likely dies off.

When a mutation is beneficial, however, that individual organism excells at survival. When it reproduces, it sometimes produces offspring with some variation of that same beneficial mutation. They excell and reproduce, so on and so forth, until that beneficial property is prevalent enough that those without it have a harder and harder time competing for the same resources.

Nowhere does any respected evolutionary theory speculate that a mutation spreads swiftly through an entire species. I don't think anybody with a half a brain and an ounce of knowledge on the subject believes that the same mutation is going to be widespread in one or two generations. . . genes are passed on via reproduction.

I gather that you're getting this a lot, but you can't disprove an argument you don't even understand. Keep at it, tho. Good times.

 

[LOki]

Yes you did, that was your whole point, my view on the chimp and the human according to your theory.

No, you lying retard.

You fatuously demanded that evolutionary scientists claim that humans are descended from chimps--you said evolutionary scientists regard chimps as ancestors of humans--your own retarded and intellectually dishonest posting indicted you then, just as it does now.

Your theory teaches we descended from mutual ancestors ...

Yes.

...and some are saying we diverged from chimps can you explain how I am wrong ?

You are wrong in the way it is wrong to say that a cousin relationship asserts ancestry of one cousin for the other. This was clearly explained to you.

I'm also pretty sure that I explained to you that closest living relation is NOT the same thing as closest ancestor, or closest common ancestor. If not, I'm telling you that now.

###A## ##B
D##|## ##|
|##|##X##C
|##|##|##|
D__|##|##E
|_____X___|
#####|
#####Y
#####|

You see, while A, B, C, D, and E above are related by common ancestry with X and Y, A is NOT the ancestor of B, an NEITHER is D. E is not the ancestor of A OR D. While A might be the closes living relation to B, C is the closest ancestor to B, and X is the closest common ancestor of A & B.

If chimps are D (and humans B), they're not our ancestors--even if you take D out of the picture. If you make them X, then yes, they'd be an ancestor, they'd be our nearest living ancestor, but NOT our nearest ancestor. But here's the thing, if chimps are X (making A=X), then it's just as valid to say that they split off from us, as it is to say we split off from them.

Sharing common ancestry with a living relative (e.g., A) does NOT make that living relative an ancestor. It doesn't necessarily make that relative's nearest ancestor (e.g., D) an ancestor. Do you get it?

Retard is a term used by immature individuals.

Not exclusively so.

Do you not understand the purpose of comparing chimps and human DNA by your side ?

Sure. What's your point?

 

[LOki]

You said natural selection leans towards more beneficial mutations and I called you on it only in your imagination does it do that.

That's what natural selection means, you retard. It means that advantageous genetics are selected for, while disadvantageous genetics are selected against.

It's not "nonsense" you retard, it's verifiable fact.

While we are on it why would a nonintelligent process think to put mechanisms in the cell to prevent mutations ?

I reject your retarded superstitiously anthropomorphic premise.

Your assertion natural selection allows beneficial mutations to exist in the gene pool while eliminating harmful mutations but like I said earlier why if that is true scientists can point to more genetic disorders then benefits from mutations ?

This is probably because pathologists concern themselves with pathological mutations rather than beneficial ones. But look, all you have to do is provide an example of the un-mutated human genome, and I'll point out some of the beneficial mutations exisiting in the entire human genome.

If that is the case why are these harmful mutations not effecting the whole human gene pool ?

CHRIST! I'm sure I've answered this question from you a half dozen times by now! BECAUSE A MUTATION DOESN'T MAGIALLY AFFECT THE WHOLE GENE POOL AT THE SAME INSTANT, YOU RETARD!

The theory of evolution is not governed by the notions of magic manifest in your superstitious paradigm. Got that?

You can't point to any beneficial mutation that has spread through the whole human population and that is what you need for evolution why is this so difficult for you to grasp ?

Somewhere in the history of human evolution, mutation occured that gave forth opposable motion in thumbs. This beneficial mutation--once arguably an abnormality--is now considered a normal part of the human genome. How about them apples?

You can't even point to a mutant gene that has spread through the whole population whether it was a benefit or harmful to the population.

I think I just did.

 

[LOki]

You said natural selection leans towards more beneficial mutations and I called you on it only in your imagination does it do that.

That's what natural selection means, you retard. It means that advantageous genetics are selected for, while disadvantageous genetics are selected against.

It's not "nonsense" you retard, it's verifiable fact.

While we are on it why would a nonintelligent process think to put mechanisms in the cell to prevent mutations ?

I reject your retarded superstitiously anthropomorphic premise.

I have already showed you why it never happened.

No. You showed how your strawman notions of evolution can never happen. Congratulations on that BTW.

I will not waste my time with you if you can't see how erroneous your belief is. Believe as you wish but you are wrong.

If this means you're going to stop misrepresenting evolutionary theory as your primary method of refuting it, I can only applaud this unprecedented effort toward intellectual honesty in you.

You don't even understand the argument you think natural selection only happens from survival of the fittest and traits are passed in this method.

I'm not sure about your use of the term "only" in this assertion; but aside from that, I'm not the one denying it.

Ask yourself if this was the case why the tranitional organisms go extinct but the transitional organisms ancestors are still living ? so much for survival of the fittest.

Why? You are aware of the concept of survival of the fittest, aren't you? Perhaps the population of transitional organisms was not fit to compete for resources against BOTH their parent organisms and their child organisms.

 

[LOki]

I could care less, Loki, if you accept it, because your acceptance or belief/nonbelief is not relevant to the conversation.

Your strawman argument is noted, dismissed, and let's move on.

What strawman? I made no strawman argument. If i did, you should be able to point it out.

Do so. I dare you.

The fact of the matter is you won't. The fact of the matter is, you are stringing along all these red-herrings in order to avoid the simple and valid request I made of you:

What is this "God" thing you keep referencing. I have been exposed to literally hundreds of self-contradictory, question-begging, special-pleading appeal-to-ignorance accounts of some "God".

All I asked for was a rationally valid explanation for this "God" thing of yours. I respectfully (it's clear now, that you don't deserve it) assumed that your "God" thing did not belong to the egregiously anti-rational variety I have already been exposed to, and I generously pointed out the reasons those anti-rational accounts were invalid.

So, this "God" thing; I have no idea what you're talking about. Why won't you explain it to me? You all seem to possess such unqualified certainty. So help me out here.

It's good to see what you are doing.

Why, thank you for saying so.

I am saying that the IDers can't disprove evolution. They can't.

I agree.

I am saying that the atheists can't disprove God. They can't.

I agree.

I am saying that evolution is not a salvation issue, becuse it isn't.

I agree.

I am saying that it takes more faith to be an atheist than a believer in deity, because it does.

Nonsense. It takes no faith at all to be an atheist.

Tuff beans, Loki.

Eat a bag of dicks, JakeStarkey.

That said, it still looks like you are stringing along all these red-herrings in order to avoid the simple and valid request I made of you:

What is this "God" thing you keep referencing. I have been exposed to literally hundreds of self-contradictory, question-begging, special-pleading appeal-to-ignorance accounts of some "God".

All I asked for was a rationally valid explanation for this "God" thing of yours. I respectfully (it's clear now, that you don't deserve it) assumed that your "God" thing did not belong to the egregiously anti-rational variety I have already been exposed to, and I generously pointed out the reasons those anti-rational accounts were invalid.

So, this "God" thing; I have no idea what you're talking about. Why won't you explain it to me? You all seem to possess such unqualified certainty. So help me out here.

 

[JakeStarkey]

Loki, so you are are getting your butt handed to you. Upsetting for you, yes.

You can't prove that God does not exist, thus atheism is a faith just like any other.

Tuff beans.

 

[LOki]

Loki, so you are are getting your butt handed to you. Upsetting for you, yes.

What the fuck are you talking about JakeStarkey?

I'm not the one making fairy-dance evasive maneuvers away from an honestly, and respectfully posed request.

You can't prove that God does not exist, ...

Never claimed I could--but you know this, I've made it clear. It's just a good thing that I don't have to.

... thus atheism is a faith just like any other.

The one, just does not follow from the other. Sorry about your superstitious luck.

Tuff beans.

Eat dicks.

 

[CandySlice]

Yet no atheist has ever proved that God did not exist, either with empirical data or with logic.

Hollie, you haven't looked everywhere in the universe in the same nth second. 'sides, girl, God ain't hiding from you, only you from God.

Let it go.

It's not the atheist's burden to "prove" that your "God" thing doesn't exist; just like it's not the atheist's burden to "prove" unicorns don't exist, or leprechauns don't exist, or Santa doesn't exist, etc.

The burden lies ENTIRELY upon those making the claim FOR existence--no matter how you want to rearrange the question.

And as far as I'm concerned, I didn't claim I had "proof" that there's no god, and I didn't ask you for "proof." Did I?

No. All I asked for was a rationally valid explanation for this "God" thing of yours. And I respectfully assumed that your "God" thing did not belong to the egregiously anti-rational variety I have already been exposed to, and I generously pointed out the reasons those anti-rational accounts were invalid. So don't try to weasel your way out with "moving the gaol posts," when you can't establish where I moved my goal posts to.

There really is no reason to try and prove God exist no matter what is presented people like you made up your mind and unfortunately it might be to late when you meet him.

Again with the threats. 'You better be good or you'll be sorry'. If God is half the guy I think he is he'll appreciate my questions, not punish me for them.

 

[Youwerecreated]

It's good to see what you are doing.

I am saying that the IDers can't disprove evolution. They can't.

I am saying that the atheists can't disprove God. They can't.

I am saying that evolution is not a salvation issue, becuse it isn't.

I am saying that it takes more faith to be an atheist than a believer in deity, because it does.

Tuff beans, Loki.

I could care less, Loki, if you accept it, because your acceptance or belief/nonbelief is not relevant to the conversation.

Your strawman argument is noted, dismissed, and let's move on.

What strawman? I made no strawman argument. If i did, you should be able to point it out.

Do so. I dare you.

The fact of the matter is you won't. The fact of the matter is, you are stringing along all these red-herrings in order to avoid the simple and valid request I made of you:

What is this "God" thing you keep referencing. I have been exposed to literally hundreds of self-contradictory, question-begging, special-pleading appeal-to-ignorance accounts of some "God".

All I asked for was a rationally valid explanation for this "God" thing of yours. I respectfully (it's clear now, that you don't deserve it) assumed that your "God" thing did not belong to the egregiously anti-rational variety I have already been exposed to, and I generously pointed out the reasons those anti-rational accounts were invalid.

So, this "God" thing; I have no idea what you're talking about. Why won't you explain it to me? You all seem to possess such unqualified certainty. So help me out here.

It could be a salvation issue if the theory is wrong which I believe there is no doubt it is.

2Ti 4:3 For a time will be when they will not endure sound doctrine, but they will heap up teachers to themselves according to their own lusts, tickling the ear.
2Ti 4:4 And they will turn away their ears from the truth and will be turned to myths.
2Ti 4:5 But you watch in all things, endure afflictions, do the work of an evangelist, fully carry out your ministry.

 

[CandySlice]

Not with scientiic evidence. Bible quotations are not scientific evidence, not binding on anyone. Just the way it is.

YWC uses the Bible in place of actually having to think.

I take offense to your assertion,care to back your claim with some sort of example ?

I submit this entire thread as evidence of your inability to take in anything new. Or for that matter even show a modicum of decency to anyone who even tries to introduce new ideas that differ from your narrow superstitious view. In the course of this thread Ive seen you call names,. threaten people and challenge them to actual fist fights in a desperate attempt to make sure people don't use their heads, don't question what you evidently see as the emmis truth, end of story, end all be all. You've tried argument, junk science and actual magical thinking to keep your narrow view front and center and your pride insists nobody knows anything more than you do, evidently about not only the Bible but the entire spectrum of scientific discoveries and speculation.

You are exactly the kind of ugly mean spirited person that drives so many of us to leave the church, ask questions and search elsewhere in the first place. You and your kind are probably responsible for turning more people away from their beliefs than any other one thing in history. Because the God you worship is evidently unbending and stiff, vindictive and evil at the same time. I'd say shame on you, but unfortunately there is no cure for people like you. You use religion as a weapon, a bludgeon to bully and corral the weak minded to embrace your vengeful nonsense and it's disgraceful.

 

[Youwerecreated]

Youwerecreated's arguments just got booted across the parking lot into the gutter.

You are a dreamer.

 

[Youwerecreated]

That's what natural selection means, you retard. It means that advantageous genetics are selected for, while disadvantageous genetics are selected against.

It's not "nonsense" you retard, it's verifiable fact.

I reject your retarded superstitiously anthropomorphic premise.

Your assertion natural selection allows beneficial mutations to exist in the gene pool while eliminating harmful mutations but like I said earlier why if that is true scientists can point to more genetic disorders then benefits from mutations ?

If that is the case why are these harmful mutations not effecting the whole human gene pool ? You can't point to any beneficial mutation that has spread through the whole human population and that is what you need for evolution why is this so difficult for you to grasp ?

You can't even point to a mutant gene that has spread through the whole population whether it was a benefit or harmful to the population.

Your assertions here demonstrate a fundamental lack of understanding regarding the basic concept of mutations as they relate to the theory of evolution.

Nowhere does any widely accepted theory of evolution contradict the fact that most genetic mutations are harmful to the individual organism displaying said mutation. However, if that mutation makes it harder for that organism to survive, that organism likely dies off.

When a mutation is beneficial, however, that individual organism excells at survival. When it reproduces, it sometimes produces offspring with some variation of that same beneficial mutation. They excell and reproduce, so on and so forth, until that beneficial property is prevalent enough that those without it have a harder and harder time competing for the same resources.

Nowhere does any respected evolutionary theory speculate that a mutation spreads swiftly through an entire species. I don't think anybody with a half a brain and an ounce of knowledge on the subject believes that the same mutation is going to be widespread in one or two generations. . . genes are passed on via reproduction.

I gather that you're getting this a lot, but you can't disprove an argument you don't even understand. Keep at it, tho. Good times.

Since you believe this you should read Dr. Spetners book Not by Chance! you will see I am right and you know very little about mutations.

You still need the mutations to affect the whole gene pool. So are you suggesting adam and eve came from apes ?

 

[Youwerecreated]

That's what natural selection means, you retard. It means that advantageous genetics are selected for, while disadvantageous genetics are selected against.

It's not "nonsense" you retard, it's verifiable fact.

I reject your retarded superstitiously anthropomorphic premise.

Your assertion natural selection allows beneficial mutations to exist in the gene pool while eliminating harmful mutations but like I said earlier why if that is true scientists can point to more genetic disorders then benefits from mutations ?

If that is the case why are these harmful mutations not effecting the whole human gene pool ? You can't point to any beneficial mutation that has spread through the whole human population and that is what you need for evolution why is this so difficult for you to grasp ?

You can't even point to a mutant gene that has spread through the whole population whether it was a benefit or harmful to the population.

Your assertions here demonstrate a fundamental lack of understanding regarding the basic concept of mutations as they relate to the theory of evolution.

Nowhere does any widely accepted theory of evolution contradict the fact that most genetic mutations are harmful to the individual organism displaying said mutation. However, if that mutation makes it harder for that organism to survive, that organism likely dies off.

When a mutation is beneficial, however, that individual organism excells at survival. When it reproduces, it sometimes produces offspring with some variation of that same beneficial mutation. They excell and reproduce, so on and so forth, until that beneficial property is prevalent enough that those without it have a harder and harder time competing for the same resources.

Nowhere does any respected evolutionary theory speculate that a mutation spreads swiftly through an entire species. I don't think anybody with a half a brain and an ounce of knowledge on the subject believes that the same mutation is going to be widespread in one or two generations. . . genes are passed on via reproduction.

I gather that you're getting this a lot, but you can't disprove an argument you don't even understand. Keep at it, tho. Good times.

Here ya go but I suggest you getting his book.

Lee Spetner/Edward Max Dialogue
Dr. Lee Spetner
continuing an exchange with Dr. Edward E. Max

© 2001 L.M. Spetner. All Rights Reserved.

fter I posted my critique of Edward E. Max’s essay, Max posted our dialogue with additional comments to my responses. The order of topics in his posting does not correspond exactly to the order of my posting, but both postings are fairly accurate representations of our dialogue. The following is my latest response (23 May 2001) in a form that reproduces his posting into which I have inserted my comments. I have identified each of our statements as he has reproduced them by putting our names in boldface followed by a colon. My new comments are inserted into the text in small caps inside square brackets and identified by "LMS".

Introduction
Spetner: I am writing this essay in response to a request from Edward E. Max to comment on his posting The Evolution of Improved Fitness (updated July 12 1999). His essay is an attempt to defend evolutionary theory against attacks by creationists. Although Max scored some points against some alleged creationist arguments, he failed to defend Darwinian evolution against my attack on it in my book Not By Chance. He did not mention my book in his posting, but he referred to my book in his request for my comments. I shall also take this opportunity to clarify some issues in my book about which some readers have written me.

The principle message of evolution is that all life descended with modification from a putative single primitive source. I call this the grand sweep of evolution. The mechanism offered for the process of modification is basically the Darwinian one of a long series of steps of random variation, each followed by natural selection. The variation is generally understood today to be random mutations in the DNA.

That primitive source of life is assumed to be sufficiently simple that it could have arisen from nonliving material by chance. There is no theory today that can account for such an event, but I shall not address that issue here. That is for another place and another time. What is relevant to this discussion is that the requirement that life arose spontaneously sets, at the very least, a stringent upper limit on the complexity and information content of the putative first organism that could reproduce itself, and thus serve as a vehicle from which to launch Darwinian evolution. The issue I address here is the alleged development of all life by the Neo-Darwinian process of random mutation and natural selection, starting from a sufficiently simple beginning.

Despite the insistence of evolutionists that evolution is a fact, it is really no more than an improbable story. No one has ever shown that macroevolution can work. Most evolutionists assume that macroevolution is just a long sequence of microevolutionary events, but no one has ever shown it to be so. (Those few evolutionists who hold that macroevolution is really different from microevolution have changed their story several times since they first came out with it, and their mechanism is so fuzzy that I cannot tell what it is. John Maynard Smith seems to be of a similar opinion.)

For the grand process of evolution to work, long sequences of “beneficial” mutations must be possible, each building on the previous one and conferring a selective advantage on the organism. The process must be able to lead not only from one species to another, but to the entire advance of life from a simple beginning to the full complexity of life today. There must be a long series of possible mutations, each of which conferring a selective advantage on the organism so that natural selection can make it take over the population. Moreover, there must be not just one, but a great many such series.

The chain must be continuous in that at each stage a change of a single base pair somewhere in the genome can lead to a more adaptive organism in some environmental context. That is, it should be possible to continue to climb an “adaptive” hill, one base change after another, without getting hung up on a local adaptive maximum. No one has ever shown this to be possible.

Now one might say that if evolution were hung up on a local Maximum, a large genetic change like a recombination or a transposition could bring it to another higher peak. Large adaptive changes are, however, highly improbable. They are orders of magnitude less probable than getting an adaptive change with a single nucleotide substitution, which is itself improbable. No one has shown this to be possible either.

Moreover, as I have noted in my book, the large mutations such as recombinations and transpositions are mediated by special enzymes and are executed with precision - not the sort of doings one would expect of events that were supposed to be the products of chance. Evolutionists chose the mechanism of randomness, by the way, because we can’t think of any other way beneficial mutations might occur in the absence of a law that might govern them. Genetic rearrangements may not be really random at all. They do not seem to qualify as the random mutations Neo-Darwinists can invoke whenever needed to escape from a local adaptive Maximum.

Evolutionists can argue, and rightly so, that we have no way of observing long series of mutations, since our observation time is limited to a relatively short interval. Our genetic observations over the past 100 years are more like a snapshot of evolution rather than a representative interval in which we can search for the required long series of changes. But our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist.

Max: I agree that there are no definitive examples where a macroevolutionary change (such as the development of cetaceans from terrestrial mammals) has been shown to result from a specific chain of mutations. And I agree with your further comment that “we have no way of observing a long series of mutations.” But you go on to say that “our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist.” An equally reasonable conclusion, in my view, would be that our inability to observe such series cannot be used as a justification for the assumption that such a series of mutations did NOT occur.

Spetner: Now Ed, that’s ridiculous! Those two statements are not symmetrical. I don’t have to assume the series did not occur to make a case for the inadequacy of NDT. You, who are basing your theory of evolution on the occurrence of such a series, are required to show that it exists, or at least that it is likely to exist. You are obliged to show an existence. I am not obliged to prove a non-existence.
[LMS: IN MAX’S POSTING HE MOVED THIS REMARK OF MINE TO A LATER POINT IN THE DIALOGUE. I ORIGINALLY HAD IT HERE, AND HERE IS WHERE IT BELONGS.]

Max: In the absence of conclusive data defining such a series, if we want to distinguish between various hypotheses to explain the origin of species we must rely on other data, such as from various laboratory model systems that show adaptations in short enough timeframes that we can observe them. Then we must extrapolate as best we can the information learned from these model systems to the questions of species origins. This extrapolation from laboratory model systems to systems unobservable in the laboratory is the method of science common to medicine, astronomy, chemistry, meteorology, physics, etc.

I think there is some semantic confusion here about the word “justification” in Spetner’s sentence “But our inability to observe such series cannot be used as a justification for the assumption that the series Darwinian theory requires indeed exist.” He is correct that acceptance of the NDT implies the belief that a series of successive mutations (including duplications and translocations) occurred in the evolution of an ancient primitive genome into the complex genome of a modern species. Because we can access only genomes of modern (or very recent) species, we can never obtain the direct evidence—i.e., a complete list of those mutations—that some anti-evolutionists (e.g. Behe) seem to think would be necessary to support NDT.
[LMS: MAX’S STATEMENT HERE IS A DISTORTION OF MY ARGUMENT INTO AN EXTREME POSITION. I NEITHER SAID NOR IMPLIED THAT EVOLUTIONISTS MUST “OBTAIN...A COMPLETE LIST OF THOSE MUTATIONS” REQUIRED FOR NDT. I DO MAINTAIN, HOWEVER, THAT THEY SHOULD AT LEAST ACCEPT THE RESPONSIBILITY OF SHOWING THAT NDT IS REASONABLY SUPPORTED BY EVIDENCE. THEY HAVE NOT DONE THAT. THE MECHANISM OF NDT CONSISTS OF TWO BASIC STEPS. AN ADAPTIVE MUTATION MUST BE ACHIEVED, AND THEN NATURAL SELECTION MUST OPERATE TO ENABLE IT TO TAKE OVER THE POPULATION. EVOLUTIONISTS ARE OBLIGATED TO SHOW THAT BOTH THESE STEPS ARE REASONABLY SUPPORTED BY EVIDENCE IF THEY ARE TO MAKE A CASE FOR NDT. MOST OF THEIR EFFORTS ALONG THESE LINES HAVE BEEN LIMITED TO ARGUING FOR NATURAL SELECTION. THEY USUALLY DO NOT DEAL WITH THE PROBABILITY OF ACHIEVING AN ADAPTIVE MUTATION. THEY MERELY ASSUME ONE WILL BE AVAILABLE WHENEVER IT IS NEEDED.]

In the absence of such direct evidence, it seems pointless to argue which side is “obliged” to provide what indirect evidence; certainly neither side can hope for anything close to “proof.” Although Spetner denies that he is “obliged to prove a non-existence” of such a chain of mutations, his whole effort in the correspondence seems to be directed to just that aim. Evolutionists have the job of defending the reasonableness of such a series of mutations. I believe that Spetner would agree with this.
[LMS: RIGHT. EVOLUTIONISTS DO HAVE THAT JOB AS AN OBLIGATION, AND THEY HAVE FAILED TO FULFILL IT. I AM NOT OBLIGED TO PROVE A NON-EXISTENCE. BUT IN MY BOOK, I HAVE MADE A GOOD CASE FOR THE UNREASONABLENESS OF THE EVOLUTIONISTS’ TACIT ASSUMPTIONS OF THE UNIVERSAL AVAILABILITY OF ADAPTIVE MUTATIONS, AND I HAVE GIVEN SOME OF THOSE ARGUMENTS IN THIS DIALOGUE.]

Spetner: But the argument against Darwinian theory is considerably stronger than that. The theory requires there be a vast number of possible point mutations which, coupled with natural selection, can produce the evolutionary advances that could produce the grand sweep of evolution. Because there must be a large number of qualifying mutations, at least a few of them should have been observed in some of the many genetics laboratories around the world. All the mutations in these long series must not only confer selective advantage on the organism but they must, on the average, also contribute to the information, or complexity, increase that surely distinguishes present-day life from the putative primitive organism.

These mutations must have whatever characteristics are necessary for them to serve as elements of the grand sweep of evolution. Thus, for a mutation to qualify as a representative member of the required multitude of long series that are supposed to produce evolution, it must bring new information not just to the genome of the organism, but the information must be new to the entire biocosm. The horizontal transfer of a gene from one species to another is not information new to the biocosm. To show evolution in action, one must at least demonstrate examples of a mutation that can serve as a prototype of those required by the theory. Such a mutation must be one that could be a contributing member of a series of mutations that could lead to the vast increase in information required by the theory. Thus, for example, a mutation that disables a repressor gene causing a constitutive synthesis of an enzyme might be advantageous to an organism under special circumstances, but the disabling of a gene does not represent the mutations required by the theory.

Max devotes a good portion of his essay to refuting what he calls the “creationist” argument against evolution. Although some opponents of evolutionary theory may have advanced the arguments he attacks, those arguments are in large measure straw men that Max busies himself with refuting. If some creationists have claimed that all mutations are harmful, they would be wrong, but Max’s observation that there are mutations that are beneficial, while true, is hardly a telling argument for evolution.


The B-Cell Hypermutation Model
Max: The next major point of discussion in the correspondence has been about how well the model of immunoglobulin gene somatic hypermutation in B cells serves as an analog to genomic mutation in evolution. The following section contains the salient points of our exchange about this question, beginning with Spetner’s initial response to my essay on Talk.Origins.

Spetner: Max’s pièce de résistance was the somatic mutations in B lymphocytes (B cells) of the vertebrate immune system as examples of random mutations that add information. He implied that Evolution could follow this method to achieve baboons from bacteria. I agree with him that these mutations add information to the B-cell genome. I also agree that they are random, but they are random only in the base changes they make; they are not random in where in the genome they can occur. More important, I do not agree that the grand sweep of evolution could be achieved through such mutations.

Although the somatic mutations to which Max referred are point mutations that do indeed add information to the genome of the B cells, they cannot be applied to Darwinian evolution. These are not the kind of mutations that can operate as the random mutations required by NDT that can, through chance errors, build information one base change at a time.

For one thing, the rate of the somatic mutations in the immune system is extremely high - more than a million times normal mutation rates. For this reason they are called hypermutations. If an organism had a mutation rate that was even a small fraction of this rate it could not survive. For a second thing, the hypermutations in the B cells are restricted to a specific tiny portion of the genome, where they can do no harm but only good. The entire genome of the B cell could not mutate at this rate; the hypermutation must be restricted only to the portion that encodes selected portions of the variable part of the antibody.

The mutation rate of the hypermutating part of the B cell’s genome is about one per thousand base pairs per replication (Darnell et al., 1986, Molecular Cell Biology, Scientific American Books, p. 1116.), and it can be as high as one in 500 base pairs per replication (Shen, 1998 Science 280: 1750). These rates are incompatible with Darwinian evolution. If an organism’s genome were to mutate at this rate, there would be, on the average, about one mutation in every gene, with a high probability that many of them would be fatal for the organism. No, Darwinian evolution could not occur with such rates.

These high rates are essential for the working of the immune system. In each replication of a B cell, about 30 of the 300 or so gene regions encoding the CDR’s will have a mutation. A lower mutation rate would make for a less efficient immune system. The high mutation rates, so necessary for the immune system, if applied to an entire organism for evolutionary purposes, would be fatal many times over.

Note that these hypermutations are limited to a restricted portion of the genome. Moreover, the hypermutations are mediated by special enzymes. Thus, although the hypermutations are random in the changes they make in the bases of the genome, they are not random in the positions in which they occur. They occur only in the small region in which they are needed, and occur there through enzymes that apparently play only that role. Furthermore, they occur only when they are switched on by the controlling mechanism of B-cell maturation. Thus it is clear that the hypermutations in B cells cannot serve as a prototype for the random mutations required for NDT.

Max: You agreed with me that the model system of random somatic mutations and selection that occurs in immunoglobulin genes in B lymphocytes can “add information to the B-cell genome.” I am glad that you accept the idea that random mutation and selection can lead to an increase in information, since this idea directly refutes the notion of Dembski and others who believe that there is some theoretical bar that would prevent achieving what they call “complex specified information” through random mutation and selection. (Incidentally, I don’t think they would appreciate your characterization of them as “straw men.") However, you then go on to declare that the B cell example is a poor model for what happens in “Darwinian” evolution, and you cite two reasons: (1) the mutation rate in this model is much higher than what is seen in non-immunoglobulin genes and in non-B-cells; and (2) these “hypermutations” are mediated by “special enzymes.” With regard to your first point, I agree that the mutation rate is higher in the B cell example than in evolution, but I fail to see why that fact weakens the usefulness of the example as a model for evolution. If adaptive mutations that increase information in the genome of a B lymphocyte population can occur over one week given a high mutation rate, what theoretical argument would lead you to reject the idea that adaptive mutations that increase information in the genome of a germ cell population could occur over many millions of years given a much lower mutation rate?

Spetner: [LMS: IN HIS POSTING, MAX MOVED MY ANSWER FROM HERE TO A LATER POINT IN THE DIALOGUE, BUT THIS IS WHERE I ORIGINALLY PUT IT, AND THIS IS WHERE IT BELONGS.]
The theoretical argument is the following. Evolution requires a long series of steps each consisting of an adaptive mutation followed by natural selection. In this series, each mutation must have a higher selective value than the previous. Thus, the evolving population moves across the adaptive landscape always rising toward higher adaptivity. It is generally accepted that the adaptive landscape is not just one big smooth hill with a single Maximum, but it is many hills of many different heights. Most likely, the population is on a hill that is not the highest in the landscape. It will then get stuck on a local Maximum of adaptivity and will not be able to move from it. This is particularly likely because the steps it takes are very small - only one nucleotide change at a time. The problem is compounded by the lack of freedom of a single nucleotide substitution to cause a change in the encoded amino acid. A single nucleotide substitution does not have the potential to change an amino acid to any one of the other 19. In general, its potential for change is limited to only 5 or 6 others. To evolve off the “dead point” of adaptivity, a larger step, such as the simultaneous change of more than one nucleotide, is required. Moreover, the probability is close to 1 that a single mutation in a population, even though it is adaptive, will disappear without taking over the population (see my book, Chapter 3). Therefore, many adaptive mutations must occur at each step.

The hypermutation in the B cells does this. It achieves all possible single, double, and triple mutations for the immune system, which allows them to obtain the information necessary to match a new antigen. Ordinary mutations, at the normal low rate, cannot add this information - even over long times. I shall explain why. Consider a population of antigen-activated B cells of, say, a billion individuals. In two weeks, there will be about 30 generations. Let’s say the population size will remain stable, so in two weeks there will be a total of 30 billion replications. With a mutation rate of 1 per 1000 nucleotides per replication, there will be an average of 30 million changes in any particular nucleotide during a two-week period. The probability of getting two particular nucleotides to change is one per million replications. Thus in two weeks, there will be an average of 30 thousand changes in any two particular nucleotides. There will be an average of 30 changes in any three particular nucleotides.

How many generations, and how long, would it take to get a particular multiple nucleotide change in a germ cell to have an effect on Neo-Darwinian evolution? Here, the mutation rate is about one per billion nucleotides per replication. Let’s suppose we're doing this experiment with a population of a billion bacteria. Then, in one generation, there will be an average of one change in a particular base. A particular double base change has a probability of one per quintillion, or 10-18. To get one of these would take a billion generations, or about 100,000 years. To get a triple change would take 1014, or a hundred trillion, years. That is why a long waiting time cannot compensate for a low mutation rate. I've given numbers here for a laboratory experiment with bacteria. Many more mutations would be expected world-wide. But the same kind of thing has to happen under NDT with multicelled animals as well. With vertebrates, for example, the breeding populations seldom exceed a few thousand. Multicelled animals would have many fewer mutations than those cited above for bacteria.

Max: Your second objection to the somatic mutation model in B-cells, that “special enzymes” are involved, is unsupportable.
[LMS: ON THE CONTRARY, I HAVE SHOWN IT IS WELL SUPPORTED (SEE BELOW).]
As far as I can tell from my reading of the literature, the mechanism of somatic hypermutation in B-cells is not currently known.
[LMS: TO WHAT EXTENT THE MECHANISM IS KNOWN IS IRRELEVANT TO THIS DISCUSSION. THE POINT IS THAT THE CONSENSUS AMONG EXPERTS IS THAT SUCH A MECHANISM EXISTS FOR B-CELL MUTATION, AND DOES NOT EXIST FOR GERMLINE MUTATION.]
The mechanism could perhaps involve “special” enzymes that create mutations, but an alternative possibility is that the high rate of accumulation of mutations simply reflects selective inhibition of normal proof-reading mechanisms. But again, I fail to see why the source of the random mutations should influence the general validity of the conclusion that random mutations and selection can increase genomic information, or why you feel that these mutations cannot serve as a model for evolutionary adaptations.

Indeed, both the rate and predominant mechanism of mutation may be different in different species of organisms, depending on whether they have more or less exposure to cosmic rays and other environmental mutagens, and depending on the nature and robustness of their genomic error-correction mechanisms. Therefore, if we accept your argument against extrapolation from B cell adaptation to species adaptation, should we reject the extrapolation of any information learned from studying one organism to understand adaptations in a second organism, unless it is shown that both the rate and mechanism of mutation are the same in both organisms?
[LMS: HERE AGAIN, MAX DISTORTS MY ARGUMENT INTO AN EXTREME POSITION AND THEN RESPONDS TO THAT EXTREME POSITION.]
In my view this would be like refusing to use the gravitational constant determined in laboratories on earth to analyze stellar physics. Such a reluctance to extrapolate would certainly prevent the use of modern organisms as a basis for understanding evolutionary events that occurred millions of years ago (which may be precisely your intent). I sometimes hear arguments like yours from creationists who are demanding rigorous “proof” of evolution. These creationists do not seem to understand the distinction between mathematics, where a rigorous proof is expected, versus most experimental and observational science, where all we are seeking is the best theory that explains observed data. Of course it is possible to extrapolate unreasonably, but I do not see that you have shown how evolutionary theory (or my essay) does this.

Spetner: Extrapolations made in astrophysics and cosmology may not be entirely valid, but at least they are reasonable based on everything we know. The extrapolation you propose from B-cell hypermutation to Neo-Darwinian evolution is unreasonable based on present knowledge, and it is therefore unjustified.
[LMS: THIS ANSWER OF MINE SOMEHOW GOT MOVED AWAY FROM THIS PLACE WHERE IT BELONGS.]
Yes, Ed, the hypermutation in the B cells cannot be a prototype of the kind of mutation required by NDT for Evolution A for the two reasons I gave. You question both those reasons, so I shall elaborate to explain to you why they are valid reasons for rejecting your example of B-cell hypermutation as support for NDT.

One of my arguments to invalidate hypermutation as a model for NDT is that this kind of mutation requires “special enzymes", and is not the kind of mutations held to be responsible for the variation required in NDT. You rejected that argument as unsupportable, but that rejection is unjustified. These mutations, unlike ordinary errors in DNA replication in the germline, are turned on precisely when they are needed and turned off when they have done their job. They are accurately targeted to the very small regions of the genome where they can provide variability to the CDR’s, which form the antibody binding site. Although the mechanism of this precisely targeted phenomenon is not yet known in complete detail, enough is known to say that there has to be a “mechanism” - it doesn’t just happen by chance.

Max: {At this point Spetner quotes a number of speculative statements in the scientific literature, to the effect that B cell somatic hypermutation involves a “special mechanism.”
[LMS: MAX DID NOT REPRODUCE HERE THE REFERENCES I CITED. I WON’T REPEAT THEM HERE, BUT THEY CAN BE SEEN IN MY PREVIOUS POSTING. MAX CALLS MY CITED REFERENCES “SPECULATIVE", AND THAT MIGHT CREATE THE IMPRESSION THAT THEY ARE NOT REPRESENTATIVE OF RELIABLE SCIENTIFIC OPINION. THAT IMPRESSION IS FALSE. THE REFERENCES ARE FROM MAINSTREAM EXPERTS IN THE FIELD, ALL AGREEING THAT THERE IS A SPECIAL MECHANISM FOR HYPERMUTATIONS THAT IS NOT AVAILABLE TO GERMLINE MUTATIONS. THEY ARE “SPECULATIVE” ONLY IN THE SENSE THAT THESE PAPERS WERE SPECULATING ABOUT WHAT THE MECHANISM COULD BE. BUT THERE IS NO SPECULATION ABOUT THE EXISTENCE OF THE MECHANISM. ALL AGREED TO THAT, WHICH IS THE ONLY POINT I INTENDED, AND NEED, TO MAKE.]
The enzymes involved in somatic hypermutation in B cells remain unknown, so if Spetner is correct that “special enzymes” is supportable, he is correct only in the sense that the idea of “special enzymes” is supported by speculation in the literature. It is unsupported by any evidence, which is what I meant by “unsupportable.”
[LMS: MAX IS WRONG. THE EXISTENCE OF A MECHANISM IS SUPPORTED BY A LOT OF EVIDENCE, AS REFERRED TO IN THE PAPERS I CITED.]
To be fair I should note that an enzyme known as Activation Induced Deaminase (AID), reported after my initial comments to Spetner, has been shown necessary for somatic hypermutation to occur, but it is not clear whether this enzyme participates directly in the introduction of mutations. Indeed, since absence of AID also blocks isotype switch recombination, a phenomenon not obviously related to hypermutation, and also leads to enlarged germinal centers, it is possible that this enzyme is required for a step in B cell developmental maturation that triggers both hypermutation and switch recombination, and that the enzyme plays no direct role in mutating DNA. In any case, I never have questioned the idea that somatic hypermutation in B cells involves a “special mechanism"; the question of whether unique enzymes are directly involved in creating the mutations seems to me rather tangential to the present discussion, but it is accurate to say that this question has not been settled as of yet.}
[LMS: SINCE MAX HERE ACKNOWLEDGES THAT HYPERMUTATIONS MAKE USE OF A “SPECIAL MECHANISM” NOT AVAILABLE TO GERMLINE MUTATION, HE IS LOGICALLY OBLIGATED TO CONCEDE TO ME THAT HIS EXAMPLE OF HYPERMUTATIONS CREATING INFORMATION IN THE B-CELL GENOME BY RANDOM MUTATIONS AND SELECTION CANNOT BE USED TO DEMONSTRATE THE POSSIBILITY THAT RANDOM MUTATIONS IN THE GERMLINE CAN CREATE INFORMATION FOR EVOLUTION. THIS CONCESSION ON HIS PART SHOULD LOGICALLY END OUR DEBATE. THE PRECISE NATURE OF THE MECHANISM OF HYPERMUTATION IS NOT SETTLED, BUT THE EXISTENCE OF SUCH A MECHANISM IS A CONSENSUS AMONG THE EXPERTS. FURTHERMORE, THE EXISTENCE OF A SPECIAL MECHANISM WITH ITS SPECIAL ENZYMES THAT PERMITS THE HYPERMUTATIONS TO DO THEIR JOB IN THE IMMUNE SYSTEM IS NOT TANGENTIAL TO OUR DISCUSSION. THE MECHANISM, WHATEVER ITS NATURE, IS WHAT PERMITS HYPERMUTATIONS CREATE INFORMATION FOR THE IMMUNE SYSTEM. SUCH A MECHANISM IS NOT AVAILABLE FOR GERM LINE MUTATIONS TO MAKE EVOLUTION POSSIBLE, AND THEREFORE MAX’S EXAMPLE OF B-CELL HYPERMUTATION TO SHOW THAT INFORMATION CAN BE GENERATED IN EVOLUTION IS INVALID.]

Spetner: It thus seems quite clear to me that informed opinion in this field supports my contention and rejects your suggestion that “an alternative possibility is that the high rate of accumulation of mutations simply reflects selective inhibition of normal proof-reading mechanisms". Please let me know if you agree or disagree.

Max: {As indicated above, I disagree.}
[LMS: MAX IS, OF COURSE, WRONG IN DISAGREEING, AS EXPLAINED ABOVE]

Spetner: You ask, why does the existence of a special mechanism for the hypermutation in B cells preclude the example from being a model of mutations for NDT? The simple answer is that if you really want to suggest that mutations for NDT are capable of hypermutations as are the B cells, you have to show two things. First you have to show that such a highly complex system with its requisite enzymes actually exists in germ cells, where they can play a role in evolution. As far as I know, there is no such mechanism in germ cells. If you know of anything like this please let me know.

Max: {I have pointed out that the enzymatic mechanisms creating somatic mutations in B cells is not known. I have never claimed that it is the same mechanism as causes mutations in germ cells where they play a role in phylogenetic evolution, so I am not obligated to show what Spetner says I am.}
[LMS: THIS IS ANOTHER EXAMPLE OF DISTORTING THE ARGUMENT. IF MAX WANTS TO USE B-CELL HYPERMUTATIONS AS A DEMONSTRATION OF THE CAPABILITY OF GERMLINE MUTATIONS TO GENERATE THE INFORMATION REQUIRED FOR EVOLUTION (WHICH WAS THE MAIN PURPOSE OF HIS ESSAY) THEN HE IS OBLIGATED TO SHOW THAT GERMLINE MUTATION HAS THE SAME CAPABILITY AS B-CELL MUTATION. THAT IS NOT TO SAY THAT IT HAS THE SAME MECHANISM, BUT IT MUST HAVE A COMPARABLE MECHANISM. SINCE NO SUCH MECHANISM IS KNOWN FOR GERMLINE MUTATIONS, THE MAIN THESIS OF MAX’S ESSAY FALLS.]

Spetner: Furthermore, according to the evolutionary paradigm, you must account for the origin and development of such a mechanism in the germline, or at the very least, you must suggest how such a development could reasonably occur. You are obligated to do this because you hold that all characteristics of life have evolved through random variation and natural selection.

Max: {Here Spetner, like Behe, seems to demand that I provide an “origin and development” scenario that he knows he will be able to disparage as another “just-so story.”
[LMS: I HAVE ASKED HIM TO BRING AN ARGUMENT. I DIDN’T ASK FOR A “SCENARIO". HIS PROBLEM, BUT NOT MY PROBLEM, IS THAT A FICTIONAL SCENARIO IS THE ONLY KIND OF ARGUMENT HE HAS, AND IT’S NOT SCIENTIFIC.]
Furthermore, the question of how somatic hypermutation evolved is totally irrelevant to the question of whether it is a good model for the efficacy of random mutation and selection in promoting “increased fitness,” which is the subject of my Talk.Origins essay.}
[LMS: THIS IS AN OTHER DISTORTION OF MY STATEMENT ABOVE. I DID NOT ASK FOR A DESCRIPTION OF HOW HYPERMUTATION EVOLVED. I ASKED FOR ONE ABOUT HOW A COMPARABLE MECHANISM IN THE GERMLINE COULD EVOLVE. IT’S NOT IRRELEVANT BECAUSE IF ONE IS TRYING TO JUSTIFY NEO-DARWINIAN THEORY (NDT), THEN ONE WOULD BE ON SHAKY GROUND TO SUGGEST IT DEPENDS ON THE EXISTENCE OF A MECHANISM WHOSE OWN ORIGIN CANNOT BE ACCOUNTED FOR BY NDT]

Spetner: You are not entitled to postulate a mechanism that could not have evolved. Such a mechanism of germline mutation would have to produce accurately targeted mutations that could play a role in evolution. For such a system to develop by Neo-Darwinian evolution, a long series of evolutionary steps in ordinary evolution would have to play the role of a single step in the evolution of this mechanism, because selection here is based on successful evolution of the ordinary kind. Thus if a million generations are necessary for the evolution and perfection of a new phenotypic character, then a million times that, or a trillion generations, would be required for the evolution and perfection of this mechanism.

Max: {These are totally unsupported quantitative speculations.}
[LMS: MAX MUST THINK HE CAN DISPARAGE MY QUANTITATIVE ESTIMATES BY THIS STATEMENT. MY ARGUMENT ABOVE IS A TYPICAL KIND OF ARGUMENT USED IN ANY QUANTITATIVE SCIENCE TO ACHIEVE SOME ROUGH QUANTITATIVE ESTIMATES, USUALLY REFERRED TO AS “BACK-OF-THE-ENVELOPE” CALCULATIONS. IT PROVIDES AN ADEQUATE ESTIMATE FOR OUR DISCUSSION, EVEN THOUGH IT IS NOT PRECISE.]

Spetner: It seems to me that any selective pressure to raise the spontaneous mutation to benefit evolution would be overwhelmed by the selective pressure to keep the mutation rate low. Perhaps I’ll look into the mathematics of such a phenomenon and prepare a paper on it.

Max: I still fail to see how the particular enzymes involved have any bearing on the applicability of the model to Darwinian species evolution. Indeed, a variety of laboratory mechanisms for generating mutations in antibody genes (chemical mutagens, randomized oligonucleotides, etc.) all lead to pools of mutated antibody genes from which higher affinity proteins can be obtained, so the principle that random mutation and selection can lead to improved function appears to be independent of the mechanism of generating the mutations.

There is no logical reason why mutation and selection in species adaptation should be strictly dependent on the mechanism of mutation either; indeed, a variety of different mechanisms are known to contribute to varying extents under different conditions, including copying errors, radiation, chemical mutagens, slipped mispairing, deamination, etc.
[LMS: THE IMPORTANT FEATURE OF THE MECHANISM OF HYPERMUTATIONS IS ITS ABILITY (1) TO TURN THE MUTATIONS ON WHEN THEY ARE NEEDED, AND OFF AGAIN WHEN THEIR JOB IS DONE, AND (2) TO CONFINE THE MUTATIONS TO A RESTRICTED PORTION OF THE GENOME WHERE THEY CAN DO NO HARM, AND CAN ONLY DO GOOD. HYPERMUTATIONS HAVE A MECHANISM WITH THESE CHARACTERISTICS AND GERMLINE MUTATIONS DO NOT. SEE MY NEXT COMMENT. THE MECHANISMS MAX CITED HERE FOR GERMLINE MUTATIONS DO NOT ADDRESS THESE QUESTIONS AND IS THUS IRRELEVANT TO THE DISCUSSION.]

Spetner: You are missing my point. I am not focusing on the source of mutation as the distinguishing factor between the somatic mutations and germline mutations, but I am noting that the hypermutations do have a special mechanism that controls them whereas the germline mutations have no such mechanism available. The important features of the somatic mutations that are unavailable to germline mutations include some (unknown) trigger that turns them on at the right time and directs them to the right place on the genome. Without these controls, hypermutations would destroy the B cells.

Max: Clearly, the lower rate of mutation that occurs in the germline does not destroy genomes for the next generation. Is this rate high enough to generate enough mutations to account for adaptive phylogenetic evolution? This is a critical issue, and while I don’t have a quantitative answer, I don’t find Spetner’s negative answer to this question supported by convincing logic. He makes reference to his book as offering some arguments, but has not discussed this evidence in our correspondence.
[LMS: AGAIN, MAX DODGES THE POINT. MY POINT IS NOT ONE OF ABSOLUTE MUTATION RATES. HE SAYS WE DON’T KNOW IF THE NORMAL GERMLINE MUTATION RATE IS ENOUGH TO PRODUCE THE ADAPTIVE MUTATIONS. ALTHOUGH WE DON’T KNOW ANY HARD STATISTICS ON ADAPTIVE MUTATIONS, THERE IS GOOD EVIDENCE THAT THERE ARE NOT ENOUGH OF THEM OCCURRING AT RANDOM TO MAKE NDT WORK, AS I HAVE NOTED IN MY BOOK. BUT THAT IS NOT THE POINT IN THIS STAGE OF THE DIALOGUE. THE POINT HERE IS THAT MAX IS TRYING TO USE THE EXAMPLE OF THE GENOMIC INFORMATION GENERATED BY HYPERMUTATIONS IN THE IMMUNE SYSTEM TO DEMONSTRATE THAT GERMLINE MUTATIONS CAN LIKEWISE GENERATE THE INFORMATION NEEDED BY NDT. I HAVE SIMPLY POINTED OUT THAT HYPERMUTATIONS HAVE SOME ADVANTAGES THAT GERMLINE MUTATIONS DO NOT. AND THESE ADVANTAGES ARE PRECISELY WHAT MAKES HYPERMUTATIONS ADD INFORMATION TO THE GENOME. THAT POINT IS SUFFICIENT TO DISQUALIFY HIS EXAMPLE AND NULLIFY ITS FORCE.]

On the question of the frequency of mutation, in your last posting you included numerical models for B cell hypermutation and for species mutation, and arrived at conclusions by reasoning that I find illogical. You calculate the time required for one, two or three particular nucleotide changes to occur as though these calculations would be relevant to the times required for changes to occur in either B cell or species adaptations. Your reasoning seems to be predicated on the following logic. (1) By single nucleotide mutations, most triplet codons of amino acids can be mutated to code for only “5 or 6” different altered amino acids out of the 20 amino acid constituents of proteins. (2) This limitation would restrict the changes available by single nucleotide changes, such that certain adaptive changes would require two or three particular nucleotide mutations in order avoid getting “stuck on a low local Maximum of activity” in the “adaptive landscape.”
[LMS: MAX IS LEAVING OUT THE NEXT IMPORTANT STEPS IN THE LOGIC. THEY ARE: (3) THE RESTRICTION ON THE CHANGES THAT COULD BE MADE IN ONE MUTATION RESTRICT THE FIELD OF MUTATIONS HAVING SELECTIVE VALUE. (4) A TRIPLE MUTATION CAN REACH ANY ONE OF THE FULL FIELD OF 19 AMINO-ACID CHANGES. FOR THIS FIELD TO BE AVAILABLE TO A CHAIN OF THREE SINGLE MUTATIONS, EACH OF THEM WOULD HAVE TO HAVE POSITIVE SELECTIVE VALUE, A REQUIREMENT NOT NECESSARY FOR A TRIPLE MUTATION.]
Your reasoning seems flawed to me in part because you are considering the time to achieve a particular change rather than the time necessary to achieve an improvement in function. The illogic of this is similar to that of equating the odds of being dealt any hand that beats a “bust” hand with the odds of being dealt a particular poker hand that beats a “bust” hand.

Spetner: I am considering in my analysis what would be analogous to being dealt any hand that beats (i.e., that has a higher selective value than) a given hand.

Max: This seems to be contradicted by the following sentences Spetner wrote (quoted a few paragraphs back): “With a mutation rate of 1 per 1000 nucleotides per replication, there will be an average of 30 million changes in any particular nucleotide during a two-week period. The probability of getting two particular nucleotides to change is one per million replications. Thus in two weeks, there will be an average of 30 thousand changes in any two particular nucleotides. There will be an average of 30 changes in any three particular nucleotides.”
[LMS: I DO NOT SEE ANY CONTRADICTION.]
“Particular nucleotides” will be generated by mutation at a far lower frequency than adaptive mutations, as discussed below.}
[LMS: THE READER CAN SEE THAT MAX MUST HAVE MISUNDERSTOOD THE POINT I MADE. SEE MY COMMENTS ABOVE.]

The B-cell system selects for improvements in function and not for particular sequences. Furthermore, there is no reason to assume that the highest theoretical peaks on the adaptive landscape are ever achieved - either by the B cell system or Darwinian species evolution. Finally, there is no reason to assume that functional improvements cannot arise from the small subset of amino acid replacements accessible from single nucleotide changes.

Spetner: On the contrary, there is no justification in assuming that one can always obtain a selective advantage with one nucleotide substitution.

Max: I am not assuming a priori that one can ALWAYS obtain a selective advantage with one nucleotide substitution. But where this has been investigated by experimentally mutating immunoglobulin genes to introduce single mutations corresponding to changes observed in natural somatic hypermutation, it has been found that improvements in antibody affinity can be attributed to specific single nucleotide changes; so it is reasonable to assume that this potential is not so rare as to require the assumption that most increases in antibody affinity require multiple simultaneous mutations.

Indeed, if one looks at actual sequences of somatically mutated antibody genes (e.g. Cumano and Rajewsky EMBO J 5:2459, 1986, Figure 2), one finds plenty of single nucleotide mutations that change amino acids, and their presence at a frequency higher than would be predicted by random mutations suggests that most have been selected for on the basis of improved antigen binding. (In this study of nine somatically mutated antibodies, there were 23 amino acid changes caused by single mutations within a codon, and only 4 caused by double mutations; in addition there were only 6 silent single mutations, i.e., not causing amino acid changes.)

Spetner: This is all consistent with what I have written. I do not say that an adaptive mutation cannot be achieved by a single mutation. I only say that the target set of single mutations is smaller than that for single plus double mutations, which in turn is smaller than that for single plus double plus triple, etc. I do not claim that functional improvements cannot be achieved by single mutations, only that the choice is much wider for multiple mutations. For example, three single mutations are not the equivalent of a triple mutation. The first mutation will not remain in the population unless it has a selective advantage. I am sure you will agree that it is possible for a triple nucleotide substitution to have a selective advantage without any single one of them having an advantage. In fact, I would say that is the most likely case.

Max: If single nucleotide changes can lead to selection for improved function, then if one wants to calculate the time necessary to achieve the even greater improvement that might be achieved by three mutations, this time would be found not by a calculation like yours, based on the product of the odds for a single mutation, but rather by multiplying the time for a single adaptive nucleotide mutation by three. Suppose it would take one week for the first adaptive change. By the selection mechanism in the germinal center, the population of B cells would soon be overtaken by B cells with this first change, so that the time required for the second adaptive change would again be one week; and similarly the third change would require a third week to yield a protein of even greater affinity than could be achieved by one or two amino acid replacements.

Spetner: You are assuming that the single mutation will be selected. I say that is unlikely. The time to achieve a triple change would be equal to the sum of the times necessary to get a single one only if all those single changes had selective value, and that is too unlikely to bank on.

Max: What is the basis for your judgment that such selectable single nucleotide mutations are “too unlikely"?
[LMS: MAX IS THE ONE WHO IS TRYING TO SHOW THAT HIS EXAMPLE OF B-CELL HYPERMUTATIONS DEMONSTRATES THE ABILITY OF GERMLINE MUTATIONS TO ACHIEVE DARWINIAN EVOLUTION. HIS ARGUMENT IS BASED ON THE TACIT ASSUMPTION THAT GERMLINE MUTATIONS CAN DO ANYTHING THE SOMATIC HYPERMUTATIONS CAN DO. I HAVE NOTED THAT HYPERMUTATIONS HAVE ADVANTAGES THAT GERMLINE MUTATIONS DO NOT HAVE. WITHOUT THESE ADVANTAGES, B CELLS CANNOT GENERATE THE INFORMATION THE ANTIBODIES NEED. ONE OF THESE ADVANTAGES IS THE ABILITY TO GENERATE A LARGE NUMBER OF DOUBLE AND TRIPLE MUTATIONS. IS MAX HERE TRYING TO ARGUE THAT THREE SINGLE MUTATIONS AT THE LOW RATE OF THE GERMLINE MUTATIONS ARE AS LIKELY TO PRODUCE AN ADAPTIVE IMPROVEMENT AS A TRIPLE MUTATION AT THE HIGH RATE IN THE B CELL? HE CANNOT SHOW THAT. IF THAT IS HIS THRUST, HE IS WRONG. CLEARLY THE FORMER IS LESS LIKELY TO PRODUCE ADAPTIVITY IN ALL OF THREE SUCCESSIVE MUTATIONS THAN THE LATTER IS TO PRODUCE IN ONLY ONE MUTATION. DOES HIS ARGUMENT REST ON CHALLENGING ME TO SHOW JUST HOW “UNLIKELY” ARE THREE ADAPTIVE MUTATIONS IN A ROW? IF SO, IT IS A POOR ARGUMENT.]

A similar argument would apply to estimates for adaptive mutations in bacteria. Because of the flawed assumptions built into your approach it seems to me that your calculations grossly overstate the time required for evolving adaptive changes by random mutation and selection.

Spetner: My assumptions are not flawed. You just don’t understand them. Read again what I wrote above and see if you don’t agree with me.

Max: {I have reread what Spetner wrote. He agrees that single nucleotide changes can lead to selectable advantages (even if the available codons are restricted so the scope of amino acid changes is less than would be possible with multiple simultaneous mutations). Such selectable single mutations could spread throughout the population, to be followed by successive additional selectable point mutations. By this model, three selectable point mutations could occur in a time frame measured by three times the time for a single mutation, rather than taking the time necessary for three simultaneous mutations as Spetner has calculated. We both agree that simultaneous double and triple mutations have greater scope for amino acid replacement, but are very rare. I honestly do not understand the basis for our disagreement here, but perhaps Spetner will clarify why he considers evolution by successive single selectable point mutations “too unlikely” even though he agrees that single point mutations leading to selectable advantage can occur.}
[LMS: I AM DISAPPOINTED THAT MAX DOES NOT UNDERSTAND MY POINT. IT IS NOT THAT I NECESSARILY CLAIM HERE THAT SUCCESSIVE POINT MUTATIONS ARE “TOO UNLIKELY", ALTHOUGH THEY ARE AND THERE IS EVIDENCE FOR IT. BUT THE POINT HERE IS THE AVAILABILITY TO B CELLS OF A HIGHER RATE OF MULTIPLE MUTATIONS PROVIDES THEM WITH GREATER SCOPE FOR ACHIEVING ADAPTIVE IMPROVEMENTS THAN ARE AVAILABLE TO GERMLINE MUTATIONS. THE POINT THAT MAX SEEMS TO MISS HERE IS THAT A TRIPLE MUTATION CAN BE ADAPTIVE EVEN THOUGH EACH NUCLEOTIDE CHANGE INDIVIDUALLY IS NOT. THESE MUTATIONS ARE AVAILABLE TO HYPERMUTATION, BUT NOT TO GERMLINE MUTATION. UNLESS EACH INDIVIDUAL CHANGE IS ADAPTIVE, A TRIPLE CHANGE CAN BE ACHIEVED BY THREE SINGLE MUTATIONS ONLY IF THE THREE OCCUR BY CHANCE WITHOUT SELECTION. THIS IS WHY SUCH AN EVENT HAS A PROBABILITY OF THE CUBE OF THAT OF A SINGLE MUTATION, AND THAT IS WHY THE TIME TO ACHIEVE SUCH AN UNLIKELY EVENT IS SO ENORMOUS. I HOPE I HAVE NOW MADE IT SUFFICIENTLY CLEAR FOR MAX TO SEE MY POINT.]



The Role of Gene Duplication
Max: In his first response to my essay, Spetner was critical of the role he thought I claimed for gene duplication in evolution. When he understood that he had originally misread the essay, he had no quarrel with this aspect. Here is the short discussion of this point.

Spetner: Max cited gene duplication as an example of a mutation that increases information. A favorite scenario for molecular evolution is that a gene gets duplicated and then gradually mutates to become something useful that did not exist before. Such a proposed scenario does not constitute evidence for evolution, it proves nothing, and indeed such a scenario itself requires proof. I do not, of course, mean to say that one has to prove that genes can be duplicated. That is well known. But gene duplication alone does not constitute an increase of information in the biocosm or even in the genome of the organism itself. Two copies of today’s newspaper contain no more information than one copy. Gene duplication, in any case, cannot play the role of the mutations that could produce the grand sweep of evolution.

Gene duplication alone cannot add information to the genome. The purpose of the gene duplication in the above scenario is simply to provide raw material from which a new gene could evolve without having to give up any functions the organism already had. New information would then supposedly be built up by point mutations and natural selection. And this is precisely the process I discussed in my book and about which I said that all known examples of these mutations lose information rather than gain it. Note that I did not say that it is impossible in principle for random mutations to add information to the genome. But it just turns out that that is what has been found.

Max: You state: “Max cited gene duplication as an example of a mutation that increases information.” On the contrary, I believe that I was careful to avoid saying that gene duplication alone increases information. I do not believe such a statement is correct and agree fully with your statement that “Two copies of today’s newspaper contain no more information than one copy.". Please let me know exactly what words in my essay (or in my letter to you) suggested that I believed duplication by itself increases information, and I will try to change the phraseology so as to reduce the likelihood that other readers will misconstrue my meaning.

On the other hand - and this is the major point of all that follows - I do believe that gene duplication is a critical component of what I will call the evolutionary triad: namely gene duplication, random mutation and selection. To illustrate the role of gene duplication in this triad, let’s extend your own newspaper analogy. Suppose we have a copy of the early edition of today’s newspaper and a copy of the final edition. In the final edition several paragraphs of certain articles have been altered to include late breaking events. Each article has remained the same length in the two editions because certain less important information in each article was deleted to make room for the late breaking news. Now it is clear that having these two copies of today’s newspaper does give us more information than either copy alone, since the early edition lacks the late breaking events and the late edition lacks the information that was deleted to make room for the late breaking news.

You seem to allude to this possibility in evolution when you suggest that in the evolutionary model, after gene duplication “[n]ew information would then supposedly be built up by point mutations and natural selection."

Spetner: You deny suggesting that gene duplication alone adds information. I accept your denial and I apologize for incorrectly attributing that view to you. What led me to believe that you did suggest this is the statement in point 1 of your letter to me, saying. “Gene duplications occur, and there is no reason to postulate supernatural processes to account for them. ...Does the ID argument about impossibility of naturalistic information increase include an assumption that naturalistic gene duplications cannot occur?” This is what led me to think that you were suggesting gene duplications as a method of adding information.
[LMS: IN MY FIRST POSTING OF OUR DISCUSSION, I LEFT OUT THIS PART OF THE DISCUSSION, BECAUSE IT WAS MY MISUNDERSTANDING OF WHAT HE WROTE. MAX WAS UPSET ABOUT MY LEAVING THAT OUT. IF HE WANTS TO ENJOY A SMALL TRIUMPH IN NOTING THAT I MISUNDERSTOOD HIM, THEN I AM MORE THAN HAPPY TO LET HIM DO SO.]


Interpretations of the Word “Evolution”
Max: Spetner tried to clarify different interpretations of “evolution” that frequently cause people confusion if one meaning is intended but another is meant. (For the text of Spetner’s comments on this issue, I have taken his True.Origins posting, which begins with this discussion.) I countered that there were several more identifiable meanings of evolution, and that Spetner seemed to be avoiding the burden of having to defend his position by being intentionally vague about where he stood. My response to this point has not been answered.
[LMS: I FRANKLY DO NOT SEE WHAT MAX WANTS TO ARGUE ABOUT HERE. IT SEEMS TO ME THAT HE IS NIT PICKING. MY PURPOSE IN NOTING THE TWO EXTREME USES OF THE WORD “EVOLUTION” WAS SIMPLY TO CLARIFY A CONFUSION POPULAR WITH EVOLUTIONISTS, AS CAN BE SEEN FROM MY COMMENTS BELOW. THERE IS NO NEED FOR ME TO CONSIDER ALL OTHER USES OF THE WORD “EVOLUTION". THE TWO EXTREMES ARE SUFFICIENT FOR MY PURPOSE. I REALLY DON’T KNOW WHAT IS BOTHERING MAX HERE. I DON’T KNOW WHY HE THINKS I MUST WRITE A TREATISE ON ALL POSSIBLE USES OF THE TERM EVOLUTION.]

Spetner: At the outset, I shall establish an important and necessary guideline in this discussion of evolution. The word evolution is generally used in at least two different senses, and the distinction between them is important. On the one hand, the word evolution is used to denote the descent of all life from a putative single primitive source. It is the grand sweep of evolution that is supposed to have led from a simple beginning, something perhaps simpler than a bacterium, to all organisms living today, including humans. This descent is supposed to have occurred through purely natural means. Neo-Darwinian theory (NDT), which is the prevailing theory of evolution, teaches that this development occurred through random heritable variations in the organisms followed by natural selection. I shall denote the word evolution used in this sense as Evolution A. When evolution is discussed for popular consumption, it is most often Evolution A.

The second sense in which the word evolution is used is to denote any kind of change of a population. The change can sometimes occur in response to environmental pressure (artificial or natural selection), and sometimes it can just be random (genetic drift). I shall denote the word used in this second sense as Evolution B. Evolution B has been observed. Evolution A is an inference, but is not observable. The distinction between these two meanings of evolution parallels the distinction between macroevolution and microevolution, but the two pairs of terms are not identical. Evolution A is certainly what is called macroevolution, but what is called macroevolution is not identical with Evolution A. In any case, I prefer to use the A and B to avoid having to carry whatever baggage might go with the macro/micro distinction.

The distinction between these two meanings of evolution is often ignored by the defenders of Neo-Darwinian evolution. But the distinction is critical. The claim is made for Evolution A, but the proof offered is often limited to Evolution B. The implication is that the observation of Evolution B is a substantiation of Evolution A. But this is not so. Since Evolution A is not an observable, it can only be substantiated by circumstantial evidence. This circumstantial evidence is principally the fossil record, amino-acid-sequence comparisons, and comparative anatomy. Circumstantial evidence must be accompanied by a theory of how it relates to what is to be proved. NDT is generally accepted to be that theory. The strength of the circumstantial evidence for Evolution A can therefore be no better than the strength of NDT.

Max: I can’t tell exactly what you accept in your distinction between Evolution A and Evolution B. I actually think that there are finer distinctions between the various meanings of evolution than encompassed by your A vs B.
[LMS: YES, FINER DISTINCTIONS CAN BE MADE, BUT THEY ARE IRRELEVANT TO THE POINT I WAS TRYING TO MAKE.]
I would distinguish several more possible meanings:

Living forms are different now from what they were in the past. This seems to be well documented by fossil evidence. This slow change is sometimes referred to as evolution.

Random mutation and selection can lead to “microevolution,” i.e., small changes in gene frequencies that follow an environmental shift and leave a population on average more fit to cope with the new environment. I think you accept this, since I think it corresponds to what you mean by Evolution B. I certainly accept it.

Various different modern species share a common ancestry. Since the time of the common ancestor, the divergence into the various modern species has involved changes much greater than microevolution. This is the idea of “common descent.” I am really not sure whether you accept this notion. I think there is excellent evidence for common descent of some groups of species, as outlined in my essay. If you do not accept common descent, at least for the cases I cite in my essay, I would be interested in hearing what alternative interpretations you can offer for the observations I cite in that essay. [I do not have that essay handy to check what you say. If you want my critique of that essay, ask me, and if I find the time I shall write one. Meanwhile, let’s stick to my critique of your fitness essay.]

All of the nucleotide discrepancies between modern species, or between a modern species and its ancestral species, arose as a result of random mutation (including gene duplications, insertions and deletions caused by naturalistic processes) and natural selection, without the intervention of an “intelligent designer.” I do not believe that there is any evidence for the preceding statement, and indicate as much in my essay. Nor do I believe that an “intelligent designer” can be ruled out as an explanation for hurricanes, disease, or stock market fluctuations. However, I have never seen a convincing argument that an intelligent designer must be hypothesized in order to explain any of these kinds of events, or to explain species change through time.
[LMS: MAX IS THE ONE WHO IS BRINGING IN AN “INTELLIGENT DESIGNER.", NOT ME. I DID NOT BRING IN THE NOTION OF AN “INTELLIGENT DESIGNER,” IN MY CRITIQUE OF MAX’S ESSAY, AND I DON’T THINK IT BELONGS IN THIS DISCUSSION. MY POINT IS THAT MAX’S ESSAY DOES NOT LEND ANY SUPPORT TO NEO-DARWINIAN THEORY. THE GRATUITOUS INTRODUCTION OF AN INTELLIGENT-DESIGNER THEORY DOES NOT HELP HIS DEFENSE OF HIS ESSAY.]
The origin of life came about through exclusively naturalistic processes operating on prebiotic chemicals, which evolved into replicating life forms. We have almost no scientific evidence about the origin of life and so there is no scientific evidence to support a purely naturalistic origin of life. I feel the same way about this meaning of “evolution” as I do about #4.
In my judgment, there is good scientific evidence for #1, #2 and #3. From your dismissal of evidence for what you call Evolution A, I can’t tell what you believe about #3. On #4 and #5 I assume we are in agreement on the insufficiency of scientific evidence to support a purely naturalistic mechanism, but we obviously differ on whether arguments such as yours are sufficient to rule out a purely naturalistic mechanism. I think that it would be an improvement in the dialogue/ document to clarify both of our opinions on these finer distinctions. Incidentally, I am not clear exactly on the difference you see between Evolution A and macroevolution.
[LMS: WHAT I CALLED EVOLUTION A IS A SUBSET OF WHAT IS CALLED MACROEVOLUTION. NOT ALL MACROEVOLUTION QUALIFIES AS EVOLUTION A. BUT LET’S LEAVE THAT. I INTRODUCED THE TERM EVOLUTION A TO MAKE THINGS CLEARER. IF IT’S ONLY MAKING THEM MORE COMPLICATED, THEN LET’S DROP IT AND SUBSTITUTE FOR IT “THE GRAND SWEEP OF EVOLUTION FROM SOME PUTATIVE PRIMITIVE ORGANISM TO ALL THE LIFE OF TODAY.” SUBSTITUTE FOR EVOLUTION B “THE SMALL CHANGE IN POPULATIONS THAT ARE ACTUALLY OBSERVED.]
I don’t know what version of creation you accept, but it seems to me that even if the supernatural played a role in past events, those past events leave traces. By refusing to specify an alternative scenario that you consider more believable than evolution, you hide behind vagueness in order to avoid having to defend potential contradictions between your scenario and the traces from the past that point in a different direction.
[LMS: HERE MAX IS TRYING TO DRAW THE DISCUSSION OFF COURSE. THE POINT IS THAT HIS ESSAY OFFERS NO SUPPORT FOR NDT. I DID NOT INTRODUCE CREATION OR THEOLOGY INTO MY CRITIQUE OF HIS ESSAY BECAUSE THEY HAVE NO PLACE IN A SCIENTIFIC DISCUSSION. THEOLOGY IS NOT WITHIN HIS EXPERTISE, NOR DO I CLAIM IT TO BE WITHIN MINE. THIS STARTED OUT AS A SCIENTIFIC DISCUSSION AND I THINK IT SHOULD REMAIN SO.]


Information Content of Proteins
Max: The central theme of Spetner’s position, and the focus of his book, is that information theory can shed light on the likelihood of the evolutionary scenario envisioned by the NDT. In particular, he believes that observed mutations do not provide increases in information that would be required by the NDT to produce what he calls Evolution A. Spetner included several graphic Figures in his discussion of ribitol dehydrogenase (section 6.1 below) which I have not been able to reproduce in the text below. I feel that the essence of his arguments is comprehensible even without the Figures, but I will attempt to insert them in the future.
[LMS: I HAVE REPRODUCED THAT SECTION HERE WITH THE FIGURES AND EQUATIONS IN PLACE OF HIS]

Spetner: Mutations have indeed been observed that confer an adaptive advantage, but that alone does not qualify them to serve as components of a series of Neo-Darwinian steps. In my critique, I included for pedagogical purposes the following short explanation of information and its measurement:

I shall emphasize again: There is no theorem requiring mutations to lose information. I can easily imagine mutations that gain information. The simplest example is what is known as a back mutation. A back mutation undoes the effect of a previous mutation. If the change of a single base pair in the genome were to change to another and lose information, then a subsequent mutation back to the previous condition would regain the lost information. Since these mutations are known to occur, they form a counterexample to any conjecture that random mutations must lose information. An important point I make in my book, and which I emphasize here, is that no mutations observed so far qualify as examples of the kind of mutations required for Evolution A.

In discussing mutations in my book I noted in each case in which the molecular change was known, that it could not serve as a prototype for the mutations required by NDT. In all the cases I discussed, it was the loss of information that prevented the mutation from serving as a prototype of those required by NDT. The back mutation likewise cannot serve as a prototype of the NDT-required mutations. Here, the reason is not that it loses information - it actually gains information. But the information it gains is already in the biocosm and the mutation contributes nothing new. Evolution cannot be accounted for if the only information gain was by back mutations.

In my book, I did not quantify the information gain or loss in a mutation. I didn’t do it mainly because I was reluctant to introduce equations and scare off the average reader. And anyway, I thought it rather obvious that a mutation that destroys the functionality of a gene (such as a repressor gene) is a loss of information. I also thought it rather obvious that a mutation that reduces the specificity of an enzyme is also a loss of information. But I shall take this opportunity to quantify the information difference before and after mutation in an important special case, which I described in my book.

The information content of the genome is difficult to evaluate with any precision. Fortunately, for my purposes, I need only consider the change in the information in an enzyme caused by a mutation. The information content of an enzyme is the sum of many parts, among which are:

Level of catalytic activity
Specificity with respect to the substrate
Strength of binding to cell structure
Specificity of binding to cell structure
Specificity of the amino-acid sequence devoted to specifying the enzyme for degradation
These are all difficult to evaluate, but the easiest to get a handle on is the information in the substrate specificity.

To estimate the information in an enzyme I shall assume that the information content of the enzyme itself is at least the maximum information gained in transforming the substrate distribution into the product distribution. (I think this assumption is reasonable, but to be rigorous it should really be proved.) We can think of the substrate specificity of the enzyme as a kind of filter. The entropy of the ensemble of substances separated after filtration is less than the entropy of the original ensemble of the mixture. We can therefore say that the filtration process results in an information gain equal to the decrease in entropy. Let’s imagine a uniform distribution of substrates presented to many copies of an enzyme. I choose a uniform distribution of substrates because that will permit the enzyme to express its maximum information gain. The substrates considered here are restricted to a set of similar molecules on which the enzyme has the same metabolic effect. This restriction not only simplifies our exercise but it applies to the case I discussed in my book.

The products of a substrate on which the enzyme has a higher activity will be more numerous than those of a substrate on which the enzyme has a lower activity. Because of the filtering, the distribution of concentrations of products will have a lower entropy than that of substrates. Note that we are neglecting whatever entropy change stems from the chemical changes of the substrates into products, and we are focusing on the entropy change reflected in the distributions of the products of the substrates acted upon by the enzyme.

The entropy of an ensemble of n elements with fractional concentrations f1,…,fn is given by (1)
and if the base of the logarithm is 2, the units of entropy are bits.

As a first illustration of this formula let us take the extreme case where there are n possible substrates, and the enzyme has a nonzero activity on only one of them. This is perfect filtering. The input entropy for a uniform distribution of n elements is, from (1), given by (2)
since the fi's are each 1/n. The entropy of the output is zero, (3)
because all the concentrations except one are zero, and the concentration of that one is 1. Then the decrease in entropy brought about by the selectivity of the enzyme is then the difference between (2) and (3), or
Another example is the other extreme case in which the enzyme does not discriminate at all among the n substrates. In this case the input and output entropies are the same, namely (4)
Therefore, the information gain, which is the difference between HO and HI, in this case is zero, (5)


We normalize the activities of the enzyme on the various substrates and these normalized activities will then be the fractional concentrations of the products. This normalization will eliminate from our consideration the effect of the absolute activity level on the information content, leaving us with only the effect of the selectivity.

Although these simplifications prevent us from calculating the total entropy decrease achieved by action of the enzyme, we are able to calculate the entropy change due to enzyme specificity alone.



The Dangers of Conclusion Jumping
Spetner: As a final example let me take part of a series of experiments I discussed in my book, which demonstrate the dangers of conclusion jumping. This subject bears emphasis because evolutionists from Darwin on have been guilty of jumping to unwarranted conclusions from inadequate data. I shall here take only a portion of the discussion in my book, namely, what I took from a paper by Burleigh et al. (1974, Biochem. J. 143: 341) to illustrate my point.


Ribitol is a naturally occurring sugar that some soil bacteria can normally metabolize, and ribitol dehydrogenase is the enzyme that catalyzes the first step in its metabolism. Xylitol is a sugar very similar in structure to ribitol, but does not occur in nature. Bacteria cannot normally live on xylitol, but when a large population of them were cultured on only xylitol, mutants appeared that were able to metabolize it. The wild-type enzyme was found to have a small activity on xylitol, but not large enough for the bacteria to live on xylitol alone. The mutant enzyme had an activity large enough to permit the bacterium to live on xylitol alone.

Fig. 1 shows the activity of the wild-type enzyme and the mutant enzyme on both ribitol and xylitol. Note that the mutant enzyme has a lower activity on ribitol and a higher activity on xylitol than does the wild-type enzyme. An evolutionist would be tempted to see here the beginning of a trend. He might be inclined to jump to the conclusion that with a series of many mutations of this kind, one after another, evolution could produce an enzyme that would have a high activity on xylitol and a low, or zero, activity on ribitol. Now wouldn’t that be a useful thing for a bacterium that had only xylitol available and no ribitol? Such a series would produce the kind of evolutionary change NDT calls for. It would be an example of the kind of series that would support NDT. The series would have to consist of mutations that would, step by step, lower the activity of the enzyme on the first substrate while increasing it on the second.


But Fig. 1 is misleading in this regard because it provides only a restricted view of the story. Burleigh and his colleagues also measured the activities of the two enzymes on another similar sugar, L-arabitol, and the results of these measurements are shown in Fig. 2. With the additional data on L-arabitol, a different picture emerges. No longer do we see the mutation just swinging the activity away from ribitol and toward xylitol. We see instead a general lowering of the selectivity of the enzyme over the set of substrates. The activity profiles in Fig. 2 show that the wild-type enzyme is more selective than is the mutant enzyme.

In Fig. 1 alone, there appears to be a trend evolving an enzyme with a high activity on xylitol and a low activity on ribitol. But Fig. 2 shows that such an extrapolation is unwarranted. It shows instead a much different trend. An extrapolation of the trend that appears in Fig. 2 would indicate that a series of such mutations could result in an enzyme that had no selectivity at all, but exhibited the same low activity on a wide set of substrates.

The point to be made from this example is that conclusion jumping from the observation of an apparent trend is a risky business. From a little data, the mutation appears to add information to the enzyme. From a little more data, the mutation appears to be degrading the enzyme’s specificity and losing information. Just as we calculated information in the two special cases above, we can calculate the information in the enzyme acting on a uniform mixture of the three substrates for both the wild type and the mutant enzyme. Using the measured activity values reported by Burleigh et al. we find the information in the specificities of the two enzymes to be 0.74 and 0.38 bits respectively. The information in the wild-type enzyme then turns out to be about twice that of the mutant.

The evolutionist community, from Darwin to today, has based its major claims on unwarranted conclusion jumping. Darwin saw that pigeon breeders could achieve a wide variety of forms in their pigeons by selection, and he assumed that the reach of selection was unlimited. Evolutionists, who have seen crops and farm animals bred to have many commercially desirable features, have jumped to the conclusion that natural selection, in the course of millions of years, could achieve many-fold greater adaptive changes than artificial selection has achieved in only tens of years. I have shown in my book that such extrapolations are ill founded because breeding experiments, such as those giving wheat greater protein content or vegetables greater size, result from mutations that disable repressor genes. The conclusions jumped to were false because they were based on data that could not be extrapolated to long sequences. One cannot gain information from a long sequence of steps that all lose information. As I noted in my book, that would be like the merchant who lost a little money on each sale, but thought he could make it up on volume.


Antibiotic Resistance as an Example of Evolution
Spetner: Continuing his effort to show the evolutionary efficacy of beneficial mutations, Max presented in his essay the acquisition of antibiotic resistance by microorganisms as an example of evolution. He said one can “demonstrate a beneficial mutation … with laboratory organisms that multiply rapidly, and indeed such experiments have shown that rare beneficial mutations can occur. For instance, from a single bacterium one can grow a population in the presence of an antibiotic, and demonstrate that organisms surviving this culture have mutations in genes that confer antibiotic resistance.” Such an experiment shows that “de novo beneficial mutations” can arise.

My response to this is that I have shown in my book that mutations leading to antibiotic resistance fail the test of representing the mutations necessary for evolution. I summarize that argument here. All antibiotics are derived from microorganisms. Recall the story of the serendipitous discovery of penicillin by Alexander Fleming in 1928, when he noticed that his plate of Staphylococcus bacteria was clear in the vicinity of a bread-mold contaminant. The mold was found to produce something that could lyse and kill the bacteria. That something was a molecule later named penicillin. Afterwards, other antibiotics were found to be produced by other microorganisms, such as soil bacteria. Soil has long been recognized in folk medicine as a cure for infections.

The antibiotics produced by these microorganisms serve them as a defense against attack by other microorganisms. Some microorganisms are endowed with genes that grant resistance to these antibiotics. This resistance can take the form of degrading the antibiotic molecule or of ejecting it from the cell. Unfortunately for human health care, the organisms having these genes can transfer them to other bacteria making them resistant as well. Although the resistance mechanisms are specific to a particular antibiotic, most pathogenic bacteria have, to our misfortune, succeeded in accumulating several sets of genes granting them resistance to a variety of antibiotics.

The acquisition of antibiotic resistance in this manner qualifies as evolution only in the sense that it is an adaptive hereditary change. It is an example only of Evolution B. It is not the type of evolution that can make a baboon out of a bacterium. The genetic change is not the kind that can serve as a prototype for the mutations needed to account for Evolution A. The genetic changes that could illustrate the theory must not only add information to the bacterium’s genome, they must add new information to the biocosm. The horizontal transfer of genes only spreads around genes that are already in some species.

It turns out, however, that a microorganism can sometimes acquire resistance to an antibiotic through a random substitution of a single nucleotide, and this is the kind of example Max presented. Streptomycin, which was discovered by Selman Waksman and Albert Schatz and first reported in 1944, is an antibiotic against which bacteria can acquire resistance in this way. But although the mutation they undergo in the process is beneficial to the microorganism in the presence of streptomycin, it cannot serve as a prototype for the kind of mutations needed by NDT. The type of mutation that grants resistance to streptomycin is manifest in the ribosome and degrades its molecular match with the antibiotic molecule. This change in the surface of the microorganism’s ribosome prevents the streptomycin molecule from attaching and carrying out its antibiotic function. It turns out that this degradation is a loss of specificity and therefore a loss of information. The main point is that Evolution A cannot be achieved by mutations of this sort, no matter how many of them there are. Evolution cannot be built by accumulating mutations that only degrade specificity.

In the final paragraph of my original critique, I said the following:

The mutations needed for macroevolution have never been observed. No random mutations that could represent the mutations required by NDT that have been examined on the molecular level have added any information. The question I address is: Are the mutations that have been observed the kind the theory needs for support? The answer turns out to be NO! Many have lost information. To support NDT one would have to show many examples of random mutations that add information. Unless the aggregate results of the genetic experiments performed until now is a grossly biased sample, we can safely dismiss Neo-Darwinian theory as an explanation of how life developed from a single simple source.


Dr. Lee Spetner's continued exchange with Dr. Edward E. Max