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University indoctrination program launched, but one professor sees the light

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Biologist Stanely Salthe at Binghamton University is at the top of the Discovery Institute’s Dissent from Darwin honor roll.

Stanley Salthe

I am a critic of Darwinian evolutionary theory — which was my own erstwhile field of specialization in biology. My opposition is fundamentally to its sole reliance on competition as an explanatory principle (in a background of chance). Aside from being a bit thin in the face of complex systems, it has the disadvantage, in the mythological context of explaining where we come from, of reducing all evolution to the effects of competition. …
….
Being materially empty, it appears capable of explaining almost anything, and so we need to be cautious about its use. Is it a Borgesian cognitive poison?

The irony is this “cognitive poison” is being indoctrinated into young minds at his school:

Evolution for Everyone: How to Increase Acceptance of, Interest in, and Knowledge about Evolution

Evolution is famously controversial, despite being as well established as any scientific theory. Most people are familiar with the dismal statistics, showing how a large fraction of Americans at all educational levels do not accept the theory of evolution [1], how efforts to teach evolution often fail to have an impact [2], and how constant vigilance is required to keep evolution in the public school curriculum [3]. Even worse, most people who do accept the theory of evolution don’t relate it to matters of importance in their own lives. There appear to be two walls of resistance, one denying the theory altogether and the other denying its relevance to human affairs.

This essay reports a success story, showing how both walls of resistance can be surmounted by a single college course, and even more, by a university-wide program. It is based on a campus-wide evolutionary studies program called EvoS (http://bingweb.binghamton.edu/~evos/), initiated at Binghamton University in 2002, which currently includes over 50 faculty members representing 15 departments. Enthusiasm at all levels, from freshmen students to senior administrators, makes EvoS a potential model for evolution education that can be duplicated; the basic ingredients are present at most other institutions, from small colleges to major universities.

Students who indicate exceptional interest are referred to books that are both authoritative and accessible, such as Daniel Dennett’s Darwin’s Dangerous Idea [10–15].

What theory of physics or chemistry requires an indoctrination program to maintain it’s acceptance? Do theories of gravity and electricity require an indoctrination campaign like this to get students to accept it?

Thankfully, while students are indoctrinated at Binghamton, brilliant minds, like Salthe’s remain open.

Stanley Salthe

The following is a wonderful essay by Salthe. I don’t get the feeling however, that this essay will be studied by most students who sign up for university indoctrination into Darwinian evolution. Salthe makes a devastating critique of the idea he once espoused and studied diligently:

Analysis and critique of the concept of Natural Selection (and of the Darwinian theory of evolution) in respect to its suitability as part of Modernism’s origination myth, as well as of its ability to explain organic evolution.

(thanks to Teleologist for alerting me to the developments at Binghamton)

Comments
[...] Stanley Salthe, a known dissenter from Darwin, trashed by Darwinists, appears in the film. [...]Uncommon Descent | Hindu-sponsored ID book team now offers documentaries as well
May 28, 2012
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[...] Stanley Salthe, a known dissenter from Darwin, trashed by Darwinists, appears in the film. [...]God's iPod - Uncommon Descent - Intelligent Design
May 23, 2012
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[...] And another signatory of the Discovery Institute’s Dissent from Darwin list, Stanley Salthe, pointed out: The internal contradiction in its [Darwinism’s] major theoretical cornerstone — Fisher’s fundamental theorem. As mentioned above, Fisher’s theorem has it that population variance in fitness is exchanged over the generations for population fitness increase — that is, for adaptedness. A corollary would be that traits having been subjected to heavy selection pressures, because of their importance in the lives of the organisms, should be less variable than less important traits. ….note that when asked which traits are most likely to be able to evolve, evolutionary biologists, again citing Fisher’s theorem, will reply, “those that have more variability in fitness”. That is to say, traits that have been most important in the lives of organisms up to this moment will be least likely to be able to evolve further! … So Fisher’s theorem is “schizoid” when one compares its postures facing the future or the past. [...]An eloquent but bogus non-review by Dawkins | Uncommon Descent
July 3, 2007
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Regarding (not necessarily the studies you cited) my deep concern here is the selection inference is often derived though the degree of similarity and amount of material “conserved”. This leads to circular reasoning (ie. high similarity implies natural selection, natural selection proven because of high similarity).
I don't think you're characterising the situation correctly: the reason we can infer selection is that we can compare the patterns we see to the patterns we would expect under neutrality.
In fact, I expect high degrees of deeply conservered regions that don’t have immediate function, and which will be in violation of neutral theory. We have the situation where the neutralist and selectionists views are finding fatal flaws in each other’s theories. If then the two theories have mutually destroyed each other, IDers argue that leaves an opening for them.
I don't think the theories won't mutually destroy each other: what I expect to happen is that we'll settle down to a position where we assess the relative strengths of the different forces acting on the genome. Different parts of the genome will be subject to differing amounts of selection, drift, mutation etc. and the task will be to assess the strengths on a case by case basis. This is more or less what's happening in evolutionary ecology now, and I don't see why it should be any different in evolutionary genomics. Thanks for being a polite discussant! BobBob OH
June 25, 2006
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With the advent of genomics, there’s a lot of data being produced, and we’re still trying to synthesise the results. But there is certainly evidence for selection at several genes.

I would expect there to be some selection. That has not been in question.

Regarding (not necessarily the studies you cited) my deep concern here is the selection inference is often derived though the degree of similarity and amount of material "conserved". This leads to circular reasoning (ie. high similarity implies natural selection, natural selection proven because of high similarity).

In fact, I expect high degrees of deeply conservered regions that don't have immediate function, and which will be in violation of neutral theory. We have the situation where the neutralist and selectionists views are finding fatal flaws in each other's theories. If then the two theories have mutually destroyed each other, IDers argue that leaves an opening for them.

In any case, thank you for your technical comments!

Salvador

scordova
June 24, 2006
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Hartl & Clark is an excellent undergraduate text. For the more mathematically inclined go for Crow & Kimura (1970) or Gale (1990), both great introductions to population genetic modelling. Big parts of the second volume of Lynch & Walsh can be downloaded from the authors' website.Raevmo
June 24, 2006
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IDers argue that natural selection is not the sole directive to evolution,...

Good. It's nice to know that we all agree. In evolutionary biology, we recognise that there are many factors that influence evolution: drift, selection, demographics, mutation, environmental variation etc. One of the tasks in modern evolutionary biology is to tease apart the different factors and see, for example, whether the observed divergence between populations is due to selection, or if drift would be enough.

I’m not saying Kimura’s findings necessarily imply ID, or that his netural theory is completely correct, but I believe his refutation of natural selection as the major force driving evolution is theoretically sound.

However theoretically sound it might be, it's liable to run up against a major problem: the real world. Fortunately, his ideas can be tested. And indeed they are frequently: in the last couple of weeks there have been reviews about investigating selection in both humans and thale cress. With the advent of genomics, there's a lot of data being produced, and we're still trying to synthesise the results. But there is certainly evidence for selection at several genes.

As Will Provine, at Cornell, recently said at the Woodstock of Evolution

Natural selection does not…really do anything at all.”

I think I'll leave a discussion about the way we assign causation (which is what Provine was on about) to another time!

Bob

Bob, does evolutionary biology acknowledge any source of heritable change that isn't ultimately devoid of planning? -ds Bob OH
June 24, 2006
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BobOH Raevmo, I have looked through the table of contents of Lynch and Walsh's book, and it seems the material of interest to me will be in their yet unpublished Volume 2. I have various texts on Population Genetics, but Hartl and Clark seem to be the most usable in my collection. If there are other titles you use, feel free to specify them. For the readers, there was some discussion of Haldane and Kimura in this thread, I will quote from my copy of a collection of 30 years of Kimura's selected papers with a foreword by James Crow.
Kimura first presented his neutral theory of molecular evolution in 1968. This proposal was blasphemy to evolutionists accustomed to thinking of natural selection as being the sole directive force in evolution...needless to say the neutral theory does not contradict the Darwinian theory as the basis of changes in form and funciton. The detailed reconciliation of molecular and phenotypic changes is a major agenda item for future research James Crow
and from Ohta and Kimuras book, Theoretical Aspects of Population Genetics, regarding Haldane's 1957 paper, The Cost of Natural Selection
page 25: This gives a rate of nucleotide substitution per generation of at least 20, making the contrast still grater with Haldane's (1957) estimate of 1/300 per generation as the standard rate of gene subsittuion in evolution. Considering the amount of selective elimination that accompanies the process of gen substitution(substitutional laod, see Chapter 5), the most natural interpretation is, we believe, that a majority of molecular mutations that participate in evolution are almost neutral in natural selection
IDers argue that natural selection is not the sole directive to evolution, it could not even be the majority directive, and in fact it could not even be a few percent of the directive to evolution based on the inferences of population genetics available in existing professional literature. The attribution of the majority of evolution to Darwin's theory natural selection, I believe at this stage, is only obligatory and ceremonial. I'm not saying Kimura's findings necessarily imply ID, or that his netural theory is completely correct, but I believe his refutation of natural selection as the major force driving evolution is theoretically sound. As Will Provine, at Cornell, recently said at the Woodstock of Evolution
Natural selection does not...really do anything at all."
Salvadorscordova
June 24, 2006
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The basic breeders equation for artificial seleciton which you cited stated: h^2 = R/S does not have an explicit noise term.
Write heritability out in full: h^2 = V_A/(V_A + V_D + V_M + V_E) (there could be other terms as well). And lo! V_E is the "noise term". And V_M as well, if the noise is affecting whole families. BobBob OH
June 23, 2006
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Sure Salvador, I’d be willing to read Sanford’s book if you can get me a free copy. You got my email from the registration, so contact me and I’ll tell you where to send it. Thanks for the offer.

I'll be e-mailing you soon to get your address.

Incidentally, Kimura did use Haldane’s argument in favor of his proposition that most molecular evolution must be neutral or nearly. Some theorists now consider the debate closed after the work of, e.g. Ewens, but others (see the book of eminent biologist GC Williams 1992) don’t think so. I am not confident to call it settled.

I VERY much appreciate your candor here!

For the other readers, Walter ReMine had his work reviewed by Warren Ewens incidentally. His account is here:
Haldane's dilemma and peer review

Salvador

scordova
June 23, 2006
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Dave, you know of course very well that evolution has been demonstrated in the lab. Not macro-evolution in the sense referred to above. I suppose a necessary condition for demonstrating macro-evolution in the lab would be to dramatically speed up evolution in the lab, otherwise it would take too much time. Maybe future developments in genetic engineering will make this possible. I certainly hope so. I don't really care whether one can call something science only if it can be demonstrated in the lab in theory. As long as the grants pay for it, I say go for it.Raevmo
June 23, 2006
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Environmental issues like nurture and luck are not factored. Environmental noise terms are not there. Sorry, this is simply factually incorrect. Quantitative genetic models include nurture (maternal effects), luck (drift) and environmental noise (both common environment, which can also be nurture, and within environmnt effects). Check a quantitative genetics text book, like Lynch & Walsh (and check the notes for Volume II as well). I’ll agree that we don’t yet understand all of the details, but we’re working on it. Science would be boring if we knew everything!
BobOH, I believe we are talking past each other and part of the issue is that I did not articulate my position in a clear manner. One could observe heretability in an artificial environment and then compare the heretability in a natural environment. The basic breeders equation for artificial seleciton which you cited stated: h^2 = R/S does not have an explicit noise term. The value of an explicit noise term is one has a marginal method of relating heretability values in various environments. In any case, I thank you for the references to Lynch and Walsh books. I will atempt to purchase them. I thank you for the time you invested in responding to my comments. Your comments will help me improve future presentations of my ideas. Thank you. Salvadorscordova
June 23, 2006
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Dave, what happened to my post answering Salvador? I'm asking because a later post has already shown up here.

I think I deleted it but I don't recall why now. It's been a busy day. -ds Raevmo
June 23, 2006
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Not quite true: it’s the noise in the environment where the trait was measured.

But that is exactly the point, the environmental noise term is not explicitly expressed in the derivation h^2 it is only post dictively derirved and not segregated from the organismal issues.

The inexatness is understandable given the difficulty of the measurement, but that does not detract from what I was trying to say.

To get a measure of environmental noise:

calculate h^2 in an artificial breeding environment

then calculate h^2 in the natural environnment

One can then derive an idea of the environmental noise for that environment.

PS: even without environmental noise, for complex triats Kimura estimated the heretability values at (.004) often approaching zero, this is a signal-to-noise ratio of 1/250. 99.6% of phenotypic selection for fitness is wasted. It would be expected environmental noise would make this worse.

scordova
June 23, 2006
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I said, “Environmental noise terms are not there”, but let me clarify. The h^2 term is analogous to S/N ratio ( signal strength divided by amount of noise), the environmental noise is not given as this is an equation for realized heretibility in artificial selection not natural selection!

Not quite true: it's the noise in the environment where the trait was measured. There are now several examples where this has been done in wild populations (e.g. Soay sheep, swans, red deer, flycatchers). Do a literature search for people like Kruuk, Coltman, and Sheldon.

Bob

I don't know about these but I'll make a prediction based upon ID - they're all still sheep, swans, deer, and flycatchers. Am I right? -ds Bob OH
June 23, 2006
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"So the claim that random mutation plus natural selection can create novel cell types, tissue types, organs, and body plans isn’t verifiable? It isn’t science in that case my friend. It’s an article of faith. Faith is fine for religion but science is about demonstration. -ds"

Indeed science is about demonstration. And indeed it hasn't been shown conclusively (at all if you like) that novel cell types, tissue types, organs and body plans can be created by RM+NS alone. That doesn't mean it's unverifiable. Right now I don't see that being replicated in a lab anytime soon, but what do I know. Maybe it can be verified or falsified some day. I don't see why it would be impossible in principle. In fact, if in a petri dish a colony of bacteria would evolve, say, a nucleus, from one day to the next, a lot would be falsified, wouldn't you agree?

Actually it does mean it's unverifiable until such time as a method of verification in principle can be outlined. Hypotheses don't get a free lunch of being verifiable until proven unverifiable. They're unverifiable until some investigator comes up with a plausible method of verification or at least falsification. None exists for the macroevolutionary claims of RM+NS. One is asked to take it as a matter of faith that RM+NS to the Nth power equals macroevolution. Faith is for religion. Demonstration is for science. Show me the evolution! -ds Raevmo
June 23, 2006
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Environmental issues like nurture and luck are not factored. Environmental noise terms are not there.

Sorry, this is simply factually incorrect. Quantitative genetic models include nurture (maternal effects), luck (drift) and environmental noise (both common environment, which can also be nurture, and within environmnt effects). Check a quantitative genetics text book, like Lynch & Walsh (and check the notes for Volume II as well). I'll agree that we don't yet understand all of the details, but we're working on it. Science would be boring if we knew everything!

"Dumb luck" has been considered in population genetic models since the 1920s: Sewell Wright argued that it was important, for example. And of course that's what Kimura's neutral theory is all about.

Bob

Bob OH
June 23, 2006
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I said, "Environmental noise terms are not there", but let me clarify. The h^2 term is analogous to S/N ratio ( signal strength divided by amount of noise), the environmental noise is not given as this is an equation for realized heretibility in artificial selection not natural selection! What S/N is basically one number, it is not decomposed into signal and noise, simply the composite ratio.

scordova
June 23, 2006
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Rubbish! You’ve been discussing uantitative genetics, where the “noise term” is the environmental variation (depending on which way you want to strain the analogy, it could be the non-additive genetic variation as well). It’s right there in the calculation of heritability.

If you’re talking about the simpler population genetic models, where the allele frequencies are measured, then the effect of the noise would be to shrink the relative fitness towards 1. So, it’s there if you know where to look!

Environmental issues like nurture and luck are not factored. Environmental noise terms are not there. Large amounts of elimination and preservation are not do to any sort of abundance of selectively beneficial mutation, but just dumb luck. This is hard to model, but it does not mean it does not exist. Quite the contrary. See: Extinction: Bad Genes or Bad Luck by Raup.

Salvador

scordova
June 23, 2006
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Ah, so evolution doesn’t happen in domesticated horses.

I did not say that or imply that, I was referring to proportion of selectively beneficial mutations. Lenski estimates 1 per 1,000,000

Sorry, that was a joke about your refernce to stables.

Bob

Bob OH
June 23, 2006
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Sure Salvador, I'd be willing to read Sanford's book if you can get me a free copy. You got my email from the registration, so contact me and I'll tell you where to send it. Thanks for the offer.

I agree with Bob OH that noise has been taken into account, at least to some extent, in population genetics (PG)/quantitative genetics (QG). In PG there has been work on selection in stochastically fluctuating environments, and Kimura's work (and of many others) has focussed very much on the stochastic aspects of selection in finite populations. One of Kimura's main tools is diffusion theory, now a standard technique in PG, as in other fields that rely on stochastic modelling (lots of physics of course). Incidentally, Kimura did use Haldane's argument in favor of his proposition that most molecular evolution must be neutral or nearly. Some theorists now consider the debate closed after the work of, e.g. Ewens, but others (see the book of eminent biologist GC Williams 1992) don't think so. I am not confident to call it settled.

In QC the signal to noise ratio is right there in the h^2=VA/VP, VA additive genetic variance and VP phenotypic variance, the latter including all sources of noise. Like Bob said, h^2 has been measured numerous times in the field, and values are all over the place from low to high (there was an interesting paper in Nature a couple of years back where they showed average measured h^2 is actually increasing over the years in publications, evidence of publication bias).

However, the PLOS paper from the Kruuk and Clutton-Brock groups you're referring to shows that h^2 may vary a lot from year to year (and probably from place to place), and this might be a source of noice that's not sufficiently acknowledged. But remember, it takes a huge amount of work to collect that kind of data, and unfortunately there isn't much $$ to support long-term projects such as the great work on sheep and deer on the Scottish islands.

Raevmo
June 23, 2006
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Bob,

The argument [kimura] was that a lot of evolution could be neutral, and hence much of the variation we see in the wild could be neutral. This has nothing to do with cost.

I believe it was stronger than that. In the book he co-authored with ohta, he pointed out the majority of evolution had to be concealed from selection. I used the word cost, but there are equivalent formulations of the same argument using cost (ReMine). Simply because a different terminology or conceptual description of the same issue is offered, does not imply it has nothing to do with "cost". One can define Newtons second law in terms of force or changes in momementum. In comparable manner, the issues of the limits which natural selection can participate can be defined in temrs of cost.

Haldane described it in his 1957 paper in something of a speed limit, information engineers understand information infusion in terms of bit rates....

Ah, so evolution doesn’t happen in domesticated horses.

I did not say that or imply that, I was referring to proportion of selectively beneficial mutations. Lenski estimates 1 per 1,000,000

Salvador

scordova
June 23, 2006
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A few comments:

1. the most basic equations of population genetics don’t speak to the likelihood of novelty emerging, the equations are generally agnostic to the issue

True: of course that was never the purpose of the models.

2. the more advanced theories of population genetics (Kimura, Crow, etc.) argue selection can not be statistically justified as the major driver of evolution because of the cost issues (one would be having to hack to death too much of the population and make too many babies to achieve the changes!)

I think you're conflating two very separate issues. Kimura's most famous work was on neutral evolution, i.e. when htere is no difference in fitness. The argument was that a lot of evolution could be neutral, and hence much of the variation we see in the wild could be neutral. This has nothing to do with cost.

The cost issues were initially raised by J.B.S. Haldane, and are an entirely different issue. I think Crow might have done some work on it, but I'm not sure. Anyway, this is something that has disappeared from the radar now: it's not seem as an issue.

3. Sanford argues selectively beneficial mutations in a stable have not theoretically and empirically been demonstrated to provide sufficient novelty to create biological innovation in geological time.

Ah, so evolution doesn't happen in domesticated horses. :-)

More seriously, I don't know Sanford's argument, so I can't comment further.

4. Sanford show that all this is further complicated by the signal-to-noise problem. The “h” (heritability, mentioned in the equations above) is the signal strength, and it is too small to overcome the noise of the real world. If a radio receives too weak a signal amonst all the “static” it can not be heard. A similar situation applies with the selection signal.

(minor quibble: heritability is h^2, not h)
I don't see this as a problem: a lower heritability will mean that evolution will proceed more slowly. Rerasonably sized heritabilies are now regularly measured from wild populations, so the necessary variation does exist.

There is not term for noise in most population genetic equations (something unthinkable in the world of information systems engineering, ala Claude Shannon). Sanford is among the first to address this oversight.

Rubbish! You've been discussing uantitative genetics, where the "noise term" is the environmental variation (depending on which way you want to strain the analogy, it could be the non-additive genetic variation as well). It's right there in the calculation of heritability.

If you're talking about the simpler population genetic models, where the allele frequencies are measured, then the effect of the noise would be to shrink the relative fitness towards 1. So, it's there if you know where to look!

Bob

It sure seems there are alot of epicycles required to make the phlogiston of accidental evolution work out in the details. And more epicycles are needed to fill in the many gaps in the neoDarwinian aether. This would be comical if it wasn't being forced down the throats of impressionable youngsters through legal chicanery. -ds Bob OH
June 23, 2006
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I should add, this topic of genetic variance in a highly selective environemnt as a twist I just realized: Interference Selection That is if were selecting heavily for one beneficial trait, we're potentially annihilating simultaneously numerous other beneficial traits. The persistence of sickle-cell anemia in a strongly selective environment of high rates of malaria is a strong (albeit unfortunate) example. Salvadorscordova
June 23, 2006
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In reading my earlier postings, let me try to clarify things a bit more in the discussion of genetic variance.

If, for example, a population underwent extreme selection pressure for small weight. What will happen? Well, they will all evolve to be the minimum size feasible, and presumably hit some sort of limit. When that happens the degree of difference from one oranism to the next will be a lot less than before the selection pressure was applied.

Statistical measure of the degree of difference can be expressed as standard deviations or variance (standard deviation squared). As Mendel discovered, the actual morphological (and other) features of an organism are not 1-for-1 with the genes, even though genes are highly influential. The non-genetic aspects of an organism are roughly referred to as the phenotype and the genetic aspects as the genotype.

We can approximately partition the organism into a phenome (the collection of phenotypic features) and the genome (the collection of genotypic features).

When there is a change in a phenotype, there may or may not be a change in the genotype.

"Additive genetic variance" is a measure of the differences in the genomes.

additive genetic variance = Summation [ 2pq[a + (q-p)d]^2

Phenotypic variance would be a measure of the differences in the population of a particular trait such as body weight, and it is easier to measure.

I point out 4 things:

1. the most basic equations of population genetics don't speak to the likelihood of novelty emerging, the equations are generally agnostic to the issue

2. the more advanced theories of population genetics (Kimura, Crow, etc.) argue selection can not be statistically justified as the major driver of evolution because of the cost issues (one would be having to hack to death too much of the population and make too many babies to achieve the changes!)

3. Sanford argues selectively beneficial mutations in a stable have not theoretically and empirically been demonstrated to provide sufficient novelty to create biological innovation in geological time.

4. Sanford show that all this is further complicated by the signal-to-noise problem. The "h^2" (heritability, mentioned in the equations above) is the signal strength, and it is too small to overcome the noise of the real world. If a radio receives too weak a signal amonst all the "static" it can not be heard. A similar situation applies with the selection signal.

There is not term for noise in most population genetic equations (something unthinkable in the world of information systems engineering, ala Claude Shannon). Sanford is among the first to address this oversight. I mentioned partial empirical validation of Sanford's thesis in passing here: Darwinist chastised

Indeed, after 50 years of investigation, we can’t convincingly demonstrate selection for most of the red-blood-cell diseases, other than sickle-cell anaemia, that are probably coevolving with the strong selective force of malaria. Other best-case scenarios for human genetic adaptation, such as adult lactase persistence and skin colour, are also incomplete.

This is not soley because we don't know enough, it is because of the noise problem.

That said, I think Salthe's argument are not phrased as effectively as they could have been, and I'm appreciative of Bob OH and Raevmo's comments. I will explore ways of getting that section of Salthe's argument improved for use in future discussions. In the meantime, if micro evolution is restrained, that is a restriction on macro evolution. I still think one should ponder the meaning of this in light of Salthe's comments:

Harsh environmental conditions were associated with strong selection for increased birthweight but low genetic variance, and vice versa. Consequently, the potential for microevolution in this population is constrained by either a lack of heritable variation (in poor environments) or by a reduced strength of selection (in good environments). More generally, environmental dependence of this nature may act to limit rates of evolution, maintain genetic variance, and favour phenotypic stasis in many natural systems. Assumptions of environmental constancy are likely to be violated in natural systems, and failure to acknowledge this may generate highly misleading expectations for phenotypic microevolution.

Salvador

scordova
June 23, 2006
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Raevmo, Thank you for your technical inputs, though we disagree, I value your input. Most of the contributers to our weblog are involved in other scientific and technology disciplines outside of biology. Like William Dembski, I use the internet to iron out kinks in materials I intend to publish and distribute, and thus, these sort of interaction are highly beneficial to me... Let me make an offer. If you'd be willing to read John Sanford's book, I'd be willing to make arrangements to get you a free copy. I'm highly recommending the books to the IDEA chapters, and I would be appreciative of a review over technical issues from a non-IDer. sincerely, Salvadorscordova
June 23, 2006
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I’m curious if anyone thinks I’m making sense here. Or have I over-simplified the science?

Sorry to say, but I think you're mangling it.

First, your quote from me says nothing about speciation: it's just about adaptation. I don't understand your comment about STOP patterns: .

For specific traits, it can be possible to see if a popuation is 'well adapted' by estimating the fitness of individuals with different values of the trait. One can then look to see if the distributiuon of the trait values in the population is at/near a maximum. In practice this isn't so easy, for example because you need a lot of data, and you have to be sure that there's a constant environment.

Speciation is caused by divergence, not by adaptation per se. Adaptation can have a role in speeding up divergence, but it's not necessary: if Darwin's finches are speciating, then it's probably because they are drifting apart. Whether this will lead to speciation will depend on the ecology of the species. I'm sure someone has modelled this, but it's not a literature I've looked at.

Bob

I don't know of any serious claims that evolution has stopped I don't know of any serious evidence that evolution beyond the production of sub-species is still in progress. Plenty of extinctions in recorded history. Extinctions are happening on a daily basis if you believe the tree huggers. Name just one novel species that evolved to replace any of the very many recently extinct ones. I'm not talking about polyploid mutations but an actual new species that can be identified by the traditional method of unique anatomical features. -ds Bob OH
June 23, 2006
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One shoudln't forget that macro-evolution takes quite a bit of time. Even the cambrian explosion took millions of years. Asking for it to be produced in the lab is a bit like asking an astronomer to produce a supernova in the lab. However, if you can point out an agency that gives away grants for million-year research projects, please let me know.

Here's an example of a very recently evolved frog species:
http://www.brightsurf.com/news/headlines/view.article.php?ArticleID=21625

So the claim that random mutation plus natural selection can create novel cell types, tissue types, organs, and body plans isn't verifiable? It isn't science in that case my friend. It's an article of faith. Faith is fine for religion but science is about demonstration. -ds Raevmo
June 23, 2006
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Bob says,

"Once something has become well adapted, there’s little improvement that can be made (to be technical, it’s at/near the top of a fitness peak), so it’s not going to be able to evolve anyway."

So how do evolutionist know Darwin's finches were truly becoming a new species? How do you predict with confidence any level of evolutionary STOP patterns in a finch? Why would a beak size indicate a new species is evolving? Give me the math that predicts it would evolved into a new species. And then in the lab, produce macro-evolution of the finch. If we know there are FULL levels of evolution, then we should know the intermediate levels and there should be clarity.

What about reptiles today? Are they evolving into birds? Do you consider the present reptilian representation as still evolving or fully evolved? If they're still evolving, then shouldn't RM&NS mechanisms experimentally explored in laboratory conditions create new steps in evolution on the way to the creation of birds?

It is not readily apparant to me you can predict anything at all based upon RM&NS. It appears that definitions are being made in the present for STOP points and data is just being interpreted from extinctions. Extrapolations are being made but there is no real consistency in the science. If RM&NS is a true mechanism for developmental structure of morphology. And as you say certain species are fully evolved. The we should identify the ones that are 1) Stopped evolving, 2) in intermediate steps, 3) those forms which can be experimented on to bring about final evolution to a stopping point.

I'm curious if anyone thinks I'm making sense here. Or have I over-simplified the science?

You're making plenty of sense. No one can demonstrate that evolution hasn't stopped except for the generation of sub-species. That's one of the more painful truths Darwinists have to admit to themselves. They're in denial. -ds Michaels7
June 22, 2006
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Actually h^2 = additive genetic variance/total *phenotypic* variance (*phenotypic* replaces *genetic*). This is an important distinction, since it says something about the proportion of *observed* phenotypic variance that can be transmitted to offspring in the form of additive genetic variance. Even if all genetic variation is of the additive kind, heritability can still be low if swamped by phenotypic variance. Another technical note: strictly speaking Fisher's theorem is only valid for a single gene locus. For multiple loci, mean fitness need not increase from one generation to the next, and in fact it typically does not.Raevmo
June 22, 2006
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