| 1. | Introduction
Charles Darwin wrote in the Origin of species
that species are not fixed as Linneaeus taught,
but that all species descend from one or a few ancestral life forms;
and the mechanism underlying the transformation of species
was heritable variation and natural selection. This is still accepted by the majority of
biologists today. Regarding the nature of mutations, scientists universally accept that
mutations are copying errors
of the bases in DNA and further (with a few exceptions) that these mutations are random.
'Random' means that those mutations are unrelated to the effects they may have for the organism.
It is also generally accepted that most mutations are harmful and will disappear, and that
a small percentage is beneficial. This fraction of positive mutations will be selected and
will be represented in the next generations. Just enough to drive evolution.
However there is a small minority of scientists who claim that there are simply not
enough positive mutations to drive evolution. Dr. Lee Spetner is one of them.
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| 2. | Neo-Darwinism: Could it work ? | |
| 2.1 | Richard Dawkins' weasel experiment as a test case
Let's start with Spetner's criticism of one of the well-known examples of Richard Dawkins.
Dawkins described a computer experiment to demonstrate the difference between one-step and cumulative selection (1).
He started with a random string of 28 letters.
He programmed the computer to change at random one letter at a time and let the computer operator select a letter
until the string reads:
METHINKS IT IS LIKE A WEASEL
The random substitution of a letter simulates random mutation of DNA and the selection of a letter
that matches the target string simulates natural selection.
Spetner's acknowledges the point of Dawkins weasel example:
"there is a much larger chance for cumulative selection to occur than for one large
adaptive step" (p.162).
Despite the fact that Spetner knows what the purpose of Dawkins example is and that Dawkins admits that his weasel
experiment is not realistic, Spetner spells out the reasons why it is not realistic:
- in real life selection has no long-range goal
- in real life mutation frequency cannot be so high (1/28)
- in real life selection pressure cannot be so high
- in real life selection is not immediate and certain
- in real life good mutations disappear because of random effects
- in real life DNA sequences are very much longer than 28
Spetner attacks Dawkins' computer simulation because it is too easy to have success with that
model. The computer simulation cannot fail to reach the target within a finite time.
However, Dawkins himself warns that "evolution has no long-term goal" and there is no "distant ideal" (p50, 1991), but does
not discuss mutation rate and other factors.
Despite Dawkins' disclaimer, Spetner pointed out all the shortcomings of the simulation in great detail and with pleasure.
John Maynard Smith (2) used the weasel experiment to provide students with practice in calculating probabilities.
"The weasel experiment illustrates the power of selection to generate highly improbable results."
He added as a student problem: "What, in your opinion is the least realistic feature of this model, regarded as a model
of evolution by natural selection?". The answer in the addendum reads:
"Perhaps it is the fact that the program has a representation of the optimum message and determines the 'fitness' of
actual messages by comparing them to the optimum. No analogous process occurs during natural selection." (p.307).
So, what JMS should have said is that the weasel experiment illustrates the power of artificial selection.
Spetner continues with
"Dawkins choice of a large mutation rate is one reason that his simulation works".
In nature the mutation rate is a billion times lower: 1/10,000,000,000.
Indeed, it needs to be low otherwise organisms will not survive. But it cannot be too low,
otherwise adaptation to changing environments is not possible. Further, mutation must not be too low, because
evolution has only 3 billion years to create humans from nothing.
Spetner argues that if a realistic simulation were run with a mutation rate of
1/10,000,000,000 (10-10) and a sequence length of 500, then the simulation would
take 70 billion steps just to get the mutations.
Spetner's criticisms have such a strong eye-opening effect, because the weasel experiment is so attractive.
It is so successful that one forgets that it was not intended as a proof of evolution.
Perhaps the weasel experiment could have been made more realistic by introducing a series of viable
intermediates that serve as short term goals for selection. But that would not make it more easy to understand.
It is obvious now that Dawkins used a simplified example to illustrate cumulative artificial selection.
However Spetner's model is too simple too, because
- in real life mutation rate is in the range from 10 - 4 to 10 - 6 per gene per generation
- in real life organisms have genomes much larger than 500 nucleotides and many genes have duplicates
- in real life there are large populations of organisms all subject to mutation and selection
Both Spetner's and Dawkins' experiments must be seen as a warming up for the serious study of population genetics.
Population Genetics tends to be a boring subject because it is so abstract.
Dawkins introduced an educational device; Spetner makes it exciting, fascinating, and gripping again
by asking critical questions.
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| 2.2 |
Could accumulation of many random mutations create new species?
Spetner's central question (in chapter 4) is:
How many small random mutations are needed 'to get a new species' ? In the scientific literature
'to get a new species' is known as speciation.
Spetner doesn't use the word; it is not in the index.
Speciation is defined as splitting up of one species into two.
In the literature one can easily find:
(1) what happens to mutations in populations under the influence of selection and chance,
(2) a lot about speciation mechanisms,
(3) how many generatons are needed to produce reproductive isolation, but not:
(4) how many mutations are needed for speciation.
Yet it seems to be a legitimate scientific question.
For if neo-Darwinism claims that mutations arise with a certain (low) frequency,
and if they are entirely random (that is: unrelated to the needs of organism),
and if only a fraction of them is positively selected,
and if 500 point mutations are needed to create a new species,
and if the resulting probability is too low, then that particular
collection of assumptions plus model is falsified.
Logically the theory could still be right and any of the assumptions could be wrong.
Spetner devotes chapter 4 to this calculation and gives all the assumptions, steps and details
supplemented with notes. He takes care to get the figures from the scientific literature,
although not always recent literature. For example Stebbins(1966) estimated that 'to get to a
new species' would take about 500 steps (=point mutations) (3).
So far the textbooks. But then Spetner takes over. He calculates the total probability
that all 500 steps occur successfully in a row.
The extreme small probability 2.7x10-2739 Spetner arrives at, results from
multiplying the probability of each step 1/300,000 by itself 500 times (p103).
Spetner concludes that it is impossible that a new species could ever originate in this way.
There are just not enough favourable mutations in the time available to produce new species.
I think that Spetner's model is wrong because his underlying speciation model is wrong.
- His speciation model conflicts with his own data and with the literature.
"It is likely that the inversions themselves were the genetic
change that led to the formation of Drosophila species" (p185).
This is the first
alternative to his 500-step-model presented earlier in his own book.
(It is an example of chromosomal changes). Elsewhere is his book Spetner says:
"Differences in DNA between species seem to be unrelated
to their supposed evolutionary divergence [McDonald 1990]. There are two frog species,
which are very much alike, but differ greatly in their genomes. The mammals, however, which
have great differences in phenotype, differ little in genotype." (p198) [emphasis mine].
This means that there need not be big genetic differences between species, which casts doubt
on his own 500-step-speciation model.
Furthermore there is a speciation mechanism which does not depend on the gradual accumulation
of many small mutations between populations and which can lead to the immediate establishment
of a new species: hybridisation followed by a doubling of chromosome number: polyploidy
(well known in plants) (4).
According to Ridley (5) "chromosomal changes may be
exceptionally important in speciation." (p457). A chromosomal change such as an inversion
involves many genes at a time.
That's a type of mutation (in Drosophila) discussed by Spetner himself (page 185).
It is clear that no textbook presents the '500-step-model' as a speciation model.
I am not saying that the textbooks are always right. And Spetner is permitted to disagree.
But Spetner does not argue against the standard view. He ignores the role of chromosomes
in speciation.
- Spetner mixes up 'reproductive isolation' and 'genetic distance'
Speciation according to the textbooks is different.
According to textbooks (4,5,6)
the most important step in speciation is reproductive isolation and this is achieved by
geographic isolation or natural selection. Not necessarily the accumulation of many small mutations.
Spetner, being a physicist, seems to think about the origin of new species as a physical
process. Something like a 'phase transition': if water is cooled down nothing visible happens
until freezing point, then suddenly ice forms. Spetner thinks species originate likewise:
if a species accumulates 499 mutations nothing happens and at 500 suddenly a new species
is born. This is not how biologists think about speciation.
"To be sure, the differences between species are due to mutation and selection, but demonstrating
that does not explain how species split" (6).
In fact reproductive isolation between populations, the crucial event in speciation, could be
caused by only two genes (7).
Recently scientists found evidence for a 'speciation gene' in Drosophila which probably
contributes to reproductive isolation(8).
Spetner assumes that any mutation would be suitable for speciation.
This is not so: the mutations that contribute to reproductive isolation are the
crucial type of mutations. And one doesn't need 500 of those! These facts were not known to
Stebbins in 1966.
After reproductive isolation between populations has arisen, genetic
differences can and will accumulate. They built up a 'genetic distance'. The populations diverge.
In the end thousands of those genetic differences could accumulate.
So Spetner needs to distinguish between the number of mutations that two species differ currently
(genetic distance) and the number of mutations required for initial reproductive isolation.
- Reproductive isolation can be fast
There is now (Oct 2000) new evidence showing that reproductive isolation only takes a dozen generations
(15).
Recently (Oct 2003) there is evidence for singel-gene speciation in a Japanese snail (17).
- We need new experimental data to resolve Spetner's problem.
Spetner's only source of the 500 steps is an estimate
of the botanist Stebbins(1966) (3).
To solve Spetner's problem we need (a) more data about the origin of reproductive isolation and
(b) comparisons of complete genomes of closely related living species.
Up till now data about species differences were based on less than 100 genes
or based upon extrapolations. However whole genomes contain 1000 - 100.000 genes.
Only the last few years techniques became available to 'read' whole genomes fast enough.
We need to know how much two closely related living species differ genetically,
in order to calculate how much time is needed or how many steps are needed to built up the
difference. That would be exciting information. That would be a real test.
But this is really another thing than the establishment of reproductive isolation.
The outcome will strongly depend on which species pair one choses,
because the difference will simply reflect how many years ago the two species got reproductively
isolated. Even 'closely related' species differ in the amount of genetic difference.
And there is the complicating factor of chromosomal differences between species.
Finally data from small animals (mice) and big (horses) should be distinguished, because
smaller animals reproduce faster and have larger populations.
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| 3. | Non Random variation. | |
| 3.1 | Spetner's Non Random Evolutionary Hypothesis (NREH).
Well, if Spetner thinks random mutations could never cause macro-evolution, what is his
alternative ? Please note that nobody is obliged to come up with an alternative in order to criticise
Darwinism, but Spetner happens to have an alternative theory.
His alternative is: the Non Random Evolutionary Hypothesis (NREH).
He claims that NREH produces some large-scale evolution (macro-evolution), but gives no
the details. He is silent about common descent (9).
Remarkably Spetner does not straightforward deny macro-evolution, he claims that
neo-Darwinism (accumulation of small changes) cannot account for macro-evolution.
This would imply macro-evolution exists.
What is clear that he denies that macro-evolution is an extension of micro-evolution.
Further he claims that NREH is a better explanation for micro-evolution.
Spetner accepts that micro-evolution occurred. He disagrees about its causes.
When evolutionists say genetic variation is random, they mean variation is unrelated to
the fitness of the organism. Here is Spetner's alternative:
- When I say a variation is not random, I mean that the chance of it occurring
has something to do with how the organism adapts to its environment (p175).
Spetner claims his hypothesis explains many observed phenomena that neo-Darwinism does not explain.
One advantage of the NREH would be that the evolutionary process need not be prohibitively slow.
In fact an adaptation would occur instantaneously on an evolutionary time scale!
There would be no cumbersome selection process over many generations.
It this is true, why doesn't the fossil record show human fossils a few hundred million years earlier?
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| 3.2 |
What is the evidence for Non Random Variation ?
Spetner mentions mutation in the flagellin proteins of Salmonella and
transposable genetic elements, but most detailed are the reports of Barry Hall (p187).
Dormant ("cryptic") genes becoming active in E. coli in response to
the presence of lactose in the environment (Barry Hall,1982).
The remarkable fact is that two mutations occurred in the same bacterium, both needed for survival,
and that the probability of that event is 10-18! Which is extremely small.
If the mutations did occur at random, he would have to wait a hundred thousand years.
But in the presence of lactose he found 40 of them in just a few days. Neither of the
two mutations is of any use by itself.
Spetner interprets this as non-random adaptive mutations. Hall continued his research in 'adaptive mutation'
and published in 1997,1998 and 1999 about it (10).
The facts are not controversial, but their interpretation is. |
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| 3.3 |
Non Random mutations: Could it work?
Does Spetner apply the "Could-it-work?"-formula to his own
Non Random Evolutionary Hypothesis? No!
So, is Spetner using a double standard? He forgot to ask these 3 questions:
- How can mutations be adaptive?
- Are these 'adaptive mutations' adequate in principle to explain macro-evolution?
- Do these mutations add information to the genome? (a prerequisite for macro-evolution
according to Spetner's own criteria).
One of the main obstacles that could keep NREH from working is: how does one guarantee that
the environment selects the right dormant gene to express itself? Recent HIV-research
(11) suggests that dormant retroviral DNA in human genome can be switched on by HIV
with the damaging result that it blocks anti-HIV drugs, thereby worsening the chances of the
patient's survival.
This highlights the main obstacle of Spetner's whole idea of adaptive mutations:
how does one guarantee that mutations are adaptive in stead of harmful?
Inducing dormant genes to express themselves is one thing, but to ensure
beneficial effects is another. Spetner does not tell us.
And: how did this beautiful
adaptation originate ? Where does it come from ? Of course the answer that genomes were
set up to behave like this (p183), is not
particularly satisfying! Even if one accepts Spetner's interpretation of Hall's experiments,
then the question remains: "Are these mutations in principle the right kind for macro-evolution?"
Spetner's examples are from physiology (food metabolism), not from morphology, anatomy or embryology.
Are mutations in the metabolism of an organism the right kind to produce reptiles, birds, mammals and humans (=macro-evolution)?
Spetner does not tell us. Of course Darwinists need to answer this most difficult question too.
The third unanswered question is: assume that 'adaptive mutations' exist, are they adding
information to the genome ? Spetner does not tell us. But he devotes a whole chapter on
this issue when talking about random mutations!
Activation of dormant ("cryptic") genes by definition adds no information to the genome,
because those genes already exist in the genome.
Spetner claims that only 'adaptive mutations' can explain macro-evolution, but they fail
to pass his own tests for macro-evolution!
Spetner is honest enough to state that the experiments with bacteria are controversial and
that the problem has not yet been resolved.
Spetner is also realistic enough to understand that science needs to be conservative "
to prevent science from fitfully chasing after every harebrained experiment" (p190).
So far Spetner's 'adaptive mutations' are miracles. Not the right kind of stuff to build an
alternative theory on.
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| 4. |
Can random variation build information?
Can random mutations really build something good and something new?
Could random mutations build the photoreceptors, the muscles for focusing, etc of the eye? asks Spetner.
Spetner investigates the answers he found in the literature. He uses an increase in information
as a criterion for the adequacy of the mutations for macro-evolution:
do those mutations add information to the genome? If not, they are not the right type.
Everybody agrees that humans have more information in their genomes than bacteria.
So we must see this increase in information in individual mutations argues Spetner.
Although Spetner later (9) recognises that the mathematical concept of information is
not very helpful in clarifying biological problems, the increase in genetic information is real.
He is not satisfied with often-mentioned examples such as resistance to streptomycin and DDT,
because "all point mutations that have been studied on the molecular level turn out to
reduce the amount of information" (p138).
I think the problem with the examples he examined (and those presented by Darwinists) is
that they are all short-term 'solutions' to environmental problems of bacteria and insects.
Of course these cannot show the real long-term innovations of vertebrates (the eye, brain,
placenta) or the construction of 35 unique body plans in the Cambrian Explosion.
Mutations detected in experimental conditions start with phenotypes (resistance to antibiotics),
and go back to the enzymes involved, and further back to the gene. However that is the wrong
approach and the wrong place to look.
Everything we find out about mutations in living organisms in nature
or in the laboratory tends to be irrelevant for the problems of macro-evolution,
because neither we, nor natural selection, know in advance what future use can be made of a
mutation.
One has to look at complete genomes, identify genes
(for example) for the eye and subsequently find organisms with similar genes that are not
yet used for building an eye.
Those genes are the precursors. Only then can we trace the path that genes followed in building
new organs. Unless one believes in a miracle every time an eye develops in an embryo,
an eye is built by genes just like any other organ. Those genes are similar to other genes.
For example the fact that we can see red and green
colours is caused by two opsin genes. The two genes are identical for 96% and this points
to a recent gene duplication.
Another example: lactation is an 'innovation' of mammals. How did it originate?
Lactalbumin, one of the main proteins in mammalian milk, has been considered to have arisen
de novo in the ancestor of mammals. Molecular studies, however, have shown that
lactalbumin is not a mammalian innovation, but rather a modification of lysozyme, a ubiquitous
enzyme found in a wide range of organisms from bacteria to plants, and a very ancient protein (12).
How would Spetner recognise this, if he only looks at mutations in bacteria?
Only with hindsight one could say that certain mutations
in lysozyme would 'add information' because they are halfway towards lactalbumin.
Spetner and many Darwinists did not realise they were looking at inadequate
evidence to verify or falsify the neo-Darwinistic theory of macro-evolution.
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 5. |
What kind of creationist?
Spetner is a theist. The Judaica Press is religious. Spetner published an online article
about the relation between Darwinism and the Torah (13).
It is clear that Spetner has a motive, but that does not make him 'guilty'.
Calculations cannot be Jewish. Clearly Richard Dawkins, being an atheist, has a motive.
But calculations cannot be atheist either.
There is no religion in Not By Chance, except in his Epilogue where Spetner discusses
the Torah concept of creation. He even claims that his Non Random Evolutionary Hypothesis is
derivable from Talmudic sources. That explains his motives behind the NREH.
Furthermore his motives also influenced the contents and the nature of his own
hypothesis:
- The NREH, on the other hand, postulates nonrandom variation.
It does not fulfill the neo-Darwinian agenda in that it does not contribute to a
natural explanation of the origin of life. (p210) (my emphasis).
So he considers his own NREH a non-natural explanation.
That makes him a creationist, not a Young Earth Creationist of course.
A difference with creationist Phillip Johnson is that Johnson typically attacks Dawkins' atheism, while
Spetner typically attacks Dawkins' weasel simulation.
Moving religious matters to an Epilogue does prevent mixing science and religion, and
is probably the best a creationist can do, but doesn't prevent Spetner from being a Creationist.
Further hints of 'design' in his book are:
- "The genome were set up for an adaptive change" (p183).
- "I am suggesting here that organisms have a built-in capability of adapting to their environment". (p200).
The only way to explain an instantaneous adaptive mutation without a trial and error process,
is a magic set up of the genome. The crucial question is of course What caused this
'set up'? If it was not a trial and error process, then what was it? A Designer ?
By the way: if such a 'set up' causes an immediate and correct adaptive response,
why do species ever get extinct ? Was there an incorrect 'set up' of the genome ?
If adaptive mutation worked, it would only speed up evolution.
If there was a 'correct setup', why did it take billions of years to create reptiles, birds,
mammals ? It could be done in a few generations. Of course Spetner's 'set up' idea is a
question-begging idea, a skyhook (14).
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| 6. |
Conclusion
Lee Spetner, a physicist, presented a scientific (mathematical) critique of neo-Darwinism
and scientific, but controversial alternatives.
He has religious motives, and religious escape routes.
He asked non-orthodox but stimulating questions (18)
and presented some unorthodox answers.
Spetner published in mainstream peer-reviewed scientific journals: Journal of Theoretical Biology
in 1964, and Nature in 1970. In that sense he is an insider and contributed to science.
At the same time he makes himself an outsider, by ignoring knowledge about speciation.
He accepts controversial results about nonrandom mutation and builds his own theory: the
'Non Random Evolutionary Hypothesis' on those controversial results.
Spetner explains these results by a mysterious 'set up' of the genome.
Spetner is not a Young Earth Creationist. He probably accepts the
Big Bang, but avoids questions such as the age of the earth and the chronological order of fossils
in the fossil record, so he doesn't need to explain that the fossils are in the right order.
He avoids mentioning the universality of the genetic code, so he doesn't need to explain why all
life on earth has the same genetic language. He avoids discussing the hierarchic structure of
life, so he misses crucial evidence for the common descent of all life.
Furthermore he misses the central task of biology: explaining the existence of a million species.
He constructed his 500-step speciation model as a disproof of neo-Darwinism
and macro-evolution, but the situation is more complex than that.
Evidence for the common descent of life (fact) does not depend upon the truth of neo-Darwinism
(mechanism), because there is a difference between the fact and the mechanism
of evolution.
His criticism of Dawkins weasel experiment shows that a defence of evolution is incomplete without a full
account of the conditions that make evolution work.
Spetner himself pretended to give a full scientific account of population genetics in a short popular book.
The value of Spetner's 'Could it work?'-approach is that it stimulates
critical thinking about the problems and solutions of neo-Darwinism. Especially because he is trying to refute neo-Darwinism.
An approach which is absent from introductory textbooks. Textbooks present established facts
and omit nasty unsolved problems. Textbooks and to a lesser degree scientific journals tend to ignore crucial questions
of how new genes are created and focus on neutral or slightly deleterious mutations and
'purifying' selection (16).
The title 'Not By Chance!' is misleading, because evolution has a random component (mutation) and a non-random
component (natural selection).
Spetner's dream: a physicist falsifies the foundations of modern biology, or in his own words
"shattering the modern theory of evolution", did not come true.
Notes:
- The weasel example is in The Blind Watchmaker, chapter 3. Ian Musgrave made a collection of computer programs simulating the "weasel"-experiment.
- John Maynard Smith (1998) Evolutionary Genetics, (second edition), Oxford University Press. This book is intended as a text for advanced undergraduates and graduate students.
- G Ledyard Stebbins is the author of Variation and Evolution in Plants(1950) and Chromosomal Evolution in Higher Plants(1971). Stebbins' expertise was chromosomal evolution in higher plants and was not a population-geneticist.
- John Maynard Smith: The Theory of Evolution, 1997. p267.
- Mark Ridley: Evolution, second edition, 1996, Blackwell Science Inc.
- Ernst Mayr: Populations, Species and Evolution, second printing, 1971, Harvard University Press, p296.
- W. J. Swanson and V. D. Vacquier: "Concerted Evolution in an Egg Receptor for a Rapidly Evolving Abalone Sperm Protein", Science, 31 July 1998.
- Chau-Ti Ting et al: A Rapidly Evolving Homeobox at the Site of a Hybrid Sterility Gene, Science 281 Nov 1998 pp1501-1504.
- In a letter Spetner explained to me that he rejects common descent of all life.
- The most recent publication is: Hall, B.G (1999) "Experimental evolution of ebg enzyme provides clues about the evolution of catalysis and to evolutionary potential". FEMS Microbiology Letters 174, 1-8. His work is also discussed by Michael Behe of the Discovery Institute.
- Nell Boyce: Dangerous liaison, New Scientist 19/26 Dec 1998, p21.
- Dan Graur and Wen-Hsiung Li(2000) Fundamentals of Molecular Evolution, p304.
- Lee Spetner: Evolution, Randomness, and Hashkafa.
- Daniel Dennett used 'skyhook' (an imaginary contrivance for attachment to the sky) to explain what supernatural explanations are. See review on this site.
- Joanna Marchant(2000) "Darwin strikes back", NewScientist, p11, 28 Oct 2000.
- Hirsh and Fraser(2001) Nature 411, 1046-1049 (2001) start with:
"If protein evolution is due in large part to slightly deleterious amino acid substitutions,
then the rate of evolution...". As if slightly deleterious mutations explain the evolution of complex life!
The focus on deleterious mutations is obvious in Mark Ridley(2001) Mendel's Demon.
- Rei Ueshima nd Takahiro Asami (2003) Evolution: Single-gene speciation by left-right reversal. Nature, 425, 679 (16 October 2003)
- Compare what Frank Close wrote about John Wheeler: "Wheeler's gift has been in asking questions that are outside the box". Nature, 434, 438-439, 24 Mar 2005. The difference is that Wheeler is a scientific giant.
Further Reading
- Review by Carl Wieland,1998. Carl Wieland is a Creationist Medical Doctor.
- Population Genetics Made Simple by David A. Plaisted.
- Mark Perakh: A Lost Chance. Dr. Spetner derives non-random evolution from the Talmud [January 2002]. Mark Perakh is a physicist. The review is not as bad as the title suggests.
- A statistical analysis of Neo-Darwinian theory: A summary of Spetner's arguments on a Baptist Church site. [no author; no date]
 Email from Paul Andrew King about errors in Spetner's calculations. 12 Feb 2003
- Email from Jason Rosenhouse about my description of Spetner's criticism of Dawkins. 10 Jun 2003
- Spetner and Biological Information by Ian Musgrave, Version 1.9 18/7/03. Focusses on biochemistry and information.
- David Whitehouse (2004) Scientists 'see new species born' (BBC News Online science editor) is about the origin of new Drosophila species.
- "Speciation" by Jerry A. Coyne and H. Allen Orr, 2004. Paperback, Sinauer Associates, 545 pages. Up-to-date overview of the literature on the origin of new species by two experts. Among many other things the authors conclude that reproductive isolation and speciation may be a by-product of ecological differences and disruptive selection on a surprisingly small number of phenotypic traits, which are controlled by an equally small number of underlying genes. This refutes Spetner's idea that many genes are necessary for the origin of new species. [2-10-2004]
- Tamra C. Mendelson and Kerry L. Shaw (2005) "Rapid speciation in an arthropod.", Brief cummunications, Nature, 433, 375, (27 Januar 2005). "The highest speciation rate, 4.17 species per million years, was found in a monophyletic clade from Hawaii Island." "We have shown that the highest rate of speciation recorded so far in arthropods belongs to a group of crickets that differ primarily in secondary sexual traits, indicating that divergence in sexual behaviour may cause this rapid speciation. AFLP technology allows high resolution of species relationships and unprecedented insight into the early stages of speciation. The best context in which to investigate the origin of species is provided by the early stages of speciation, before subsequent diversification. [ 28 Jan 2005]
- Edward E. Max (2001) The Evolution of Improved Fitness. Correspondence with Critic Lee Spetner on the TalkOrigns archive.
- Elizabeth Pennisi (2006) Two Rapidly Evolving Genes Spell Trouble for Hybrids, Science, 314, 24 Nov 2006. "Evolutionary geneticists are pinning down pairs of genes that help promote speciation; these genes are rapidly evolving, but not in response to ecological pressures". 24 Nov 2006
- Lee Spetner/Edward Max Dialogue by Dr. Lee Spetner (2001). The True.Origin Archive.
- L. M. Spetner (1964) 'Natural Selection: an information-transmission mechanism for evolution', J. Theor. Biol. 7 (1964), 412.
Postscript
The claim of forgery of the London and Berlin Archaeopteryx specimens seems to have been started
by Dr. Lee Spetner at a meeting of orthodox Jewish scientists in Jerusalem in July 1980. (source: Arthur Strahler(1987) Science and Earth History, p426.) [added Oct 2 1999]. See further: Paul Chambers(2002) Bones of Contention. The Archaeopteryx Scandals.
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"Not By Chance! -Shattering The Modern Theory of Evolution."