Intelligent Design vs Natural Selection as Rational Explanations to Account for the Present Diversity of Life

W.P. Hall (AKA Son of Darwin),

PhD Biology (Evolution), January 1973, Harvard University


Proposed Contents

Overall Introduction

Part 1. Philosophy of Science and What Makes Theories Scientific

Part 2. Core Concepts in the Theory of Evolution Based on Variation and Natural Selection

Part 3. Non-equilibrium Thermodynamics, Autopoiesis and the Origin and the Chemical Evolution of Life - to be written

Part 4. Origins and Early Evolution of the Anatomy of the Eukaryote Cell - to be written

Part 5. Evolution of the Earth's Atmosphere, Early Fossils and  and Origins of the Multicellular Animal Phyla - to be written

Part 2

Core Concepts in the Theory of Evolution Based on variation and Natural Selection


Progress Report

This is obviously turning into a larger project and will take substantially longer to finish than I originally intended. However it is worth my time to persevere with it for four reasons.

  1. Some of the material I am arguing here is directly relevant the areas of the hypertext project I am working on under the title: Application Holy Wars or a New Reformation: A Fugue on the Theory of Knowledge. This is a history of the (cultural) evolution of knowledge management technologies from early speech and writing, through books and libraries, up through the World Wide Web and the latest supercomputer applications in organisational knowledge management. I am currently confronting the theory of the organisations as an autopoietic entities, where organisations have 'lives' in their own rights that transcend the sum of the lives of the individuals belonging to the organisation at any one time. In my university courses I used a very similar concept to that proposed by Maturana and Varela in their 1980 book Autopoiesis and Cognition: The Realization of the Living, that now forms the basis of a lot of thinking in the areas of systems theory, artificial intelligence, and organisation theory and strategic management theory. Reviewing the autobiographical bits for the first sections is helping to recover details of what I was thinking 30 to 40 years ago when I used the arguments presented here to guide my teaching in biology..

  2. The essay may provide a case study demonstrating how the comparative method is used to guide the discovery and formulation of evolutionary theories and to help determine how realistic they might be..

  3. The present work represents a real challenge to see if I have learned enough about writing to be able to express some very difficult ideas and concepts so the interested layperson can actually understand them.

  4. I hope the contents will help readers of this forum understand how some of the hairy questions raised in this thread about evolution and evolutionary processes can be rationally answered.

  5. If this helps people see the difference between rational and critical thinking vs acceptance of dogma on faith, so much the better.

Feedback of any kind will be welcome.

Introduction to Part 2

In this section I will try to explain the main features of Darwin's Theory of Evolution by Natural Selection and how it is scientific. This section will be relatively brief because I can refer anyone who wants to know more about the theory of evolution and how it was tested and added to or modified over time to Steven Jay Gould's (2002) massive masterwork, The Structure of Evolutionary Theory. Like all good scientific theories, it is subject to criticism, and I don't agree totally with Gould's presentation - but my quibbles are out in the twigs and leaves. The massive core of the theory is as soundly formulated and tested as any physical theory, such as relativity and gravitation, and this is what I will try to explain in this section.

Ideally, I would simply refer everyone to Gould's masterwork, but ever since I first met him when he was Ernst Mayr's assistant in Harvard's Evolutionary Biology course when I was a student in it, Gould was always one to use 10 flowery words when one simple one would have done the job, and in the book there are five times as many citations of Gould's own papers than there are for any other single author including Darwin himself (I counted them). However, at 1,400 pages, the book is expensive and it would help to have a trolley to transport it  (I have been trying to read it on the commuter train!). However, despite the verbosity and ego of the writer, from what I have read so far I think it will  prove to be the pinnacle of writing on evolutionary theory in the second century following Darwin's publication in 1859.

Three Premises on which the Theory Depends

Darwin's theory of evolution is one of the towering intellectual achievements of all time. For purposes of analysis and discussion Gould resolves the structure of the theory into three major logical branches, that I will follow here:

If these three premises are accepted, then a vast array of predictions can be deduced from Darwin's theory that are imminently testable and thus subject to falsification.

Starting with the premises, each is susceptible to falsification. If any one of them can be shown to be untrue, then the theoretical edifice built on them fails.


The planet Earth offers a limited surface area for life. Most of the time most species exist in a state of dynamic equilibrium in the environment, maintaining relatively constant populations over time. Even when population sizes vary, they never become infinite, and if the population falls to zero the species becomes extinct, never to reappear. Yet, every species produces more progeny than are required to maintain a relatively constant population. Even humans, large primates, elephants and whales are capable of producing 10 to 20 or more progeny over a reproductive life time. When humans were colonizing new habitats and population can grow without restraints, i.e., in the settling of the Americas, family sizes of 10-15 were not uncommon.

Other familiar species such as dogs and cats typically have 4-8 or more offspring in a litter, with the possibility of 1-2 litters a year for a reproductive life of at least 5 years. Many insects (e.g., Drosophila, the fruit fly studied for so many years in genetics labs) typically lay several hundreds of eggs over a lifespan that may only last a few weeks. Some fish, e.g., the cod, produce many millions of eggs a year.

The premise that species' populations overproduce has the capacity to be falsified, i.e., if it could be shown that individuals or species in any one generation only ever produced the exact number of offspring required to replace themselves, then evolution as described by Darwin would be impossible. It is an observational fact that every species not on the borderline of permanent extinction produces more offspring than required to replace its individuals.

Individual Variation

The physical details of form and functioning of an individual is called its "phenotype". No two members of sexually reproducing species have identical phenotypes, saving "identical" twins or other clonally reproduced individuals (and even these will show some degree of variation). Even the very slowly reproducing humans come in a variety of sizes, skin, hair and eye colors, shapes, weights, lengths of limbs, intellectual abilities, propensity to take risks, fertility, etc. Darwin proposed that there was an underlying system of inheritance whereby heritable (i.e., persistent) information was responsible for at least some of this phenotypic variation, and that heritage passed from one generation to the next via reproductive cells independently of the actual expression of the information in the developed organism. 

The premise of individual variation also has the capacity to be falsified, i.e., if it could be shown that one could never tell apart individuals belonging to the one species, natural selection would be impossible. However, again, it is an observational fact that we can readily recognize and identify individual differences amongst our domestic pets and animals shows they do exhibit individual variation. When sufficient familiarity is gained with other species, they to are shown to be variable.

Heritability and the Genetic Theory of Inheritance

Heritability is a more difficult topic than overproduction or individual variation because it depends on much less tangible aspects of individual and population biology. 

Darwin's theory assumes 

  1. that some intrinsic form of heritable information accounts for individual differences, 

  2. that this information is passed from parent to offspring, which accounts for the tendency of progeny to more closely resemble their parents than an average for the population at random.

  3. that heritable information has a capacity to persist down through many generations independently from its action in any one generation, and

  4. that the heritable information is subject to a low rate of mutation that is "random" in the sense that specific changes take place independently of any future value or detriment of the mutation in the organism in which it occurred.

As is the case for the other two premises, the premise of heritability also has the capacity to be falsified. If it could be shown that there was no heritable basis to the observation that progeny tended to resemble their parents, then evolution according to Darwin's theory would be disproved.

The specific mechanism of heredity that Darwin himself postulated to meet the requirements of his theory of evolution was falsified. However, Mendel's genetic theory of inheritance, rediscovered in 1900 and elaborated into fundamental engineering knowledge pharmaceutical industry and animal and plant breeding by the end of the 20th Century has provided a vastly more powerful understanding of the sources of individual variation and heritability that has informed the totality of modern biology and medicine.

The genetic mechanism of inheritance includes the following aspects of direct relevance to the theory of Darwinian evolution. DNA molecules organised into linear structures called chromosomes carry genetic programs that living cells use as instructions to assemble cellular components (i.e., proteins and other macromolecules) and to control the growth and development of multicellular organisms. Development of the organism is controlled by instructions encoded in the DNA (i.e., structural genes) that specify the fabrication of RNA and protein macromolecules and regulatory codes surrounding structural genes that control when and how often that structural code is read to produce the product the gene specifies. The aggregate of an individual's genetic information is called its "genotype".

The unfolding of our understanding of genetics followed two threads, the chromosomal theory of inheritance deriving from an understanding of cellular reproduction and the process of meiosis and segregation in sex, and the chemical basis of heredity leading to the identification of the DNA molecule as the bearer of hereditary information and the unravelling of the mechanisms that control cellular metabolism, growth and development. I won't attempt to summarise the chromosomal theory of inheritance here. The subject is actually quite complex and takes a full semester course (which I have taught several times) to explain in any detail its history, logic and multiple variations. Also, adequate descriptions are provided in some of the top hits in http://www.google.com/search?q=chromosomal+theory+of+inheritance.

On the other hand, molecular genetics is much simpler to explain. Some of the critical steps in identifying DNA as the bearer of encoded hereditary information included:

  1. Griffith, who in 1928 identified a soluble fraction "the transforming principle" that could transmit hereditary information that could transform one strain of bacteria into another.

  2. Avery, McLeod and McCarty, in 1944, established that this transforming principle was nucleic acid rather than protein.

  3. It was originally believed that hereditary information would be carried in proteins because these were the most complex macromolecules. However, DNA was found only in chromosomes that were already known to carry hereditary information. A number of studies led to an increasing suspicion that hereditary information was carried by the DNA in the chromosomes rather than the proteins.

  4. Chargaff, in 1950, analysed the constituents of DNA and showed that the bases adenine:thymine, and guanine:cytosine always occurred in the ratio of 1:1, but that there was no consistent ration between the amounts of adenine+thymine compared to guanine:cytosine.

  5. Hershey and Chase, in 1952, provided convincing evidence using bacteria and virus infecting bacteria, known as bacteriophages, that the DNA component was both necessary and sufficient to infect the bacteria.

  6. In 1953 Watson and Crick provided a structural model for the DNA molecule that explained the prior observations and suggested how sufficient information could be encoded into its structure to specify the exact sequence of amino acids used to form proteins.

  7. Within another 20 years or so after Watson and Crick presented their hypothesis, all of the fundamental machinery for translating the coded sequence of DNA nucleotides into proteins forming cellular structure and controlling cellular metabolism had been identified.

Crick (1970) expressed this understanding of the flow of cellular information as the "central dogma" of molecular biology. The graphic is replicated (with some simplification) from Strickberger, M.W. 1976. Genetics, 2nd Ed. Macmillan Publishing Co., Inc., New York.

  1. Protein machines known as replicases replicate the DNA molecule and the encoded information very (but not totally) exactly for separation into daughter cells, where it provides those daughter cells the information required for metabolism, growth and development.

  2. Protein machines known as transcriptases transcribe short stretches of information on one of the paired strands of DNA into a sequence of RNA nucleotides (i.e., different chemicals, same information) called "transfer" RNA (tRNA). In general each different kind of protein molecule will be encoded by a particular tRNA.

  3. Machines comprised of both RNA and protein called ribosomes translate the information encoded in a tRNA molecule into a specific sequence of amino acids to form proteins.

In general, in today's organisms (this qualification is significant, as I will show in future sections of this essay), the information flow from DNA to RNA to protein is absolutely only one way. The sole exceptions known (which served to further inform our understanding of the molecular mechanisms involved) are certain viruses, which maintain their heredity in RNA rather than DNA. As shown by the thin line is the figure, some RNA viruses subvert cellular machinery to produce more RNA directly. A few have a "reverse transcriptase" enzyme able to transcribe the information encoded in the RNA molecule back to DNA, where the DNA is then transcribed to produce more viral RNA. With reverse transcriptase it is possible for the viral DNA to be spliced back into the host cell's chromosomal DNA. These aberrant reverse transcriptases have also given us some of our most important tools for genetic engineering and inserting human coded information back into the chromosome (i.e., some of the technology used in building transgenic organisms), but serve to further prove the genetic theory of inheritance.

Mutations result from various kinds of errors in replicating the encoded information from the parent strand of DNA to the daughter strands (molecular sources of mutation are well understood). The rates of such errors are generally very low - probably lower than once in a million copy events over the length of a whole gene for a structural protein, say 1,000 nucleotides). Copy errors range from minor ones where a single nucleotide is miscopied which may or may not result in changing a single amino acid in the structure of the protein encoded by the DNA, to duplications, deletions, inversions or splices that leave out, duplicate, rearrange amino acids within a given gene product, or perhaps even combine products from what were originally separate genes into a single new protein. Other errors in regulatory parts of the code, outside of the sequences that actually specify the proteins' amino acid sequences may change the amounts or conditions under which the protein is synthesised. Once such a mutation is occurred, it will be copied with equal fidelity into its daughter products. Sources of copy errors include ionizing radiation, chemical mutagens and quantum indeterminacy. 

Many gene mutations completely disable the functioning of the protein encoded by the gene. This may or may not disrupt development or survival of the individual carrying the gene. In such cases the gene will not survive in the population because individuals carrying the gene to not reproduce. In other cases the functioning of the protein or the timing or quantity in which it is produced may be slightly or significantly changed in ways that have slight to mild effects on the individuals carrying the genes.

It is important to note that none of the known sources of mutation are capable of conveying specific information from the environment back into the information encoded on the DNA molecule. In other words, although the frequency of mutation may be affected by environmental conditions, mutations are random and undirected in relationship to any adaptive requirement the organism carrying the genes may have.

The cybernetics of the process of cellular metabolism and development is now very well understood - to the point where within the next very few years we will actually be able to assemble a very simple bacterium from cellular building blocks and encode a minimal set of genes into a DNA chromosome which then can be inserted into the cell to create a totally new species of life. 

Deductive Predictions from Darwin's Theory of Evolution

Change through time (Descent with modification)

Evolution through natural selection is the deductive consequence from the three premises of overproduction, individual variation and heritability.

  1. A population of a species produces more individuals in a generation than can survive to reproduce themselves. It follows that only some of the individuals born are able to leave copies of the genes they carry in the subsequent generation.

  2. Some percentage of the individual variation within the population is a consequence of the specific genes these individuals carry. It follows that some variants are better able (i.e., "fitter") to survive and reproduce in the specific environment in which they live than other variants.

  3. Those variants that do survive and reproduce determine the genetic constitution of the subsequent generation. Genes from those individuals that fail to reproduce will not be passed on to subsequent generations. It follows that the genetic constitution of the subsequent generation will differ from the constitution of the prior generation; and it further follows that phenotypes will also vary through time as a consequence of the differential reproduction of some genotypes at the expense of others.

Each and all of these predictions are subject to wide varieties experimental testing from mathematical modelling to actual breeding experiments in the lab with short-lived organisms ranging from bacteria and yeast, to fruit flies and mice. The consequences of such experimentation are now central to the entire edifice of biological and medical science, to say nothing of modern agriculture.

Thus the impact certain variant genes have on the fitness of the individuals carrying them determines to some degree their frequency in subsequent generations. Generations of selection in the same direction will lead to significant changes in average genotypes and phenotypes to the degree they depend on the genotypes. Darwin argued that over geologically long periods of time that this form of natural selection was a necessary and sufficient explanation to account for the total diversity of life forms present on the earth today.

The earliest chemical and fossil evidence for life in the form of bacterial type organisms (bacteria and various forms of photosynthetic blue-green algea) are found in some of the oldest existing sedimentary rock, going back some 3.5 billion years (Schopf 1999). The very earliest dates have been disputed, but dates more than 2 billion years are not.

Compared to many protozoa, bacterial type cells are encased in fairly rigid cell walls and a reasonably stiff non-motile cytoplasm that are readily preserved. The fossils are found in a semi-transparent silica-based rock called chert, which is chemically very similar to water glass. Water glass can gel from an aqueous solution very much like the mounting media normally used to preserve minute organisms for microscopic examination. Such geological preservation is very rare, but where it occurs it is ideal for preserving microscopic fossils.

 The first presumably multicellular organisms to fossilise were the Ediacarans (named for the place in outback South Australia where they were first found), beginning approximately 580 million years ago. The first armored and shelled fossils first appeared some 530 million years ago. Given that most experimentation with animal body plans (i.e., fundamental structures used to define phyla and classes of organisms) has probably taken place with small soft-bodied sessile organisms generating thousands to millions of microscopic mobile larvae and with generation times for sexual reproduction of less than a year probably had more than 50 million years to evolve from the first multicellular organisms until the first significant fossils began to appear (in a later section I will explain why early organisms did not/could not leave fossils. Here we are talking about 50-100 million generations of selection, and survival rates from .1 % to perhaps less than .00001%, This would provide for maximum selection. By comparison, working with Drosophila fruit flies in the lab, the best we can hope for are selection (i.e., survival) rates of 1% over perhaps 25-50 generations during the active professional life of an experimenter.

More than ample time has existed to allow descent with modification to produce the presently living diversity of life.

Proliferation of Species

Darwin did not directly address the question as to when and how one species became two. However, this has been a major subject considered by developers of the modern synthetic theory of evolution during the middle of the 20th Century.

Mayr has made a very strong case that if the interbreeding population of a species becomes fragmented by the establishment of geographic isolation (i.e., geographic or ecological barriers that individuals of the species cannot cross) for a long enough time that enough genetic differences will evolve between them so that the separated populations do not interbreed when they meet again due to further geological, ecological or climatic change, or that if they do interbreed genes from the parent species do not work well enough together to produce viable or fit hybrid progeny. Once this situation is reached, the species will continue to evolve independently. People like Gould, Grant, myself, MJD White and many others have looked for circumstances that might allow speciation to take place more rapidly without the requirement for a prolonged geographic isolation. Some situations such as those involving polyploidy and parthenogenesis are generally accepted, since the circumstances leading to isolation can be replicated in the lab or controlled breeding experiments. Others, depending on "disruptive" selection within local populations, such as those I have proposed, are much more difficult to test because the proposed processes are still likely to take hundreds to tens of thousand generations, and the cases studied involve species with at best annual generations. 

However, even assuming Mayr's allopatric speciation is the only way species can proliferate, tens or hundreds of millions of years gives ample time to evolve the present diversity of life we see today.

A major test of speciation combined with descent with modification from common ancestors predicts that similar appearing species will have similar genomes (which, with the mapping of complete DNA genomes from humans, mice rice, yeast, etc...), we can now begin comparing similar species and very different species on a nucleotide by nucleotide basis. Where the total genome has not been mapped, there is a much larger number of species where DNA sequences coding for particular kinds of proteins has been mapped. All of these studies produce genomic family trees that are generally quite similar to those created by comparing physical phenotypes. If this was not the case, the prediction of descent with modification would be falsified.

Conclusion to the Part

I could go on, but I think I have shown in ample detail,

  1. That Darwin's Theory of Evolution is properly formulated as a scientific theory.

  2. That the three premises that it is based on are susceptible to falsification and have been very robustly tested and have not been falsified, such that they stand confirmed beyond a reasonable doubt.

  3. That a number of predictions follow deductively from the premises.

  4. That these predictions have also been very robustly tested and have not been falsified. Here it is worth noting that Darwinian theory underpins substantial areas of agricultural practice, the pharmaceutical industry, the biological sciences in general, and medicine in particular. (Why do we use animal models for testing drugs and surgical procedures, and to understand a variety of diseases - because they are closely related to people and because their genetics and physiologies are basically similar).

In other words, the theory of evolution has survived as stringent testing as any physical law, and on present evidence from anomalies being found on very large scales of the universe, it is at least as well founded as the law of gravity and relativity.


Theory of Evolution and Natural Selection

Darlington, C.D. 1939. Evolution of Genetic Systems. 2nd Ed. Revised and Enlarged 1958. Basic Books, Inc.

Dobzhansky, T. 1937, 1941, 1951. Genetics and the Origin of Species. Columbia Univ. Press, New York.

Dobzhansky, T. 1970. Genetics of the Evolutionary Process. Columbia Univ. Press, New York.

Eldridge, N. and and Gould, S.J. 1972. "Punctuated equilibria: an alternative to phyletic gradualism," in Models in Paleobiology. T.J.M. Schopf (ed.). San Francisco: Freeman, Cooper. pp. 82-115.

Ford, E.B. 1964, 1965, 1971, 1975. Ecological Genetics. Chapman and Hall, London.

Gould, S.J. 2002. The Structure of Evolutionary Theory. Belknap Press of Harvard University Press. Cambridge, Mass.

Grant, V. 1971. Plant Speciation. Columbia Univ. Press. New York

Mayr, E. 1942. Systematics and the Origin of Species: From the Viewpoint of a Zoologist.

_____. 1963. Animal Species and Evolution. Belknap Press of Harvard Univ. Press. Cambridge, Mass.

_____. 1970. Populations, Species and Evolution: An Abridgment of Animal Species and Evolution. Belknap Press of Harvard University Press. Cambridge, Mass.

_____. 2001. What Evolution Is. Basic Books [Phoenix Paperbacks - UK ed published 2002].

O'Neil, D. (2002). Synthetic Theory of Evolution: An Introduction to Modern Evolutionary Concepts and Theories. - http://anthro.palomar.edu/synthetic/ [http://web.archive.org/web/*/http://anthro.palomar.edu/synthetic/].

Schopf, J.W. 1999. Cradle of life: The Discovery of the Earth's Earliest Fossils. 1999. Princeton Univ. Press., Princeton, N.J.

Simpson, G.G. 1944. Tempo and Mode in Evolution. Columbia Univ. Press., New York.

_____, 1953. The Major Features of Evolution. Columbia Univ. Press, New York.

Stebbins, G.L., Jr. 1950. Variation and Evolution in Plants. Columbia University Press, New York.

White, M.J.D. 1945, 1954, 1973. Animal Cytology and Evolution. Cambridge Univ. Press, London.

____. 1970. Modes of Speciation. W.H. Freeman and Company. San Francisco

Genetic Theory of Inheritance

Avery, D.T., MacLeod, M., McCarty, M. 1944. Studies on the chemical nature of the substance inducing transformation of pneumococcal types.  Induction of transformation by a deoxyribonucleic acid fraction isolated from pneumococcus type III. Jour. Exp. Med., 79:127-158 - http://profiles.nlm.nih.gov/CC/A/A/A/M/_/ccaaam.pdf (Note: this is a big PDF file that will take a long time to download)

Chargaff, E. 1950. Chemical specificity of nucelic acids and mechanism of their enzymatic degradation. Experentia 6:201-209.

Crick, F.H.C. 1970. Central Dogma of Molecular Biology> Nature 227:561-563.

Fisher, R.A. 1929. The Genetical Theory of Natural Selection. [Dover Edition. 1958] Dover Publications, New York

Ford, E.B. 1965. Genetic Polymorphism. MIT Press, Cambridge. Mass.

Griffith, F., 1928. The significance of pneumococcal types. Jour. Hygiene 27:113-150.

Hershey, A.D. & Chase, M. 1952. Independent functions of viral protein and nucleic acid in growth of bacteriophage. Jour. Gen. Physiol. 36:39-56.

Olby, R. 1974. The Path to the Double Helix. Macmillan, London.

Watson, J.D. 1968. The Double Helix. Atheneum, New York.

Watson, J.D. and Crick, F.H.C. 1953. Molecular Structure of Nucleic Acids: A Structure for Deoxyribose Nucleic Acid. Nature, VOL 171, page737, (2 April 1953) - http://biocrs.biomed.brown.edu/Books/Chapters/Ch%208/DH-Paper.html

Wright, S. 1968. Evolution and the Genetics of Populations. Vol. 1. Genetic and Biometric Foundations. Univ. Chicago Press, Chicago