Evolution and Design

 

David Pratt

May 2004

 

Part 1 of 3

 


Contents

(Part 1)
    1. Darwinism under fire
    2. The origin of life
    3. Genes, mutation, and natural selection

(Part 2)
    4. Fossils and missing links
    5. Common descent and common design

(Part 3)
    6. Saltation, symbiosis, self-organization
    7. Chance, creation, and design
    8. Theosophy: evolution from within


 

1. Darwinism under fire


Darwinian evolutionary theory claims that all living creatures are related by descent from common ancestors, and ultimately from bacteria. All the members of any particular species show slight physical variations, which are said to result mainly from random genetic mutations. Most mutations are harmful and are eliminated by natural selection, whereas offspring who inherit characteristics that render them better adapted to their surroundings are more likely to survive and reproduce. Over the course of time, modifications in successive generations have allegedly given rise to the stunning diversity of life we see today.

Many scientists have challenged the central role that neodarwinism, or the modern synthetic theory of evolution, assigns to random genetic mutations (mostly involving errors in the replication of DNA). Robert Wesson says that ‘Many evolutionists have always been uncomfortable ... with the idea that progress is simply a matter of selection of the best mistakes’, and that ‘organisms have responded to their conditions and needs more purposefully than strict Darwinian theory can allow’.1 The same objection is echoed by Lyall Watson: ‘It is abundantly clear from the fossil record that when organisms do change, the modifications which occur are of a kind which improve fitness far more often than can be expected from changes taking place on a purely random basis.’2

There is no empirical evidence that unguided trial and error will produce anything but the most trivial results. The probability of a cell developing by chance alone is staggeringly remote. This is even more true of complex structures such as wings and feathers or the human eye and brain, which would require a long series of useful mutations in exactly the right order. Furthermore, all the intermediate, unfinished stages would have to offer some competitive advantage otherwise they would be weeded out by natural selection.

In response to this problem, darwinists are attaching increasing importance to regulatory genes. These genes can turn other genes on or off, so that new organs already encoded in the genes can appear very quickly and ‘simply’. But there is no satisfactory explanation of how such an intricate system arose in the first place, or how regulatory genes know which other genes to activate or deactivate; here too, darwinists simply fall back on their blind faith in happy accidents.

Most evolutionists still agree with Darwin that new species arise ‘solely by accumulating slight, successive, favourable variations’. But dissident scientists argue that although genetic change and natural selection partially explain variations within species, or microevolution, they are completely inadequate to explain macroevolution, i.e. the emergence of higher types. Rupert Sheldrake remarks:

The main problem that Darwin and Darwinians have always faced is to account for the origin of species themselves, or of genera, families, and the higher orders of living organization. The idea that such large-scale evolutionary processes all took place gradually over very long periods of time has been challenged again and again. ... Why do plants and animals fall into distinct types, such as ferns, conifers, insects, and birds, rather than lying on a continuous spectrum of living forms?3

A crucial problem facing gradualistic models of evolution is the conspicuous absence of a continuous series of transitional fossils between major groups of species – e.g. between invertebrates and fish, fish and amphibians, amphibians and reptiles, reptiles and birds, and reptiles and mammals. The ‘missing links’ are as absent today as they were in Darwin’s time, and the belief that this is due to the imperfection of the fossil record is becoming increasingly implausible. The fossil record simply does not give any indication of how the fins of fish became the legs and feet of amphibians, how gills became lungs, scales became feathers, and legs became wings.

Contrary to neodarwinist expectations, most species suddenly appear on the scene, live for millions of years essentially unchanged, and then inexplicably die out. Recognizing this, some darwinists now argue that, instead of emerging gradually, new species originate in sudden, rapid bursts of evolutionary creativity, with the result that no transitional fossils are left behind – a theory known as punctuated equilibrium. But this theory still accepts the dogma that new species are the result of random, undirected mutations.

Information science has clearly demonstrated that the new information needed to transform one species into another cannot emerge by chance; some form of intelligence is required. Mutations typically cause a corruption or loss of existing genetic information. Experimentally induced genetic mutations in rapidly reproducing species such as fruit flies (Drosophila) have succeeded only in producing deformed or less viable flies, e.g. flies with extra pairs of legs or extra wings. After thousands of generations fruit flies remain fruit flies and show no sign of metamorphosing into dragon flies, butterflies, or anything else.

Similarly, animal and plant breeders have been able to create many new breeds and varieties of domesticated animals and cultivated plants, but they have failed to produce any changes significant enough to give rise to a completely different species. Animals and plants showing extreme variations are usually sterile or weak and tend to revert to the ancestral type or eventually die out.

Darwinists often assume that any given feature of a species must have some adaptive value and then speculate about the ‘selective pressures’ that have given rise to it. Darwin admitted that he had exaggerated the role of natural selection and that it was wrong to assume that every detail of structure had some special survival value. ‘If adaptation alone were the core of evolution,’ writes Fritjof Capra, ‘it would be hard to explain why living forms ever evolved beyond the blue-green algae, which are perfectly adapted to their environment, unsurpassed in their reproductive capacities, and have proved their fitness for survival over billions of years.’ He says that genotypic change is only one side of evolution, the other being creativity, ‘the creative unfolding of life toward forms of ever increasing complexity’.4 But what is the source of this creativity? And is it really true that new types of organisms always descend from ancestral creatures through a series of physical modifications, whether gradual or rapid?

Conventional evolutionary theory represents life as a purely physical and mechanical process, devoid of purpose and intelligence. It is unable to explain where our bodies came from, let alone our minds. Wesson writes:

There is something of self-hate in the materialist approach. It depreciates the life of the mind and works of imagination and character. It demeans the richness and wonder of nature. It seems to make unnecessary further thinking about the mysteries of existence, of life and the universe.5

Darwinism continues to reign because most materialistic scientists cannot conceive of a less implausible alternative. Many are afraid to criticize its shortcomings too loudly for fear of giving ammunition to their great rivals, the biblical creationists. There appears to be a widespread belief that the only alternative to blind chance is the biblical Jehovah!

The defects of standard darwinism are considered in more detail in the sections that follow, and a variety of alternative ideas are examined. Theosophy, for example, rejects the materialistic assumptions on which darwinism is based and the notion of a continuous transformation of physical forms, leading from microbes to man. It regards evolution as essentially a development of the consciousness that animates successive physical forms, and sees evolutionary innovations on the physical level as a reflection of processes taking place on deeper, subtler levels of reality.


References

  1. Robert Wesson, Beyond Natural Selection, Cambridge, MA: MIT Press, 1994, pp. 224, 226.
  2. Lyall Watson, Supernature II: A new natural history of the supernatural, London: Sceptre, 1987, p. 87.
  3. Rupert Sheldrake, The Presence of the Past: Morphic resonance and the habits of nature, New York: Vintage, 1989, p. 280.
  4. Fritjof Capra, The Turning Point, London: Flamingo, 1987, p. 310.
  5. Beyond Natural Selection, p. 308.

 

2. The origin of life


Most scientists believe that the emergence of life began with the chance formation of the first self-replicating molecule in a prebiotic soup rich in organic compounds, amino acids, and nucleotides. Then, driven by natural selection, ever more efficient and complex self-reproducing molecular systems evolved until finally the first simple living cell emerged.

However, the earliest rocks fail to provide any evidence that a prebiotic soup ever existed, and the original assumption that the earth’s early atmosphere was a favourable mixture of water vapour, ammonia, methane, and hydrogen has also been called into doubt. Instead, it was probably a mixture of water, carbon dioxide, nitrogen, and oxygen. The latter would have hampered the production of amino acids and other molecules necessary for life, and broken down any organic molecules that did form.

All modern lifeforms contain genes made of DNA (deoxyribonucleic acid), which in turn is made up of nucleotides, whose sequence encodes instructions for making proteins. However, DNA is unable to manufacture proteins by itself. It first has to be translated into RNA (ribonucleic acid), which provides the blueprint for protein construction. But to translate DNA into RNA, and to make copies of DNA to pass on to daughter cells, proteins (in the form of enzymes) are needed. In other words, proteins, DNA, and RNA are all essential for life as we known it – presenting a chicken-and-egg problem.

Many biologists believe that the first organisms consisted of RNA (which is less complex than DNA), and that an early ‘RNA world’ provided a bridge from simple chemistry to the prototypes of complex DNA-based cells in modern organisms. But RNA is difficult to synthesize in the conditions prevailing when life originated and it cannot easily generate copies of itself. Several other highly speculative hypotheses have been proposed – e.g. that life originated in deep oceanic hydrothermal vents, or on the surface of clay or iron pyrite (fool’s gold) – but they are unconvincing and none has won widespread support. Some scientists, such as astrophysicist Fred Hoyle, have suggested that the first living organisms might have been carried to earth from outer space – but this merely moves the problem elsewhere.



Fig. 2.1. DNA has the form of a double helix, a spiral consisting of two DNA strands wound around each other. Each strand is composed of a long chain of nucleotides. Each nucleotide consists of a deoxyribose sugar molecule (designated by the pentagons) to which is attached a phosphate (designated by the circled Ps) and one of four nitrogenous bases: adenine (A), guanine (G), cytosine (C), and thymine (T). The two DNA strands are held together by the hydrogen bonds between pairs of bases; A only bonds with T, and C with G. Segments of DNA that code for the cell’s synthesis of a specific protein are called genes, which are packaged into threadlike structures called chromosomes. DNA replicates by separating into two single strands, each of which serves as a template for a new strand.1


Each of the 60 trillion cells in the human body contains a 1-metre-long string of DNA coiled into a tiny ball about 5 thousandths of a millimetre in diameter in the cell nucleus. DNA can store information so efficiently that all the information needed to specify an organism as complex as a human weighs less than a few trillionths of a gram. Geneticist Michael Denton remarks:

To the sceptic, the proposition that the genetic programmes of higher organisms, consisting of something close to a thousand million bits of information, equivalent to the sequence of letters in a small library of one thousand volumes, ... were composed by a purely random process is an affront to reason.2

Physicist Paul Davies has said that ‘the spontaneous generation of life by random molecular shuffling is a ludicrously improbable event’.3 Fred Hoyle and Chandra Wickramasinghe estimated that the probability of obtaining the simplest self-reproducing system by random combination of molecules is only 1 in 1040,000.4 Hoyle concluded that the probability of even the simplest known lifeform arising by accident was ‘evidently nonsense of a high order’, and ‘comparable to the probability that a tornado sweeping through an airplane junkyard would happen to assemble a flyable Boeing 747’.5

Assuming that proto-cell systems were to emerge, they would be far more prone to making translational errors when synthesizing proteins and it is difficult to see how they could be viable. In the words of evolutionary biologist Carl Woese: ‘The primitive cell was faced with the seeming paradox that in order to develop a more accurate translational apparatus it had first to translate more accurately.’ And Denton adds:

That such a cell might undergo further evolution, improving itself by ‘selecting’ advantageous changes which would be inevitably lost in the next cycle of replication, seems contradictory in the extreme. ... [A]n error-prone translational system would lead inevitably to self-destruction ...6

Scientists have spent countless hours attempting to create life in the laboratory, but all they have achieved is the production of certain prebiotic organic molecules, such as amino acids, which are essential to life as we know it.

We find ourselves in the situation in which the biochemist, with the exercise of much thought, care and purposive activity, together with the use of elaborate and intricate equipment, can duplicate in his laboratory a few of the simpler processes known to be performed at a considerably higher level of complexity by a single microscopic living cell – the activities of the cell being ascribed to hazard and chance!7

It is noteworthy that although there are thousands of kinds of amino acid, living organisms contain only 20 kinds. What’s more, although amino acid molecules occur in right-handed and left-handed forms, only left-handed amino acids are found in the protein of living organisms. The probability of this occurring by chance is only 1 in 1030.8

A typical cell contains 10 million million atoms, and is a structure of breathtaking intricacy. If we were to magnify a cell a thousand million times until it was 20 km in diameter, we would see an object of unparalleled complexity resembling an immense automated factory, larger than a city and carrying out almost as many functions as all the manufacturing activities of humans on earth. Yet it is capable of replicating its entire structure within a matter of hours. Furthermore, studies have shown that, far from moving at random, cells can respond intelligently to their environment as they possess a ‘control centre’ (a centrosphere, containing two centrioles) which is ‘capable of collecting and integrating a variety of physically different and unforeseeable signals as the basis of problem-solving decisions’.9


  Fig. 2.2.
A typical human cell.10


Geneticist Jacques Monod admitted that the origin of the genetic code and its translational mechanism was a ‘veritable enigma’, and Francis Crick, cowinner of the Nobel prize for the discovery of DNA, said that the origin of life appeared to be ‘almost a miracle’.11 Chemist Robert Shapiro has said that both DNA and RNA are too complex to have arisen spontaneously, and hoped for the discovery of ‘some new natural principle’ to explain their origin.12 Even time travel – allowing engineers from the future to seed life in the present – has been seriously proposed by some physicists! Rodney Brooks suggested in Nature that scientists might be ‘missing something fundamental and currently unimagined’ in their models of biology, and that ‘some aspect of living systems is invisible to us right now’.13

Life appeared on earth about 3.8 billion years ago, as soon as conditions were viable. This led palaeontologist Stephen J. Gould to say that the origin of life on earth was ‘a chemical necessity’ and ‘virtually inevitable given the chemical composition of early oceans and atmospheres, and the physical principles of self-organizing systems’.14 Many other scientist have adopted the same tune. For instance, Nobel laureate Christian DeDuve has said that the emergence of life and mind are ‘written into the fabric of the universe’. Paul Davies believes that above a certain threshold of complexity, new-style ‘complexity laws’ come into action, enabling a system to ‘self-organize and self-complexify’, and this could rapidly direct a system towards life.15 However, ‘complexity laws’ and ‘self-organizing principles’ are just words; the forces and operations they denote have never been satisfactorily explained in physicochemical terms.

One suggestion is that simple chemicals might possess ‘self-ordering properties’ capable of organizing the constituent parts of proteins, DNA, and RNA into the specific arrangements they now possess. But as Stephen Meyer explains, ‘biochemistry and molecular biology make clear that forces of attraction between the constituents in DNA, RNA, and proteins do not explain the sequence specificity of these large information-bearing biomolecules.’16 Mind or intelligence is the only cause known to be capable of generating the complexity and information content found in DNA.

Information theorist Hubert Yockey held that the information needed to begin life could not have developed by chance, and suggested that life be considered a given, like matter or energy.17 Astronomer Erich Jantsch wrote that ‘Life no longer appears as a thin superstructure over a lifeless physical reality, but as an inherent principle of the dynamics of the universe.’18 Physicist David Bohm believed that life and consciousness were enfolded deep in the ‘implicate’ or ‘generative’ order underlying our physical (or ‘explicate’) world, and were therefore present in varying degrees of unfoldment in all matter, including ‘inanimate’ matter.19

The theosophic tradition, too, recognizes life and consciousness as the ultimate ground of the universe, and indeed the ultimate mysteries. Rather than dead physical matter miraculously giving rise to life and consciousness when it reaches a certain level of organizational complexity, consciousness-life-substance is seen as an eternal and universal unitary essence, manifesting in infinite degrees of density and in infinitely varied forms. Physical matter is a more condensed manifestation of the finer grades of consciousness-substance that make up the subtler realms, including the subtler elements of each organism’s own constitution. Life is therefore present in all of nature’s kingdoms, but in different degrees of development.

Scientists generally regard the cell as the smallest living unit. But they do not understand how ‘dead’ matter can suddenly become alive, or why the spontaneous generation of life seems impossible today. Death is also hard to explain: Why does organization as an entity suddenly cease, sometimes without any evident cause? After all, it is the same ‘inert’ matter which composes living and nonliving things. There is clearly something missing from the scientific picture: life cannot be reduced to physicochemical processes.

The advent of ‘living’ organisms undoubtedly represents a huge advance on the more latent forms of life to be found in the mineral kingdom.

A crystal may be said to feed and grow, but it feeds upon the same single substance of which it is made, and it grows by accretion, not by assimilation of selected portions of a mixture of foodstuffs and their chemical modification into protoplasm. A crystal may serve as a nucleus for the growth by accretion of a new crystal, but this is quite different from the division of the contents of the living cell, to form a replicate daughter-cell.20

Theosophy sees the emergence of higher molecular and cellular forms of life as one of nature’s habits (‘laws’), an event that recurs in each major evolutionary cycle. But rather than physical matter organizing itself into organic forms, its activities are largely organized and coordinated from deeper levels of reality. The widely varying degrees of manifest life (and mind) displayed by the mineral, plant, and animal worlds arise from the level of sophistication of the vehicle that the animating consciousness, or monad, has to work through, as this determines how much of its inner potential can be expressed. In more complex organisms, an increasing role is played by etheric life-currents (prana or chi) which circulate through the astral model-body, thereby helping to vitalize the physical body and sustain its electric life-field. Prana can be regarded as an individualized expression of jiva, the ocean of life in which we are all immersed.


References

  1. Michael J. Behe, William A. Dembski and Stephen C. Meyer, Science and Evidence for Design in the Universe, San Francisco: Ignatius Press, 2000, p. 4; ‘DNA’, Encyclopaedia Britannica, CD-ROM 2004.
  2. Michael Denton, Evolution: A theory in crisis, Bethesda, MA: Adler & Adler, 1986, p. 351.
  3. Paul Davies, The Cosmic Blueprint, London: Unwin, 1989, p. 118.
  4. Sri Ramesvara Swami (ed.), Origins: Higher dimensions in science, Los Angeles, CA: Bhaktivedanta Book Trust, 1984, p. 35.
  5. Quoted in Alexander Mebane, Darwin’s Creation-Myth, Venice, FL: P&D Printing, 1994, p. 35.
  6. Evolution: A theory in crisis, pp. 266-7.
  7. Corona Trew and E. Lester Smith (eds.), This Dynamic Universe, Wheaton, IL: Theosophical Publishing House, 1983, p. 132.
  8. Walter J. ReMine, The Biotic Message: Evolution versus message theory, Saint Paul, MN: St. Paul Science, 1993, p. 83.
  9. Guenter Albrecht-Buehler, ‘Cell intelligence’, www.basic.nwu.edu/g-buehler/htmltxt.htm. See Rudi Jansma, ‘Cosmic mind in the microcosm’, Sunrise, April/May 2004, pp. 118-26.
  10. James P. Gills and Tom Woodward, Darwinism under the Microscope: How recent scientific evidence points to divine design, Lake Mary, FL: Charisma House, 2002, p. 43.
  11. Quoted in Evolution: A theory in crisis, p. 268.
  12. Darwin’s Creation-Myth, pp. 35-6.
  13. Rodney Brooks, ‘The relationship between matter and life’, Nature, v. 409, 2001, pp. 409-11.
  14. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the nature of history, New York: Norton, 1989, pp. 289, 309.
  15. David P. Woetzel, ‘The spontaneous generation hypothesis’, Creation Research Society Quarterly, v. 38, no. 2, 2001, pp. 75-8.
  16. Science and Evidence for Design in the Universe, p. 87.
  17. ‘The spontaneous generation hypothesis’.
  18. Quoted in Anna F. Lemkow, The Wholeness Principle: Dynamics of unity within science, religion & society, Wheaton, IL: Quest, 1990, p. 137.
  19. David Bohm and F. David Peat, Science, Order & Creativity, London: Routledge, 1989, pp. 200-1.
  20. This Dynamic Universe, p. 131.

 

3. Genes, mutation, and natural selection


Chance and selection

‘Chance is the only source of true novelty.’ – Francis Crick1

‘Darwin puts in the place of a conscious creative force, building and arranging organic bodies of animals and plants on a designed plan, a series of natural forces working blindly (or we say) without aim, without design.’ – Ernst Haeckel2

Darwinists frequently try to deny that they believe evolution to be based essentially on blind chance, and stress the role of natural selection – the survival of the fittest – in weeding out organisms and species whose form, physiology, and behaviour are least well adapted to their environment. Natural selection has been called the ‘major creative force of evolutionary change’. Darwin even spoke of it as an ‘intelligent power’, but said that he did so only ‘for brevity’s sake’. However, natural selection is a passive, automatic outcome of the universal struggle to survive and reproduce in the face of predation, competition for resources, and climatic and ecological changes. To call it ‘creative’ is disingenuous.

Darwinists do not believe that specific ‘selection pressures’ induce specific mutations. Most take the view that the variations on which natural selection acts arise from purely random genetic mutations. ‘Random’ in this context does not necessarily mean that mutations have no cause, but that they do not take place in response to an organism’s needs, and are not subject to any overriding direction or purpose; they occur haphazardly and unpredictably without regard for whether they are good, bad, or neutral for the organism in question. Jacques Monod was therefore accurately expressing the core belief of orthodox darwinism when he said that ‘Pure chance, absolutely free but blind, [is] at the very root of the stupendous edifice of evolution ...’3

Some evolutionists have said that it would be more accurate to speak of the ‘survival of the luckiest’ than the ‘survival of the fittest’. After all, even the ‘fittest’ organisms may be killed by disease, flooding, fire, famine, predation, etc. When a whale swoops up a mouthful of plankton by the thousands it is not because those individuals are all unfit; they just happened to be in the whale’s path. Furthermore, a genetically inferior organism may be larger, faster, or stronger simply because it happened to have better nourishment when it was young. Nevertheless, it is a truism that offspring with variations which improve their chances of survival will, on the whole, stand a better chance of survival and will therefore produce more offspring.

Many darwinists take the view that every new feature that emerges must in some way improve the survival chances of the organism concerned, and they then speculate about the selective pressures that must have given rise to it. Sheldrake writes:

Such speculations are usually untested and untestable; they are in fact rather like fables: how the rhino got its horn, how the peacock got its tail, and so on. One of the appeals of Darwinism is that it permits a limitless supply of stories to be spun.4

Gould considered the belief that everything is built by natural selection to be ‘the most serious and widespread fallacy’ among palaeontologists. His own ‘big idea’ was contingency – which is simply a more pompous way of saying ‘chance’!


Random mutations

Mutations occur when one DNA base is substituted for another or when one or more bases are inserted or deleted from a gene. They can occur spontaneously (the result of accidents in the replication of DNA), or they may be induced by ultraviolet light, x rays, or certain chemicals. Genetic change also arises from the seemingly haphazard breaking and recombination of chromosomes in the process of sexual reproduction. Another way in which organisms can acquire new genes is via viruses and plasmids.

Mutations are rare; for instance, each human gene has a likelihood of mutation of about 1 in 100,000 per generation. The consequences of mutations may range from negligible to lethal; as few as one in a million may be beneficial. The reason new mutations are usually harmful can be illustrated by the following analogy:

Consider an English sentence, whose words have been chosen because together they express a certain idea. If single letters or words are replaced with others at random, most changes will be unlikely to improve the meaning of the sentence; very likely they will destroy it. The nucleotide sequence of a gene has been ‘edited’ into its present form by natural selection because it ‘makes sense.’ If the sequence is changed at random, the ‘meaning’ rarely will be improved and often will be hampered or destroyed.
    Occasionally, however, a new mutation may increase the organism’s adaptation.1

It is upon these very rare ‘lucky mistakes’ that the whole edifice of neodarwinism is built. A shakier foundation is difficult to imagine!

No evolutionary biologist has ever produced any quantitative proof that the designs of nature are within the reach of chance. Richard Dawkins has claimed that blind physical forces can ‘mimic the effects of conscious design’. But as Michael Denton says, ‘It is surely a little premature to claim that random processes could have assembled mosquitoes and elephants when we still have to determine the actual probability of the discovery by chance of one single functional protein molecule!’2

Biologist Lynn Margulis has said that history will ultimately judge neodarwinism as ‘a minor twentieth-century religious sect within the sprawling religious persuasion of Anglo-Saxon biology’. She says that 99.9% of random genetic mutations ‘tend to induce sickness, death, or deficiencies’, and challenges people to name a single unambiguous example of the formation of a new species by the slow accumulation of mutations. Neodarwinism, she says, ‘is in a complete funk’.3

Richard Dawkins admits that the evolution of a complex organ like the human eye in a single step would require random spontaneous events that are so improbable as to be practically impossible. But he claims it is not so wildly improbable to get there in a series of small steps. Francis Crick dubs this the ‘statistical fallacy’. This is because the probability of step 1 being correctly followed by step 2, then step 3, and so on for 100 mutations is just as minuscule as leaping to the 100th step in one go. The greater the number of steps into which we break up the overall leap, the more improbable it becomes that they will all take place in the right order.4

Dawkins programmed a computer to generate random combinations of letters and compare them with a target sequence that forms an intelligible sentence. Any matching letters occurring in the same position as in the target sequence are retained, while the computer replaces the rest with another random selection of letters. This continues until all the letters match the target sequence. For instance, for a target sequence consisting of 28 letters and spaces (e.g. ‘Methinks it is like a weasel’), the computer takes only about 40 tries to produce the sequence, whereas it would take an average of 1040 tries (ten thousand trillion trillion trillion) to produce the entire sequence of letters and spaces simultaneously by pure chance.5 Dawkins regards this computer simulation as proof that random combinations of chemicals could gradually produce biologically functional proteins.

However, the ‘simulation’ is thoroughly unrealistic. First, it involves the existence of a target sequence, whereas darwinian evolution is supposed to be goalless, directionless, and purposeless. Second, the computer is programmed to lock in any correct hits, whereas in nature favourable mutations can be eliminated by later adverse mutations. Third, the sequences of letters selected by the computer do not all form real, meaningful words, and have no linguistic advantage over other sequences, except that they are one or two letters closer to the target sequence. In real life, each stage in the making of a complex protein would need to have some function otherwise it would not be favoured by natural selection. In other words, the only reason the simulation produced a favourable result was because Dawkins designed it to do so! Yet his computer games are widely cited as proof of the plausibility of random evolution.


Nonrandom mutations

Mutations are supposed to be accidental, undirected events that are in no way adaptive. For example, if an animal species needs thick fur to survive in a cold climate, it will not respond by growing fur; rather, any animals who undergo random genetic changes that happen to result in thick fur will survive to produce more offspring. As Robert Gilson says, ‘The doctrine of random variation is just as unprovable as is the doctrine of the Virgin Birth, and just as sacrosanct to its adherents.’1

Attempts to justify the doctrine of random mutations usually refer to a series of experiments on the bacterium E. coli in the late 1940s and early 50s. These experiments found that when bacterial cells are suddenly subjected to a particular selection pressure (e.g. the addition of a lethal antibiotic), a small proportion of cells invariably survive because they contain a mutation that confers resistance to the antibiotic. Tests were then carried out which proved that the mutations were present in the surviving cells before the antibiotic was added to the culture, and that they were therefore truly spontaneous and nonadaptive. However, the original researchers recognized that this did not rule out the possibiity of adaptive, nonrandom mutations.’2

Experiments over the past 15 years have shown that mutations can indeed occur in direct response to an environmental challenge – and have aroused great controversy.3 It has been found that bacteria which are unable to digest lactose, if given no other food, will after a few days develop new mutants that are able to handle it, the mutation rate being many orders of magnitude faster than the ‘spontaneous’, ‘random’ rate. Two independent mutations were needed, giving an ‘accidental’ explanation a probability of less than 1 in 1018. Adaptive mutations also appear to occur in yeast cells and possibly fruit flies.4 The existence of adaptive mutations is now widely accepted, though the term ‘directed mutations’ is sometimes shunned. Although some of the biochemical mechanisms involved have been identified, there is no real understanding of what lies behind the phenomenon.

According to Eshel Ben-Jacob and his colleagues, ‘a picture of problem-solving bacteria capable of adapting their genome to problems posed by the environment is emerging’; ‘It seems as if the bacterial colony can not only compute better than the best parallel computers we have, but can also think and even be creative.’5 As James Shapiro has said, even the ‘simplest’ form of life – tiny, ‘brainless’ bacteria – ‘display biochemical, structural and behavioral complexities that outstrip scientific description’.6

The rapidity with which pests, from rats to insects, acquire resistance to poisons is also hard to account for on the basis of conventional evolutionary theory. Some 500 species of insects and mites have been able to defeat at least one pesticide by genetic changes that either defensively alter the insect’s physiology or produce special enzymes to attack and destroy the poison. 17 have shown themselves capable of resisting all chemicals deployed against them. As Robert Wesson says, ‘If it is true that mutations are much more frequent where they are needed than when they are virtually certain to be harmful, they cannot be held to be random.’7

Molecular biologist Lynn Caporale points out that mutations seem to occur preferentially in certain parts of the genome while other DNA sequences tend to be conserved – which shows, she says, that evolution is not purely a game of chance. Although she believes that genomes can ‘steer’ mutations to ‘hot spots’ where they are more likely to increase fitness, and that the genome may be ‘in some way intelligent’, she does not believe that the actual mutations themselves are nonrandom in the sense of being somehow engineered by the organism in question to bring about the changes it needs.8 This is a good example of how darwinists sometimes dress up their dogmas in ‘sexy’ and even mystical-sounding language.


The overrated gene

Morphogenesis – literally, the ‘coming into being of form’ – is something of a mystery. How do complex living organisms arise from much simpler structures such as seeds or eggs? How does an acorn manage to grow into an oak tree, or a fertilized human egg into an adult human being? A striking characteristic of living organisms is the capacity to regenerate, ranging from the healing of wounds to the replacement of lost limbs or tails, together with the ability to adjust to damage during embryonic development. Organisms are clearly more than just complex machines: no machine has ever been known to grow spontaneously from a machine egg or to regenerate after damage! Unlike machines, organisms are more than the sum of their parts; there is something within them that is holistic and purposive, directing their development toward certain goals.

Although modern mechanistic biology grew up in opposition to vitalism – the doctrine that living organisms are organized by nonmaterial vital factors – it has introduced purposive organizing principles of its own, in the form of genetic programmes. Genetic programmes are sometimes likened to computer programs, but whereas computer programs are designed by intelligent beings, genetic programmes are supposed to have been thrown together by chance!

The role of genes is vastly overrated by mechanistic biologists. The genetic code in the DNA molecules determines the sequence of amino acids in proteins; it does not specify the way the proteins are arranged in cells, cells in tissues, tissues in organs, and organs in organisms. As biochemist Rupert Sheldrake remarks:

Given the right genes and hence the right proteins, and the right systems by which protein synthesis is controlled, the organism is somehow supposed to assemble itself automatically. This is rather like delivering the right materials to a building site at the right times and expecting a house to grow spontaneously.1

Genes do not even entirely explain the structure of proteins. Proteins consist of chains of amino acids, called polypeptide chains, which spontaneously fold up into highly complex three-dimensional shapes. Out of the astronomical number of possible ways a polypeptide chain could fold up, a particular protein always adopts the same one. This cannot be explained in terms of the sequence of amino acids in the protein chain and the known laws of physics and chemistry.



Fig. 3.1. The 3-dimensional structure of 2 kinds of protein molecule.2


The fact that all the cells of an organism have the same genetic code yet somehow behave differently and form tissues and organs of different structures clearly indicates that some formative influence other than DNA must be shaping the developing organs and limbs. Developmental biologists acknowledge this, but their mechanistic explanations tend to peter out into vague statements about ‘complex spatio-temporal patterns of physico-chemical interaction not yet fully understood’. Developmental (or morphogenetic) fields and gradients of chemical substances are sometimes invoked, but these are little more than vague, descriptive terms.

The fact that genetic mutations can alter an organism’s physical structure does not prove that genes themselves determine form. Sheldrake gives the analogy of a radio set:

a mutation in one of the components in its tuning circuit might cause the set to pick up another radio station: an entirely different series of sounds would come out of the loudspeakers. But [this] does not prove that these sounds are determined or programmed by the components of the set. These are necessary for the reception of the program, but the sounds are in fact coming from radio stations and are transmitted through the electro-magnetic field.3

Like morphogenesis, instinctive behaviour, learning, and memory also defy explanation in mechanistic terms. As Sheldrake remarks, ‘An enormous gulf of ignorance lies between all these phenomena and the established facts of molecular biology, biochemistry, genetics and neurophysiology.’4 He says that in this respect ‘properties are projected onto nervous systems which go far beyond anything that they are actually known to do. Brains, like genes, have been systematically overrated.’5

For instance, how could purposive instinctive behaviour such as the building of webs by spiders or the migrations of swallows ever be explained in terms of DNA and protein synthesis? Or consider the accomplishments of the monarch butterfly (shown right), whose brain is hardly visible to the naked eye:

[I]t winters at a few sites, especially in central Mexico, where hordes festoon the trees. In the spring, they migrate north, each generation going some hundreds of miles, as far as Canada. In the fall, the five-times-great-grandchildren return as much as 1,800 miles over lands they have never seen to the very grove, perhaps the very tree, from which the ancestors set forth. This ... could reasonably be called impossible.6

Wesson says that science cannot be expected to understand the origin and transmission of instincts when such a basic property of the brain as memory is impenetrable. Attempts to locate memory-traces within the brain have so far proved unsuccessful; experiments have shown that memory is both everywhere and nowhere in particular. Sheldrake suggests that the reason for the recurrent failure to find memory-traces in brains is very simple: they do not exist there. He goes on: ‘A search inside your TV set for traces of the programs you watched last week would be doomed to failure for the same reason: The set tunes in to TV transmissions but does not store them.’7 He also opposes the materialistic dogma that self-awareness and the power of thought can be reduced to the workings of the physical brain; the brain is an instrument of the mind rather than the mind itself.


Regulatory genes

Modern darwinists have assigned a major role to regulatory genes (also known as homeotic, homeobox, or Hox genes) in order to explain why we so often find innovations appearing abruptly in the fossil record, rather than being slowly fine-tuned by natural selection. Regulatory genes control developmental patterns, and seemingly minor changes in these genes can apparently have major consequences for the individuals and populations carrying them.

Homeobox genes are currently the best-known group of regulatory genes. Multicellular animals share many, if not most, of their homeobox genes. The differences between species are said to depend on where and when certain homeobox genes are activated. When particular genes are turned on for certain lengths of time and in certain regions, a worm may emerge. If the same or other genes are expressed for different lengths of time and in different regions, a more complex organism may develop. Likewise, insect wing development and vertebrate limb development are controlled by similar homeobox genes.

But as already indicated, contrary to what darwinists like to claim, genes do not carry the ‘blueprint’ for the construction of an organism; they merely code for the production of proteins. The proteins specified by structural genes provide the raw materials used in building the body, while the proteins specified by regulatory genes can carry signals that turn other genes on or off. But no genes are known to carry instructions for moulding proteins into more complex structures. Nor do they explain instinctual and learned behaviour, and the workings of the mind. Great chunks of reality are therefore missing from the materialistic darwinist theory.

For decades, fruit flies have been deliberately irradiated in the laboratory to induce genetic mutations. The mutations have succeeded mainly in producing monstrosities: the mutant flies may have varied colouring of the eyes, stunted and deformed wings, extra wings, no wings at all, or extra eyes on different parts of their anatomy. But although many mutants have been produced, they are still fruit flies, and no mutated fruit fly has ever reproduced a fruit fly with the same characteristics.



Fig. 3.2. Above: A normal specimen of the fruit fly Drosophila (top), and a mutant fly in which the third thoracic segment has been transformed so that it duplicates the second thoracic segment. Below: On the left, the head of a normal fruit fly; on the right, the head of a mutant fly in which the antennae are transformed into legs.1


In one experiment, researchers mutated the homeotic gene Pax-6, which is related to eye development, causing eyes to grow on the antennae and legs of fruit flies. Pax-6 is similar in flies and mammals (including humans), and part of the gene is also found in worms and squids. It was concluded that Pax-6 was the master control gene for eye morphogenesis. But as Jonathan Wells points out:

If the same gene can ‘determine’ structures as radically different as ... an insect’s eyes and the eyes of humans and squids then that gene is not determining much of anything. ... Except for telling us how an embryo directs its cells into one of several built-in developmental pathways, homeotic genes tell us nothing about how biological structures are formed.2

That embryonic development involves more than automatic gene regulation is shown by experimental tissue-grafting work on frog eggs and developing tadpoles. For instance, if a limb bud is removed and a tail bud grafted in its place, the tail bud is converted into a limb. And if the tissues in a developing frog egg are transposed by cutting and grafting, material that would have become skin is converted into a spinal cord, and vice versa. This suggests that there are additional, nongenetic formative influences at work.


Micro- and macroevolution

Microevolution refers to minor genetic variation in a local population, mainly resulting from the reshuffling of characteristics already present in a species’ gene pool and the influence of natural selection. Macroevolution is the emergence of entirely new and more ‘advanced’ features, leading to the emergence of species of a completely different type. Microevolution is a fact. Macroevolution, or large-scale molecules-to-man transformation, is an unproven hypothesis. As palaeontologist Keith Thompson has said:

no one has satisfactorily demonstrated a mechanism at the population genetic level by which innumerable very small phenotypic changes could accumulate rapidly to produce large changes: a process for the origin of the magnificently improbable from the ineffably trivial.1

Various examples of microevolution have been observed. For instance, the average beak size of finch populations can change over the course of a few years. Many species of moths and butterflies in industrialized regions have shown an increase in the frequency of individuals with dark wings in response to industrial soot blackening trees. More than 200 insect and rodent species have developed resistance to the pesticide DDT in parts of the world where spraying has been intense. Viruses mutate their coats to evade the human immune system. Disease-causing bacteria have made a comeback as strains evolved the ability to defend themselves against antibiotics. (As already noted, some of these changes may involve adaptive rather than random mutations.)

Microevolution can bring about the emergence of a new, but similar, species, if we adopt the orthodox definition that different species do not interbreed. For instance, a study of a species of Siberian greenish warblers that nest and breed in forest habitats encircling the Tibetan Plateau found that warblers from neighbouring habitats readily mate, though their characteristics differ slightly, but that two warbler populations living far apart did not mate and differed strikingly in other characteristics – they can therefore be considered two distinct species.*

*Defining a species as an interbreeding community of organisms is only a theoretical definition. In practice, species are almost always defined by their morphology, and sometimes by their behaviour. Some evolutionists argue that when a population varies continuously over a large range, it constitutes a single species, even though the extremes may be incapable of interbreeding. Note that some populations regarded as different species, such as dogs and wolves, do interbreed freely if allowed to.2

The differences between the two species of warblers are however trivial compared with the differences between a mouse and an elephant, or an octopus and a bee. It seems wildly improbable to expect accidental mutations to change one creature into a completely different one – but darwinists simply respond with the mantra that ‘improbable does not mean impossible’. They have an unshakeable faith in the ability of random chance to bring about wildly improbable changes (i.e. perform miracles) again and again for millions upon millions of years! If this were true, ‘chance’ would have to change its name. Recognizing this, biologist Lyall Watson asserted that, instead of acting blindly, ‘chance’ seems to have ‘a pattern and a reason of its own’ as if operating according to a ‘set of cosmic rules’!3

Since darwinists can’t even explain how the form of an organism arises from its own genetic material, anything they say about one organism being transformed into a very different organism (e.g. a fish into an amphibian) purely by random genetic mutations should be taken with a large pinch of salt!


Breeding limits

The origin of domesticated plants and animals by artificial selection and breeding is often cited as evidence for darwinian evolution. However, even with the aid of humans’ inventive genius, which permits maximum variation in the shortest time, the variation achieved is extremely limited and results in plants and animals with reduced viability.

In 1800, experiments were begun to increase the sugar content of table beets. By 1878 it had increased from 6% to 17%, but further selection failed to increase it any further. Similar techniques have been used to develop chickens that lay more eggs, cows that give more milk, and corn with increased protein content. In each case, limits were reached beyond which change has not been possible. Furthermore the breeders ended up with the same species of chickens, cows, and corn with which they began. In all cases these specialized breeds possess reduced viability, i.e. their basic ability to survive has been weakened.1

Domestic breeds of animals, if allowed to reproduce without selection, revert in not many generations more or less to the wild type. For instance, settlers introduced domesticated rabbits into Australia, where there were no native rabbits. When some of the domesticated rabbits escaped, they bred freely among themselves, and very quickly their descendants reverted to the original, wild type.

Darwin, as a breeder of pigeons and other animals, was aware that the amount of variability available was limited. Yet in the first edition of The Origin of Species he wrote: ‘I can see no difficulty in a race of bears being rendered, by natural selection, more and more aquatic in their habits, with larger and larger mouths, till a creature was produced as monstrous as a whale.’2 Although Darwin removed this statement from later editions of his book, the substance of its claim remains the central tenet of orthodox neodarwinism – that bears can become whales, or microbes can eventually become elephants by means of random mutation and natural selection.


Population genetics

It is a common mistake to assume that all advantageous mutated genes will eventually be ‘fixed’, i.e. inherited by all the members of a species and completely replace the original genes. First, in order to be inheritable, a favourable mutation must occur in sex cells, which make up only a tiny fraction of an organism’s cells. Furthermore, among sexually reproducing organisms, sex cells have half the genes of the adult; a given gene therefore has a 50% chance of getting into a sperm, and the same chance of getting into an egg, regardless of its survival value. On top of this ‘sexual lottery’, genes are also eliminated or fixed through genetic drift (random changes in the gene pool). If these processes alone were operative, most beneficial mutations would therefore never reach fixation, but would be eliminated from the population.

Genes used to be regarded as independent, noninteracting entities that can be selected more or less independently of one another – a theory known as ‘beanbag genetics’. However, we now know that a single gene may affect a wide range of traits, and most traits are determined by many genes (polygeny). The random origin and fixation of many-gene traits are even more improbable than in the case of a single-gene trait. For instance, if a new beneficial trait arises from a rare combination of five genes, due to sexual reproduction each gene has a 50% chance of being in a given offspring, so that the full 5-gene trait has 1 chance in 32 of being inherited. This is a 3% chance, rather than the usual 50% chance when only one gene is involved. If females average less than 32 offspring each (as is typical of higher vertebrates), then the many-gene trait would quickly vanish from the population.

That is why evolutionists prefer to assume that one trait equals one gene. To explain many-gene traits, they sometimes suggest that they arise in small populations with heavy inbreeding. However, heavy inbreeding typically harms species, and since genetic drift is strongest in small populations, it could easily eliminate beneficial genes necessary for a many-gene trait.

In the 1950s, evolutionary geneticist J.B.S. Haldane calculated the maximum rate of genetic change due to differential survival (survival of the fittest). He reluctantly concluded that there was a serious problem – now known as Haldane’s Dilemma.1 He found many higher vertebrate species could not plausibly evolve in the time available. Over a period of 10 million years, a population could substitute no more than 1667 beneficial mutations. This amounts to three ten-millionths of the human genome – which is hardly likely to transform an ape into a human, for example. Even this estimate is very optimistic, as it ignores the effect of harmful mutations, takes no account of deleterious processes such as inbreeding and genetic drift which remove beneficial genes, and disregards the fact that species typically spend 90% of their time in stasis where little or no morphological change occurs. Haldane’s Dilemma has remained the ‘trade secret’ of evolutionary geneticists. Textbooks continue to present the illusion that the key evolutionary processes are simple, fast, and virtually inevitable.

The idea that organisms can be radically transformed as a result of a succession of small independent changes is also undermined by the phenomenon of redundant genes: it has been found that particular organs may be generated by two quite different, genetically coded developmental mechanisms. Redundancy has the benefit that it ensures that developmental goals are achieved with a virtually zero error rate. However, ‘the greater the degree of redundancy, the greater the need for simultaneous mutation to effect evolutionary change and the more difficult it is to believe that evolutionary change could have been engineered without intelligent direction.’2 Another challenge is the discovery that if a specific gene is damaged or destroyed, its functions may be taken over, at least in part, by the remaining genes. This implies that genetic information may be spread holistically throughout the genome.3

It is clear that without some form of coordination, no evolution is likely to take place. That additional factors do exist is indicated by the phenomenon of multigene families. The genomes of nearly all organisms contain gene families, which consist of multiple identical copies of the same gene. Surprisingly, these copies are often identical not only within the genome of one individual but in the genomes of all the individuals in the species. One scientist sparked controversy by calling this phenomenon ‘molecular drive’, on the grounds that it drives evolution much more substantially and rapidly than natural selection, by permitting synchronous genetic changes in all members of a population.4


Inheritance of acquired characteristics

Until the late 19th century, nearly everyone believed that the characteristics and habits acquired by one generation in response to environmental conditions could be transmitted to the next generation. Darwin took this for granted, as did Jean-Baptiste de Lamarck, with whose name the inheritance of acquired characteristics is usually associated. Since the beginning of the 20th century, however, Lamarckian inheritance has been completely rejected. This is because the ‘central dogma’ of molecular biology states that, although environmental stimuli can alter the outward character of organisms (phenotypic change), there is no known mechanism whereby they can alter an organism’s genes in any coherent way (genotypic change). Nevertheless, there is strong evidence that acquired characteristics can be inherited.

Ostriches, for example, are born with horny calluses on their rumps, breast, and pubis, just where these will press on the ground when they sit. Likewise, warthogs have hereditary calluses on their knees, corresponding to their habit of kneeling while they root in the ground. So do camels, again in perfect agreement with their habit of kneeling. It seems reasonable to suppose that their ancestors developed these calluses through their habit of sitting or kneeling, and that the tendency for them to form was somehow transmitted to their offspring, who are now born with them. Yet darwinist theory denies that this is possible, and would have us believe that purely random genetic mutations have taken place which just happened to put callosities in just the right places, and that the animals’ habit of sitting or kneeling played no role whatsoever!

C.H. Waddington conducted experiments with fruit flies which showed that acquired characteristics could indeed be inherited. He explained this effect in terms of developmental pathways or ‘chreodes’, and called this process ‘genetic assimilation’. He attempted to account for it in terms of the selection and accumulation of mutant genes within the population, thereby providing a seemingly orthodox neodarwinian explanation for it. But recent reinvestigations have failed to support his explanation, and the effect does not seem to be explicable in traditional darwinian terms.1 Rupert Sheldrake proposes that acquired habits of behaviour and bodily development can be inherited not because of modifications of DNA but through modifications of ‘morphic fields’ (nonphysical organizing fields), which are inherited nongenetically by morphic resonance (see section 6).


References

Chance and selection

  1. Quoted in Robert Wesson, Beyond Natural Selection, Cambridge, MA: MIT Press, 1994, p. 9.
  2. Quoted in H.P. Blavatsky, The Secret Doctrine, Pasadena, CA: Theosophical University Press, 1977 (1888), 2:652.
  3. Quoted in Michael Denton, Evolution: A theory in crisis, Bethesda, MA: Adler & Adler, 1986, p. 43.
  4. Rupert Sheldrake, The Presence of the Past: Morphic resonance and the habits of nature, New York: Vintage, 1989, p. 281.

Random mutations

  1. ‘Evolution’, Encyclopaedia Britannica, CD-ROM 2004.
  2. Denton, Evolution: A theory in crisis, p. 324.
  3. Michael J. Behe, Darwin’s Black Box: The biochemical challenge to evolution, New York: Free Press, 1996, p. 26; Lynn Margulis and Dorion Sagan, Acquiring Genomes: A theory of the origins of species, New York: Basic Books, 2002, pp. 11-2, 29.
  4. Richard Milton, The Facts of Life: Shattering the myths of darwinism, London: Corgi, 1993, pp. 178-80.
  5. Michael J. Behe, William A. Dembski and Stephen C. Meyer, Science and Evidence for Design in the Universe, San Francisco: Ignatius Press, 2000, pp. 38-40.

Nonrandom mutations

  1. Robert J. Gilson, Evolution in a New Light: The outworking of cosmic imaginism, Norwich: Pelegrin Trust, 1992, p. 3.
  2. Michael J. Denton, Nature’s Destiny: How the laws of biology reveal purpose in the universe, New York: Free Press, 1998, pp. 285-6.
  3. Barbara E. Wright, ‘A biochemical mechanism for nonrandom mutations and evolution’, Journal of Bacteriology, v. 192, 2000, pp. 2993-3001; James A. Shapiro, ‘Adaptive mutation: who’s really in the garden?’, Science, v. 268, 1995, pp. 373-4; Anna Maria Gillis, ‘Can organisms direct their own evolution?’, BioScience, v. 41, 1991, pp. 202-5.
  4. Mae-Wan Ho, Genetic Engineering: Dream or nightmare?, Dublin: Gateway, 2nd ed., 1999, pp. 132-5.
  5. http://star.tau.ac.il/~inon/wisdom1/node4.html, /~inon/baccyber0.html.
  6. James A. Shapiro, ‘Bacteria as multicellular organisms’, Scientific American, v. 258, 1988, p. 82.
  7. Wesson, Beyond Natural Selection, p. 239.
  8. Lynn H. Caporale, ‘Genomes don’t play dice’, New Scientist, 6 March 2004, pp. 42-5.

The overrated gene

  1. Rupert Sheldrake, The Rebirth of Nature: The greening of science and God, New York: Bantam Books, 1991, p. 107.
  2. www2.hivolda.no/alu/fag/naturfag/Bilder/photosystem%20I%20protein.jpg; www.jenner.ac.uk/BacBix3/BIXdef.htm.
  3. Sheldrake, The Presence of the Past, pp. 89-90.
  4. Rupert Sheldrake, A New Science of Life: The hypothesis of formative causation, London: Paladin, 1988, p. 27.
  5. The Presence of the Past, p. 158.
  6. Wesson, Beyond Natural Selection, p. 72.
  7. The Rebirth of Nature, p. 116.

Regulatory genes

  1. Sheldrake, The Presence of the Past, pp. 89, 138.
  2. Quoted in Michael A. Cremo, Human Devolution: A Vedic alternative to Darwin’s theory, Los Angeles, CA: Bhaktivedanta Book Publishing, 2003, p. 69.

Micro- and macroevolution

  1. Keith S. Thompson, ‘Macroevolution: the morphological problem’, American Zoologist, v. 32, 1992, pp. 106-12.
  2. Wesson, Beyond Natural Selection, pp. 196-8.
  3. Lyall Watson, Supernature II, London: Sceptre, 1987, pp. 24-5.

Breeding limits

  1. Duane T. Gish, Evolution: The fossils still say no!, El Cajon, CA: Institute for Creation Research, 1995, pp. 32-3.
  2. Quoted in Milton, The Facts of Life, p. 162.

Population genetics

  1. Walter J. ReMine, The Biotic Message: Evolution versus message theory, Saint Paul, MN: St. Paul Science, 1993, pp. 208-36.
  2. Denton, Nature’s Destiny, pp. 338-9.
  3. William R. Corliss (comp.), Biological Anomalies: Mammals II, Glen Arm, MD: Sourcebook Project, 1996, pp. 196-7.
  4. Nature’s Destiny, p. 281; Ho, Genetic Engineering, pp. 125-6.

Inheritance of acquired characteristics

  1. Sheldrake, The Presence of the Past, pp. 140-6, 275-9.



Evolution and Design: Part 2

Evolution and Design: Contents


Homepage