Evolution and Design

 

David Pratt

May 2004, May 2014

 

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. The fossil record
    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 of the same species have allegedly given rise to new species and ultimately to the amazing diversity of life we see today.

Many scientists have challenged the central role that neo-Darwinism, 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. The same applies to 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.

Darwinists attach increasing importance to regulatory genes. These genes can turn other genes on or off, so that new organs, supposedly already encoded in the genes, can appear very quickly and ‘simply’. But there is no satisfactory explanation for 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. Moreover, DNA merely contains the code for the sequence of amino acids in proteins; it is not known to carry instructions for the assembly of proteins into cells, tissues, organs and entire body forms. In other words, genes do not contain the blueprint for the formation of organisms during embryogenesis. Many biologists now think that ‘epigenetic’ factors within the cell explain the origin of form, but this is little more than a speculative hypothesis. Some scientists invoke ‘self-organization’ – but giving the problem a name is not the same as explaining it.

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 sequence 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. Existing fossils do not give a clear 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. It is becoming increasingly implausible to attribute this problem to the imperfection of the fossil record.

Contrary to neo-Darwinist expectations, most species suddenly appear on the scene, live for millions of years essentially unchanged, and then die out. Recognizing this, some Darwinists 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 – 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?

An article in Trends in Ecology and Evolution in 2008 acknowledged that there exists a ‘healthy debate concerning the sufficiency of neo-Darwinian theory to explain macroevolution’.5 Biologist Scott Gilbert has stated: ‘The modern synthesis is remarkably good at modeling the survival of the fittest, but not good at modeling the arrival of the fittest.’6 According to palaeontologists James Valentine and Douglas Erwin, neo-Darwinism fails to account for the origin of new body plans and consequently ‘biology needs a new theory to explain “the evolution of novelty”’.7 In 2009 Eugene Koonin stated that breakdowns in core neo-Darwinian tenets such as the ‘traditional concept of the tree of life’ or the belief that ‘natural selection is the main driving force of evolution’ indicate that ‘the modern synthesis has crumbled, apparently, beyond repair’.8 About 850 scientists have signed the following statement: ‘We are skeptical of claims for the ability of random mutation and natural selection to account for the complexity of life. Careful examination of the evidence for Darwinian theory should be encouraged.’9

Conventional evolutionary theory depicts 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.10

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 arch-rivals, the biblical creationists. There appears to be a widespread belief that the only alternative to blind chance is the biblical Jehovah! The intelligent design movement presents evidence pointing to some sort of designer, without linking this concept to a specific religious faith. Most scientists dismiss any talk of intelligent, nonphysical agencies as ‘not science’ or as ‘religion masquerading as science’. Geneticist Richard Lewontin stated:

We take the side of science ... because we have a prior commitment ... to materialism. ... [W]e are forced by our a priori adherence to material causes to create an apparatus of investigation and a set of concepts that produce material explanations, no matter how counter-intuitive, no matter how mystifying to the uninitiated. Moreover, that materialism is absolute, for we cannot allow a Divine Foot in the door.’11

Another biologist put it this way: ‘Even if all the data point to an intelligent designer, such an hypothesis is excluded from science because it is not naturalistic.’12 In other words, anything that contradicts mechanistic materialism is ‘unscientific’, no matter how well supported by empirical data.

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, more mindlike 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. Michael A. Bell, ‘Gould’s most cherished concept’, Trends in Ecology and Evolution, v. 23, no. 3, 2008, pp. 121-2.
  6. John Whitfield, ‘Biological theory: postmodern evolution?’, Nature, v. 455, 2008, pp. 281-4, nature.com.
  7. Quoted in Stephen C. Meyer, Darwin’s Doubt: The explosive origin of animal life and the case for intelligent design, New York: HarperOne, 2013, p. 292.
  8. Eugene V. Koonin, ‘The Origin at 150: is a new evolutionary synthesis in sight?’, Trends in Genetics, v. 25, 2009, pp. 473-4.
  9. dissentfromdarwin.org.
  10. Beyond Natural Selection, p. 308.
  11. Quoted in Darwin’s Doubt, p. 386.
  12. Scott C. Todd, ‘A view from Kansas on that evolution debate’, Nature, v. 401, 1999, p. 423.


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 ammonia, methane and hydrogen and contained no free oxygen has also been called into doubt. Instead, it is now widely believed to have been a mixture of carbon dioxide, carbon monoxide, nitrogen and water vapour, and to have included significant amounts of free oxygen. Such atmospheric conditions would have hampered the production of amino acids and other molecules necessary for life, and broken down any organic molecules that did form.1

All modern life forms contain genes made of DNA (deoxyribonucleic acid), which contains nucleobases, whose sequence encodes instructions for making proteins. However, DNA is unable to manufacture proteins by itself. Protein synthesis requires ribonucleic acid (RNA) and a tightly integrated sequence of reactions, involving over a hundred different proteins (including enzymes, which catalyze chemical reactions). This poses a chicken-and-egg problem: which came first, nucleic acids or proteins?


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 to which is attached a phosphate and one of four nucleobases: 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. When a cell divides, its DNA replicates by separating into two single strands, each of which serves as a template for a new strand.


Fig. 2.2. Highly simplified diagram of protein synthesis (or gene expression). During transcription, the sequence of nucleobases on a strand of DNA is reproduced on a molecule called messenger RNA (mRNA) by an enzyme known as RNA polymerase. Next, mRNA migrates from the cell nucleus to a structure called a ribosome in the cytoplasm, where a process known as translation takes place. With the help of transfer RNAs (tRNAs) and specific enzymes, a chain of amino acids is built up, with each amino acid being specified by a three-nucleotide sequence (a codon) on the mRNA. The amino-acid chains then fold into functional proteins. The full complexity of protein synthesis is staggering (see animation).


RNA is less complex, but also less stable, than DNA, and uses the same chemical alphabet, except that uracil is substituted for thymine. Many biologists believe that early in the earth’s history there was an ‘RNA world’, which eventually developed into the DNA, RNA and protein world of today. It was thought that this would solve the chicken-and-egg problem, because as well as being able to store information, certain RNA molecules possess some of the catalytic properties of proteins. But the theory does not solve the problem of the origin of RNA. Synthesizing and maintaining RNA constituents, particularly ribose (a sugar) and the nucleobases, have proven either extremely difficult or impossible under realistic prebiotic conditions.2 Various additional 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 none provides a convincing explanation for the origin of the cell’s genetic code and information-processing system. Some scientists have suggested that the first living organisms might have been carried to earth from other planets (e.g. Mars) or outer space – but this merely moves the problem elsewhere.

Each of the 60 trillion cells in the human body contains a 2-metre-long string of DNA coiled into a tiny ball about 5 thousandths of a millimetre in diameter in the cell nucleus. The information storage density of DNA is many times that of our most advanced silicon chips.3 DNA can store information on protein synthesis so efficiently that all the information needed for 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.4

Physicist Paul Davies has said that ‘the spontaneous generation of life by random molecular shuffling is a ludicrously improbable event’.5 Douglas Axe calculated that the probability of producing a functional protein of modest length (150 amino acids) at random is only about 1 in 1074 (i.e. 1 followed by 74 zeroes). Moreover, chains of amino acids will only fold into a protein if they are joined by a chemical bond known as a peptide bond – with a probability of 1 in 1045. There are thousands of kinds of amino acid, but living organisms contain only 20 kinds, and although amino-acid molecules occur in both right- and left-handed forms, only left-handed amino acids are found in the protein of living organisms – the probability of this is also about 1 in 1045. This means that the odds of producing even one functional protein of modest length by chance from a prebiotic soup is no better than 1 in 10164. If we assume that a minimally complex cell needs at least 250 proteins of, on average, 150 amino acids, the probability of a living cell arising by chance is just 1 in 1041,000 – an unimaginably small number.6 Astrophysicist Fred Hoyle concluded that the probability of even the simplest known life form 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’.7

Even if 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 ...8

Beginning with the Miller-Urey experiment in 1953, scientists have spent countless hours trying to create life in the laboratory, by passing sparks through favourable mixtures of gases (now considered to be unrepresentative of the early atmosphere), but all they have achieved is the production of certain prebiotic organic molecules, such as amino acids. The experiments have been described as ‘a story of abject scientific failure’, because any desirable molecules formed invariably react with unwanted by-products, resulting in ‘tar-like goo’.9 No nucleotides of any kind have ever been produced in spark-discharge experiments. In other types of experiments chemists have managed to engineer a partially self-replicating RNA molecule, but only by exercising great ingenuity and creating unrealistic conditions.10 The irony of this has not gone unnoticed:

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!11


Fig. 2.3. There are two types of cells: prokaryotic cells contain no nucleus, while eukaryotic cells contain a nucleus and membrane-bound organelles such as mitochondria. Single-cell prokaryotic organisms are believed to have appeared about 3.8 billion years ago, and eukaryotic cells about 2 billion years ago. Eukaryotes include many unicellular organisms (e.g. protozoa) and all multicellular organisms (including plants, fungi, animals and humans).


A typical animal 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, experiments 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’.12


Fig. 2.4. A typical animal cell: 1. nucleolus; 2. nucleus; 3. ribosome (the dots); 4. vesicle; 5. rough endoplasmic reticulum; 6. Golgi apparatus; 7. cytoskeleton; 8. smooth endoplasmic reticulum; 9. mitochondrion; 10. vacuole; 11. cytosol; 12. lysosome; 13. centriole; 14. cell membrane.13


Geneticist Jacques Monod admitted that the origin of the genetic code and its translational mechanism was a ‘veritable enigma’, and Francis Crick, cowinner with James Watson of the Nobel prize for the discovery of the structure of DNA, said that the origin of life appeared to be ‘almost a miracle’.14 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.15 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’.16

Life is believed to have appeared on earth about 3.8 billion years ago, within just 10 or 20 million years of viable conditions arising. 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’.17 Many other scientists 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.18 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 constituents 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.’19 For instance, self-organizing bonding affinities cannot explain the specific arrangement of nucleobases in DNA because there are no chemical bonds between its nucleobases, and there are no differential affinities between the bases and the sugar-phosphate backbone, which means that any base can attach to the backbone at any site with equal ease.20 Physicochemical laws describe highly regular, ordered patterns, but lawlike processes cannot generate functional information, which is characterized by irregular complexity. Mind or intelligence is the only cause known to be capable of generating the complexity and information content found in DNA and RNA.

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.21 Astronomer Erich Jantsch wrote: ‘Life no longer appears as a thin superstructure over a lifeless physical reality, but as an inherent principle of the dynamics of the universe.’22 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.23

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 more ethereal 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.24

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. Stephen C. Meyer, Signature in the Cell: DNA and the evidence for intelligent design, New York: HarperOne, 2009, pp. 224-6; Simon Conway Morris, Life’s Solution: Inevitable humans in a lonely universe, New York: Cambridge University Press, 2003, pp. 61-2.
  2. Signature in the Cell, p. 301.
  3. Ibid., p. 97.
  4. Michael Denton, Evolution: A theory in crisis, Bethesda, MA: Adler & Adler, 1986, p. 351.
  5. Paul Davies, The Cosmic Blueprint, London: Unwin, 1989, p. 118.
  6. Signature in the Cell, pp. 210-3.
  7. Quoted in Alexander Mebane, Darwin’s Creation-Myth, Venice, FL: P&D Printing, 1994, p. 35.
  8. Evolution: A theory in crisis, pp. 266-7.
  9. Life’s Solution, pp. 37, 44.
  10. Signature in the Cell, pp. 302, 313-4, 334-5.
  11. Corona Trew and E. Lester Smith (eds.), This Dynamic Universe, Wheaton, IL: Theosophical Publishing House, 1983, p. 132.
  12. Guenter Albrecht-Buehler, ‘Cell intelligence’, basic.northwestern.edu. See Rudi Jansma, ‘Cosmic mind in the microcosm’, Sunrise, April/May 2004, pp. 118-26.
  13. en.wikipedia.org.
  14. Quoted in Evolution: A theory in crisis, p. 268.
  15. Darwin’s Creation-Myth, pp. 35-6.
  16. Rodney Brooks, ‘The relationship between matter and life’, Nature, v. 409, 2001, pp. 409-11.
  17. Stephen Jay Gould, Wonderful Life: The Burgess Shale and the nature of history, New York: Norton, 1989, pp. 289, 309.
  18. David P. Woetzel, ‘The spontaneous generation hypothesis’, Creation Research Society Quarterly, v. 38, no. 2, 2001, pp. 75-8.
  19. Michael J. Behe, William A. Dembski and Stephen C. Meyer, Science and Evidence for Design in the Universe, San Francisco, CA: Ignatius Press, 2000, p. 87.
  20. Signature in the Cell, pp. 240-9.
  21. ‘The spontaneous generation hypothesis’.
  22. Quoted in Anna F. Lemkow, The Wholeness Principle: Dynamics of unity within science, religion & society, Wheaton, IL: Quest, 1990, p. 137.
  23. David Bohm and F. David Peat, Science, Order & Creativity, London: Routledge, 1989, pp. 200-1.
  24. 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 (as 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’. Richard Dawkins likens it to a ‘blind watchmaker’. 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. It acts like a sieve. To call it ‘creative’ is disingenuous. As molecular biologist James Shapiro puts it, ‘Selection operates as a purifying but not creative force’.3

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: ‘Pure chance, absolutely free but blind, [is] at the very root of the stupendous edifice of evolution ...’4

Some evolutionists have said that it would be more accurate to speak of the ‘survival of the luckiest’ rather 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.5

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’!


References

  1. Quoted in Robert Wesson, Beyond Natural Selection, Cambridge, MA: MIT Press, 1994, p. 9.
  2. Ernst Haeckel, The Pedigree of Man, London: A. and H.B. Bonner, 1903, p. 34, archive.org. Quoted in H.P. Blavatsky, The Secret Doctrine, Pasadena, CA: Theosophical University Press, 1977 (1888), 2:652.
  3. James A. Shapiro, Evolution: A view from the 21st century, Upper Saddle River, NJ: FT Press Science, 2011, p. 144.
  4. Quoted in Michael Denton, Evolution: A theory in crisis, Bethesda, MA: Adler & Adler, 1986, p. 43.
  5. Rupert Sheldrake, The Presence of the Past: Morphic resonance and the habits of nature, New York: Vintage, 1989, p. 281.

Random mutations

Genetic mutations may involve the substitution, deletion or insertion of nucleotides, or the inversion or duplication of a DNA segment. 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, plasmids (DNA molecules separate from chromosomal DNA), and transposons (DNA sequences that move from one genome location to another).

Because cells possess sophisticated DNA proofreading and repair systems, mutations are rare. On average, a mistake is made only once for every hundred million nucleotides of DNA copied in a generation. Each human gene has an estimated likelihood of mutation of about 1 in 100,000 per generation. The consequences of mutations range from negligible to lethal; very few are 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 neo-Darwinism 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. 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 More recently, Douglas Axe determined experimentally that the probability of a mutation producing a new functional protein of modest length is 1 in 1077.3

Biologist Lynn Margulis stated that history will ultimately judge neo-Darwinism as ‘a minor twentieth-century religious sect within the sprawling religious persuasion of Anglo-Saxon biology’. She said that 99.9% of random genetic mutations ‘tend to induce sickness, death, or deficiencies’, and challenged people to name a single unambiguous example of the formation of a new species by the slow accumulation of mutations. Neo-Darwinism, she says, ‘is in a complete funk’.4

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.5

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.6

However, as Dawkins admits, this computer ‘simulation’ certainly does not prove that random combinations of chemicals could gradually produce biologically functional proteins. First, it involves the existence of a target sequence, whereas Darwinian evolution is supposed to be blind, 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 have been cited as proof of the plausibility of random evolution.

Other biologists have devised more sophisticated evolutionary algorithms to simulate how mutation and selection can supposedly generate new biological information. But in no case do such algorithms produce large amounts of functionally specified information entirely from scratch; such simulations succeed only if the programmer has designed them to converge on the desired solution in a manner at odds with truly Darwinian processes.7 As David Berlinski puts it: ‘Where attempts to replicate Darwinian evolution on the computer have been successful, they have not used classical Darwinian principles, and where they have used such principles, they have not been successful.’8

Key biological structures such as the inner ear, the amniotic egg, eyes, olfactory organs, gills, lungs, feathers, and reproductive, circulatory and respiratory systems depend for their function on the coordinated action of many components. As Stephen Meyer says: ‘Genetic change affecting any one of the necessary components, unless matched by many corresponding – and vastly improbable – genetic changes, will result in functional loss and often death.’9 This has led to the development of neutral theories of evolution: one set of genes becomes duplicated, and the duplicated genes, which are not immediately expressed, undergo multiple mutations without compromising the fitness of an organism, and also without any natural selection to eliminate harmful mutations. Then at some point, the existing genes are deactivated and the newly mutated genes are activated, resulting in the – magical – appearance of a viable new biological structure.10 This is typical of the woolly wishful-thinking that characterizes neo-Darwinism. Where necessary, Darwinists simply invoke the ‘fortuitous juxtaposition’ of suitable genetic sequences, the ‘hypermutability’ of genes, ‘extensive refashioning’ of the genome, or some other scientific-sounding phrase; and if all else fails, they can always fall back on the ‘de novo origination’ of new genes.11


References

  1. ‘Evolution’, Encyclopaedia Britannica, CD-ROM 2004.
  2. Stephen C. Meyer, Darwin’s Doubt: The explosive origin of animal life and the case for intelligent design, New York: HarperOne, 2013, p. 200.
  3. Michael Denton, Evolution: A theory in crisis, Bethesda, MA: Adler & Adler, 1986, p. 324.
  4. 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.
  5. Richard Milton, The Facts of Life: Shattering the myths of Darwinism, London: Corgi, 1993, pp. 178-80.
  6. 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.
  7. Stephen C. Meyer, Signature in the Cell: DNA and the evidence for intelligent design, New York: HarperOne, 2009, pp. 284-94.
  8. David Berlinski, The Deniable Darwin and Other Essays, Seattle, WA: Discovery Institute Press, 2009, p. 446.
  9. Darwin’s Doubt, p. 233.
  10. Ibid., pp. 236-7, 325-6.
  11. Ibid., p. 228.

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 possibility of adaptive, nonrandom mutations.2

More recent experiments 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 Shapiro states that ‘All careful studies of mutagenesis find statistically significant nonrandom patterns of change ...’8

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.9 This is a good example of how Darwinists sometimes dress up their dogmas in ‘sexy’ and even mystical-sounding language.


References

  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. tamar.tau.ac.il/~eshel; http://archive.is/wZmo3.
  6. James A. Shapiro, ‘Bacteria as multicellular organisms’, Scientific American, v. 258, 1988, p. 82.
  7. Robert Wesson, Beyond Natural Selection, Cambridge, MA: MIT Press, 1994, p. 239.
  8. Shapiro, Evolution: A view from the 21st century, p. 82.
  9. Lynn H. Caporale, ‘Genomes don’t play dice’, New Scientist, 6 March 2004, pp. 42-5.

The overrated gene

Morphogenesis – literally, the ‘coming into being of form’ – is 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’ or ‘genotypes’. 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. Above: The protein haemoglobin. Below: The enzyme T7 RNA polymerase (blue) producing mRNA (green) from a double-stranded DNA template (orange).


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 physicochemical 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.2

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.’3 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.’4

Simon Conway Morris, a Darwinian evolutionist, admits that ‘Claims for the primacy of the gene have distorted the whole of biology ... ’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

The American golden plover is able to fly over 2200 miles from Alaska to Hawaii without eating any food on the way. Before departing, they gain 2.5 ounces in a short time, so that they weigh about 7 ounces. By flying in a V formation, at the optimum energy-saving speed (just under 32 miles per hour), and taking it in turns to occupy the lead position, the birds use only 2.24 ounces of fat from their reserves instead of the calculated 2.9 ounces, and reach their destination with a few grams to spare. Somehow they know where the Hawaiian Islands are, and can correct their course without any visible point of reference even if a storm drives them off course. As Hornyánszky and Tasi point out, ‘We can say these are just the effects of instinct and hormones, but giving a scientific name to the wonder does not actually explain its origin.’7

There are countless other examples of instinctive animal behaviour that could not have evolved step by step. For instance, cleaner wrasses pick parasites off bigger fish, even inside their mouths, in a symbiotic relationship that provides food for the wrasse and health benefits for the other fish. Cleaner wrasses first perform a dance-like motion, and the bigger fishes adopt a specific pose to allow them access to their body surface, gills and sometimes mouth. Similarly, pilot fish often enter a shark’s mouth and clean fragments of food from between its teeth.8


Fig. 3.2. A bluestreak cleaner wrasse in the mouth of a grouper.


The courting and mating rituals of males and females of the same species, and their sexual organs, have to evolve simultaneously and match perfectly, otherwise reproduction could not take place. For example, great crested glebes seal their mate selection for life by synchronized swimming. First one of them swims underwater toward the other while the latter watches in a characteristic bent posture. The bird swimming then emerges from under the water in a vertical position and both begin to shake their heads and arrange each other’s wing feathers. ‘Out of the many similar, highly elaborate scenes, the most lyrical is the “hair-weed dance” directly preceding nesting. They both dive under the water and emerge with a bunch of hair-weed in their bills. Then they quickly swim toward each other swaying their heads, and completely emerging from the water, start dancing.’9 Both birds somehow know the exact sequence of dance steps and how to respond to the movements of their partner.

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.’10 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.


References

  1. Rupert Sheldrake, The Rebirth of Nature: The greening of science and God, New York: Bantam Books, 1991, p. 107.
  2. Rupert Sheldrake, The Presence of the Past: Morphic resonance and the habits of nature, New York: Vintage, 1989, pp. 89-90.
  3. Rupert Sheldrake, A New Science of Life: The hypothesis of formative causation, London: Icon Books, 3rd ed., 2009, p. 39.
  4. The Presence of the Past, p. 158.
  5. Simon Conway Morris, Life’s Solution: Inevitable humans in a lonely universe, New York: Cambridge University Press, 2003, p. 238.
  6. Robert Wesson, Beyond Natural Selection, Cambridge, MA: MIT Press, 1994, p. 72.
  7. Balázs Hornyánszky and István Tasi, Nature’s I.Q., Badger, CA: Torchlight Publishing, 2009, pp. 91-3.
  8. Ibid., pp. 42-5; en.wikipedia.org/wiki/Bluestreak_cleaner_wrasse; dailymail.co.uk.
  9. Nature’s I.Q., pp. 111-3.
  10. The Rebirth of Nature, p. 116.

Regulatory genes

The genome consists not only of structural, or protein-coding genes, but also of regulatory genes (also known as homeotic, homeobox, Hox, or toolbox genes), which control the expression of one or more other genes and the pattern in which different parts of an embryo or larva develop. The study of regulatory genes is part of a growing field called evolutionary developmental biology, or evo-devo for short. Evolutionary developmental biologists argue that mutations affecting regulatory genes can generate large-scale morphological change and even whole new body plans.

Homeobox genes are currently the best-known group of regulatory genes; they determine where limbs and other body segments form. In the 1990s researchers were astounded to discover that homeobox genes are almost identical in different multicellular animals; they control the development of analogous sections of the growing embryo of flies, reptiles, mice and humans – a finding entirely unanticipated by neo-Darwinism. 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.

Scientists have discovered that the cell’s regulatory system displays ‘mind-boggling complexity’ (see fig. 3.3). Biochemist Michael Behe (pronounced: BeeHee) writes:

[T]he control systems that affect when, where, and how much of a particular protein is made are becoming so complex, and their distribution in the DNA so widespread, that the very concept of a ‘gene’ as a discrete region of DNA is no longer adequate. ... In animals, a master switch sets in train a whole cascade of lesser switches, where the initial regulatory protein turns on the genes for other regulatory proteins, which turn on other regulatory proteins, and so on.1

There may be more than ten regulatory proteins controlling each protein-encoding gene used in building an animal’s body. Note that control genes, like structural genes, do not embody the instructions to build particular bodily structures – they merely mark certain areas of the body, and signal other genes to turn on or off.


Fig. 3.3. Overview of the developmental gene regulatory network (dGRN) for the construction of a tissue called the endomesoderm in sea urchins, concentrating on the network after 21 hours. The diagram strongly resembles a complex electrical or computer-logic circuit. (http://sugp.caltech.edu/endomes)


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. The elimination of certain genes may prevent the formation of a given organ but, as Stuart Pivar says, ‘this does not mean that the gene shaped the organ, any more that a lamp switch creates light’.2 Moreover, 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. 3.4. 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.3

 

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 helps regulate the development of compound eyes (composed of hundreds of separate lenses), as found in fruit flies (arthropods), and camera-type eyes (with a single lens and retinal surface), as found in squid and mice (cephalopods and vertebrates respectively). Darwinists have concluded that Pax-6 is 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.4

Moreover, Pax-6 is also involved in the development of other organs, including nose, brain, pituitary gland, gut and pancreas. It is also expressed in nematodes, which are eyeless. In at least one group of animals (flatworms), Pax-6 is involved in eye formation but if it is ‘knocked out’ during the process of regeneration (for which flatworms are famous) eyes still form.5

Here is another example of largely identical genetic sequences regulating the development of very different structures in different organisms:

In fruit flies, the gene distal-less regulates the development of compound limbs with exoskeletons and multiple joints. In sea urchins, however, the homologous gene regulates the development of spines. In vertebrates, by contrast, it regulates the development of another type of limb, with multiple joints but an internal bony skeleton. Except insofar as these structures all exemplify a broad general class, namely, appendages, they have little in common with each other. ... The gene distal-less and its homologues function as switches, but in each case a switch that regulates many different downstream genes, leading to different anatomical features, depending upon the large informational context in which the gene finds itself.6

Many biologists found this surprising because orthodox evolutionary theory had led them to assume that genes control the development of organisms and anatomical structures and that homologous genes should therefore produce homologous structures and organisms.

The evo-devo hope is that cells’ regulatory systems somehow make evolution easier. In reality, the exact opposite is the case. As Behe puts it, ‘the elaborate assembly control instructions for whole animals are a further layer of complexity, beyond the complexity of the animal’s anatomy itself’.7 Supposedly blind, random mutations need to change both structural and regulatory genes in just the right ways to produce proteins in the right places at the right times to build a new organ or body plan. But experiments have shown that mutating the genes that regulate body-plan construction tend to destroy animal forms.8

Moreover neither structural nor regulatory genes actually determine the form of any body structures. What does determine them is essentially unknown. That there are additional, epigenetic (i.e. nongenetic) formative influences at work 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. In another experiment, a portion of a newt embryo was transplanted into another developing newt embryo, which then produced two bodies, each with a head and tail, but joined together at the belly; the anatomy of the embryo was thus dramatically altered even though its DNA remained unchanged.9 Epigenetic information is thought to be contained in cell structures other than DNA, and to involve, for example, patterns in the cytoskeleton (the cellular scaffolding or skeleton in a cell’s cytoplasm) and in the cell membrane,10 but these patterns, too, are probably effects of more fundamental causes.

Darwinism therefore fails to account for the origin of both the genetic and nongenetic information necessary to produce new forms of life, and cannot explain what actually determines an organism's physical shape. As Stuart Pivar says, during embryogenesis ‘cells seem to run about helter-skelter, organizing themselves into organs as though they knew in advance where to go, all to the utter confusion of embryologists. ... It is difficult, if not impossible, to assign epigenetic, mechanically causative effects to the successive steps of observed embryology. Instead, it is as though the cells give the illusion of filling an invisible mold.’11


References

  1. Michael J. Behe, The Edge of Evolution: The search for the limits of Darwinism, New York: Free Press, 2008, pp. 101, 178.
  2. Stuart Pivar et al., The Urform Theory: Evolution without Darwin, Synthetic Life Lab, 2011, p. 5.
  3. Rupert Sheldrake, The Presence of the Past: Morphic resonance and the habits of nature, New York: Vintage, 1989, pp. 89, 138.
  4. Quoted in Michael A. Cremo, Human Devolution: A Vedic alternative to Darwin’s theory, Los Angeles, CA: Bhaktivedanta Book Publishing, 2003, p. 69.
  5. Simon Conway Morris, Life’s Solution: Inevitable humans in a lonely universe, New York: Cambridge University Press, 2003, p. 240.
  6. Stephen C. Meyer, Signature in the Cell: DNA and the evidence for intelligent design, New York: HarperOne, 2009, p. 471.
  7. The Edge of Evolution, p. 192.
  8. Meyer, Darwin’s Doubt, p. 257.
  9. Ibid., pp. 271-2.
  10. Ibid., pp. 285-6; Signature in the Cell, pp. 475-6.
  11. The Urform Theory, p. 4, 83.

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. 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, with the help of natural selection, 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

Macroevolutionary change requires changes in very early embryogenesis. During embryonic development, the appropriate genes must be turned on or off to ensure the production of the right protein products at the right time and in the right cell types. As already explained, the protein-coding regions of the genome and the non-protein-coding regions that control gene expression together function as circuits, known as developmental gene regulatory networks (dGRNs). The overall precision and complexity of this system are stunning. Not surprisingly, experiments have shown that mutations affecting the dGRNs that regulate body-plan development have catastrophic effects on the organism, leading to abnormalities or death.4 Moreover, the genetic and epigenetic information contained in cells does not explain the form of developing organisms. In short, anything Darwinists say about one organism being transformed into a very different organism (e.g. a fish into an amphibian) purely by random genetic mutations or other physical changes should be taken with a large pinch of salt.


References

  1. Keith S. Thompson, ‘Macroevolution: the morphological problem’, American Zoologist, v. 32, 1992, pp. 106-12.
  2. Robert Wesson, Beyond Natural Selection, Cambridge, MA: MIT Press, 1994, pp. 196-8.
  3. Lyall Watson, Supernature II, London: Sceptre, 1987, pp. 24-5.
  4. Stephen C. Meyer, Darwin’s Doubt: The explosive origin of animal life and the case for intelligent design, New York: HarperOne, 2013, pp. 259-70.

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 produce 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 neo-Darwinism – that bears can become whales, or microbes can eventually become elephants by means of random mutation and natural selection.


References

  1. Duane T. Gish, Evolution: The fossils still say no!, El Cajon, CA: Institute for Creation Research, 1995, pp. 32-3.
  2. Quoted in Richard Milton, The Facts of Life: Shattering the myths of Darwinism, London: Corgi, 1993, p. 162.

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 five-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. He found that 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 on the false assumption that genes determine form. 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. However, modern Darwinists like to claim – not very convincingly – that Haldane’s Dilemma has been ‘solved’, and that key evolutionary processes really are simple, fast and virtually inevitable.1

Based on the principles of population genetics, several calculations and experiments since 2004 have pointed to the inability of random mutation and natural selection to explain the evolution of life. Michael Behe and David Snoke found that if generating a new functional gene or trait required two or more coordinated mutations, it typically required either unreasonably long waiting times, exceeding the duration of life on earth, or unreasonably large population sizes, exceeding the number of multicellular organisms that have ever lived.2 The neo-Darwinian mechanism is unable to generate even two coordinated mutations in the 6 million years that have allegedly elapsed since humans and chimps diverged from a common ancestor. Two defenders of neo-Darwinism, Rick Durrett and Deena Schmidt, set out to refute this conclusion by making their own calculations. But even they concluded that it would take 216 million years to generate and fix two coordinated mutations in the hominid line.3

Some neo-Darwinists have proposed that a protein that performs one function can be transformed, or co-opted, to perform some other function. Douglas Axe and Ann Gauger decided to test this experimentally. They found that too many coordinated mutations would be required to convert one protein function to another, even in the case of extremely similar proteins. Axe found that, taking into account the probable fitness cost to an organism of carrying unnecessary gene duplicates (as was necessary to give the evolution of a new gene a reasonable chance), the probable waiting time for even three coordinated mutations exceeds the duration of life on earth. In short, ‘the neo-Darwinian mechanism cannot generate the information necessary to build new genes, let alone a new form of animal life, in the time available to the evolutionary process’.4


References

  1. Walter J. ReMine, The Biotic Message: Evolution versus message theory, Saint Paul, MN: St. Paul Science, 1993, pp. 208-36; Walter J. ReMine, ‘Cost theory and the cost of substitution – a clarification’, Journal of Creation, v. 19, no. 1, 2005, pp. 113-25, creation.com; Walter ReMine, ‘Haldane’s dilemma’, 2007, http://users.minn.net/science/Haldane.htm.
  2. MStephen C. Meyer, Darwin’s Doubt: The explosive origin of animal life and the case for intelligent design, New York: HarperOne, 2013, pp. 245-7.
  3. Ibid., pp. 248-9.
  4. Ibid., pp. 252-4.

Inheritance of acquired characteristics

Until the late 19th century, most scientists 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. At the beginning of the 20th century, however, Lamarckian inheritance was completely rejected, because according to the ‘central dogma’ of molecular biology, 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).

However, the taboo against Lamarckian inheritance began to lift at the turn of the millennium with the widespread recognition of epigenetic inheritance, which involves changes in gene expression rather than changes in the genes themselves. Mechanisms include changes in chromatin (the DNA-protein complex forming a cell nucleus), the methylation of DNA molecules, and changes to cell cytoplasm.1 Advocates of neo-Lamarckianism point out that the inheritance of epigenetic information independently of DNA allows evolutionary possibilities denied by neo-Darwinism. However, the heritability of such changes has so far proved transient, lasting from a few generations up to 40; no experiment has yet resulted in an induced epigenetic change persisting permanently in any population.2

There is plenty of evidence that acquired characteristics can be inherited. For instance, mice of the agouti strain are fat, yellow and disease prone, but females who had been given a food supplement gave birth to many offspring who were slender, brown and long-lived. There are also many examples of epigenetic inheritance in humans. For example, one study found that nutrition in male children affected the incidence of diabetes and heart disease in their grandchildren. In the 1950s C.H. Waddington conducted experiments showing that two-winged fruit flies exposed to ether fumes could produce four-winged fruit flies (known as bithorax phenocopies). The ether did not induce specific mutations in the DNA but disturbed the normal pathway of development. By exposing fruit fly eggs to ether generation after generation, the proportion of bithorax flies increased, until after 29 generations some offspring showed the bithorax character without any exposure to ether. Later experiments have confirmed that the proportion of bithorax phenocopies increases progressively in successive generations. Rupert Sheldrake proposes that acquired habits of behaviour and bodily development can be inherited not only by gene selection and epigenetic inheritance, but also through modifications of ‘morphic fields’ (nonphysical organizing fields), which are inherited nongenetically by morphic resonance (see section 6), which increases in strength according to the number of organisms whose development has already been modified.3


Fig. 3.5. The callosities of an ostrich.


Ostriches are born with horny calluses on their rumps, breast and pubis, just where these 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.4 Yet Darwinists 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.


References

  1. Rupert Sheldrake, A New Science of Life: The hypothesis of formative causation, London: Icon Books, 3rd ed., 2009, pp. 163-4.
  2. Stephen C. Meyer, Darwin’s Doubt: The explosive origin of animal life and the case for intelligent design, New York: HarperOne, 2013, pp. 329-32.
  3. A New Science of Life, pp. 162-8.
  4. Rupert Sheldrake, The Presence of the Past: Morphic resonance and the habits of nature, New York: Vintage, 1989, pp. 275-9.



Evolution and Design: Part 2

Evolution and Design: Contents


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