Genes, mutation and natural selection With Richard Dawkins Being Proven A Charlatan

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 ...’ – 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 ...’³
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.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

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 

Dawkins A Charlatan 

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

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.

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.’⁹Both 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.

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

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.

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.’²Although 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.

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 theyconcluded 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

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

Chance and selection

1. James A. Shapiro, Evolution: A view from the 21st century, Upper Saddle River, NJ: FT Press Science, 2011, p. 144.
2. Quoted in Robert Wesson, Beyond Natural Selection, Cambridge, MA: MIT Press, 1994, p. 9.
3. Quoted in H.P. Blavatsky, The Secret Doctrine, Pasadena, CA: Theosophical University Press, 1977 (1888), 2:652.
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

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. Denton, Evolution: A theory in crisis, 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

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. Wesson, Beyond Natural Selection, 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

1. Rupert Sheldrake, The Rebirth of Nature: The greening of science and God, New York: Bantam Books, 1991, p. 107.
2. Sheldrake, The Presence of the Past, 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. Wesson, Beyond Natural Selection, 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

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. Sheldrake, The Presence of the Past, 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. Morris, Life’s Solution, p. 240.
6. Meyer, Signature in the Cell, 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

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.
4. Meyer, Darwin’s Doubt, pp. 259-70.

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; 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. Meyer, Darwin’s Doubt, pp. 245-7.
3. Ibid., pp. 248-9.
4. Ibid., pp. 252-4.

Inheritance of acquired characteristics

1. Sheldrake, A New Science of Life, pp. 163-4.
2. Meyer, Darwin’s Doubt, pp. 329-32.
3. A New Science of Life, pp. 162-8.
4. Sheldrake, The Presence of the Past, pp. 275-9.

An article published by David Pratt. @  http://davidpratt.info/evod1.htm