A critique of Richard Dawkins’ The Greatest Show on Earth: The evidence for evolution - cont...

4. Half-truths about proteins

It is clear Richard Dawkins realises that the complexity of embryological development poses a serious challenge to the theory of evolution, so he goes out of his way to gloss over the realities. The cornerstone of his approach is to try to argue that embryological development proceeds simply through the natural operation of local rules i.e. without an overall plan that would need a designer. I will explain subsequently how his attempted sleight of hand doesn’t work. Meantime ...

Unfortunately (for him), he tries to build up his case with reference to the structure of proteins; but it is his undoing because exposing his half-truths here makes it all the easier to explain the fallacy of trying to apply a similar approach to embryological development. As he says, proteins comprise linear sequences of amino acids, which fold up into a 3-dimensional structure which is essential for their biological function.

Protein molecules, simply by following the laws of chemistry and thermodynamics, spontaneously and automatically twist themselves into precisely shaped three-dimensional configurations. ... Any given sequence of amino acids dictates a particular folding pattern. (p236)

What he fails to say is that, simply because of the laws of chemistry and thermodynamics (his local rules), the vast majority of amino acid sequences will not fold at all. By not acknowledging this, he gives the false impression (false, but no doubt deliberate, as he must surely know this) that most amino acid sequences will fold in this way. Whereas in fact very few do - Douglas Axe estimated that only about 1 in 10^77 sequences have the potential to fold (Estimating the prevalence of protein sequences adopting functional enzyme folds; J Mol Biol 341(5):1295

Dawkins mentions only the specificity of proteins in terms of their ability to selectively bind their substrates (compounds they act on). What he ignores is their active sites - the parts of the proteins that have just the right chemical groups (derived from the right amino acids) in just the right places in relation to the bound substrates so as to catalyse reaction between them. Needless to say, taking these features on board as well, further compounds the specificity required of the amino acid sequence for e.g. an enzyme, and hence reinforces the prohibitive improbability against their arising by chance.

Dawkins comments that at present we are able to predict how some amino acid sequences will fold; and quite likely we will be able to do this for all before too long. But that’s only one side of the coin. What’s required is to identify an amino acid sequence that will fold, and once folded will perform a required biological function. Thanks to increased computing power and some ingenious programming, I expect that one day we will be able to design proteins to fold in a particular way, and maybe perform a particular function. But that will serve only to reinforce the case that functional proteins require a designer.

The nonsense that proponents of evolution would have us believe is that biologically active proteins, with their highly specific and hence improbable sequences, could arise by chance. Dawkins of course rolls out the usual evolutionary article of faith that complex proteins evolved from shorter/simpler precursors. But, as discussed more fully in my book, there are substantial objections to such a scenario.

1. First is the question of folding. The forces between the packed amino acids (Dawkins’ local rules) that hold a protein in its folded state are so weak that there needs to be many amino acids involved, typically requiring a protein to be at least 70 amino acids long (see Protein structure and function by Jack Kyte) So it’s utter nonsense to suggest as some textbooks do, and Dawkins would have us believe, that proteins could have started off with just a handful of amino acids.
2. Second is that key amino acids, such as those contributing to the active site, are generally scattered throughout the linear sequence of the protein, and are brought together only once the protein is folded. If proteins had evolved from short sequences, one would have thought that at least these critical amino acids (which necessarily would need to have been close together in a short protein) would still be grouped together; because to disperse them during the course of subsequent evolution would require constant restructuring of the protein.

It’s all very well for Dawkins to argue that proteins fold merely through the operation of local rules / natural forces. But what he fails to acknowledge is that operation of those rules results in something useful only if the underlying components are right - so far as proteins are concerned, that they have the right amino acid sequence. And the evidence clearly shows that natural selection acting on random mutations could not generate such sequences. Evolutionists merely cling to this hope as a drowning man clings to a straw.

A critique of Richard Dawkins’ The Greatest Show on Earth: The evidence for evolution - cont...

3. The case for ID vindicated

In chapter 5 Dawkins describes various examples of natural selection of which, as I said in the preceding post, all but one are comparable with artificial selection: all that's happening is selection from an existing gene pool; there's no production of new or altered genes. The exception is a long-term experiment using bacteria (by Lenski et al. at Michigan State University) specifically designed to investigate the evolution of new characteristics.

The long-term evolution experiment (LTEE)

For more information about the overall long-term evolution experiment see myxo.css.msu.edu/ecoli/, and for the emergence of the ability to utilise citrate it’s useful to read their paper which is available from www.pnas.org/content/105/23/7899.abstract

The LTEE involves propagating 12 lines of E. coli bacteria, all initially identical (except that 6 had a genetic marker), but then each strain allowed to develop independently. They were grown in a glucose-limiting medium, and initially the experiment was designed to see how their growth adapted to this. The experiment has run since 1988, now exceeding 50,000 bacterial generations.

All strains improved their ability to utilise glucose, evidenced by increased initial rate of consumption, this effect reaching a plateau after about 20,000 generations (typical of selection from a gene pool). On the other hand, all showed reduced ability to utilise other sources of carbon such as maltose or lactose. This is similar to most instances of the acquisition of resistance to antibiotics, discussed in Evolution under the microscope pp235-244, where such resistance is generally at the expense of reduced overall fitness.

Utilisation of citrate

E. coli cannot normally utilise citrate under aerobic conditions, and a surprising discovery was that one strain evolved the ability to do this (citrate was present in the growth medium, and the ability to utilise it resulted in a marked increase in the bacteria’s growth), emerging after about 30,000 generations. Further investigation showed that this development was contingent on an earlier mutation, arising in this strain after about 20,000 generations.

The mutations have yet to be characterised. The authors suggest several possibilities, including enabling the expression of a carrier protein to enable citrate to pass through the cell membrane; as it is transport into the cell that normally limits its use - once inside the cell it is readily metabolised.

Because this evolution required at least two distinct mutations, Dawkins vaunts it as disproving the intelligent design concept of irreducible complexity. But that is merely his spin on the facts; a closer look shows that the results from the experiment actually support the ID case.

Advantageous mutations

A typical mutation rate is approx 10^-9 (1 in 10⁹ per cell per generation) for any particular base in DNA (the authors cite the slightly lower figure of approx 5 x 10^-10 for E. coli). As they say, despite this low rate, given the high numbers of bacteria and generations it can confidently be assumed that during the course of the experiment all possible single point mutations in the bacterial genome will have occurred, probably many times. Of course, as they comment, only a small number of these will become ‘fixed’ in the genome - even advantageous ones will not be fixed automatically but have only a small chance of spreading throughout the population (contrary to many of Dawkins’ comments, for an explanation see a text-book on population genetics).

It is therefore not surprising that not only have the same genes been affected in several of the strains, but that in some cases the same point mutations have been fixed, especially those that improved the ability to metabolise glucose. This too is analogous to the emergence of some antibiotic (and insecticide) resistance where the same point mutation has arisen independently.

Even where two mutations are required (i.e. neither alone confers resistance, so both must arise together, with a probability of doing so of just 1 in 10¹⁸), e.g. some resistance to penicillin, bacterial populations and their reproduction rate are so high that these can occur, albeit at a low frequency.

In a similar way, even after the potentiating mutation, the probability of the citrate-enabling mutation was estimated by the authors at about only 10^-13, which they say indicates the change involves multiple point mutations or a rarer type of mutation.

And the preceding potentiating mutation also had a very low incidence - occurring in only one strain, even after efforts by the researchers to reproduce it. They suggest it may be a neutral mutation, which would have been be fixed only by genetic drift.

Geological time isn't enough

In Evolution under the microscope - based on the rate of occurrence of point mutations, the size of bacterial populations and their rate of reproduction, and supported by the observed instances of resistance - I suggest that the upper limit for multiple dependent mutations that could arise in the course of a year is likely to be 3 or maybe 4. And I went on to point out that, given the mutation rate is about 1 in a billion, this implies that the upper limit for mutually dependent mutations arising throughout the whole of geological time (e.g. a billion years) is only 4 or 5.

So, although it may be possible to switch a gene on or off with just a few point mutations, or modify its performance, this cannot be extrapolated to producing genes in the first place, as typically they require hundreds of specific base pairs e.g. to code for the many essential amino acids in the protein product.

In discussing the possible nature of the citrate-enabling mutation(s) the authors consider reactivation of a cryptic transporter, but think this unlikely because they would expect such a cryptic gene to have been degraded beyond recovery after millions of years of disuse. It begs the question - if they consider it so likely that the effect of random mutation is to degrade genes, how do they think useful genes arose in the first place?

Dawkins frequently emphasises the immense length of geological time, suggesting that this is more than enough to overcome the improbability of advantageous mutations. It is time he did a few simple calculations and started to look at geological time objectively. If he did so, he would realise that it is not the answer to evolution's problems that he makes it out to be.

ID vindicated

And this is why, as I indicated above, far from defeating the case for intelligent design based on irreducible complexity, the LTEE results actually support it - because they demonstrate how limited is the ability of random mutations to generate useful sequences. And - unfortunately it needs to be repeated often - natural selection is dependent on being fed the right raw material on which it can work.

Further, it should be noted that the above-mentioned rate of finding useful mutation combinations applies to such as bacteria which have very large population sizes (at least billions) and high rates of reproduction (more than one generation per day). In organisms with smaller populations and slower reproduction rates, what can be achieved will be so much less.

Which is why, yet again, Dawkins misleads his readers by saying:

So whatever evolutionary change Lenski may have clocked up in the equivalent of a million years of bacterial generations, think how much more evolution might happen in say 100 million years of mammalian evolution (p119)

because the size of the human population will be so much smaller than the bacterial populations of the LTEE.

The ID argument is not that an advantageous mutation cannot occur, or even that a few mutually dependent ones cannot - but that the complexity and specificity of molecular biology would require so many mutually dependent ones that it is not credible they could have occurred.

A critique of Richard Dawkins’ The Greatest Show on Earth - cont..

2. Macroevolution?

Darwin used the artificial selection of domestic breeding to introduce the concept of natural selection. Dawkins follows this, in particular using the breeding of the various types of dog from the wolf to illustrate the range of characteristics that can be achieved. Indeed, he points out that with almost any plant or animal we can breed for almost any trait we wish, such as maize for high or low oil content (p67) or rats for low or high susceptibility to tooth decay (p68). He also observes that in all such cases, though rapid change can be achieved in the first few generations, before long it tails off - not just because e.g. low oil content trends to zero, and you can't get any lower than that, but also the cultivation for high oil content tends to plateau.

Dawkins recognises that domestic breeding is through losing or subtracting genes, comparing it with removing pieces of stone in making a sculpture (p37). And this, of course, is why there is a limit to the degree of change achievable - because once all of the genes available in the original species that favour the desired trait are retained, and all those that detract from the trait are bred out, then no further change is possible through conventional breeding (ignoring genetic engineering which is now available).

So he is completely unjustified to extrapolate from the changes possible through domestic breeding (which involves the loss of genetic information) to macroevolution (which would require the emergence of new genes), yet this is how he tries to mislead his readers:

If so much evolutionary change [referring to dog breeding] can be achieved in just a few centuries or even decades, just think what might be achieved in ten or a hundred million years. (p37)

And this isn’t just a momentary oversight or over-enthusiasm on his part, for he repeats this false extrapolation at the end of chapter 3:

if so much difference can be achieved in breeding such different breeds of dogs in just a few centuries, think how much can be achieved over geological time.

From what he has written in these first chapters he must surely be aware that this is a misleading comparison. Of course, he says that the gene pool is added to by mutation (p37); but this is merely the evolutionary dogma. It is clear that he does not see this as taking place in the course of domestic breeding (certainly not to the extent of producing new characteristics), because he recognises (p56):

Domestically bred songs are longer, louder and more frequent than the wild ancestral type. But all these highly prized songs are made up of elements that occur in wild canaries, just as the habits and tricks of various dogs come from elements found in the behavioural repertoire of wolves.

He claims to be a science educator and is not slow to berate creationists for any misrepresentation of scientific facts - yet this is exactly what he's doing here!

The title of his chapter 3 is 'The primrose path to macroevolution'; but it's nothing of the sort - all but one of his examples of natural selection are comparable with the changes achievable through domestic breeding - i.e. merely through selection from an existing gene pool - whereas macroevolution would require new genes to arise. (The exception relates to bacteria, which I will discuss subsequently.)

Unfortunately this is typical not only of Dawkins, but of many evolutionary writers: the unsupported presumptions required to support the overall (macro)evolutionary theory (notably that new useful genes arise through mutation) are tucked away among the facts of microevolution (that substantial morphological change can be achieved merely using existing genes) - no doubt to give the impression that the unsupported assumptions are valid too.

It's interesting that in chapter 1 he discusses the dictionary definition of a fact:

... a particular truth known by actual observation or authentic testimony, as opposed to what is merely inferred ... (p14)

and he takes issue with 'inferred', arguing that although the overall theory of evolution is inferred from limited observations, the inference is as sound as any observed fact (p16):

... I shall show the irrefragable power of the inference that evolution is a fact. (p16)

But I think the definition is right, and particularly apposite here: it highlights the fact that the whole theory of (macro)evolution (which would require new genetic information) is an inference from the observed facts of microevolution (which merely involves the use of existing genetic information).

Evolutionists are keen to promote the notion that macroevolution is nothing more than accumulated microevolution. But this is wrong. There is a fundamental distinction that microevolution is based merely on existing genes (even though sometimes this may result in large morphological changes, such as the different dog breeds) and macroevolution which would require new genes.

A critique of Richard Dawkins' The Greatest Show on Earth

1. Looking at the evidence

Although Richard Dawkins published his The Greatest Show on Earth: The evidence for evolution in 2009 to celebrate the 150th anniversary of Darwin’s Origin of Species, it’s only recently that I’ve got around to reading it. He’s right that nature is indeed the greatest show on earth, and his book includes good descriptions and photographs of some of the wonders of biology.

His aim in this book is, of course, to present the evidence for evolution, mistakenly thinking (or, at least, implying) that this proves the overall theory of (macro)evolution must be true (p9).

Evolution is fact ... no unbiased reader will close the book doubting it.

What he fails to take on board - though it is well known in the philosophy of science, so surely he is aware of it - is that no amount of supporting evidence can prove a theory true; what matters is whether there is contrary evidence that shows it to be false - Karl Popper’s falsifiability, which I’ve dealt with previously, so I won’t dwell on it here. I realise that some may think I am just raising this as a sort of smoke screen to try to avoid considering the supporting evidence. But this is not so, and you can judge for yourself from my subsequent comments whether this is the case. I will show (a) that the evidence presented by Dawkins (and others) is not as convincing as he would have you believe, and (b) there is substantial contrary evidence that shows the theory to be false.

One final introductory comment: It is a travesty that he lumps together those, such as myself, who have exclusively scientific objections to the theory of (macro)evolution, with those who reject evolution primarily for religious reasons; and it is utterly ridiculous that he then labels such as ‘history deniers’ and compares them with those who deny the holocaust - this does him no credit at all. I wonder if the main reason he does this is to fabricate an excuse to avoid taking seriously the scientific arguments against (macro)evolution, because he has no answer to them.

Homology refutes evolution

Homology is commonly cited as demonstrating, or even proving, common descent and evolution. But there is substantial evidence showing that supposedly homologous structures in fact are not; and in doing so this provides compelling evidence against both common descent and macroevolution. Let me explain:

Homology - what is it?

Historically, homology is simply similarities of biological structure. Probably the most widely-used example to illustrate this is the skeleton of vertebrates, especially the forelimb of tetrapods (vertebrates with four limbs): despite the substantial differences in overall appearance of e.g. a horse’s foreleg, human arm, bird’s wing and whale’s flipper - the underlying bone arrangement is remarkably similar.

The theory of evolution seems to provide an elegant explanation for these similarities. It proposes that the tetrapod leg, from its first appearance with the early amphibians, as their descendants diversified, was itself progressively modified to adapt to differing uses. Similarly, the supposed evolution of tetrapods from fish is supported by the similarities of skeleton of all vertebrates. This evolutionary explanation has become so widely accepted that it now defines homology as referring to those organs which have been derived from the same structure in a common ancestor.

That is, over the course of evolution, modifications of the embryological developmental processes have resulted in divergence from the common embryological source to give the range of modern day organs. And with this evolutionary account of homology, embryology acquired an important role in identifying and interpreting homologies. The point being that, even if adult structures look rather different (wing, flipper, arm), if they are homologous then they will be derived from equivalent embryological sources.

Conversely, even if structures from different species look similar, if they have developed from different embryological tissues then they would not be regarded as homologous, but due to convergent evolution. A good example of this is the vertebrate eye and that of the cuttlefish (a mollusc related to squid). In overall structure they closely resemble each other, notably in having a lens and iris, are equally specialised and with comparable performance. But they are not considered to be homologous, as there is no doubt they have arisen quite independently in separate phyla (chordates and molluscs) which have completely different body plans. And there was no common primitive eye from which they have both evolved.

Homology - the inconvenient truth

Although most evolutionary texts convey a consistent and hence persuasive picture of homology, there are in fact many substantial anomalies. In particular, as we discover more of how tissues are formed embryologically, increasing doubt is being cast on much of the homology that has been perceived for so long at the morphological level.
Notably, in view of the importance attached to the apparent homology of the vertebrate skeleton, and the weight given to embryology for identifying homology, it is especially relevant that vertebrae – a major component of the vertebrate skeleton – form embryologically in significantly different ways for different classes of vertebrate (such as mammals, birds, amphibians and fish), and even from different groups of early embryonic cells. (For example, see Vertebrates: Comparative anatomy, function, evolution by K. Kardong.) This clearly shows that the vertebrae of these different vertebrate classes are not, in fact, homologous - and hence that these different groups of vertebrate do not in fact share a common vertebrate ancestor, despite their superficial similar appearance and contrary to the commonly held view.

Taking this further, in the course of embryological development the members of different classes of vertebrate pass through a similar-looking stage (called the phylotypic stage), which is seen as clear evidence of their common ancestry. However, what is confounding (from an evolutionary perspective) is that even though the phylotypic stage looks similar, and we would have expected it to be formed from a fertilised egg in substantially the same way, there is, in fact, remarkable diversity, including some fundamental anomalies. The fact that the phylotypic stages are formed in different ways prima facie at least undermines, if not completely negates, the notion that they are derived from a common ancestor. And there are similar anomalies in other phyla, not only the vertebrates.

This is not just putting an anti-evolutionary spin on the facts. Here’s what evolutionary biologist Rudolf Raff had to say:

The process of early development from the egg to the phylotypic stage should be at least as conserved as the pattern of the phylotypic stage. One might reasonably expect mechanisms of early development to be especially resistant to modification because all subsequent development derives from early processes.

Homology - why the evidence is important - and hence ignored!

The evidence from homology - or, rather, the lack of it - is very important. Although some people try to dismiss the ‘intelligent design’ case against evolution as a ‘gap’ argument, this excuse is not available over homology. The fact that apparently homologous organs such as the vertebrae in fact have proved not to be, not only removes circumstantial evidence in support of evolution - it constitutes clear counter-evidence against the organisms concerned having evolved from e.g. a common vertebrate ancestor. This evidence unequivocally refutes the theory of evolution.

And this no doubt is why so few, including professional biologists, know about these anomalies - they are kept safely out of the limelight so as not to upset the applecart. As mentioned above, textbooks on evolution only cite the evidence that supports evolution. How many who are reading this article knew previously about the anomalies of so-called homology?

Peer Review

In the preceding post (below) I mentioned what I think is a key failing of evolutionary scenarios, such as that of the eye by Nilsson & Pelger - they completely ignore what we now know of the genetic and molecular mechanisms that are essential for forming biological tissues. And along with this they ignore the fact that the evolution of substantially new biological structures, such as eyes and feathers, would require new genes to arise.

And my point here is this: this knowledge has been well known for at least a generation; yet, not only did N&P (and authors of comparable scenarios for other organs) feel free to ignore this, but presumably the reviewers of their paper were happy to overlook this oversight too. And, we should note, it wasn’t published in some minor or obscure journal, but in the prestigious Proceedings of the Royal Society of London.

Before I comment further on peer review, let me also mention another serious flaw in the authors’ rationale. Their aim was not only to show what they considered to be a plausible scenario for the evolution of an eye, but also to estimate how long it would take - to show that there was plenty of geological time for it to happen. But their method was seriously flawed: their calculations used an equation (in Falconer’s Introduction to Quantitative Genetics) formulated to estimate the time to effect change through domestic breeding.

First of all, this reinforces the point I made previously - that their model for the evolution of an eye is based on selection from an already existing gene pool - completely ignoring the fact that a new organ such as an eye will require very many new genes (which are prohibitively improbable to arise - a central theme of my book).

Second, their model assumes that only those organisms having a variation that confers at least a 1% improvement in vision will contribute to the next generation. This is the sort of thing a breeder can put into practice, but totally unrealistic to think that natural selection (which of course is what the evolution of the eye would have had to rely on) will operate this way - most of the mature individuals (even those with reduced visual acuity) in a population will have some offspring.

So these criticisms completely undermine their claim that their calculations are a ‘pessimistic’ estimate of the time for an eye to evolve. Quite the opposite!

This also gives some insight into peer review: Presumably the reviewers were so happy with the overall message of the paper that either (a) they didn’t examine it too closely, and/or (b) they were aware of its serious shortcomings but chose not to stand in the way of a paper which said what they want to hear. At very least It shows that ‘peer review’ is not the independent objective assessment it’s claimed to be.

And its not just the reviewers who are at fault. This paper is referred to widely to support the notion that eyes could have evolved readily. Have none of these bothered to take a careful look at what N&P actually proposed?

Eye Evolution

A good example of where belief in evolution is maintained because people aren’t prepared to look at the detail is in the supposed evolution of new organs such as the eye.

The eye is the classic example of a highly specialised organ, considered by many pre-Darwinian scientists such as John Ray as incontrovertible evidence of design in biology. Even Darwin recognised that the eye was a challenge to his theory, but in the Origin speculated how it might have arisen progressively from a simple light-sensitive tissue through a series of variations.

In the 1990s a couple of Swedish scientists, Dan-E Nilsson and Susanne Pelger (Proceedings of the Royal Society of London Series B - Biological Sciences, 256:53-9), expanded on this sort of scenario, illustrated as follows:

Starting from a patch of light-sensitive cells (which is a huge presumption in itself, though I can’t expand on that here) it is envisaged that an eye evolves by a flat patch of cells becoming a depression, which gradually deepens into a small pit (a to c), the neck of which then narrows (d). Each of these stages, taking place over several generations, is driven by the advantage of increased optical acuity (better resolution). When this stage has been reached, further improvement can be achieved only by addition of a lens (e), and the authors boldly assert that ‘Even the weakest lens is better than no lens at all, so we can be confident that selection for increased resolution will favour such a development all the way from no lens at all to a lens powerful enough to focus a sharp image on the retina.’

The totally unjustified assumption in this scenario is that if a variation will offer some advantage, then we can be sure that it will arise. No thought whatsoever is given to the crucial question of how those variations will arise. I think this blind spot (!) has arisen for two reasons.

First, before we knew about genetic and molecular mechanisms, it was thought that biological tissues were innately plastic in the sense that variations would arise spontaneously, and favourable ones could then be passed on. However, we now know that the formation of morphological structures – whether it be an eye, feather or leaf – is not by some sort of vague plasticity, but through the closely orchestrated action of many genes. So new structures need new genes. But in the above scenario, all that we have learned in the last 50 years about the biochemistry of tissues and the molecular mechanisms involved in forming tissues is totally ignored.

The second reason arises from the fact that much variation is possible through the mixing of genes that are already available. For example, it’s been known since well before Darwin that domestic varieties of crops and animals can be developed by breeding selectively from those individuals which have the desired variations (which have arisen naturally). But it was also well-known that there are limits to the amount of change that can be achieved this way. Which is why, although artificial selection could validly help to illustrate natural selection, Darwin’s contemporaries also knew that domestic breeding could not support changes such as the evolution of new organs. We now know why: new organs need new genes and molecular mechanisms to construct them - which are not available in the genomes of the original parents.

This oversight is illustrated by the fact that the above-mentioned authors’ calculation of the rate of eye evolution is based on selection from an existing pool of genes. Whereas there can be no doubt at all that the evolution of an eye would require very many new genes – for several proteins used exclusively in the eye, and for the molecular mechanisms that construct the eye in the course of embryological development. So their comment about a lens arising simply because it would be advantageous to do so is just ignorant wishful thinking - scarcely science at all.

There are so many speculative scenarios for the evolution of new structures - whether they be for eye, wing, feather, limb or whatever - but they are no better than those available in the 19th century - because they are based on the assumption that biological tissues are plastic, and completely ignore the genetic and molecular implications. If proponents of evolution want their scenarios to be taken seriously then they really do need to take on board the genetic and molecular detail.