Saturday, 28 September 2013

Chapter 7: Colin Patterson

In his discussion of transitional fossils (page 106), Sarfati uses a quote by the late Colin Patterson (who was a palaeontologist at the British Museum of Natural History:
I fully agree with your comments on the lack of direct illustration of evolutionary transitions in my book. If I knew of any, fossil or living, I would certainly have included them...I will lay it on the line – there is not one such fossil for which one might make a watertight argument.

Patterson's quote comes from a personal letter of 1979, written to Luther Sunderland (a creationist, although Patterson was unaware of this at the time).  Sunderland had written to Patterson asking why his recently published book, Evolution, did not feature illustrations of transitional fossils from which modern species were descended.  Adding the sentences before and after the second part of the quote clarifies Patterson's point:
You say that I should at least "show a photo of the fossil from which each type of organism was derived."  I will lay it on the line – there is not one such fossil for which one could make a watertight argument.  The reason is that statements about ancestry and descent are not applicable in the fossil record.  Is Archaeopteryx the ancestor of all birds?  Perhaps yes, perhaps no: there is no way of answering the question.  It is easy enough to make up stories of how one form gave rise to another, and to find reasons why the stages should be favoured by natural selection.  But such stories are not part of science, for there is no way of putting them to the test.

Patterson was explaining to Sunderland that, of the transitional fossils that were known, he could not make a watertight argument for any of them being the direct ancestor of a living species group.  Archaeopteryx, for example, is not necessarily the direct ancestor of modern birds.  It may have been a species on a side-branch.

Patterson's quote has been used extensively by creationists over the years, and creationists and anti-creationists have argued about its proper use.  Consequently, creationists now tend to accompany their quotation of Patterson by suggesting his meaning was clear (they usually argue the clear meaning is that suggested by their edited quote, complete with the ellipses!) and any subsequent comment or clarification (including any by Patterson himself!) on the quote is a distortion of its true intent.

In The Greatest Hoax on Earth, Sarfati accompanies the Patterson quote with a footnote that says, "Patterson later tried to backtrack somewhat from this clear statement, apparently alarmed that creationists would utilize this truth."  Patterson's own words are the best defence to such a claim.  He made some strong statements in favour of evolution and against creationism in his second edition of Evolution, including comment on creationists' fondness for misquoting evolutionary biologists:
Because creationists lack scientific research or evidence to support such theories as a young earth (10,000 years old), a world-wide flood (Noah's), and separate ancestry for humans and apes, their common tactic is to attack evolution by hunting out debate or dissent among evolutionary biologists.  When I published the first edition of this book I was hardly aware of creationism but, during the 1980s, like many other biologists I learned that one should think carefully about candour in argument (in publications, lectures, or correspondence) in case one was furnishing creationist campaigners with ammunition in the form of 'quotable quotes', often taken out of context.
I see the general historical theory, common descent, as being as firmly established as just about anything else in history.  We have compelling reasons to believe that Napoleon and the Roman empire existed, although we don't know every detail of what went on in Napoleon's life or in Rome and its colonies; it is much the same with evolution.  There is abundant documentary evidence for Napoleon and the Roman empire; there is abundant evidence for common descent in the hierarchy of homologies at both the structural and morphological level, though those documents may not be so easy to read.


Colin Patterson, Evolution (second edition) The Natural History Museum: London (1998), pages 122-3.

Lionel Theunissen, 'Patterson Misquoted: A Tale of Two 'Cites'' (1997)

Gary Bates, 'That quote!-about the missing transitional fossils' (2006)

Richard Dickerson, 'Creationism and Evolution', Los Angeles Times (8 November 1989)

Thursday, 26 September 2013

Chapter 5: Embryos, Self-Assembly and the Evolution of Multicellular Life

The origin of multicellular life is the focus of chapter five of The Greatest Hoax on Earth.  Sarfati's main scientific point in this short chapter is that "Evolutionists have no explanations for the enormous changes needed to transform a single-celled organism into a multi-celled one" (page 87).

Actually, evolutionists have a few explanations.  See, for example, the chapter 'From Single Cells to Multicellular Organisms' in Molecular Biology of the Cell, one of the leading cell biology textbooks.[1]  John Tyler Bonner, a developmental-evolutionary biologist at Princeton University, has written a whole book on the evolution of multicellular life.[2]
There are three main theories for the evolution of 'multicellularity'[3]:

The colonial theory: this holds that the symbiosis (cooperation) of many organisms of the same species led to a multicellular organism.  This theory has the most support in the scientific community and has the advantage of aspects of it being observable.  Some species of algae form colonies of thousands of cells, only a fraction of which reproduce.  Cooperation between cells and formation of groups of cells has also been observed in bacteria.[4]

The symbiotic theory: this suggests the first multicellular organisms resulted from symbiosis of different species of single-cell organisms, each with different roles. Over time these organisms became so dependent on each other they could not survive independently and were incorporated into one multicellular organism.  The problem with this theory is it is not clear how each organism's DNA could be incorporated into a single genome.[5]

The cellularisation theory: this states that a single unicellular organism, with multiple nuclei, could have developed internal membrane partitions around each of its nuclei.[6]  The problem with this theory is that while there are some existing single-cell organisms with multiple nuclei, these nuclei are either the result of the fusion of uninuclear cells or each nucleus has a specific function (making it unlikely the nucleus could split from within the single cell).

Since the publication of The Greatest Hoax on Earth there has been some interesting research on the evolution of multicellular organisms.  William Ratcliff and his colleagues at the University of Minnesota conducted an experiment in which they evolved multicellularity in unicellular yeast.[7]  The unicellular yeast in their experiment formed multi-celled organisms that stayed multi-cellular and reproduced as a multicellular organism.
Critics of Ratcliff's experiment have pointed out that many yeast strains naturally form colonies, and because yeast has ancestors that were multicellular, the experiment might merely have activated a vestigial gene already present in the yeast.  In other words, Ratcliff's experiment may only have demonstrated the reversion of a unicellular organism to multicellularity, rather than the evolution of multicellularity.[8]  This latter point was also picked up by creationists, as it supports their claim that evolution cannot produce 'new' genetic information.[9]

Ratcliff maintains the traits that evolved in the yeast in his experiment were novel and they improved the fitness of whole clusters, not their component cells, which demonstrates evolution in a multicellular manner.[10]  Furthermore, much of evolution proceeds by using existing traits in new ways, which is what Ratcliff's yeast did.  Ratcliff and his team now intend to repeat the experiment with algae (that has no multicellular past) and they are continuing with the yeast strains to see if they evolve further into true multicellular organisms.

So Sarfati's actual point is that evolutionists don't yet understand exactly how single-celled organisms evolved into multicellular ones.  Much of the rest of chapter five (Sarfati's discussion of the programming and organisation of information) is really a variation of the argument about the origin of life, which is the focus of chapter 13 of The Greatest Hoax on Earth


[1] Bruce Alberts, et al., 'From Single Cells to Multicellular Organisms', in Molecular Biology of the Cell (third edition), New York: Garland Science (1994); available online at  (The book is now in its fifth edition, published in 2007, but this is not freely available online).

[2] John Tyler Bonner, First Signals: The Evolution of Multicellular Development, Princeton: Princeton University Press (2001).

[3] My summary of the theories is adapted from Wikipedia:

[4] Gregory Velicer and Yuen-tsu Yu, 'Evolution of novel cooperative swarming in the bacterium Myxococcus Xanthus', Nature, Vol 425 (2003), pp 75-8; Paul Rainey and Katrina Rainey, 'Evolution of cooperation and conflict in experimental bacterial populations', Nature, Vol 425 (2003), pp 72-74

[5] Lynn Margulis, Symbiotic Planet: A New Look at Evolution, New York: Basic Books (1998), p 160.

[6] C Hickman and F Hickman, Integrated Principles of Zoology (fifth edition), Mosby (1974), p 112.

[7] William Ratcliff, et al., 'Experimental evolution of multicellularity', Proceedings of the National Academy of Sciences (17 January 2012); for a simple summary by Ratcliff, see

[8] Bob Holmes, 'Lab yeast make evolutionary leap to multicellularity', New Scientist, Issue 2818 (23 June 2011)

[9] Elizabeth Mitchell, 'News to Note' (2 July 2011)

[10] Carl Zimmer, 'Evolving Bodies: A Storify Follow-up' (18 January 2012)

Wednesday, 11 September 2013

Chapter 3: 'Human Genome Decay': Kondrashov and Sandford

Selective use of Kondrashov

Sarfati cites the evolutionary geneticist Alexey Kondrashov in support of the claim that the human genome is accumulating harmful mutations at such a rate that the human race cannot be tens of thousands of years old.
[B]ad neutral mutations accumulate till the point of damage. These mutations are accumulating much faster than previously thought—at least 100 nucleotide substitutions (single-letter 'typos') per person per generation, according to geneticist Kondrashov—and the rate might be as high as 300....Evolutionist Kondrashov himself asked, "Why aren't we dead 100 times over?" (p 57)

Sarfati's selective use of Kondrashov suggests he is citing Kondrashov for rhetorical effect ("This presents such a challenge to evolution that even a prominent evolutionist is expressing doubts!").

A look at the Kondrashov papers cited by Sarfati presents a different picture. Kondrashov's question ("Why have we not died 100 times over?") is part of the title of his 1995 paper[1], which sets out to answer that question. The paper outlines several possible resolutions, including soft selection[2] and synergistic epistasis (discussed below).

Sarfati also cites a 2002 paper[3] by Kondrashov, which has the figure of 100 new mutations per human genome per generation. Sarfati presents this in a way that gives the impression all 100 of these mutations are harmful. Howevever, Kondrashov's article states that the ratio of harmful mutations is around 10 percent of the 100 ("Comparison of human and murine [mouse] orthologous intergenic regions suggests that at least 10% of these mutations are deleterious"). He then adds that "deleterious mutation rates in excess of 1 do not necessarily lead to prohibitively high genetic load, as long as selection against mutations involves synergistic epistasis"[4].

Theoretical models and synergistic epistasis

The following paragraphs are from an extensive review of Genetic Entropy and the Mystery of the Genome (the book by plant geneticist John Sanford, which Sarfati is summarising in this section of The Greatest Hoax on Earth) by chemical engineer Scott Buchanan[5].
Much of the confusion in Sanford's book is due to his failure to distinguish models from reality.  He seizes on the predictions of oversimplified models when they suit his case, and ignores the fact that these models obviously do not represent the real world.
There is general agreement among geneticists that a simple model of mutations, with high rate of deleterious mutations operating independently, would predict that a population's fitness and genome will deteriorate fairly rapidly. The cost of eliminating each mutation would be too high for the population to bear.
There is also general agreement that if mutations interact such that several mutations together decrease fitness more than predicted by the sum of their individual effects, then the genome will not deteriorate.[6]
The effect is that individuals with say four or five mutations have a much higher probability of dying young or otherwise producing few offspring, compared to the individuals with just one or two mutations. This reduces the cost to the population of eliminating the bad mutations. This is known as "synergistic epistasis". The opposite trend is "antagonistic epistasis", where just one mutation can have a large effect, and additional mutations have diminishing effects[....]
Sanford addresses the experimental evidence for synergistic epistasis with a single sentence on page 110: "At least one paper provides experimental evidence that the concept is not valid (Elena and Lenski, 1997)."  As we have come to expect from Sanford, this statement is formally true, but grossly misleading for the general reader. Sanford claims to be most concerned about the genomes of higher organisms like animals and humans, yet he ignores the studies which show synergistic epistasis in multi-cellular eukaryotes[7] and cites only a single study on the bacteria E. coli.[8]
We have already noted that prokaryotes like bacteria are likely to show no epistasis. Further, this particular study used artificial insertion mutations rather than random natural mutations. Dickinson has pointed out that these insertion mutations are unlikely to show epistasis.[9] So again Sanford has cherry-picked one study which is largely inappropriate yet shows the results he wants, and ignored the body of evidence that points in the opposite direction.
Buchanan's review is worth reading in full to see all of the problems in Sandford's approach. Here are a few other good points made by Buchanan that are relevant to Sarfati's use of Sandford.
For all Sanford's hand-wringing over the inescapable declines in genomes everywhere, his lack of concrete examples shows that the scientific facts are not on his side. Microbes have existed for untold millions of generations, and even small mammals like mice and rabbits which reproduce one or more times a year have existed with humans for thousands of generations in historic times, and many more thousands of generations in prehistoric times. If genomes of these rodents were declining by say 0.1% per year, then in 3000 years since 1000 BC, they should be down to 5% of their original fitness (0.999 raised to 3000 power = 0.05) So where is the evidence of super-rabbits in 1000 BC or even 1000 AD?
Humans carry around 100-200 new mutations per generation[10]. That seems like a lot, but that is only about one mutation in each 15 to 30 million nucleotides. While a few of these mutations can have devastating health effects, most of these mutations have no apparent physical impact. Most of these mutations fall in regions of the genome with no known function, and many mutations in protein coding regions are "silent" mutations which do not alter the protein which is ultimately formed. Even within the coding for proteins, many of amino acids can be altered without appreciable harm to the individual[11].


[1] Alexey Kondrashov, 'Contamination of the genome by very slightly deleterious mutations: why have we not died 100 times over?', Journal of Theoretical Biology, Vol 175, No 4 (1995), pp 583-94 [only the abstract is available free online]
[2] For a definition, see here:

[3] Alexey Kondrashov, 'Direct Estimates of Human per Nucleotide Mutation Rates at 20 Loci Causing Mendelian Diseases', Human Mutation, Vol 21, Issue 1 (2002), pp 12-27; available in full online at:
[4] Kondrashov (2002), p 22.

[5] Scott Buchanan, 'Assessing Limits to Evolution and to Natural Selection: Reviews of Michael Behe's Edge of Evolution and John Sanford's Genetic Entropy' (2010)

[6] James Crow,'The high spontaneous mutation rate: Is it a health risk?', PNAS, Vol 94 (1997), pp 8380-6; Kondrashov (1995); M W Nachman and S L Crowell, 'Estimate of the mutation rate per nucleotide in humans', Genetics, Vol 15, No 6 (2000), pp 297-304.

[7] Rafael Sanjuán and Santiago Elena, 'Epistasis correlates to genomic complexity', PNAS, Vol 103, No 39 (2006), pp 14402-5; W C Whitlock and D Bourguet, 'Factors affecting the genetic load in Drosophila: synergistic epistasis and correlations among fitness components', Evolution, Vol 54, No 5 (2000), pp 1654-60;
 Victoria Ávila, et al, 'Increase of the Spontaneous Mutation Rate in a Long-Term Experiment With Drosophila melanogaster', Genetics, Vol 173 (2006), pp 267-77; Gregory Kryukov, Steffen Schmidt and Shamil Sunyaev, 'Small fitness effect of mutations in highly conserved non-coding regions', Molecular Genetics, Vol 14, No 15 (2005), pp 2221-9; W Joseph Dickinson, 'Synergistic Fitness Interactions and a High Frequency of Beneficial Changes Among Mutations Accumulated Under Relaxed Selection in Saccharomyces cerevisiae', Genetics, Vol 178 (2008), pp 1571-8

[8] S F Elena and R E Lenski, 'Test of synergistic interactions among deleterious mutations in bacteria', Nature, Vol 390 (1997), pp 395-8

[9] See Dickinson (2008) in reference 7.

[10] Wellcome Trust Sanger Institute, 'We are all mutants: measurement of mutation rate in humans by direct sequencing' (2009) 

[11] Michael Lynch, 'Simple evolutionary pathways to complex proteins', Protein Science, Vol 14 (2005), pp 2217-25

Tuesday, 10 September 2013

Chapter 3: Haldane's Dilemma

On pages 54-5 of The Greatest Hoax on Earth Sarfati mentions engineer Walter ReMine and his use of the work of geneticist John Haldane.  The problems with both Haldane's "dilemma" and ReMine's use of it are summarised here:

Another useful discussion of the subject can be read here:

Monday, 9 September 2013

Chapter 3: Michael Behe and John Sanford

On pages 51-2 of The Greatest Hoax on Earth Sarfati summarises biochemist Michael Behe's book The Edge of Evolution, which argues human evolution is not possible even over millions of years.  On pages 56-8 Sarfati summarises plant geneticist John Sanford's book Genetic Entropy and the Mystery of the Genome, which argues that the accumulation of bad mutations means the human genome cannot be very old.

Both of these books (and their problems) are addressed in an extensive review by chemical engineer Scott Buchanan: 

'Assessing limits to evolution and to natural selection: reviews of Michael Behe's Edge of Evolution and John Sanford's Genetic Entropy' (2010)

Wednesday, 4 September 2013

Chapter 3: Natural selection, mutations and information

"[T]o change microbes into men requires changes that increase the genetic information content." (The Greatest Hoax on Earth, page 43)
"[R]andom changes act mainly to degrade information." (page 44)"All the alleged proofs of 'evolution in action' to date do not show that functional new information is added to genes. Rather, they involve sorting and/or loss of information." (page 44)

In Chapter 3 Sarfati argues that mutations are unable to add new genetic information and he suggests they are ultimately unhelpful to populations.

Sarfati distinguishes between re-ordering existing information to produce something new and producing entirely new information (pp 43-4).  From his point of view, the new information produced by point mutations, frameshift mutations and gene duplication does not count as truly 'new' because it is produced by re-sorting existing information.

The argument comes down to how you define 'new' and 'information'.  This is conceded in
an article by Sarfati's organisation, Creation Ministries International (
Can mutations produce new information? Yes, depending on what you mean by 'new' and 'information'. Can they account for the evolution of all life on Earth? No!
Effectively, an act of supernatural creation is needed to meet Sarfati's definition of new information, which may be fine theologically but isn't particularly helpful scientifically.  (On the topic of information and creationists' use of information theory, including a critique of the work of Werner Gitt – who is cited in this chapter by Sarfati – see:

There are studies on bacteria (which are useful for observing mutation and natural selection because they reproduce and die quickly and in such large numbers) that demonstrate mutations producing new (in the sense of 'different') genetic information.

For example, the E coli experiment by Barry Hall and his colleagues at the University of Rochester. Hall began by deleting a gene from E coli bacteria. This gene produces an enzyme that allows the bacteria to break down the sugar lactose into subunits that can be used as food. The 'geneless' bacteria were then put in an environment containing lactose as the only food source. Initially, of course, they lacked the enzyme and couldn't grow. But after only a short time, the function of the missing gene was taken over by another enzyme that, while previously unable to break down lactose, could now do so weakly because of a new mutation.  Eventually, yet another adaptive mutation occurred: one that increased the amount of the new enzyme so that even more lactose could be used.  Finally, a third mutation at a different gene allowed the bacteria to take up lactose from the environment more easily.

An objection might be that such mutations may be helpful in a stressful environment (such as one with a single food source), but they make the bacteria less fit for its original environment.  This does not, however, discredit evolution.  If the original bacterium has had thousands of years to adapt to its normal environment, it is likely to perform optimally in that environment, so it's not surprising that (a) nearly any change to it will make it less-than-optimal for that original environment, or that (b) further spontaneous beneficial mutations are rarely observed for that environment.

Another example is the Pseudomonas bacteria that evolved the new ability to digest nylon.  This process has occurred in the wild and in the laboratory.  Nylon was invented in 1935. It didn't exist before then, and neither did this organism.  In the 1970s Japanese scientists noticed bacterial mats growing on nylon waste in ponds.  In 1984 Susumu Ohno found that these bacteria had a new enzyme that allowed them to digest nylon.  In 1995 Irfan Prijambada reported that researchers at Osaka University had observed the evolution of nylon metabolism in their laboratory cultures of Pseudomonas, after ensuring the original culture had no ability to digest nylon.  This new and useful genetic information arose from the standard evolutionary processes of mutation, natural selection, and reproduction.  The genetic mutation that produced the new enzyme probably occurred countless times in the past, and would most likely have been lethal, until the environment changed and nylon was introduced.


Scott Buchanan, 'STAN 1: Fossils, Runaway Subduction and Bible Interpretation' (2010),

Robert Carter, 'Can mutations create new information?', Journal of Creation, Vol 25:2 (2011), pp 92-8

Jerry Coyne, Why Evolution is True, Viking: New York, 2009, p 140.

Kenneth Miller, Finding Darwin's God: A Scientist's Search for Common Ground Between God and Evolution, Cliff Street Books, 1999, pp 104-6, 143-6.

Kenneth Miller, Only a Theory: Evolution and the Battle for America's Soul, Penguin 2008, pp. 79-84.

Ian Musgrave, 'Nylonase Enzymes' (2004)

Ian Musgrave, Rich Baldwin, et al, 'Information Theory and Creationism' (2005

Dave Thomas, 'Evolution and Information: The Nylon Bug' (2004)   
"In this case, a mutation has clearly produced new information. That is, unless you want to quibble that the detailed three-dimensional structure and composition of a protein that reacts specifically to nylon is not "information.""