@Professor Kent: It’s quite different because multiple valid criteria can …

Comment on Southern Adventist University opens Origins Exhibit by Sean Pitman.

@Professor Kent:

It’s quite different because multiple valid criteria can be applied. One species concept works in some cases and fails in other cases–for good reason that I don’t have time to elaborate.

Exactly. Thank you for admitting that there simply is no universally consistent single definition of the “species” concept in mainstream literature. It all depends upon which one among many potential definitions one chooses…

I still haven’t seen from you an explanation of what would qualify different human groups as being distinct species.

I never said that they were different species. What I said is that according to some definitions of species different groups of humans, or even domestic dog breeds, might qualify.

What are these functionally distinct differences? Let me guess: skin color and tolerance to sun? (No…a continuum exists.) Language? (No…its a learned and culturally-transmitted trait.) Ability to catch a fish bare-handed? (Right.) Mathematical and spatial skills versus linguistic and relational skills? (No…these categorize different sexes, not races). I am sooooo intrigued…please do tell!

There are both phenotypic as well as genetic differences that are used to defined species concepts in literature. It all depends upon where you draw the line as to what does and does not qualify.

You tell me. At what point is a distinct species realized? For example, just how different does one have to be, genetically, to be classified as a different species? How many mutations, for a given stretch of DNA, does it take to consistently define a novel species with universal application?

I’d be most interested in your answer to this question…

Sean Pitman

Sean Pitman Also Commented

Southern Adventist University opens Origins Exhibit

I agree with Prof Kent. I think you have a few problems

1] You have used an arbitrary statistical limit to define a universal limits of evolutionary development and speciation

The limitation is not arbitrary. It is both observed in real time and can be calculated to show that it (a minimum requirement of 1000 specifically arranged residue positions) is the most likely limitation this side of trillions of years of time – from the perspective of RM/NS.

2] You have conceded that 80-90% of the genetic variation between species has been acquired over 4000 years. (I am surprised that you feel able to extend this to 5000 years given EG White’s writings.

It depends upon what type of variation you’re talking about. Certainly all variation at lower levels of functional complexity could easily be realized in this period of time.

3] You allow for rapid development of phenotype and novel repurposing of proteins in the development of evenomation

DNA can and does rapidly mutate – true.

4] You claim some value for a limit of 1000fsaar but do not seem able to identify concrete examples of this during speciation.

Speciation is not based on producing novel functional complexity beyond very low levels of functional complexity. In fact, speciation can be based on functionally neutral genetic changes. Also, there are no examples of evolving beyond the level of 1000 specifically arranged amino acid residues because it is statistically impossible to do so. Only variations at low levels of functional complexity can be or ever have been demonstrated.

5] Indeed comparative genomics between man and apes suggests that the differences between these species is mostly at the single nucleotide level and in gene duplications

and that there seems to be none of the barriers of 1000fsaar complexity that Sean suggests to limit evolution of homo sapiens from an hominid ancestor common with great apes.

Humans and apes are quite different in various respects, to include brain structure and function – which is thought to be based on numerous differences in genetic regions that code for miRNAs (around 8% of which are human specific).

“miRNAs recently have been implicated in synaptic development and in memory formation. As the species specific miRNAs described here are expressed in the brain, which is the most complex tissue in the human body, with an estimated 10,000 different cell types, these miRNAs could have a role in establishing or maintaining cellular diversity and could thereby contribute to the differences in human and chimpanzee brain … function.”

Eugene Berezikov, Fritz Thuemmler, Linda W van Laake, Ivanela Kondova, Ronald Bontrop4, Edwin Cuppen & Ronald H A Plasterk, “Diversity of microRNAs in human and chimpanzee brain”, Nature Genetics, Vol 38 | Number 12 | December 2006 pp. 1375-1377.

The Y-chromosome is even more unique. A study published by Nature in early 2010 showed many striking differences between human and chimp chromosome structure, gene content, and even qualitatively unique genes between the two species. As far as looking at specific genes, the chimp and human Y-chromosomes seem to have a dramatic difference in gene content of up to 53 percent. In other words, the chimp is lacking approximately half of the genes found on a human Y-chromosome. Because genes occur in families or similarity categories, the researchers also sought to determine if there was any difference in actual gene categories. They found a shocking 33 percent difference. The human Y-chromosome contains a third more gene categories, entirely different classes of genes, compared to chimps.

Hughes, J.F. et al. 2010. Chimpanzee and human Y chromosomes are remarkably divergent in structure gene content. Nature. 463 (7280): 536-539.

For further discussion see:


6] You define species classification as being arbritary but have some nebulous concept of a barrier of complexity for potential changes induced by the acquired changes which you concedes occurs rapidly and frequently.
This limit to complexity you relate to some theoretic 1000fsaar limit.

Again, this limit is both observable and calculable based on known distributions and densities of viable sequences in sequence spaces at various levels of functional complexity.

You seem to support models of rapid evolution by Darwinian mechanism inside a 1000fsaar limit; if you think them scientific they must be tested by reference to reality and real data. I suggest you look at the genomic data and point out the genetic differences that correspond to your 1000 FSAAR limit.

I’ve given you numerous examples already of systems that require a minimum of far more than 1000 specifically arranged residues. How many more examples do you need?

You might like to also comment on you model of evolution of all Y chromosome variation that exists today from a single Y chromosome 4000 years ago at the time of flood.

In case anyone suggests there were 4 males on the boat and therefore there were 4 Y chromosomes, Noah and his 3 sons would all have the one identical Y chromosome because of transmission from Noah to his sons. Humans in terms of Y chromosomes are equivalent to a breeding pair.

The variation in the Y chromosome in humans today, like all other unclean animals must therefore date to mutations in the last 4000 years.


All this genomic sequence is now freely available so there is no excuse for not testing it except the paucity of value you see in your arguments.

What testing would you want? Low level genetic changes can and do take place very fast – especially in larger populations. There are no examples of higher level changes because, statistically, they are impossible this side of a practical eternity of time.

Both Jeff Kent and I have both offered advice in publication of these experiments in the peer reviewed literature.

Until you give me some real evidence based on experimental data you seem to be simply doing what Bob Ryan abhors; telling just so stories.

Sit down. Do the math for yourself. Then, come back and talk to me about who is telling the just-so stories regarding the creative potential of random mutations and natural selection (RM/NS).

Sean Pitman

Southern Adventist University opens Origins Exhibit

Thanks for that. Wise choice, that I knew given your intelligence you would make despite you vigorous defence of your near perfect pair model of origins. We will pass over the assumption that there are no deleterious mutations and that you discriminate against animals with variant expression of FGF4 and consider it deleterious. Why the prejudice against short legs?

When you disrupt a pre-existing system and this disruption has a beneficial effect, that doesn’t mean that this benefit wasn’t the result of a loss of pre-existing genetic information. It’s like a population of cave fish who have lost the ability to grow eyes. Such a mutation, in certain environments, is beneficial. It takes a lot of energy to maintain eyes that aren’t beneficial in the dark. Yet, mutations that result in the loss of ability to grow eyes are degenerative in nature in that they remove or disrupt pre-existing genetic information.

The same thing is true of mutations that disrupt the normal expression of FGF4 – which results in the abnormal structure of the stumpy legs of certain breeds of dog. Such mutations are degenerative in nature in that they aren’t based on anything new; they are based on the disruption or loss of pre-existing systems of function.

In short, your argument there is no such thing as a degenerative mutation, informationally speaking, is clearly mistaken. A correct understanding of this concept is vital to understanding the creative potential and very clear limits of the Darwinian mechanism of RM/NS.

Lets recap what we do agree on

1] A genetically bottle-necked population such as 2 Daschunds lacks the genetic diversity to allow rapid selection of phenotypic novelty by selection among allelic variants. imposing a bottleneck on a non-bottle-necked population of wolves is also suspect so you choose 100 pairs.

This is not the reason why I would choose 100 pairs vs. a single pair of wolves with non-degenerative gene pools. The reason, as already explained, is only a timing issue. The 100 pairs would be more rapidly adaptive in the near term. However, in the long term the offspring and larger population from single pair of genetically perfect wolves would be just as adaptive . . . due to the evolution of novel alleles over the course of time.

2] In this you seem to be accepting the conventional scientific view that a bottle-necked population is undesirable as it has dramatically decreased repertoire in their gene pool and high levels of homozygosity. Lack of variation rather than deleterious mutation is the issue.

Not true. Deleterious mutations are far more problematic for modern gene pools than is the lack of allelic diversification. It is the enhanced expression of recessive detrimental mutations that is the primary threat.

Sure, modern environments have far more virulent pathogens than did the original environment when all gene pools were still perfect or near perfect. Various alleles have evolved over time to more effectively deal with these pathogens. The loss of these allelic variations would make modern bottlenecked populations more susceptible to disease. However, as already explained, this was not the problem it is today right after the Flood since pathogens had not yet evolved to their current levels of virulence.

3] You accept that wolves and their subfamily dogs, foxes, jackal and coyotes are all derived from 2 animals living 4000 years ago. This by definition is a genetic bottleneck

Yes. And their allelic diversification since that time is not miraculous since it can be explained by rapid low-level allelic evolution.

4] These animals had 2 genomes and maximum of 4 haplotypes and alleles for every gene. Any additional alleles has arisen subsequently as random or non-random mutations.

Yes . . . although I don’t exactly know what you mean by “non-random mutations”?

5] The vast majority of the SNP (>2.5million) arose in the progeny of this pair by mutations over a period of 4000 years.

Give or take a thousand years or so, yes.

5] The multiple DLA alleles at the class II arose denovo since these 2 animals provided the 4 original alleles.

You mean HLA alleles? – yes.

6] Similarly in man [assuming 8 people on the ark and that Noahs sons were the progeny of he and his wife, and that his daughter in laws were unrelated to each other and to Noah and his wife and were heterzygous] there were a total of 10 alleles at HLA B. this means that 1590 of the HLA-B alleles currently recognized by genotype in man have arisen denovo over the last 4000 years.


7] In this case if we accept Seans value of 1600 HLA-B allels then 99.3% of the variation seen today has arisen by chance mutations and selection.


8] If we conservatively estimate the HLA-B serological specificities associated with amino acid changes and differences in peptide binding are 60 and all of the 10 HLA-B alleles in the 8 people on the boat were associated with serological specificity then we can assume that at least 83% of the variation in the highly functional amino acid changes in HLA-B seen the current population were derived by chance mutations.

That’s right.

9] There seems little reason to argue that the same process that must occur in highly polymorphic systems such as the MHC do not occur in other gene systems.

Other genes also experience random mutations and allelic variations – more rapidly in larger populations.

9] If between 83% and 99% of the variation in the progeny of 2 animals and 8 humans arose rapidly over 4000 years and in the case of canines this acquired variation was able to generate at least the species wolves, coyote, foxes and Jackals, it is hard to then mount a consistent criticism that species can never arise by acquired mutations.

That’s right. It’s not that different “species” can’t evolve because the species concept isn’t based on measures of novel functional complexity within different gene pools. All genetic definitions of species are based on non-functional aspects of genetic mutations, or at least don’t take into consideration the level of functional complexity involved. Given these species definitions which are not based on functionality, on levels of functional complexity, it is very easy to rapidly evolve novel species via the mechanism of RM/NS.

That is why the Biblical concept of unique “kinds” of gene pools is more accurate as far as the limits of evolutionary divergence is concerned. Unique kinds of gene pools that are based on qualitatively unique functional elements beyond very low levels of functional complexity are isolated from each other. These lines of complexity cannot be transgressed by any mindless evolutionary mechanism.

10] You can of course invoke miracles. Indeed I think it is the only logically consistent conclusion given your premises.

Why would I need to do that? I ask you again, where is the need to invoke miracles here? beyond the original creation of the various “kinds” of gene pools and their potential for rapid genetic and phenotypic diversity over time?

1] All species variation arose over 4000 years from an extremely bottle-necked population

Within the same “kind” of gene pool, yes.

2] Mutations account for any variation not present in the original near perfect pair.

Yes . . . without the need to invoke additional miracles of intelligent design.

3] These mutations cannot generate anything useful or novel that can contribute to the phenotypic development of breeds or species.

Not true. Mutations can and do contribute useful as well as novel elements to the phenotypic development of breeds and “species”. I’ve specifically explained this concept several times to you.

I have great faith in your ability to reconcile these but I do not have the intellectual horsepower to do so except by invoking miracles.

That is because you draw no distinction between levels of functional complexity within gene pools.

Sean Pitman

Southern Adventist University opens Origins Exhibit

A pubmed search for “sequence space” AND “functional complexity” yielded 30 publications none of which convey your perspective but do follow the scientific tradition of testing models against biological data in order to understand the operation of the natural world.

That’s right. There are no papers, of which I am aware, that detail the limitations of the Darwinian mechanism of RM/NS when it comes to levels of functional complexity.

Of course, the basic concept of different levels of functional complexity is fairly well defined in literature. However, no one has gone to the next step and detailed the limitations that this concept presents to Darwinian mechanism of RM/NS. No one has published anything at all about the average time necessary for random mutations to find anything qualitatively novel at various levels of functional complexity.

Yet, this concept is not beyond reach for scientific investigation. In fact, there is enough information for anyone interested in this question to sit down and work out the math for him/herself. The results are quite surprising – from an Darwinian perspective anyway. There is a very clear exponential decline in evolutionary potential with each linear increase in the level of functional complexity under consideration.

Now, don’t take my word for it. Do the math yourself. Don’t simply rely on what you read in literature. Why not actually do some of your own investigation into this question?

For example for speciation

1] We say that with time there is accumulation of genetic change or mutations by a variety of mechanisms including point mutations, indels, duplication events and within a population there is thus variation and selection for a phenotype that reflects a favourable genotype. With time pheotypic selection leads to genetically isolated populations which you can call a species.

Great! I have no problem with this except for the fact that it details no limitations to the potential for producing qualitatively novel systems of function beyond very low levels of functional complexity.

2] You start with a model of all possible protein sequences. Calculate the possibility that anything big and complex is statistically impossible within your sequence space matrix and then decide this is the basis of limitations of “RM/NS” and the limit of speciation. You may well be right but you do not seem to appreciate that at least to me without anchoring your model to real data and observations it appears just theory and conjecture over reality, an instance of argument from incredulity that does nothing to advance science.

My model is anchored to real data and observations. The data is available. You can determine the density of potentially viable protein sequences in sequence spaces at various levels of functional complexity. From this density, you can determine the most likely minimum Hamming distance between any one viable island cluster of protein sequences and the next closest viable/potentially beneficial sequence. Then, you can determine the average number of mutations necessary to get across this minimum likely gap distance…

As it turns out, the minimum likely gap distance increases in a linear manner with each linear increase in the level of functional complexity under consideration. With each linear increase in the gap distance, the average number of mutations needed to cross the gap increases exponentially…

I’ve explained this all in detail on my website.


Sean Pitman

Recent Comments by Sean Pitman

Science and Methodological Naturalism
Very interesting passage. After all, if scientists are honest with themselves, scientific methodologies are well-able to detect the existence of intelligent design behind various artifacts found in nature. It’s just the personal philosophy of scientists that makes them put living things and the origin of the fine-tuned universe “out of bounds” when it comes to the detection of intelligent design. This conclusion simply isn’t dictated by science itself, but by a philosophical position, a type of religion actually, that strives to block the Divine Foot from getting into the door…

Revisiting God, Sky & Land by Fritz Guy and Brian Bull

Why is it that creationists are afraid to acknowledge the validity of Darwinism in these settings? I don’t see that these threaten a belief in God in any way whatsoever.

The threat is when you see no limitations to natural mindless mechanisms – where you attribute everything to the creative power of nature instead of to the God of nature.

God has created natural laws that can do some pretty amazing things. However, these natural laws are not infinite in creative potential. Their abilities are finite while only God is truly infinite.

The detection of these limitations allows us to recognize the need for the input of higher-level intelligence and creative power that goes well beyond what nature alone can achieve. It is here that the Signature of God is detectable.

For those who only hold a naturalistic view of the universe, everything is attributed to the mindless laws of nature… so that the Signature of God is obscured. Nothing is left that tells them, “Only God or some God-like intelligent mind could have done this.”

That’s the problem when you do not recognize any specific limitations to the tools that God has created – when you do not recognize the limits of nature and what natural laws can achieve all by themselves.

Sean Pitman

Revisiting God, Sky & Land by Fritz Guy and Brian Bull
@Bill Sorensen:

Since the fall of Adam, Sean, all babies are born in sin and they are sinners. God created them. Even if it was by way of cooperation of natural law as human beings also participated in the creation process.

God did not create the broken condition of any human baby – neither the physical or moral brokenness of any human being. God is responsible for every good thing, to include the spark or breath of life within each one of us. However, He did not and does not create those things within us that are broken or bad.

“The owner’s servants came to him and said, ‘Sir, didn’t you sow good seed in your field? Where then did the weeds come from?’ ‘An enemy did this,’ he replied. “The servants asked him, ‘Do you want us to go and pull them up?'” Matthew 13:27-28

Of course, all humans are indeed born broken and are in a natural state of rebellion against God. However, God is not the one who created this condition nor is God responsible for any baby being born with any kind of defect in character, personality, moral tendency, or physical or genetic abnormality. God did not create anyone with such brokenness. Such were the natural result of rebellion against God and heading the temptations of the “enemy”… the natural result of a separation from God with the inevitable decay in physical, mental, and moral strength.

Of course, the ones who are born broken are not responsible for their broken condition either. However, all of us are morally responsible for choosing to reject the gift of Divine Grace once it is appreciated… and for choosing to go against what we all have been given to know, internally, of moral truth. In other words, we are responsible for rebelling against the Royal Law written on the hearts of all mankind.

This is because God has maintained in us the power to be truly free moral agents in that we maintain the Power to choose, as a gift of God (Genesis 3:15). We can choose to accept or reject the call of the Royal Law, as the Holy Spirit speaks to all of our hearts…

Remember the statement by Mrs. White that God is in no wise responsible for sin in anyone at any time. God is working to fix our broken condition. He did not and does not create our broken condition. Just as He does not cause Babies to be born with painful and lethal genetic defects, such as those that result in childhood leukemia, He does not cause Babies to be born with defects of moral character either. God is only directly responsible for the good, never the evil, of this life.

Sean Pitman

Revisiting God, Sky & Land by Fritz Guy and Brian Bull

Again, your all-or-nothing approach to the claims of scientists isn’t very scientific. Even the best and most famous of scientists has had numerous hair-brained ideas that were completely off base. This fact does not undermine the good discoveries and inventions that were produced.

Scientific credibility isn’t based on the person making the argument, but upon the merits of the argument itself – the ability of the hypothesis to gain predictive value when tested. That’s it.

Sean Pitman

Gary Gilbert, Spectrum, and Pseudogenes
Don’t be so obtuse here. We’re not talking about publishing just anything in mainstream journals. I’ve published several articles myself. We’re talking about publishing the conclusion that intelligent design was clearly involved with the origin of various artifactual features of living things on this planet. Try getting a paper that mentions such a conclusion published…

Sean Pitman