@Professor Kent: And here is just a smattering of the

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

And here is just a smattering of the evidence for the second failed prediction:

AMPHIBIANS

How did 400 species of plethodontid salamanders (almost the entire family) and 100 species of leptodactylid frogs (the entire family) end up in the New World, with just species of plethodontid and no leptodacylids in the Old World? As amphibians, they could not have survived salt water or swam across the ocean after leaving Noah’s ark. Most or all had to have evolved in the New World from ancestors that left the ark. In the Caribbean Islands, as far removed from Mt. Ararat as one can get, every one of the 170 amphibian species found there is confined to those islands without members occuring elsewhere. Where did they all come from?

Besides the fact that there were numerous land bridges after the Flood, especially during the ice ages when ocean levels dropped dramatically, this situation is not at all unique. For example, most of the species on the island of Madagascar are unique to the island.

Again, speciation and unique local adaptations can be achieved very quickly via Mendelian-style variation within a particular “kind” of gene pool. That is why essentially all modern breeds of dogs could be realized within 300 years or so.

Also, local environments may support certain kinds of creatures while elsewhere they’ve gone extinct…

BIRDS

Even more puzzling, some 300 species of trochilids (the entire hummingbird family), 500 species of tyranids (an entire flycatcher family), and 300 species of funariids (the entire ovenbird and woodcreeper family) occur strictly in the New World, without a single representative (apart from a fossil hummingbird) in the Old World. These birds can potentially fly from one continent to another, so you would expect a few of the millions upon millions of descendents to remain in the Old World before heading to the New World, or at least fly back to whence they came–but there are none!

Obviously hummingbirds were in the Old World post-Flood since you yourself cite the fossil evidence (rare as it may be – which is also telling). The fact that they went extinct in the Old World and did not repopulate it is pretty much beside the point – – that they were once there. There are, of course, many potential explanations for this lack of repopulating old habitats – such as the current difficulty of actually making it across the vast distances of inhospitable terrain that would be required (huge oceans, ice sheets, etc), the fact that birds tend to remain in established habitats as long as they remain viable, etc.

SNAKES

There are some 30+ species of rattlesnakes in the New World that had to evolve their distinct features here and speciate in less than 4,000 years, as none–even as fossils–occur in the Old World. I could add that, for the rattlesnakes, it was a heckuva crawl from Mt. Ararat in such a short time. Curiously, Geanna Dane tells me they originated in Mexico of all places, according to the same DNA-based analyses that Sean Pitman insists are valid for testing the ancestry of North American indians (I had to laugh when she brought this up!). So how did they get to Mexico before acquiring their rattles and other features, and how did they spread so far from there and diversify into so many forms in just a few thousand years?

It doesn’t take nearly as long as you imagine for a turtle or a snake to get from one part of the globe to the opposite side. Do the math.

As far as rattle snakes appearing only in Mexico and North America, not in the Old World, again, this is not unique as already noted. Many species are isolated from other regions because they went extinct in other regions for whatever reason or evolved specializations in isolated regions over time (at low-levels of functional complexity or via a loss of ancestral genetic information). In fact, currently, 18 genera and 151 species of “pit viper” are recognized: 7 genera and 54 species in the Old World, against a greater diversity of 11 genera and 97 species in the New World. The original front-loaded genetic information within this subfamily of venomous vipers could easily explain their rapid diversity as well as cases of isolated diversity.

And these animal groups are just the tip of the iceberg, as there are many others that show no evidence of having originated in the old world. Neither Sean Pitman nor David Read can explain the lack of an “out of Ararat” pattern.

There are many potential reasons for the patterns that currently exist. Your arguments do not remotely falsify the Biblical claim for a single origin for all land animal life. This is hardly the strongest argument for neo-Darwinism…

And these groups have evolved hundreds of new species–at spectacularly rapid rates–within just a few thousand years. Makes you wonder who the “true” evolutionists are, as we require far more rapid rates than evolutionists believe to be possible.

That is because most evolutionists do not seem to understand that changes that are not dependent upon the gain of novel genetic elements can and do happen very very quickly. They don’t understand the concept of front-loaded information and the speed of diversification that this allows – to include various forms of Mendelian variation for instance.

Sean Pitman
www.DetectingDesign.com

Table of Contents

1 Sean Pitman Also Commented
- 1.1 Recent Comments by Sean Pitman
2 Related

Sean Pitman Also Commented

Southern Adventist University opens Origins Exhibit
@pauluc:

If I may summarize our previous posts on allelic variation, SNPs and speciation
You suggest

1] There was frontloading of genetic information in a breeding pair for most species 2349-2348 BC.

The frontloading was at the time of creation by the Creator (less than 10,000 years ago), with a genetic bottleneck at the time of the Noachian Flood some 4,000 or so years ago . . .

2] Variation leading to speciation within kinds was by genetic mechanisms of allelic variation from the original gene pool. Maybe 10-20% of the variation can be attributed to this front loading.

It depends what type of variation you’re talking about. All of the variation beyond very low levels of functional complexity is the result of frontloading . . .

3] Most of the allelic variation and SNPs seen in species today has arisen by random mutation within the populations derived from this starting population of 4 haplotypes. ie 80-90% of the variation within species derived from “kind” ancestor.

At low levels of functional complexity, yes, the vast majority of allelic variations are the result of random mutations.

4] Most (80-90%) of the phenotypic differences seen between species has occurred by natural selection and genetic drift.

Within the same basic “kind” of gene pool – yes.

5] Any differences due to RM/NS after selecting the front-loaded pair can only confer very very low level complexity.

That’s right.

6] There is a barrier of 1000fsaar that limits any ability to generate anything novel and complex within this 80-90% of new mutations.

Yes.

Apropos of the recent paper:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3310774/?tool=pubmed

How do you modify your model of constraint by 1000fsaar to account for the role of SNPs in determining the effects of non-coding regulatory elements? In this context any discussion of hamming distance is really examining the edge effect of minimal relevance. I should not have to explain how this is particularly germane and impacts your discussion about genetics of feathers and the regulation of genes controlling feathered phenotype.

Non-coding regulatory elements are key to the building of complex systems within living things – far more important than are the protein-coding genes themselves (which function more like bricks and mortar that can be used to create many different types of buildings). SNPs can affect these regulatory elements, obviously. However, SNPs cannot affect these regulatory elements in a way that causes them to produce a qualitatively novel type of “building” with the “bricks and mortar” – beyond very low levels of functional complexity of course. In other words, you have to ask yourself the odds that a single point mutation to a regulatory non-coding sequence, or any other type of mutation, will result in a change in the location of the final product to an entirely novel island in sequence space that has a qualitatively unique function that requires a minimum of more than 1000 specifically arranged amino acid parts? That just doesn’t happen. There are no examples of this anywhere in literature – period.

If you would actually sit down and do the math, you’d see why. Sequence space has a fairly uniform distribution of potentially viable sequences/structures. As the minimum size and or specificity of the system under consideration increases in a linear manner, what do you think happens to the ratio of potentially viable/beneficial vs. non-viable/non-beneficial sequences in sequence space? The number of non-viable sequences increases in an exponential manner compared to the potentially viable sequences. The means that the viable sequences become more and more isolated in sequences space, dramatically so, with each step up the ladder of minimum size and/or specificity requirements. This means, of course that the minimum likely gap distance between viable sequences in different island clusters increases in a linear manner with each increase in the minimum size and/or specificity requirements. And, this means, of course, that the average time needed for any kind of random mutations needed to traverse the linearly increasing gap distances increases exponentially.

Now, tell me, how do you solve this sequences/structure space problem at increasing levels of functional complexity? Do you really not see the exponential nature of the problem? There is really no point in further discussion if you will not discuss this particular question. I really don’t understand your continued reluctance to substantive address such problems or consider the statistical basis for your own evolutionary assumptions. Why don’t you sit down and actually do a few calculations? Why not calculate the odds, for yourself, of any kind of mutation or series of mutations in any kind of coding or non-coding region evolving any kind of qualitatively novel system at various levels of functional complexity?

Give it a shot already. What could it hurt?

Sean Pitman
www.DetectingDesign.com

Southern Adventist University opens Origins Exhibit
@pauluc:

Since you havent responded to my request to identify in the genomic comparison of mammalian species or primates with the instances of where the 1000fsaar criteria limiting the sequence differences, I suggest an alternative.

But I have responded to this question at least a couple times in this thread. Please go back and review these responses to you and Jeff Kent.

Please provide insights on this recent paper from Kate Sullivans group on Human Accelerated Regions that are proposed to be contributors to the differences between humans and Chimps particularly in limb and brain development. Im interested in the comparison between human SNPs and the varying presence of these SNPs in chimp, Neandertal and Denisova genomic sequences.

Differences between human and ape brain development are based on more than SNPs (which would produce quantitative differences in form and function, but not produce qualitative changes beyond very low levels of functional complexity).

As already noted a few posts above in this thread, 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:

http://www.detectingdesign.com/pseudogenes.html#Key

I am sure you see P Troglodyes as entirely unrelated to man but I am a little unclear on your model of origins in terms of relatedness of Neandertal and Denisova hominids to man. Are they the children of Adam, Noah or neither? How do you account for any sharing of SNPs, the HAR and the development of pehnotypic differences by SNPs?

Neandertals and Denisova are human, descendants of Noah. They are simply ethnic variations of humans. Even mainstream scientists think that they could interbreed with each other to produce viable and virile offspring.

Of course there will be SNP differences between modern humans and Neandertals and other ancient ethnic groups – as there are between modern ethnic groups. And, these SNPs may be associated with functional differences – but not beyond low levels of functional complexity (usually only quantitative differences of the same basic type of gene function).

As far as the HAR-1 RNA, there are 18 character differences between humans and chimps (out of 118 characters/nucleotides). These differences are thought to play some role in the development of our brain differences, but no one knows exactly what role. Obviously, there are many structural and functional brain differences at high levels of functional complexity. However, there are also many unique non-coding genetic elements that seem to be involved with these differences (as already explained). No single point mutation or small cluster of mutations is going to be able to cross the gap between any qualitatively novel higher level system of function. Again, there are no examples of this in literature – for very good statistical reasons.

Another paper that cries out for your interpretation including the point at which ignorance about the 1000fsaar limit has blinded this group of scientist.

http://www.ncbi.nlm.nih.gov/pubmed/22398555

Critique below the abstract would be most helpful in seeing the errors.

Where in this paper is there any discussion of levels of functional complexity and how mutations can generate qualitatively novel systems at high levels of functional complexity? Remember, we aren’t just talking about quantitative differences in functionality here. We are talking about qualitatively novel differences beyond low levels of functional complexity. We need some actual math here – a few statistical calculations as to the odds that the just-so stories in papers like this might or might not actually be likely to be realized in a given span of time. Please do quote for me the relevant portion of this or any other paper along these lines.

Don’t just give me a bunch of references without any quotes or commentary (aka: reference mining). Show me that you actually understand the problem under discussion by, well, discussing it for a change with the use of quotes that you think are relevant. That would be most helpful…

Sean Pitman
www.DetectingDesign.com

Southern Adventist University opens Origins Exhibit
@Professor Kent:

Again, the question is why does one accept the Bible among so many compete options as the real Word of God? If this choice is based on blind faith without any rational basis or appeal to the weight of empirical evidence, what you have is nothing much more useful than wishful thinking… not the kind of faith that has the power to provide a solid hope in the future for most rational people – especially in the face of very difficult trials or even the threat of torture and death.

What you’re asking people to do is to accept the Bible without really considering the weight of empirical evidence or any additional evidence that may contribute to the current weight of evidence for or against the Bible’s credibility. That’s simply not a rational expectation. Certain God does not expect anyone to believe without a rational basis for belief or faith set upon the weight of evidence that would appeal to the candid mind.

In this line, we are talking about what paid representatives of the SDA Church are teaching and/or preaching in the name of the Church. The Adventist Church, as an organization, simply cannot afford to pay people to go around teaching our young people that the best we have to support the Adventist position on origins is faith that is effectively blind to the otherwise overwhelming scientific basis for neo-Darwinism. That simply isn’t helpful to Adventism. Those who believe in neo-Darwinism, however honest and sincere they may be (and there are many in this category) cannot effectively represent the Adventist perspective on several fundamental doctrinal positions within our schools…

Sean Pitman
www.DetectingDesign.com