Is all TRUTH scientifically knowable?

[Scott J]

Originally posted by UTEOTW:
"So in other words, this phenomenon that we have wasted a great deal of time discussing has nothing at all to contribute to macroevolution?"

It is strong evidence that it happened.

No. It is purely coincedental. Can I prove that? No... no more than you can prove it is "strong evidence".

You do not accept the mechanisms when presented so it seems that maybe we should focus solely on some of the evidence for it for a while.

That is actually an untrue statement. I have not argued with the supposed mechanisms on the whole. Many are observed realities. I have argued against the notion that any of these mechanisms or all of them together account for common "ascent"- the mass increase of information via natural processes.

Any alternate ideas must be able to explain the details of our observations.

An alternative is not necessary to prove that the idea given by you fails.

There is, as yet, no parsimonious explanation for the details outside of common descent.

Actually I gave you one. You can call it improbable if you want but you cannot call it impossible any more than I can call naturalistic evolution impossible.

BTW, how many inserts do you assert that man shares with apes? Out of how many total?

Also, you said that the type you are talking of are rare. That would seem to suggest a level of novelty that defies a hard and fast rule that cannot be experimentally confirmed.... and a level of novelty that at least opens the door to the notion that the retrovirus itself is the cause of the similarity rather than the hosts.

One that can be considered to be beyond a reasonable doubt.

Frankly... nope.

That there are numerous such shared insertions is an even tighter case.

Again, you seem to be contradicting yourself. However, if indeed there are many of these shared insertions, I would argue that it is evidence of common design, not common ancestory.

Given the size of vertebrate genomes (>1 × 109 bp) and the random nature of retroviral integration (22, 23), multiple integrations (and subsequent fixation) of ERV loci at precisely the same location are highly unlikely (24).

This presumes something that was not addressed to my knowledge... and that I contended before. The common location could be a function of a genetic blindspot common to several species.

Otherwise, we could be talking about a specific capability of the retrovirus itself.

Common design is ruled out because these are functionless bits of junk.

Not at all. Common designs will react to common stimuli in common ways.

BTW, as much as possible, I would like to keep this only on the level of data involving humans only.

A common design that littered the genomes with random bits of viral DNA would be a sloppy design indeed.

Of course this is a straw man.

First, I have not argued that viral DNA have not infected species at all. I have argued that since common design attributes were used there would be similar or common reactions to environments.

Second, we don't actually know enough about the gene to say that anything is necessarily "junk" or "useless".

 

[Scott J]

BTW, I ran across an interesting bit of information that you might want to respond to.

Accord to Stephen Meyer, the Cambrian explosion was "top down" in terms of evolution/speciation. He said, "Instead, however, fossils from the Cambrian explosion show a radically different 'top down' pattern. Major differences in form and body plans appear first, with no simpler transitions before them. Later, some minor variations arise within the framework of these separate and disparate body plans."

Now he still apparently believes that this occurred during a "short" 5 million year or less time period about 530 million years ago. Nonetheless, contrary to your contention, evolution is not the system that best explains the fossil record. Gradual evolution would require that ever greater levels of variation occur as time went on.

I agree with Meyer that a sudden infusion of "information" from an Intelligent Designer is a far more rational assumption than anything proposed by evolutionists.

With that in mind, I would like to place my idea on an apples to apples basis with evolution (for argument's sake only).

I believe that a smaller number of parent animals with rich genomes appeared suddenly in the past and that all animals with the exception of man are "descended" from them. Like evolution asks for faith that a means for the appearance of the first organism(s) will be given later... I claim the same privilege. The "how" of the application of ID at the beginning of this initial group of animals may be discovered later but is not important with regard to the discussion of later events.

Of course, I still disagree with an OE approach. However, Meyer's testimony if true provides another piece of my foundation.

Here's the basic outline. God created the original types with very rich genomes. The immediate descendents of this group speciated quickly and with great diversity. One of the characteristics of this process was that the great variability was not passed on in equal measure thus hardening-off the species. At the time of the flood, Noah did not take one of every species but rather just a representative of each kind. These animals while far more adaptable than animals today were not as rich as the original copy. Thus, a huge number of species went extinct in the flood. The flood was then followed by a more modest and declining level of speciation. Today, the last vestiges of this ability to "evolve" are adaptations.

Can I fill in all of the gaps? Nope. I don't have the time, money, or the total expertise. However, until a better theory comes along... I will maintain this one. It accounts for everything you have argued including the viral inserts. It employs the same mechanisms you claim except it concludes in ways that are actually consistent with what we observe in nature.

Mutation more often (by a wide margin) produces a loss of information and/or function rather than any kind of benefit. Even your vitamin C example illustrates this. The information used by living things is overwhelmingly derived from its parents... not unidentified external sources.

 

[UTEOTW]

"No. It is purely coincedental. Can I prove that? No... no more than you can prove it is "strong evidence". "

I find it incontrovertible.

You must remember that we are never talking proof in science. We are merely looking for what explanation best fits the data. Young earths often like to throw out some really big numbers and say that those odds mean that evolution could not have happened. Usually such things are short on details of how the odds are calculated or they make faulty assumptions.

But in this case we can derive the odds for coincedence rather easily, at least for part of the procedure.

Now, there are 10^9 locations that a given insertion can take place so an insertion shared between two species at the same location has odds against of 10^9. Now, just this paper discusses twelve specific inserts. So the odds for all twelve being shared between two species is (10^9)^12 or 10^108. I counted ten different species in the list so the odds of the twelve being shared among all ten is (10^108)^(10-1) or 10^972. That is 1 followed by 972 zeros! By comparison there are about 10^85 total protons, neutrons and electrons in the entire visible universe.

Quite long odds for a coincidence!

The odds get longer when you consider that it is only a select group of viruses out of all those that can infect. The odds get longer when you consider the long odds against a given insert becoming fixed in the population. The odds become longer when you consider the likelyhood of the patterns of the mutations in the sequences.

"An alternative is not necessary to prove that the idea given by you fails."

Well, then at least show a place where the ERV data fails!

I contend that you are not out to merely disprove an old earth but to also show a young earth. In that case you DO need to provide an alternative.

"Actually I gave you one."

I must have missed it.

Which mechanism did you propose that accounts for the particular combination of shared viral insertions that we see out of the thousands of different viruses that can infect apes? What data supports your claim?

Which mechanism do you propose that accounts for all the insertions being located at the same locations in the genome? What data supports your claim?

What mechanism do you propose for fixing only these insertions? What data supports your claim?

What mechanism do you propose for all the insertions accumulating mutations in a pattern that matches trees from other methods? What data supports your claim?

"BTW, how many inserts do you assert that man shares with apes? Out of how many total?"

It is a complicated question. There are thousands of such insertions. But most are so old that they are shared not just by all apes, but also by all vertebrates or even all eukaryotes. The total makes up as much as a few percent of the geneome. If you want to talk about apes specifically, I am not sure of the exact number but from what I have read the number is in the dozens for how many inserts the apes share that are not shared by other vertebrates. Finally, I think around one or two inserts have been found in each species that are not shared with other species.

"Frankly... nope."

I disagree. I think the evidence is beyond a reasonable doubt. It is not and never will be beyond an unreasonable doubt. That is to say that you do not find absolute proof in sceince.

"Again, you seem to be contradicting yourself. "

Not when taken in context. Given how rare such events are, having dozens in common for the apes is a fair number. Having thousands in common among the vertebrates is significant.

"However, if indeed there are many of these shared insertions, I would argue that it is evidence of common design, not common ancestory... This presumes something that was not addressed to my knowledge... and that I contended before. The common location could be a function of a genetic blindspot common to several species. Otherwise, we could be talking about a specific capability of the retrovirus itself. "

No, this was addressed. Observation shows that the insertions are truely random.

Varmus, H. E. & Swanstrom, R. (1984) in RNA Tumor Viruses, eds. Weiss, R., Teich, N. M., Varmus, H. E. & Coffin, J. M. (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 369-512.

Brown, P. O. (1997) in Retroviruses, eds. Coffin, J. M., Hughes, S. H. & Varmus, H. E. (Cold Spring Harbor Laboratory Press, Plainview, NY).

"First, I have not argued that viral DNA have not infected species at all. I have argued that since common design attributes were used there would be similar or common reactions to environments."

Not possible for it to be coincidental. See above. It would have to be on purpose.

"Second, we don't actually know enough about the gene to say that anything is necessarily "junk" or "useless"."

But we do. We know they are viral in origin. We know that they are generally not expressed. And we know that they accumulate mutations in a pattern consistent with sequences that have no function.

 

[Scott J]

Now, there are 10^9 locations that a given insertion can take place so an insertion shared between two species at the same location has odds against of 10^9. Now, just this paper discusses twelve specific inserts. So the odds for all twelve being shared between two species is (10^9)^12 or 10^108. I counted ten different species in the list so the odds of the twelve being shared among all ten is (10^108)^(10-1) or 10^972. That is 1 followed by 972 zeros! By comparison there are about 10^85 total protons, neutrons and electrons in the entire visible universe.

This counts on the event being a purely random, chance occurrence. I have given at least two possibilities that would undermine that assumption.

I am not arguing for chance. Expressing things in odds like this assumes a random incident. This applies very well to the claims of evolution. It fails miserably when you introduce design as the basic premise.

BTW, how many are the shared inserts between humans and apes? I have only understood you to claim one.

 

[UTEOTW]

"This counts on the event being a purely random, chance occurrence. I have given at least two possibilities that would undermine that assumption."

There are OBSERVED to be random. These references discuss that observation.

Varmus, H. E. & Swanstrom, R. (1984) in RNA Tumor Viruses, eds. Weiss, R., Teich, N. M., Varmus, H. E. & Coffin, J. M. (Cold Spring Harbor Lab. Press, Plainview, NY), pp. 369-512.

Brown, P. O. (1997) in Retroviruses, eds. Coffin, J. M., Hughes, S. H. & Varmus, H. E. (Cold Spring Harbor Laboratory Press, Plainview, NY).

"BTW, how many are the shared inserts between humans and apes? I have only understood you to claim one."

There are thousands. Most of these, however, are quite ancient and are also shared with the other vertebrates. The number of shared inserts unique to apes are on the order of dozens. I do not know the exact number. It is possible that not all have been found.

The paper that I referenced for you discusses twelve specific inserts.

 

[Scott J]

Not possible for it to be coincidental. See above. It would have to be on purpose.

This is not true and you know it. It remains within the realm of possibility. I have consistently been honest enough to acknowlege that your beliefs remain possible though I consider them extremely unlikely. Courtesy demands that you not be overreaching on your conclusions.

If the preponderance of probability is all that is needed to affirm or negate a proposal then evolution is false. It is far more improbable than the odds you propose above against common design. You still have not bridged the gaps between mutation, accummulation of information, and the emergence of new functioning biological. The odds against even a very simple, novel function arising dwarf those given above by you. Mutation and time simply don't do it... and that's assuming 100's of millions of years not the compressed time asserted by Meyer.

Again, design answers this improbablity completely... even if it turns out to be arbitrary as you claim. Non knowing the reason someone chooses something is not the same as their not having a reason to do it. If, as you believe, God chose evolution to create everything then that would be a completely arbitrary and unnecessary choice- not to mention a mammoth waste of time. Using 13.5 billion years to prepare an earth for a few thousand years of human history? I don't think so.

 

[UTEOTW]

OK. Improbable.

We are looking for the most parsimonious explanation. Something so improbable does not fit that description.

 

[Scott J]

Does that go for macroevolution as well?

When we see a complex, functioning, encoded machine, the most parsimonious explanation is that its origin required intelligence and a direct creative act.

We would consider some complete irrational if they found a PLC and said "I wonder what processes over the last 13 billion years led to the construction of this thing." Evolution cannot account for the origin of information... and every living system and structure requires a ton of it.

The assumption of an intelligent creator by the way is very much scientific. In fact, its mechanisms are all about us. It is only the assumption of naturalism and the attached arbitrary definition of science restricted to that means that disallows science from exploring the most "parsimonious", observable line of inquiry.

[ February 02, 2005, 01:20 PM: Message edited by: Scott J ]

 

[Scott J]

Oh... I ran across a very interesting piece of info today. You claim that my contention for "descent" from a rich genome is without basis. Read the story "Genes evolving downward" on this site: http://creationsafaris.com/crev200502.htm

In spite of the dogged efforts to force fit this info into the evolutionary paradigm by these authors, please note this conclusion:

Intron losses outnumber gains over a large range of eukaryotic lineages. These results show that early eukaryotic gene structures were very complex, and that simplification, not embellishment, has dominated subsequent evolution.

... and this...

These results contradict the assumption that genome complexity has increased through evolution. Instead, species have repeatedly abandoned complex gene structures for simpler ones, questioning the purpose and value of intricate gene structures. These results suggest a reconsideration of the genomics of eukaryotic emergence [sic].

Here's the reference: Scott W. Roy and Walter Gilbert, “Complex early genes,” Proceedings of the National Academy of Sciences

Of course you will follow up and say that they still support evolution and long time periods. But they aren't looking for these facts to point anywhere but back toward their assumption of evolution. Further, this part is telling to me:

Two-thirds of bilateran introns were present in the bilateran ancestor [sic]; 40% of opisthokont introns were present in the ophisthokont ancestor; and 40% of plant, animal, and fungal introns were present in the plant?animal ancestor. This is quite different from what is commonly assumed and surprising in light of relatively fast rates of intron turnover observed in nematodes and flies

There seems to be a reasonable answer to this problem... the first ancestor wasn't millions of years ago and was created as a fully functional type.

 

[UTEOTW]

"You still have not bridged the gaps between mutation, accummulation of information, and the emergence of new functioning biological. The odds against even a very simple, novel function arising dwarf those given above by you."

I think we have a major difference of opinion on that matter. I assert that observed genetic process involving such things as duplication, point mutations, frame shifts, recombination, exon shuffling and the like are sufficient to generate new information. (I asked on the last page for a definition of information and an example of what you would consider to be new information. Answers might help bridge the gap. It is possible that you are laboring under an uneccesary definition and it is possible that there may be examples of what you would find acceptable so long as you do not try to move the goalposts and ask for direct observation of something that takes place in geologic timescales.) You assert that it is not sufficient though I am unsure what your basis for claiming this is. In my opinion, it sounds like you are asserting that it is not possible without showing why it is not possible.

I have tried to reason through this, but to no avail. So I have a different tact to try. If I the amateur cannot make a good case then I will let the professional. Please read the following two papers. (I am not sure you ever looked at the paper I referenced you on ERVs because you kept asking questions that were spelled out clearly in the text.)

Jianzhi Zhang, "Evolution by gene duplication: an update," TRENDS in Ecology and Evolution Vol.18 No.6 June 2003.

http://www.anthro.utah.edu/~rogers/bio5410/Readings/Zhang-TRE-18-292.pdf

The second may be more applicable but the pdf has disappeared from the web. I can give an abstract and an HTML cache but the figures will be missing and the formatting may be a bit off.

Long, M. 2001. “Evolution of novel genes.” Curr Opin Genet Dev 11(6):673-80.

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6VS0-448YP2P-G&_coverDate=12%2F01%2F2001&_alid=243045236&_rdoc=1&_fmt=&_orig=search&_qd=1&_cdi=6248&_sort=d&view=c&_acct=C 000050221&_version=1&_urlVersion=0&_userid=10&md5=bd5c5b78a754a2e9573cbf7b7bf1cc3e

http://scholar.google.com/scholar?hl=en&lr=&q=cache:aG7lJxTjrXEJ:[url]www.csb.yale.edu/people/gerstein/zl/papers/Evolution-Molecular/long-curr01-evolution-novel-gene.pdf+%22Evolution+of +novel+genes%22+long[/url]

 

[UTEOTW]

Let's also continue this by giving some more examples of new functions evolving.

Copley, S. D. (2000). “Evolution of a metabolic pathway for degradation of a toxic xenobiotic: the patchwork approach.” Trends Biochem Sci 25(6): 261-265.

The pathway for degradation of the xenobiotic pesticide pentachlorophenol in Sphingomonas chlorophenolica probably evolved in the past few decades by the recruitment of enzymes from two other catabolic pathways. The first and third enzymes in the pathway, pentachlorophenol hydroxylase and 2,6-dichlorohydroquinone dioxygenase, may have originated from enzymes in a pathway for degradation of a naturally occurring chlorinated phenol. The second enzyme, a reductive dehalogenase, may have evolved from a maleylacetoacetate isomerase normally involved in degradation of tyrosine.

Anandarajah K, Kiefer PM Jr, Donohoe BS, Copley SD (2000) "Recruitment of a double bond isomerase to serve as a reductive dehalogenase during biodegradation of pentachlorophenol," Biochemistry. 2000 May 9;39(18):5303-11.

Since maleylacetoacetate isomerase is involved in a common and presumably ancient pathway for catabolism of tyrosine, while tetrachlorohydroquinone dehalogenase catalyzes a more specialized reaction, it is likely that tetrachlorohydroquinone dehalogenase arose from a maleylacetoacetate isomerase. The substrates and overall transformations involved in the dehalogenation and isomerization reactions are strikingly different. This enzyme provides a remarkable example of Nature's ability to recruit an enzyme with a useful structural scaffold and elaborate upon its basic catalytic capabilities to generate a catalyst for a newly needed reaction.

Johnson, G. R., Jain, R. K. and Spain, J. C. (2002). “Origins of the 2,4-dinitrotoluene pathway.” J Bacteriol 184(15): 4219-4232.

The degradation of synthetic compounds requires bacteria to recruit and adapt enzymes from pathways for naturally occurring compounds. Previous work defined the steps in 2,4-dinitrotoluene (2,4-DNT) metabolism through the ring fission reaction. The results presented here characterize subsequent steps in the pathway that yield the central metabolic intermediates pyruvate and propionyl coenzyme A (CoA)... The presence of the transposon remnants and vestigial genes suggests that the pathway for 2,4-DNT degradation evolved relatively recently because the extraneous elements have not been eliminated from the region.

Long, M., Betran, E., Thornton, K. and Wang, W. (2003). “The origin of new genes: glimpses from the young and old.” Nat Rev Genet 4(11): 865-875.

from the summary, not the abstract

Direct and indirect observations of new genes in eukaryotic genomes show that genes with new functions are not as rare as was previously thought.
Analysis of the repeated new gene origination by retroposition in the Drosophila genome has uncovered a pattern in which new genes tend to avoid the X-chromosome linkage and most of the X-chromosome-derived autosomal new genes have evolved male-specific functions.

Nurminsky, D., Aguiar, D. D., Bustamante, C. D. and Hartl, D. L. (2001). “Chromosomal effects of rapid gene evolution in Drosophila melanogaster.” Science 291(5501): 128-130.

Rapid adaptive fixation of a new favorable mutation is expected to affect neighboring genes along the chromosome. Evolutionary theory predicts that the chromosomal region would show a reduced level of genetic variation and an excess of rare alleles. We have confirmed these predictions in a region of the X chromosome of Drosophila melanogaster that contains a newly evolved gene for a component of the sperm axoneme. In D. simulans, where the novel gene does not exist, the pattern of genetic variation is consistent with selection against recurrent deleterious mutations. These findings imply that the pattern of genetic variation along a chromosome may be useful for inferring its evolutionary history and for revealing regions in which recent adaptive fixations have taken place.

So we have a new metabolic pathway (sounds irreducibly complex to me), followed by another new metabolic pathway, followed by another new metabolic pathway, followed by sevel new genes formed by retroposition, followed by another new gene where before and after is compared by looking at populations with and without the new gene.

 

[UTEOTW]

More...

This one may be too speculative for your taste as it involves interpreting data from the past, but I would suggest that we do need to know why a designer would make it look like He invented through tinkering. It is another example of evidence for the mechanisms proposed though I doubt you will accept it.

Patthy, L. (2003). “Modular assembly of genes and the evolution of new functions.” Genetica 118(2-3): 217-231.

Modular assembly of novel genes from existing genes has long been thought to be an important source of evolutionary novelty. Thanks to major advances in genomic studies it has now become clear that this mechanism contributed significantly to the evolution of novel biological functions in different evolutionary lineages. Analyses of completely sequenced bacterial, archaeal and eukaryotic genomes has revealed that modular assembly of novel constituents of various eukaryotic intracellular signalling pathways played a major role in the evolution of eukaryotes. Comparison of the genomes of single-celled eukaryotes, multicellular plants and animals has also shown that the evolution of multicellularity was accompanied by the assembly of numerous novel extracellular matrix proteins and extracellular signalling proteins that are absolutely essential for multicellularity. There is now strong evidence that exon-shuffling played a general role in the assembly of the modular proteins involved in extracellular communications of metazoa. Although some of these proteins seem to be shared by all major groups of metazoa, others are restricted to certain evolutionary lineages. The genomic features of the chordates appear to have favoured intronic recombination as evidenced by the fact that exon-shuffling continued to be a major source of evolutionary novelty during vertebrate evolution.

Prijambada I. D., Negoro S., Yomo T., Urabe I. (1995). “Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolution.” Appl Environ Microbiol. 61(5):2020-2.

Through selective cultivation with 6-aminohexanoate linear dimer, a by-product of nylon-6 manufacture, as the sole source of carbon and nitrogen, Pseudomonas aeruginosa PAO, which initially has no enzyme activity to degrade this xenobiotic compound, was successfully expanded in its metabolic ability. Two new enzyme activities, 6-aminohexanoate cyclic dimer hydrolase and 6-aminohexanoate dimer hydrolase, were detected in the adapted strains.

Ranz, J. M., Ponce, A. R., Hartl, D. L. and Nurminsky, D. (2003). “Origin and evolution of a new gene expressed in the Drosophila sperm axoneme.” Genetica 118(2-3): 233-244.

Sdic is a new gene that evolved recently in the lineage of Drosophila melanogaster. It was formed from a duplication and fusion of the gene AnnX, which encodes annexin X, and Cdic, which encodes the intermediate polypeptide chain of the cytoplasmic dynein. The fusion joins AnnX exon 4 with Cdic intron 3, which brings together three putative promoter elements for testes-specific expression of Sdic: the distal conserved element (DCE) and testes-specific element (TSE) are derived from AnnX, and the proximal conserved element (PCE) from Cdic intron 3. Sdic transcription initiates within the PCE, and translation is initiated within the sequence derived from Cdic intron 3, continuing through a 10 base pair insertion that creates a new splice donor site that enables the new coding sequence derived from intron 3 to be joined with the coding sequence of Cdic exon 4.

Seffernick, J. L. and Wackett, L. P. (2001). “Rapid evolution of bacterial catabolic enzymes: a case study with atrazine chlorohydrolase.” Biochemistry 40(43): 12747-12753.

The text of the abstract eludes me. The title should be informative enough. A bacteria evolved to make new enzymes to process a new class of chemicals.

More examples of new genes and new functions arising through the very processes that you assert cannot produce such.

 

[UTEOTW]

"BTW, I ran across an interesting bit of information that you might want to respond to.

Accord to Stephen Meyer, the Cambrian explosion was "top down" in terms of evolution/speciation. He said, "Instead, however, fossils from the Cambrian explosion show a radically different 'top down' pattern. Major differences in form and body plans appear first, with no simpler transitions before them. Later, some minor variations arise within the framework of these separate and disparate body plans."

Now he still apparently believes that this occurred during a "short" 5 million year or less time period about 530 million years ago. Nonetheless, contrary to your contention, evolution is not the system that best explains the fossil record. Gradual evolution would require that ever greater levels of variation occur as time went on."

Could you please flesh out what your objection to evolution based on this are?

For anyone following this thread, Meyer is an ID advocate if that helps to know where he is coming from.

YEers generally make two contradictory criticisms of the Cambrian. One, they will say too many new things appeared too quickly for evolution to have produced it all. Or they will take the opposite approach and say that there was too much variation at the beginning of the Cambrian.

In an interesting anecdote, Well's apparently tries to burn both ends of that candle in his Icons of Evolution. I am not sure how he not his readers manage to miss that he is claiming contradictory things side by side.

"Major differences in form and body plans appear first, with no simpler transitions before them."

Except that there are transitions before then. They are harded to document because the beginning of the Cambrian was also about when the chemistry of the oceans and the increase in predation led to hard body parts that preseved more easily. But there are earlier transitions. The Edicharian fauna and the Burgess shale both show transitional forms beforehand. They also show that there was a very diverse amount of body plan experimentation going on. Many body plans were tried during this period that died out as unsuccessful in the long run. I can hardly see how these experiments going extinct before and during the Cambrian can be considered evidence against it.

"Later, some minor variations arise within the framework of these separate and disparate body plans."

Minor variations? Like all amphibians, reptiles, mammals, birds, and most fish?

He really has to be kidding. I know what he is saying. These are just variations on the bilateral body plan, but he misleads to suggest that all tetrapods are simple variations on this plan and should not be considered macroevolution.

"Now he still apparently believes that this occurred during a "short" 5 million year or less time period about 530 million years ago."

Glad you put the quotes in there because 5 million years is still an enormity. But he also quotes the extreme end of the range of the Cambrian. Most put it at more like 50 million. Ten times as long does change the perception a bit. Consider, for example, all of the mammalian evolution in the last 50 million years. There has been a lot of change in that time.

"Gradual evolution would require that ever greater levels of variation occur as time went on."

For the most part it does increase. Meyer was using a very strained definition to say it did not.

"Here's the basic outline. God created the original types with very rich genomes. The immediate descendents of this group speciated quickly and with great diversity. One of the characteristics of this process was that the great variability was not passed on in equal measure thus hardening-off the species. At the time of the flood, Noah did not take one of every species but rather just a representative of each kind. These animals while far more adaptable than animals today were not as rich as the original copy. Thus, a huge number of species went extinct in the flood. The flood was then followed by a more modest and declining level of speciation. Today, the last vestiges of this ability to "evolve" are adaptations."

Not consistent with observations.

The bottleneck at the flood would be visible in the genomes of todays organisms. Since essentially would have gone through a bottleneck of two individuals, there would be very little diversity within the genomes of todays species. At most there could be four different version of a given gene within populations. Such is not seen.

A rich genome would mean that variation between species would have to occur by the loss of function of certain genes in each species. This is not what we observe. Closely related species are different in the variation of the same genes. This is contradictory to both a rich genome and to having had a recent bottleneck.

If there was a diversification of life before the flood and then another after, then there would be little connection between the fossils of the past and the animals of today. It does not fit observations. (Not to mention that the fossil record itself is inconsistent with having been created largely in a big flood.)

 

[UTEOTW]

To return briefly to the subject of the ERVs.

I have mentioned several times my opinion that common descent is the best explanation for the endogenous retroviral inserts. But there is another contrast to be made here. The power of prediction.

Knowing that certain viruses insert their genes into the host of their genome and knowing from other sources that humans and the other apes share a common ancestor, it is a simple prediction to say that there should be wide agrement between the various ape species on the sequence and location of these inserts. The prediction comes directly out of the premise.

And as geneticists search the genomes, they do indeed find that the species share the location and sequence of such inserts and that the patterns of mutations match that predicted from other means. Whenever they look, the predictions are matched to the observations.

Now, where is this power of prediction from any other explanation? Other ideas offered thus far reach no further than guesses. Perhaps it is coincidental (despite the very low odds). Perhaps there is a preference for a specific location (despite the observations to the contrary. Perhaps they are beneficial (despite them being viral in origin, despite them not coding for proteins and despite them accumulating mutations in the manner that useless DNA does so). No YE theory explains the details of the observation and further no YE theory would predict the observations.

What would we predict for the inserts in a young earth? Well, if we trust observations which say that such insertions that get passed on are rare, then we should expect that there would be few if any insertions at all. In addition, because of the short time period, what insertions there may have been would not have time to have become fixed throughout populations. So, at most, an individual would expect only a couple of insertions and these should not even be shared widely within a species, much less between species. But this is not what we observe. There are thousands of inserts and they are widely shared within and between species.

Well, what if you assume that insertions are accuaaly common and that our observations are wrong? Then you might be surprised by the large number of such inserts but you would expect that individuals would have combinations of inserts that varied widely within a species and even more so between species as far as sequence goes and location would be different as well. This would be because new inserts would be frequent and starting separate lines that did not have chances to merge and fix specific insertions throughout the population. Again, this is not what we observe. The sequence and the location of insertions are highly conserved within and between species.

So, while ERVs are very much what you would expect if common descent were true and common descent can make successful predictions about what else will be found, the same cannot be said of the alternatives. The alternatives make no correct predictions about what else should be found and fail to account for a mechanism to give the current state of observations.

 

[Scott J]

Not consistent with observations.

It is more consistent than macroevolution.

Did you not read the other post? That citation comes from evolutionists writing in the Proceedings of the National Academy of Science. They say that the greatest genetic complexity occurred at the beginning and has since been simplifying.

Without regard to timeframe for now, this is exactly what I have been arguing for and you have been arguing against.

Meyer's quotes are further confirmation of this trend.

Both of these work against the macroevolutionary model of slowly accummulating genetic complexity that results in higher biological systems.

BTW, with the exception of the inclusion of man, this also allows for your ERV objection to be true yet not supportive of macroevolution.

You know that I have not discluded the possibility that many current species share a parent ancestor. In fact, I count on it. What I have argued is the mechanism best supported by the evidence is literal "descent", not "ascent" as required by the TOE.

Animals derive their genetic make up and variability from their parents. Your ERV examples do not disprove this. You have yet to give a real world example that supports any other theory. All of the things you list above are ultimately speculation... educated guesses. Almost all external influence on genes at the molecular level are harmful or benign. The few that are deemed beneficial would never amount to anything close to the ascendency of a new biological system.

 

[Scott J]

BTW, Have you found the number of shared ERV inserts between men and apes? I would be interested in how many there are compared to those shared between apes species as well.

Again, the only one I have seen you post as shared between man and ape is the one effecting Vitamin C production.

 

[Scott J]

The bottleneck at the flood would be visible in the genomes of todays organisms.

No more nor less than the Cambrian bottleneck proposed by evolution.

 

[Scott J]

A rich genome would mean that variation between species would have to occur by the loss of function of certain genes in each species. This is not what we observe. Closely related species are different in the variation of the same genes. This is contradictory to both a rich genome and to having had a recent bottleneck.

Two things.

First, that isn't a necessary outcome of a rich genome... and if it is then you still have a problem because evidence of a rich ancient genome has now been found.

Second, it isn't the closely related descendents that are most in question. It is the more distant ones... though I contend that they may not be that much further from the initial parent. Information loss would quickly give the appearance of distance when all you are really seeing is one line of descent preserving one set of traits while another preserves another with only a small shared subset. A third line might have a much larger subset in common with one or the other.

I don't believe that these two methods for speciation, deletion and variation, are contradictory but rather complimentary. Together, they make speciation much more robust than evolution would predict.

 

[Scott J]

If there was a diversification of life before the flood and then another after, then there would be little connection between the fossils of the past and the animals of today.

That's not at all true. There should be significant connection but also disconnects... and that is what the fossil record shows.

(Not to mention that the fossil record itself is inconsistent with having been created largely in a big flood.)

I have read some well educated men who disagree with you. Of course, you would have a kneejerk bias against them for bucking the popular paradigm. Their ideas never the less account for the known facts.

Do the account for them as well? That is subjective enough to simply leave it unresolved. However they do a better job of accounting for the fossil record than naturalism does for explaining complexity or the origin of information.
[/quote][/qb]

 

[Phillip]

Originally posted by UTEOTW:
For anyone following this thread, Meyer is an ID advocate if that helps to know where he is coming from.

UTEOTW, I find this statement quite enlightening. I spend a lot of time analyzing testimony and statements and this one has disturbed me.

You claim to believe in God and God's hand in creation (even if it is through evolution), you claim to believe in the virgin birth, Jesus as diety and His miracles, and miracles of the disciples.

Then you make a blatant open ended statement that says that "Meyer is an ID advocate". Setting the tone that "Meyer" obviously has a problem with his theories because he uses an intelligent design factor in his studies.

Does this mean that you do not take into consideration "intelligent design"?