Southern Adventist University opens Origins Exhibit

 
By Sean Pitman

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For those who aren’t already aware, Southern Adventist University opened up its new long anticipated Origins Exhibit on April 15, 2012.   It took over four years of planning and some $300,000 in donations to produce the first two of three phases of the project:  1)  hire professors who had origins experience.  2)  find a way to provide origins education outside of the classroom. 3) expand the hallway exhibit into an institute that provides information for all who are looking to learn about the short-term creation worldview.

Before work began on the second phase of the project, the “hallway phase”, Dr. Keith Snyder, Biology Department Chair, wrote to 20 prominent scientists who support the Biblical perspective on origins and asked them what they felt was the strongest evidence supporting short-term creation?  Dr. Snyder then used this information to produce an exhibit that features 25 hallway displays which highlight three main categories of evidence:  the living cell, the geologic column, and intelligent design.

So, why does the biology department at SAU hope to achieve with their project?

We wanted the finished product to be professional, but not overpowering.  Our goal is not to tell people that their beliefs are wrong, but to provide scientific evidence that substantiates the Bible’s account of creation.

Dr. Keith Snyder, Biology Department Chair

 

Also, Ron Hight, the art director for the project, says that he felt called by God to help with this exhibit.  He spent the last 15 years working as an artist for The Institute for Creation Research, and believes his experience there was excellent preparation for this work.

“Our goal,” says Hight, “is to present the creationist viewpoint in an attractive, professional, and educational way.  It is a challenge because no one has ever done this kind of thing before.”

 

This is all reflected in the general attitude toward the Biblical view of creation at SAU among professors in all departments.  Dr. Greg King, dean of the School of Religion and Professor of Biblical Studies, explains:

“Our campus has a commitment to creation.  We are unapologetic creationists, but we do not claim to have all the answers.  Religion and science don’t need to be at odds. We as scientists and theologians have a camaraderie. Our belief in the biblical perspective on origins is what binds us together.”

 

 

SAU Origins Exhibit – From the spring issue of Columns – the magazine of SAU:

For more information, visit:  Southern.edu/FaithandScience

 

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725 thoughts on “Southern Adventist University opens Origins Exhibit

  1. Bob Helm: However, I must take issue with your statement that low-elevation environments in today’s world are loaded with vertebrates. That may be true of terrestial environments, but actual low elevation environments are found on the sea floor, and these environments are loaded with invertebrates, along with some rather bizarre fish – like eels.

    I was speaking only of terrestrial biomes. And I know you won’t take exception with the facts there.




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    • @Professor Kent: No, Professor Kent, I won’t take issue with the fact that low elevation terrestial biomes contain many vertebrates. And I hope you agree that the ocean floor is the home of many invertebrates. Now the interesting thing is that the lower Paleozoic column contains abundant marine invertebrates and fish. And this is exactly what the ecological zonation theory would predict. Please bear in mind that I agree with you that the EZT has some problems and cannot account for all the order we find in the fossil record. But it accords nicely with the lower Paleozoic fossil record.




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  2. Sean, Bob, David, Eddie, and Holly,

    In just one sentence, please tell me whether Genesis informs your interpretation of the fossil record, or whether the fossil record informs your interpretation of Genesis.




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    • @Professor Kent:

      Faith and science inform each other. Without Genesis certain features of the fossil record would be much harder to interpret. I think that’s a given. It’s always good to have an eye-witness account in hand when investigating historical evidence. Such eye-witness accounts help fill in many details that would otherwise be very very difficult to determine.

      However, even without Genesis it should be clear that the fossil record and geologic column are records of recent shortly-spaced watery catastrophes.

      It is only because of the philosophical influence of neo-Darwinism that the catastrophic nature of the fossil record, to include its recent and rapid formation, has not become the standard interpretation in mainstream science. It’s similar to what happened to J Harlen Bretz and his theory for a flood or series of floods as the origin for Washington’s Scablands. He was rebuffed by mainstream scientists until it was discovered that the floods were local floods, not the Noachian Flood…

      Sean Pitman
      http://www.DetectingDesign.com




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    • @Professor Kent: I agree with Bob and Sean that it works both ways, but I believe more the former than the latter. Because of the Genesis narrative, I interpret the fossil record, at least the great bulk of it, as the residue of the Flood. Were it not for the Genesis narrative, I might interpret the fossil record, or the bulk of it, according to the principle of uniformity, ala Lyell. So clearly, the primary determinant is Scripture, not unaided examination of the raw data.

      For an example of how the fossil record can add depth of meaning to the interpretation of Scripture, consider Genesis 8:3. The King James Version renders it “And the waters returned from off the earth continually: . . .” The Hebrew word translated “from off” is usually translated “upon” or “above.” Two Hebrew words are translated together as “continually.” The first is yalak, which means, “to go.” The second is shuwb, which means, “to return.” The text might better be translated, “And the waters returned upon the earth, going and returning.” The floodwaters surged in and retreated in a repeating cycle. One commentator explains it as follows:

      “In Genesis 8:3, “continually” is a translation of two Hebrew verbs: shuwb, which means “to turn about, to return,” and yalak, which means “to go.” Together they present us with a graphic picture of the powerful churning action of the flood waters! A going is followed by a returning. Both verbs are set in the infinitive absolute form, indicating emphasis and duration. The flood waters did not tranquilly seep into the soil. This was a moving Flood, carrying back and forth vast amounts of water, soil, vegetation, and sediments. Gradually, layer after layer of sediments, vegetation, and other materials were laid down and covered over. The infinitive form means that it kept happening over a period of time (instead of only once if the imperfect form had been used). Terrific hydraulic forces were at work. Massive erosional and depositional actions were taking place. Gradually, layer after layer of sedimentary deposits were laid down.”

      The fact that the sedimentary deposits testify so strongly to this back and forth deposition pattern brings to our attention a detail in Scripture that we probably would not have noticed otherwise. The implication of back and forth action was always there in the Bible, but we would not have noticed it or attached any significance to it were it not for a very prominent characteristic of the stratigraphic record. So that’s an example of the fossil record enhancing our knowledge and interpretation of the Genesis record.




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      • @David Read: Dear David,
        I agree with everything you have stated. The reason I said it works both ways is that the Biblical account, while true, is only a sketch. In fact, Genesis moves very fast through its first 11 chapters and then slows down when it arrives at Abraham. Furthermore, Genesis is not written in scientific jargon; it is written in language that even children can understand, which is as it should be, because the Holy Spirit has wanted to communicate with all people in all ages, not just modern scientists. So scientific concepts like ecological zonation, catastrophic plate tectonics, and post-flood glacial theory are not touched on in Genesis, but they give us a broader picture of how the events described in Genesis probably took place.

        I do have to agree with Sean on one thing. The Phanerozoic fossil record looks very catastrophic to me, and I would have a hard time keeping an open mind and applying the principles of uniformitarianism to it. With what we know today, it can only be interpreted that way if we are already committed to the philosophical presuppositions of Lyellism and are trying to force nature to conform to that model. An objective interpretation of the fossil data yields catastrophism of some sort, and the Genesis account of the flood helps us to be more specific in identifying the catastrophic process that was involved.




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  3. David Read: God has provided plenty of evidence to confirm our faith, but He’s not going to remove the necessity of faith. There will always be hooks for skeptics to hang their doubts on, but if you cannot ultimately overcome your doubts and exercise faith, you cannot be a Christian believer. Only people of faith can be saved, that is, only people who are willing to trust God and put away doubts can be saved.

    I say a big “Amen” to this.




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    • @Professor Kent:

      I also agree. Science is dependent upon faith. God is not going to remove the need for faith because faith is more than just a knowledge of what is true. Satan has great knowledge, but no faith. Faith is a combination of knowledge of and desire or love for the truth.

      However, faith is also linked to knowledge. Did the faith of the disciples of Jesus increase or decrease after the Resurrection? Did the empirical evidence of Jesus’ deliberate fulfillment of Biblical prophecy regarding his birth, life, death, and resurrection add to the faith of those investigating His claims to be God? How about His demonstrated ability to raise the dead? Would such a demonstration tend to increase or decrease faith?

      Clearly, faith and empirical evidence are inextricably linked together – yet, faith goes beyond evidence to include the motive of love…

      Sean Pitman
      http://www.DetectingDesign.com




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      • @Sean Pitman: New Testament faith is always based on evidence – especially prophetic evidence. It was only during the 18th century Enlightenment, when the idea arose of science and spirituality being in two “airtight” compartments, that faith was defined as being a blind leap in the dark. If we take the New Testament seriously, there is a pressing need for Christian apologetics.




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  4. Professor Kent: In just one sentence, please tell me whether Genesis informs your interpretation of the fossil record, or whether the fossil record informs your interpretation of Genesis.

    The Bible informs my world view and that by definition for all observers informs my interpretation of the fossil record.

    But even without that super advantage available to the Christian and even more so to the Seventh-day Adventist Christian we have examples of atheist scientists themselves admitting to the paucity in scientific method that can be seen among the by-faith-alone believers in evolutionism.

    How sad that any Adventist would choose blind faith evolutionism over the Bible.

    It is one thing to treat the Bible as a book of good moral instruction, to be heeded so far as is consistent with the spirit of the times and our position in the world; it is another thing to regard it as it really is—the word of the living God, the word that is our life, the word that is to mold our actions, our words, and our thoughts. To hold God’s word as anything less than this is to reject it. And this rejection by those who profess to believe it, is foremost among the causes of skepticism and infidelity in the youth. {Ed 260.1}

    in Christ,

    Bob




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  5. Nice to see folks, including Sean Pitman, admit that their interpretation of the fossil record is influenced by their understanding of Genesis.

    For this reason alone, it’s difficult to defend a position that one must find and acknowledge God through the objective, rational, unbiased study of fossils. And it’s difficult to claim that one’s belief in God is anchored entirely in empirical evidence such as the fossil record when one’s interpretation of it is biased by faith in what scripture tells us.




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    • @Professor Kent:

      It is not mysterious or inconsistent to suggest that the Bible influences one’s interpretation of the fossil/geologic records and that empirical evidence influences our understanding of the Bible as the true Word of God.

      The same thing is true for any historical document thought to be a genuine description of real historical events – like documents describing the life of Alexander the Great. The credibility of such accounts are based on empirical evidence that, once established, affects our modern view of other forms of empirical evidence since the document is able to fill in details regarding history that could not otherwise be known…

      Sean Pitman
      http://www.DetectingDesign.com




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  6. BobRyan: How sad that any Adventist would choose blind faith evolutionism over the Bible.

    It’s hilarious that the basic assumption of naturalism–there is no God–gets turned into “blind faith evolutionism” by those who openly proclaim their faith in God. Naturalism applies the evidence to understand scripture, and creationism applies scripture (in no small part) to understand the evidence. But only one group could possibly have uninformed faith? It’s premeditated pejorative propagandizing.

    Is there such a thing as a kind, gentle, and gracious Christian?




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    • @Professor Kent: “Naturalism applies the evidence to understand scripture, and creationism applies scripture (in no small part) to understand the evidence.”

      Jeff, your clauses are not parallel. Naturalism first assumes that there was no Creator God (a faith assumption) and then uses that assumption to interpret the data of nature. It then uses its (atheistic) interpretation of nature to re-interpret Scripture. But since Scripture is all about miracles, all about an omnipotent Creator God, why would anyone who rules out such a God in his interpretation of the data of nature even be interested in the Bible?




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      • @David Read:

        After reading your Dinosaur book I can see you know about science as a non-participant but do not really know about the practice of science or of scientists.

        Your statement

        “Naturalism first assumes that there was no Creator God (a faith assumption) and then uses that assumption to interpret the data of nature. It then uses its (atheistic) interpretation of nature to re-interpret Scripture.”

        bears no resemblence to the reality of the history of science or of current scientific practice of scientists

        The comments by 2011 Nobel winner Brian Schmidt whose work on the supernova project are typical of most scientists I know.

        http://www.abc.net.au/tv/qanda/txt/s3522732.htm

        Look at his response to the question on science and creation at 20:26 and on science deniers at 33.39.

        Science is predicated on 2 things.
        1] Admission of ignorance and
        2] attempt to understand the physical universe based only on natural law.
        To know all the answers a priori deprecates the first. To consider that the world is ruled by a capricious God that intervenes constantly minimizes the second.
        This has been the approach from Newton to Darwin to any contemporary scientist publishing in the peer reviewed literature. It is very clear that many might believe that those natural laws have a orderly God behind them but this does not stop the attempt at understanding the world as a product of natural law.

        That you do not understand this scientific process is clear from your book in that you privilege the cryptic words of prophet some 150 years ago over any scientific view based on natural law and at the same time do not allow for any criticism or assessment of the validity of that source of knowledge. I do not think that you have any credibility to offer criticism of Jeff Kent.




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  7. Eddie,

    It’s hard to find your comments where they appear beneath a prior comment. Could you respond in a way that they appear as the most recent comment?

    I like your approach. You have a very forthright, honest, and balanced approach in the way you craft your remarks. The SDA colleagues I know personally assure me that your views are held by the majority of SDA biologists. I agree with them myself.




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  8. FLOOD MODEL PREDICTIONS

    There are two major predictions that derive from the flood model:

    1. Plants and animals that lived together should be buried together in the geological column. The evolutionary model, in contrast, predicts that order exists, with the simplest organisms appearing first and increasingly complex life forms appearing only higher in the geologic column.

    2. The biogeography of contemporary plant and animal groups should reveal a pattern of dispersal originating from Mt. Ararat. The evolutionary model, in contrast, predicts that large taxonomic groups are restricted to the area of origination by barriers to dispersal.

    As the next two posts make crystal clear, these two major predictions fail badly. Virtually all SDA biologists and geologists agree that these are two HUGE problems for creationism, as our explanations to account for these failures are embarrassingly weak. Others will brush them off as unimportant, if only because, well, we know what really happened.

    The question is what to do with the evidence: follow where it leads–to accept the evolutionary model–or reject the evidence in favor of inspired history?




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  9. Here is the evidence for the first failed prediction: the incontestable succession of simple to complex organisms that exists in the geological column:

    SUCCESSION FOR VETEBRATE ANIMALS

    Quaternary (post-flood)
    Tertiary (post-flood) – no humans below this
    Cretaceous (flood)
    Jurassic (flood)
    Triassic (flood) – no birds or mammals below this
    Permian (flood)
    Pennsylvanian (flood) – no reptiles below this
    Mississippian (flood)
    Devonian (flood) – no amphibians below this
    Silurian (flood)
    Ordovician (flood)
    Cambrian (flood)
    Precambrian (pre-flood)

    SUCCESSION FOR INVERTEBRATE ANIMALS

    Quaternary (post-flood)
    Tertiary (post-flood)
    Cretaceous (flood)
    Jurassic (flood)
    Triassic (flood)
    Permian (flood) – no trilobites or rugose corals above this
    Pennsylvanian (flood)
    Mississippian (flood) – no graptolites above this
    Devonian (flood) – no pentamerus brachiopods or cystoid crinozoans above this
    Silurian (flood)
    Ordovician (flood)
    Cambrian (flood) – no archaeocyathids (primitive sponge-like organisms) above this
    Precambrian (pre-flood)

    SUCCESSION FOR PLANTS

    Quaternary (post-flood)
    Tertiary (post-flood)
    Cretaceous (flood) – no angiosperms (flowering plants) below this
    Jurassic (flood)
    Triassic (flood)
    Permian (flood)
    Pennsylvanian (flood)
    Mississippian (flood) – no gymnosperms (coniferous plants) below this
    Devonian (flood) – no psilopsid plants (whisk ferns–primitive vascular plants) above this
    Silurian (flood)
    Ordovician (flood)
    Cambrian (flood)
    Precambrian (pre-flood)

    No matter how loud a few protest by pointing out that the sequence is consistent with ecological zonation (a spectacularly failed explanation), or that there are one or two exceptions (like fossil pollen in the precambrian, the decades-old evidence for which only creationists accept), the simple fact is that the order is undeniably real. Even Sean Pitman and David Read will concede this, if begrudgingly.




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  10. 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?

    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!

    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?

    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.

    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.




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    • @Professor Kent:

      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
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        Once again I cant help but respond to your most egregious claims.

        You are absolutely right science practitioners skilled in genetics do not understand the concept of front-loaded information. It is not a concept that is even mentioned in the indexed bioscientific literature. In trying to understand it from the lay literature I see that it can refer to a washing machine or a concept from economics that seems to find favour with Stephen Meyers and understandably you then seem to have borrowed uncritically. I suppose you are referring to some concept of allelic variation in a population that can then allow for rapid shift in gene frequency within a generation. What is completely baffling is how you can have a huge amount of front-loaded information (allelic variation?) in the face of the most astounding instance of genetic bottle-necks in every species required in the global flood model. You must accept a population of 2 snakes and hummingbirds at around 3000 BC which I am finding difficulty understanding as a high degree of front loaded information.

        Maybe you have some other concept to which I am naive but I would appreciate if you could explain in simple terms using the concepts and terminology I can read in any textbook of genetics what exactly and precisely you mean by front-loaded information in genetics.

        Of course you could resort to magic or a gnostic approach and dismiss me completely as unworthy to received the information.

        On another issue that piqued my interest. Can you give me the references for the data that shows that there were land-bridges across the Atlantic or Pacific oceans during the period from 3000-2500 BC when the northern half of North America and presumably also Asia was covered by Ice during the 500 years of the last ice age as David Read so cleverly argues in his dinosaur book. I presume you think that the Atlantic or Pacific trenches were bridged at some point within the last 4000 years? Or maybe the tectonic plate movements have all occurred after the flood and after the animals moved in an Easterly direction across Eurasia across the temperate zone pacific land bridges or maybe in a Westerly direction across the Atlantic ocean over temperate zone land bridges.

        Astonishing claims really deserve some solid supporting data.




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        • @pauluc:

          The basic concept of front-loaded information is the basis of Mendelian and polygenic forms of variation where the potential for all of the various phenotypic differences or traits among the offspring of two parents was all contained within the parental gene pool.

          Also, it doesn’t take a large population to achieve a very high degree of potential phenotypic variety among offspring. Even a pair of individuals can have pre-programmed potential for a huge amount of phenotypic variety – as demonstated by the fact that most modern breeds of dog were produced from a very small “bottlenecked” population of ancestors within very short order (around 300 years or so).

          Additional allelic variety via various forms of genetic mutations at lower levels of functional complexity can also be rapidly achieved and introduced into the gene pool as time progresses and the population size increases.

          Sean Pitman
          http://www.DetectingDesign.com




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        • @Sean Pitman:

          Sorry I am still baffled by the logic of your response.
          1] It is a basic principle of genetics that you can at the maximum get only one of 2 alleles from each parent. A population of 2 has only 4 allelic options in the gene pool for that population. No matter how many bases or aa may differ between the alleles there is only 2 options.
          2] Recombination is rare in intragenic region so there is little chance for generation of new recombinant alleles.
          3] You can obvious argue anything by divine intervention but a gene pool is extremely small in a population of 2.
          4] It is extremely unlikely that the current wide range of dog breeds comes through a bottleneck. Since the domestication of wolves by human populations, dogs have been associated with human populations and likely represent a very large gene pool. Further any dog breeder knows that at some point you may well have to backcross to maintain low levels of deleterious traits. Indeed there is evidence that black colour in wolves derives from breeding of domestic dogs into wild populations of wolves.
          You will have to argue against the history of dog domestication to maintain your spurious argument that the current derivation of canis lupus familaris is via some genetic bottleneck. For this there is absolutely no evidence.

          As always I imagine that you are truly genuine in your desire for data. I offer some references on domestication of dogs for you to consider, although from past experience it seems you are relatively impervious to new data that does not fit your front-loaded paradigm.

          Vilà, C. et al (1997). Multiple and ancient origins of the domestic dog. Science 276, 1687–1689. http://www.ncbi.nlm.nih.gov/pubmed/9180076

          Lindblad-Toh, K., et al. (2005). Genome sequence, comparative analysis and haplotype structure of the domestic dog. Nature 438, 803–819. http://www.ncbi.nlm.nih.gov/pubmed/16341006

          Vonholdt, B.M., et al. (2010). Genome-wide SNP and haplotype analyses reveal a rich history underlying dog domestication. Nature 464, 898–902. http://www.ncbi.nlm.nih.gov/pubmed/20237475

          Wayne, R.K., and vonHoldt, B.M. (2012). Evolutionary genomics of dog domestication. Mamm. Genome 23, 3–18. http://www.ncbi.nlm.nih.gov/pubmed/22270221

          Do a search on pubmed for some of the primary data on dog domestication and genomics if you are not afraid of what you might find. If you read a little you will see that there is really little need for spurious concepts like front loaded information there is simply variation and selection based on well known principles of genetics. It is really much more interesting and exciting than simply dreaming of what might have happened in alternative reality.

          http://www.ncbi.nlm.nih.gov/pubmed/21338479
          http://www.ncbi.nlm.nih.gov/pubmed/20711490
          http://www.ncbi.nlm.nih.gov/pubmed/22022279




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        • @Pauluc:

          Sorry I am still baffled by the logic of your response.

          1] It is a basic principle of genetics that you can at the maximum get only one of 2 alleles from each parent. A population of 2 has only 4 allelic options in the gene pool for that population. No matter how many bases or aa may differ between the alleles there is only 2 options.

          Many features, of dogs for example, are polygenetic – such as height or color, etc. For example, the determination of coat color and pattern is a polygenic in that these features are controlled by more than one gene or gene complex. A dog with the gene for black color expression may also have the gene for suppression of black and so have a red or yellow coat. Or a dog with the brindle gene may have one or more of the genes for large areas of white and so have little or no brindle coloring visible. A dog with the dominant black gene may have genes for color fading and appear gray or merle.

          Such polygenetic traits can be additive or non-additive.

          Additive polygenes have a cumulative effect. This refers to genes simply adding up to increase the expression of a trait… such as making a dog taller. Additive traits can have a low hertibility, such as litter size or birth weights. Or, additive traits can have a high hertibility, such as height or growth rate. It is important to remember that many traits with low heritability are still under considerable genetic control. That is, litter size is highly genetic but it is not highly heritable.

          For non-additive polygenes it is the combination of genes that makes the difference. This means that different sets of genes can combine in different ways to produce dogs who appear identical with regard to a given trait. Furthermore, a dog who is superior in any one respect may owe that superiority to his particular combination of genes more than to the specific genes themselves. Unfortunately, such outstanding animals are unable to pass on their own particular gene combinations; they simply pass on a sample of the individual genes that make up those combinations. Those genes may combine quite differently in their offspring producing very different results.

          2] Recombination is rare in intragenic region so there is little chance for generation of new recombinant alleles.

          Beside the fact that new alleles can be produced by many different kinds of mutations (besides intragenic recombination) and are fairly common in larger populations, they simply aren’t needed to produce a huge variety of phenotypic variations starting from just two parents.

          3] You can obvious argue anything by divine intervention but a gene pool is extremely small in a population of 2.

          Indeed, but the potential of such a small gene pool for phenotypic variety of offspring can be truly enormous.

          4] It is extremely unlikely that the current wide range of dog breeds comes through a bottleneck. Since the domestication of wolves by human populations, dogs have been associated with human populations and likely represent a very large gene pool. Further any dog breeder knows that at some point you may well have to backcross to maintain low levels of deleterious traits. Indeed there is evidence that black colour in wolves derives from breeding of domestic dogs into wild populations of wolves.

          I’m not arguing that the current range of dog breeds actually came through a recent bottleneck. What I’m saying is that the offspring from a single pair of wolves could actually be bred to produce a very wide variety of domesticated dogs, very similar to what we have now, in relative short order – i.e., just a few hundred years. The current diversity of domesticated dog breeds simply doesn’t require long periods of time or very many novel allelic options beyond what can be found within an original pair of wolves.

          Do a search on pubmed for some of the primary data on dog domestication and genomics if you are not afraid of what you might find. If you read a little you will see that there is really little need for spurious concepts like front loaded information there is simply variation and selection based on well known principles of genetics. It is really much more interesting and exciting than simply dreaming of what might have happened in alternative reality.

          I’m afraid you’re the one living in an alternate reality where functionally complex features can evolve from pre-existing systems without having to have been in the original ancestral gene pool. That just doesn’t happen. It has never been observed and is statistically impossible this side of eternity when it comes to anything beyond very very low levels of functional complexity. Also, genetic deterioration is quite evident in slowly reproducing creatures. The death rate required by natural selection to keep up with the rapid buildup of slightly deleterious mutations is far far too high for your theories to be tenable (as I’ve already discussed with you extensively).

          It seems to me like your main problem here is that you think every trait is governed by only two alleles. This simply isn’t true. Many if not most traits are governed by multiple genetic elements. This makes for huge phenotypic variety from what might otherwise seem like a very limited parental gene pool…

          Sean Pitman
          http://www.DetectingDesign.com




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  11. I recognize that many of you are angry that I would point out these problems, or even admit that they are problems. But problems they are.

    Now Sean Pitman and David Read will argue vociferously that the weight of the evidence–if not overwhelming evidence– favors Young Life Creationism (YLC). Yes, there certainly is evidence that supports it, but the weight or strength of this evidence will depend on how one chooses to “weigh” the varied pieces of evidence. Obviously, if you weigh heavily the two predictions most scientists think are critical, and which fail spectacularly, then it would be easy to conclude that the Genesis account is not literal.

    There are SDAs who do exactly what Sean Pitman advocates–they follow the evidence and conclude from this evidence in particular that the Genesis account of origins and the flood cannot be literal. And there are SDAs who do exactly what Professor Kent advocates–they admit the evidence is problematic but continue to trust in God’s word, conceding there is much that remains to be understood.

    We all get to decide which approach we use (prioritizing evidence vs. faith), and how we choose to weigh the different pieces of evidence, but it’s really sad that so many of you hate Professor Kent’s approach and think he has no right to call himself a Seventh-day Adventist. Bob Ryan, for example, loves to insinuate Professor Kent is an evolutionist, which he most certainly is not. Another anonymous soul recently referred to Professor Kent as a “fool.” These are undoubtedly fine SDAs who are, unfortunately, possessed by a spirit which encourages them to mock a fellow believer. But is this antagonism really necessary? Is Professor Kent truly dispicable because he honestly points out the key problems with flood theology? Because he chooses God’s word when it conflicts with the evidence? Because he disagrees with the goal of Educate Truth to publicly mock and humiliate fellow SDA Christians?




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  12. Having yet to see responses from Sean Pitman, David Read, or others, I’ll anticipate a few additional arguments as to why the fossil record provides overwhelming support for Young Earth Creationism.

    GENERAL LACK OF BIOTURBATION

    There is a “general lack” of bioturbation between successive layers of the fossil column. Bioturbation would be expected if there were millions of years between some layers, and a complete lack would be expected if there were, at most, only days to months between successive layers.

    Well, this argument certainly oversimplifies reality. In the real world, bioturbation is certainly present and scientists find it throughout the geological column.

    A book published in 2004 provides a nice compilation of articles on the topic of bioturbation (The Application of Ichnology to Palaeoenvironmental and Stratigraphic Analysis, by D. McIlroy, editor). As one author put it, “The use of trace fossils for palaeoenvironmental analysis is commonplace, and can be applied to ALL PARTS of the geological column, including extinction-recovery intervals (emphasis supplied).” The book provides detailed examinations of bioturbation in many layers of the geologic column and at many localities. Yet, the authors point out that our understanding of bioturbation in the fossil record remains rudimentary. As the same author quoted above noted, “We have only just begun to scratch the surface.”

    Another more recent book (Ichnology: Organism-Substrate Interactions in Space and Time, by Luis A. Buatois and M. Gabriela Mángano, 2011) summarizes our current understanding further. A simple literature search at ISI Web of Science yields >200 articles with the keywords “bioturbation, fossil.” Seems to be a LOT of scientists finding a LOT of material to study in the fossil record.

    Are you comfortable taking a stand on the bioturbaton argument? In your judgment, if we use the argument of a “general lack” of bioturbation in the fossil record as evidence in support of a recent creation, and we eventually learn that there is a lot more bioturbation present than we formerly believed, and that there are bona fide reasons why significant bioturbation might be absent under certain ecological conditions associated with preservation events, should we then abandon our faith? In other words, should we allow science to dictate what we believe?

    GLOBAL COVERAGE OF THE FLOOD

    We find evidence throughout much of the planet that water-deposited sediments are present. Therefore, there was a single global flood.

    Unfortunately, this argument lacks traction because there is nothing in evolutionary theory that precludes the possibility of major floods. As Eddie has pointed out (several times), secular geologists believe there were two major floods. Not one, but two really, really big floods.

    Is there evidence that there was one major flood that covered every single piece of earth at one point in time. No. Of course not. There is no evidence ANYWHERE to support the view that 100.0% of land was covered, as opposed to 80% or 70% or even 50%.

    Again, there is physical evidence that much of the planet at one time or other was covered by water, but there is NO physical evidence to support the literal interpretation of Genesis that a single flood covered the entirety of the planet.

    UNIFORMITY OF PALEOCURRENTS

    Paleocurrents are vectors indicating the direction of flow of currents depositing sediments on the earth’s surface. Supposedly, the majority of paleocurrents established by studies flow in just one direction.

    There are a number of factors that influence the direction of water flow, chief among them being topography (elevation change). It’s unclear how one would could conclude a priori from scripture, or Ellen White, why “flood geology” would predict primarily unidirectional flow. Why would the preflood global topography favor this more than the topographies evolutionists posit to have existed over the millenia?

    Unfortunately, this entire argument hinges on the unpublished analyses of one individual, Dr. Arthur Chadwick, of Southwestern Adventist University. Have you, the reader, analyzed the data yourself, or are you going to place your faith in Dr. Chadwick’s analysis and conclusions? Chadwick’s argument has not been challenged because the argument remains a private conclusion that has yet to be vetted to scientists capable of assessing the claim. (Of course, Sean Pitman believes this claim wholeheartedly, not because he has analyzed the data independently, but because, well…maybe he should tell us.)

    IN SUM

    Look folks, I believe as most of you do, but not because we’ve got this “overwhelming” or even “weight” of fossil and geological evidence supporting our position. As even Sean Pitman and David Read have admitted in this thread, they interpret this evidence based on their understanding of Genesis. Clearly, we as SDAs accept the Genesis account for reasons other than evidence arising from so-called flood geology.

    Considering the difficulties we have supporting our view with flood geology, it seems all the more remarkable that Dr. Pitman maintains that an SDA scientist must be fired if they fail to tell students that our position is supported by overwhelming evidence. I imagine most of you think a scientist should be fired for sharing the facts that I have just related.




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  13. My position is that the students should be exposed to truth, rather than have it hidden from them. Further, if the students are on their knees daily, cementing a relationship with God as strong as any other relationship in their life, then their faith will withstand even mountains moved into their path.

    Yes, I know, my position on faith is reckless, dangerous, anti-SDA, and heretical. Good thing I’m not employed by the SDA Church!




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    • @Professor Kent: Anyone who is on his knees daily, cementing a relationship with God as strong as any other relationship in their life (hopefully stronger) will believe what God has told him about our origins, and will interpret the evidence accordingly, not accept interpretations, and rules of interpretation, that make God a liar.

      Armed with proper principles of interpretation, he will proceed to interpret the data bearing on origins accordingly, and turn the mountains of data against his faith into mountains of evidence that support his faith.




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  14. Professor Kent,

    Of course students should be told about all the information in hand.

    The issue here is that there are many, the vast majority of mainstream scientists in fact, who believe that the information in hand definitively proves that life has existed and evolved, in a Darwinian manner, over the course of millions of years of time. They simply ignore or do not substantively discuss or understand the very strong evidence that effectively falsifies the Darwinian mechanism of RM/NS beyond very low levels of functional complexity, the rapid genetic deterioration of all slowly reproducing creatures (like all mammals for instance), the recent and catastrophic nature of the geologic and fossil records, the preservation of complex proteins and soft tissues within dinosaur bones and other fossils where kinetic chemistry says that such proteins and tissues should not survive more than 100kyrs at best, the general lack of bioturbation (not a complete lack despite your misunderstanding of this argument – just much much less than would be expected if the mainstream perspective where actually true), the discovery of “first appearance” of many different kinds of creatures lower and lower in the fossil record that previously thought, the discovery of more and more “Lazarus” taxa thought to be long extinct during their “last appearance” within the fossil record (like the coelacanth which is still alive and well today), and on and on and on.

    This is what is not explained by those, like you, who actually believe that the neo-Darwinian perspective has the clear weight of evidence on its side. This simply isn’t so. Despite the fact that there are still unanswered questions, the basic features of geologic, fossil, and genetic evidence that are currently in hand strongly support the Biblical perspective on origins and effectively disprove or falsify the neo-Darwinian perspective.

    Of course, if you still believe that the neo-Darwinian perspective has the overwhelming weight of evidence on its side, that’s fine. You, like everyone else in this country, is welcome to such opinions. It is just that you would not then be able to effectively represent the Adventist perspective in one of our schools and should not be hired to do so… because of your apparent ignorance of the science, of the weight of evidence, in favor of the Biblical perspective…

    Sean Pitman
    http://www.DetectingDesign.com




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  15. @ Sean Pitman

    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.

    Domesticated dogs do not exemplify speciation. Not even remotely close. And where did you come up with 300 years? Surely not from the original stock. Archaeological evidence shows that humans were domesticating dogs long before Jesus was born. Secular scientists date it to 20,000 years or more.

    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 there.

    What’s more parsimonious: An Old World group of hummingbirds (of multiple genera) departed the ark and spread to the New World, whereupon all the Old World populations vanished while other Old World bird groups fared perfectly well? Or a New World radiation of hummingbirds spread to the point where one species invaded the Old Word, whereupon it became extinct while the New World population continued to thrive? Think statistical probabilities (which you seem to think are important). But I do understand; parsimony is meaningless when the evidence has to fit informed faith.

    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)…

    I did a quick Google Scholar search for annual movement of rattlesnakes. I found a mean annual displacement of 3.5 km for timber rattlesnake and 4.6 km for prairie rattlesnake. Given the larger value, my math says they could travel 18,400 km. The bigger problem you don’t get is why the animals moved outward from the ark, reproducing after their kind, establishing new populations in all directions from the ark (across much of Asia and Africa)–and then they all died off without leaving a post-flood fossil trace except for those that managed to make it to the New World, where they absolutely thrived. Remarkably, other non-rattlesnake vipers persisted in the Old World without any problem whatsoever. I know, this evidence is no problem for your informed faith. I shouldn’t have to explain to you that your explanation, of course, is ad hoc and faith-based.

    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.

    Depends on what you mean by “falsify.” If you accept statistical parlance, it’s a big huge FAIL. The evidence does not support the flood geology prediction. Not even remotely. Somehow I don’t think you want to go with the evidence.




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    • @Professor Kent:

      Domesticated dogs do not exemplify speciation. Not even remotely close.

      This is only by convention since the very definition of “species” is quite subjective – as you surely know (Link). Different breeds of dogs are produce by placing them in reproductive isolation to select for certain phenotypic trait expressions. This also produces genetically unique breeds which can be identified, with a very high degree of accuracy, by genetic analysis alone. If these very same breeds of dog were produced in the wild in different environments instead of by human design, they would indeed be classified by various definitions of “species” as distinct species that have been produced by various forms of breeding isolation. Certainly cryptic species are far more similar, morphologically, than are certain breeds of dog.

      And where did you come up with 300 years? Surely not from the original stock. Archaeological evidence shows that humans were domesticating dogs long before Jesus was born. Secular scientists date it to 20,000 years or more.

      Why don’t you at least try to look this stuff up before you comment on it? A simple Google search would tell you that most modern breeds of dogs are very new, produced by human breeding over the last 300 years or so.

      Most dog breeds have been created by humans over the past 300 years, and each breed has clearly defined standards for an animal’s behavior and physique.

      http://www.genomenewsnetwork.org/articles/2004/05/20/dog.php

      See, was that so hard?

      But I do understand; parsimony is meaningless when the evidence has to fit informed faith.

      You mean parsimony is indeed effectively meaningless when there are so many factors involved where animals are migrating and evolving different morphologies within the same gene pool at very rapid rates over thousands of years? – when groups are isolated from other groups from the same original gene pool over extended periods of time? All these things are not unexpected, even predictable, from a Biblical perspective.

      I did a quick Google Scholar search for annual movement of rattlesnakes. I found a mean annual displacement of 3.5 km for timber rattlesnake and 4.6 km for prairie rattlesnake. Given the larger value, my math says they could travel 18,400 km.

      Half the circumference of the globe is just over 20,000 km. Also, you are considering current average annual displacement rates when you should be talking about maximum displacement rates per region or colony per year. Also, you’re not taking into account how far snakes can migrate when encouraged to do so… as in cases with increasing local competition, or changes in the environment, etc.

      I shouldn’t have to explain to you that your explanation, of course, is ad hoc and faith-based.

      Again, we know that many animals died off in many areas without leaving much if any trace – despite having lived there for long periods of time. Why you put so much stock in this argument is therefore a mystery to me. It simply isn’t a useful argument at all against the Biblical account of origins.

      Depends on what you mean by “falsify.” If you accept statistical parlance, it’s a big huge FAIL. The evidence does not support the flood geology prediction. Not even remotely. Somehow I don’t think you want to go with the evidence.

      This simply isn’t true. The fact that animals would change rapidly over time with isolation and would go extinct in certain areas while thriving in others is actually predictable from the Biblical model of origins. I really don’t see why you think anything else should expected or predictable over a few thousand years of time?

      Sean Pitman
      http://www.DetectingDesign.com




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  16. @ Sean Pitman

    The vast majority of mainstream scientists…simply ignore or do not substantively discuss or understand the very strong evidence that effectively falsifies the Darwinian mechanism of RM/NS beyond very low levels of functional complexity

    Falsifies? Your “falsification” is statistical probability at best. You’re right: we can’t falsify whether Jesus’ body came back to life (we don’t have access to that event nearly 2,000 years ago). But using your criterion of statistical probability, human brain cells simply cannot revive even one day after cellular death. If you think your statistical inferences regarding RM/NS equate to falsifiable evidence supporting scriptural claims, then scripture’s claim regarding resurrection of a 3-day-old corpse is as falsifiable as anything else. Statistical probability declares the resurrections of Lazarus and Jesus (not to mention the others at Christ’s resurrection) to be a fairy tale. And you know it.

    the rapid genetic deterioration of all slowly reproducing creatures (like all mammals for instance)

    Mere statistical probabilities. Sorry to point this out to you.

    the recent and catastrophic nature of the geologic and fossil records

    All physical evidence suggests old dates, as many honest YLCs forthrightly concede. Multiple dating systems based on different assumptions yield similar results. Catastrophic? The secular scientists completely agree with you on the catastrophic conditions leading to fossil preservation, so how is this evidence supporting a literal versus non-literal Genesis account?

    the preservation of complex proteins and soft tissues within dinosaur bones and other fossils where kinetic chemistry says that such proteins and tissues should not survive more than 100kyrs at best

    Published empirical evidence shows that the assumptions of kinetic chemistry do not apply to the preservation conditions within bone. With this argument, you latched onto an apparent candy bar before you discovered what was actually inside it.

    the general lack of bioturbation (not a complete lack despite your misunderstanding of this argument – just much much less than would be expected if the mainstream perspective where actually true)

    Oh…”much less than would be expected” by whom? Right. The problem is that you’ve hitched yourself to a factoid that continuing research can’t support. You need to get up to date.

    the discovery of “first appearance” of many different kinds of creatures lower and lower in the fossil record that previously thought, the discovery of more and more “Lazarus” taxa thought to be long extinct during their “last appearance” within the fossil record (like the coelacanth which is still alive and well today)

    None of which contradicts evolutionism. You fail to recognize this is a simple statistical expectation: with additional research, fossil groups will be found to be more widespread than was apparent with a smaller sample size. But showing, for example, that birds actually make it into the Triassic (one level lower) does not change the bigger, unassailable evidence for the sequential deposition of fossil life forms from simple to complex. And it’s completely inconsistent on your part–I won’t use the word ignorant–to emphasize the discovery of more widespread taxa while dismissing the discovery of more widespread bioturbation. How do you fail to see this logical fallacy? As many have pointed out, you cherry pick your evidence to “weigh” that which fits your faith-based expectations.

    Despite the fact that there are still unanswered questions, the basic features of geologic, fossil, and genetic evidence that are currently in hand strongly support the Biblical perspective on origins and effectively disprove or falsify the neo-Darwinian perspective.

    You’ve convinced yourself, that’s quite clear. But you haven’t effectively disproved or falsified anything other than your straw man construct of the neo-Darwinian perspective. The only reason you’ve convinced yourself is that you have used scripture to interpret the evidence–and cherry-picked evidence at best. I know you can’t bring yourself to admit it, but your faith supercedes your objective assessment of evidence. I congratulate you, Dr. Pitman.




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  17. I’m sure that the vast majority of scientifically-informed Adventists will thank Dr.Kent for his every effective and rational approaches to the views expressed by Dr. Pitman and others on this misnamed web site. There is little that needs to be added. Dr. Kent has done a masterful job of exposing the misunderstandings of scientific data dealing with geology and evolutionary biology that has been offered by Dr. Pitman on this and his own web site.




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    • @Ervin Taylor:

      I literally have not logged on to this website in years. It looks like the same arguments are going back and forth which means that if you haven’t been able to solve them by now, you aren’t going to convence each other of your points. What is really amazing to me and anyone intersted in the topic, however, is the tone of the comments, which usually reveal the maturity of the writer especially if they include absolutes:

      Examples:
      “vast majority of scientifically-informed Adventists will thank Dr.Kent ”

      “this misnamed web site”

      “Dr. Kent has done a masterful job”

      These are usually tip-offs to a lot. Also, it makes me wonder that if Sean Pitman is so ill-informed, and he operates on such a mis-leading web site, why does the good Dr. Taylor waste his time coming to this website, reading the material and then commenting on it? In fact I can bet that Dr. Taylor has spent more time on this web site then I have in the last year – and that speaks volumes about what Dr. Taylor really thinks of this website – perhaps the good Dr. Kent as well.




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    • @Ervin Taylor:

      really? Do you have some actual evidence for that assertion (for our unbiased objective readers) or is it simply another example of musing on your part intended only for your own following?

      Critical thinking people here who pay attention to detail – would like to know where you come up with those sweeping assertions.

      in Christ,

      Bob




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  18. Sean Pitman: If these very same breeds of dog were produced in the wild in different environments instead of by human design, they would indeed be classified by various definitions of “species” as distinct species that have been produced by various forms of breeding isolation. Certainly cryptic species are far more similar, morphologically, than are certain breeds of dog.

    Cryptic species are not identified on the basis of morphological differences. They are delineated on the basis of molecular divergence–after all, they’re called “cryptic” for a reason. Dogs show extremely shallow genetic divergence. No mammalogist considers the different breeds to be distinct species for good reason. I do know of a physician, though, who insists he knows things about taxonomy that no taxonomist understands.

    Sean Pitman: Why don’t you at least try to look this stuff up before you comment on it? A simple Google search would tell you that most modern breeds of dogs are very new, produced by human breeding over the last 300 years or so.

    I did look it up. That’s why I wrote “And where did you come up with 300 years? Surely not from the original stock.” Yes, I wrote “original stock.” Again, archaeological evidence shows human domestication of dogs long before Christ. Molecular analyses suggest 15,000+ years ago. Look these up yourself. Domestication has resulted in multiple species? That’s a pretty fantastic claim, Dr. Pitman. Multiple species have not resulted in 300 years, nor in several thousand years.

    Sean Pitman: Also, you’re not taking into account how far snakes can migrate when encouraged to do so… as in cases with increasing local competition, or changes in the environment, etc.

    And what do you know about this? Do you think local competition was greater as populations were spreading than they are now? Doesn’t matter. You didn’t address the other issues I mentioned that are far more problematic. Hugely problematic! You won’t concede one inch–and not because of the evidence, but because of your faith. You’re becoming increasingly transparent.

    Sean Pitman: [Professor Kent wrote] The evidence does not support the flood geology prediction. Not even remotely. Somehow I don’t think you want to go with the evidence.

    This simply isn’t true. The fact that animals would change rapidly over time with isolation and would go extinct in certain areas while thriving in others is actually predictable from the Biblical model of origins.

    Are you serious? You actually believe that contemporary biogeography SUPPORTS the flood narrative and the Biblical model of origins? And by predictable, I assume you mean falsifiable, since you use these in the same phrase often. You amaze me, Dr. Pitman.




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    • Cryptic species are not identified on the basis of morphological differences. They are delineated on the basis of molecular divergence–after all, they’re called “cryptic” for a reason.

      That’s right. However, molecular divergence (which has no significant functional and/or phenotypic effect) isn’t the only definition of “species” in use. There are also phenotypic definitions – among many others. That is why the “species” concept is still quite subjective…

      Dogs show extremely shallow genetic divergence. No mammalogist considers the different breeds to be distinct species for good reason. I do know of a physician, though, who insists he knows things about taxonomy that no taxonomist understands.

      Again, you know as well as I do that if the history where not known, if various types of dogs were found in the fossil record or even on an isolated island without first knowing how their phenotypic and/or genetic differences were derived and in what time frame, they would be classified as different species.

      After all, it has often been the case that male and female forms of the same type of animal were originally classified as different “species” until it was later discovered that they were in fact the same type of creature. So, don’t tell me that the concept of “species” is consistently reproducible or is free from subjective determinations. It isn’t.

      I did look it up. That’s why I wrote “And where did you come up with 300 years? Surely not from the original stock.” Yes, I wrote “original stock.” Again, archaeological evidence shows human domestication of dogs long before Christ. Molecular analyses suggest 15,000+ years ago. Look these up yourself. Domestication has resulted in multiple species? That’s a pretty fantastic claim, Dr. Pitman. Multiple species have not resulted in 300 years, nor in several thousand years.

      What I said was that most modern breeds of dog have been produced within the last 300 years or so – which is true.

      Are you serious? You actually believe that contemporary biogeography SUPPORTS the flood narrative and the Biblical model of origins? And by predictable, I assume you mean falsifiable, since you use these in the same phrase often. You amaze me, Dr. Pitman.

      I would certainly predict a rather randomized pattern to arise over relatively short periods of time for animals that can rapidly adapt to local environments with a huge variety of phenotypic modifications in combination with widespread extinction events and the rarity of fossil formation outside of large-scale catastrophic events…

      I’m not sure why you or anyone else would think otherwise. Your “falsified” model simply isn’t one that I would predict. In short, what you’ve “falsified” here is simply a strawman of your own creation – not an actual prediction from the Biblical perspective.

      Sean Pitman
      http://www.DetectingDesign.com




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  19. Science, if it is accurate, will confirm the truth of our origins. (a week of creation and an earth roughly 6,000 years old.)

    Amazing that the debate here is a dispute about that. That is the true Adventist position and basically the world disagrees. So what?

    It seemed to me the original intent of this site was not so much about debating our origins but was about discussing whether or not one or more of our (SDA) educational institutions was teaching something contrary to the Adventist position? Yes? No?

    Seems to me, that question has been well settled here. If you indeed believe that the earth is millions of years old and that we evolved from lower forms of life, you are in the majority. But you most certainly are not an SDA. (call yourself what you like.)




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  20. We know that Abraham Lincoln lived based upon faith. We have to believe that those who have written the books and taken the photos were not lying to us. We have to trust that they are telling us the truth. in other words we have to believe by faith that what we have heard about Lincoln is real. There is not one scientific experiment that could be done that can prove that Lincoln existed.

    The same thing goes for Creation. We have to believe by faith that God is telling us the truth. Science cannot prove that creation happened. It cannot prove that it didn’t happen. This is because Creation is not a hypothesis. It is a fact of faith.

    Scientific methodology is simply a logical process by which we can study creation. But without the philosophical foundation of Biblical truth, science cannot prove what happened in the past.




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  21. @Professor Kent
    “FLOOD MODEL PREDICTIONS
    “There are two major predictions that derive from the flood model:
    1. “Plants and animals that lived together should be buried together in the geological column.

    False straw-man prediction. This is based on a flawed understanding of what the flood was like. It was far more catastrophic than you imagine.

    2. “The biogeography of contemporary plant and animal groups should reveal a pattern of dispersal originating from Mt. Ararat.
    False straw-man prediction. It assumes that one would find such pattern in the fossil record, which is contrary to creationary flood models where the fossil record is the record of the flood, not post-flood events. And it assumes that fossils lived where they were buried, again not a flood model assumption

    “Virtually all SDA biologists and geologists agree that these are two HUGE problems for creationism, as our explanations to account for these failures are embarrassingly weak.”

    This is a “Huge problem” in your eyes only because you are all bound up in the blinders of naturalism..

    The question is what to do with the evidence: follow where it leads–to accept the evolutionary model–or reject the evidence in favor of inspired history?

    WRONG! The question is how do you interpret the evidence within the Biblical world view of creationism. Creationism is not an hypothesis or theory to be tested by science. Rather it is the philosophical paradigm within which science MUST be done.

    Allen




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  22. David Read said:

    “Ellen White’s statements about larger antediluvian life forms are well attested with regard to many different types of flora and fauna. They’re not even controversial…

    Hi David,

    As you know, I took advantage of your kind offer and I read your manuscript as well as I purchased 3 of your books, one for me, one for my sisters, and one for the church library. It took me a week to finish the book, and I and my sisters are very impressed with it. My one sister calls it “one incredible book”. It has answered a lot of the questions we had on the subject of evolution vs creation science, and, yes, I believe we (you and I and my sisters) are on the same page in our beliefs. We have immensely enjoyed discussing the various aspects of the subject as we read. It makes perfect sense to us.

    I still have a couple of questions–new ones will probably always keep popping up–but I would say you have covered the subject admirably. Thanks so much for this book.

    I agree with Elder Wilson, this is something every Adventist should read. In my opinion it should be used as required reading for science courses. It is exactly the way I would want science courses in the universities to treat the Creation/evolution debate in the classroom. And if the professors at LSU and the other SDA institutions would do this we wouldn’t be constantly losing our young people and, for that matter, our professors, to skeptisism.

    Thank God someone has the courage to publish the truth and expose error.

    God Bless you, David.




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    • @Faith: Thank you so much for your gracious and kind comments, Faith. I am humbled and gratified to know that you and your sisters were blessed by the book, and I am confirmed in thinking that God impressed me to write the book.

      Also, I am appropriately impressed that you read it [over 600 pages] in a week. You’re obviously a highly literate and intelligent person, with a strong to desire to learn about origins.




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  23. Further to my comment on skeptism and our professors, I’ve got to tell you that I found Prof Kent to be extremely annoying in his comments on EGW. He seems to think that she is an embarrassment to the church when she speaks on Science.

    Personally I find people who dis her to be the embarrassment to the church. I really don’t see how they dare to contradict and mock God’s prophet. By doing this they undermine a lot of our church’s beliefs to outsiders as well as church members. God will hold them accountable for that.

    Furthermore, David’s unpublished manuscript plus other books I have read on archaeology have reported skeletons of the type that EGW mentions. Also found were artifacts such as huge iron bedsteads made for and buried with kings of huge stature.

    Just because you haven’t done your research, PK, don’t jump to the conclusion the evidence isn’t there. It’s there, all right, and you make yourself look a little foolish for not knowing about it.




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  24. Mr Taylor,

    After reading your comment above, I must say PK isn’t the only one in that boat.I would make some comment as to how I really feel about you, but I know Sean will only delete it and you won’t benefit from my insight anyway–seeing as Sean is more concerned about other people’s feelings than you seem to be.

    How you have the nerve to come to this website and call us all a bunch of morons (which is really what you are doing) is beyond me. You and your cronies are the ones drowning in error. Anyone who dares to accept man’s opinions over the Bible or SOP isn’t to be trusted to define truth for anyone.

    Too straight-forward in my comment? Trust me, I have restrained myself admirably. If you only knew….




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  25. Roger Seheult: @Ervin Taylor: I literally have not logged on to this website in years. It looks like the same arguments are going back and forth which means that if you haven’t been able to solve them by now, you aren’t going to convence each other of your points. What is really amazing to me and anyone intersted in the topic, however, is the tone of the comments, which usually reveal the maturity of the writer especially if they include absolutes

    Roger, Your comments are very true. Look at the title of this article, and then look at the vast majority of the posts–they have no direct connection to the topic!

    Why does Shane allow Sean, Kent, Ron, Taylor etc. to drone on and on about something that is not related to the topic of this article? They should take their personal opinions and personally email each other, and not bore the rest of us to death.

    How about this, Shane?




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  26. Sean Pitman: That’s right. However, molecular divergence (which has no significant functional and/or phenotypic effect) isn’t the only definition of “species” in use. There are also phenotypic definitions – among many others. That is why the “species” concept is still quite subjective…

    Phenotypic definitions are based on molecular divergence. But I give up.




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  27. All academics look forward to the end of the spring semester (or quarter). With the break, they are able to indulge things that pique their interest. For many, however, the ensuing summer term beckons. My time here is up, and I must move on to other things.

    I am certainly relieved that my tour of flood geology has not tarnished the faith of any readers. I appreciate and applaud the vigorous defense of our core beliefs. Before departing, I would like to share some personal wishes for those I have become acquainted with here.

    David Read – I pray for your success in your determined effort to warm the hearts and souls of fellow SDAs to Jesus.

    Faith – I love your name, and pray that the grace and unconditional love of Jesus Christ will continue to saturate all aspects of your life.

    Bob Helm – As you continue to indulge your fascination with origins and science, I pray that you will be drawn ever closer to our Savior.

    Charles – I admire your thirst for God’s second coming, and pray that you will invigorate others with your passion and longing for that wondrous day when Christ reunites us to Him.

    Roger Seheulte – As you provide daily care to your patients, I pray that you will treat each of them with the very same love and tenderness that you see in our Creator’s enduring sacrifice for us.

    Bob Ryan – As the patriarch of your family, I pray that you succeed in warming the hearts and souls of your loved ones to our redeemer, Jesus Christ.

    Allen Roy – I pray that your passion for Jesus rises above all else so that you continue to defend Scripture as God’s most remarkable gift to mankind.

    Ervin Taylor – I praise God that you continue to believe in the man, Jesus Christ, and remain willing to associate with SDAs and defend many of our beliefs.

    Eddie – As an exemplary academic, you are a voice of reason, and I pray that your witness to students creates an enduring appetite to learn more about Jesus Christ and what it means to be the sons of a Creator God.

    Sean Pitman – I pray that you will instill a greater confidence in God’s word for those who question it, and succeed in your effort to bolster our faith in Jesus with empirical evidence wherever it may be found.

    Bill Sorensen – I pray that your enthusiasm for Biblical prophecy as a key to know and understand Jesus will build the faith of many.

    Pauluc – I admire your knowledge and passion for science, and love your commitment to the Church and the fellowship of believers who profess Christ above all things.

    Wesley Kime – I pray that your trust in Jesus and all things Scripture will thorougly saturate every part of your life.

    Holly Pham – As you continue to defend your faith, I pray that you will instill in fellow SDAs a stronger confidence in the love of our Lord Jesus Christ.

    Ron – I pray that you will continue to seek Jesus wherever you find Him, and share your faith with those who need Him.

    I bid you all adieu.




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  28. @Prof. Kent, You have bidden adieu at least a dozen times on this website, and you still keep reappearing. Is this time “for good?” Or just until the summer term is over?




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  29. Professor Kent: Phenotypic definitions are based on molecular divergence. But I give up.

    I kindly asked you to delete this, but you chose to post it. I bumped the wrong button and submitted it prematurely by mistake. When I tried to edit it, I apparently ran out of time or something because the edit with a more detailed response didn’t take.

    Since you decided to post it, I’ll just say this: phylogenetic (not phenotypic) definitions are based on molecular divergence. Everyone recognizes the limitations of the phenotypic species concept, so I was surprised you even brought it up.

    What amuses me is that no other taxonomist on this planet recognizes, accepts, or has even heard of the species concept you have put forth at other threads here at ET. It’s very difficult to dialogue with someone who rejects the lexicon others use in favor of their own private one. You might as well be speaking Cuneiform.




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    • @Professor Kent:

      I’m sorry, but I didn’t see where you asked for this comment to be removed. If you still wish it to be removed, since it clearly isn’t accurate, I will do so. Just say the word…

      Everyone recognizes the limitations of the phenotypic species concept, so I was surprised you even brought it up.

      Every definition of “species” has limitations and subjective elements – even genetically based definitions of species. Genetic definitions of the species concept also rely, to at least some extent, on human judgement as to just how much difference is enough to constitute a separate species.

      For some “cryptic species” the genetic distance required to define a new species isn’t very great. For example, take a DNA strand of 658 nucleotides. How many differences in this strand, between different groups of organisms, would qualify one group as being a unique “species”? Ten or eleven maybe? That certainly is enough for certain researchers (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0032992). Yet, certain groups of humans differ from other groups by more than this. See the problem? Also, fossils “species” determinations aren’t based on genetic analysis.

      Sean Pitman
      http://www.DetectingDesign.com




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  30. Sean

    I dont think you are really addressing the problem. You hopefully suggest

    “Many features, of dogs for example, are polygenetic – such as height or color, etc. For example, the determination of coat color and pattern is a polygenic in that these features are controlled by more than one gene or gene complex”

    Indeed that is true but at each of these polygenic sites there are only at maximum 4 possibilities in a bredding pair of 2.

    “For non-additive polygenes it is the combination of genes that makes the difference. This means that different sets of genes can combine in different ways to produce dogs who appear identical with regard to a given trait. Furthermore, a dog who is superior in any one respect may owe that superiority to his particular combination of genes more than to the specific genes themselves. Unfortunately, such outstanding animals are unable to pass on their own particular gene combinations; they simply pass on a sample of the individual genes that make up those combinations. Those genes may combine quite differently in their offspring producing very different results.”

    If you want to get taken seriously you need to provide references for these claims. I am loathe to take your word for it unless you have published it in the peer reviewed literature. Otherwise it is only hearsay.

    You then go on to provide mechanisms for genetic diversity that is quite mainstream and with which I entirely agree

    “Beside the fact that new alleles can be produced by many different kinds of mutations (besides intragenic recombination) and are fairly common in larger populations”

    But then you spoil it all with repetition of your mantra based on your particular insights that have never actually been published or subjected to peer review.

    “…they simply aren’t needed to produce a huge variety of phenotypic variations starting from just two parents.

    “.. but the potential of such a small gene pool for phenotypic variety of offspring can be truly enormous.”

    “I’m not arguing that the current range of dog breeds actually came through a recent bottleneck. What I’m saying is that the offspring from a single pair of wolves could actually be bred to produce a very wide variety of domesticated dogs, very similar to what we have now, in relative short order – i.e., just a few hundred years. The current diversity of domesticated dog breeds simply doesn’t require long periods of time or very many novel allelic options beyond what can be found within an original pair of wolves.”

    I am again confused. Are you arguing for dogs derived from 2 wolves or not? If you take the genesis account literally which I understand you do, dogs are unclean and you must consider that they are therefore derived from the most severe genetic bottleneck possible.

    It would help your argument if you could point to an example of a reintroduction program where there was success with 2 genetically isolated animals. I certainly cannot find any.

    If you care to read the paper on reintroduction of wolfs into yellowstone
    http://www.ncbi.nlm.nih.gov/pubmed/17877715
    You will see they followed the standard practice built up based on long experience and reintroducing around 40 animals. [It is argued whether sustainable populations are around 30 or if 50 are needed)

    The experience with 4 avian species again shows that populations with low genome equivalents are subject to significant and life threatening inbreeding and loss of genetic diversity
    http://www.ncbi.nlm.nih.gov/pubmed/20825445

    2 genome equivalents is clearly in the unsustainable range according to all the current practical and theoretical models of population genetics.

    If I am wrong pleas give the examples.

    I really dont know why you seem to be continually arguing for naturalistic mechanisms for scenarios around the miraculous global flood account. Cant you accept that derivation of all populations from the ark is genetically untenable and accept it as miraculous. Creation science is intrinsically miraculous; turtles all the way down. Just accept it and dont pretend it is some scientific hypothesis that can be tested by experiment. As prof Kent argues it is even worse because you not only try to argue a particular interpretation is scientifically valid but then pin your faith on your ability to argue the scientific validity. Its a miracle. Move on to the consequences and you might not find it is so foundational.




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    • I dont think you are really addressing the problem. You hopefully suggest, “Many features, of dogs for example, are polygenetic – such as height or color, etc. For example, the determination of coat color and pattern is a polygenic in that these features are controlled by more than one gene or gene complex.”

      Indeed that is true but at each of these polygenic sites there are only at maximum 4 possibilities in a [breeding] pair of 2.

      That’s right, but a polygenic trait is not governed by a single site. It might help to get a few concepts straight here. “Quantitative traits refer to phenotypes (characteristics) that vary in degree and can be attributed to polygenic effects, i.e., product of two or more genes… Polygenic inheritance refers to inheritance of a phenotypic characteristic (trait) that is attributable to two or more genes and can be measured Quantitatively… Unlike monogenic traits, polygenic traits do not follow patterns of Mendelian inheritance (separated traits). Instead, their phenotypes typically vary along a continuous gradient depicted by a bell curve… Most phenotypic characteristics are the result of the interaction of multiple genes.” (Link)

      Sometimes hundreds of genetic loci are involved in governing the expression of a given trait or feature. For example, height in humans is governed by the interaction of some 200 genetic regions. Genome-wide association studies in humans, laboratory animals, and outcrossed domesticated plants such as maize show that the genetic architecture of most phenotypes tested to date—including body size, body mass index, lipid level, and flowering time—appear to be under the control of hundreds of genes, each contributing a very modest amount to the overall heritability of a given trait. This makes a great deal of variety of expression of a given trait possible – even starting with a very small population (such a just two individuals). This is why my brother and I look so different despite having the very same parents. He has dark skin. I have light skin. He is hairy. I’m not. He has dark green eyes. I have light greenish blue eyes. etc. The is also why two dogs can produce a mix of very different looking puppies within the same litter – to include significant differences in color, hair texture, size, etc…

      Of course, it not always the case that a wide variety of a phenotypic trait expressions is the result of a large number of genes. When it comes to modern dog breeds in particular, it seems like relatively few genetic regions of large phenotypic effect underlie most traits.

      For example, dog size (the variation of which is greater across dog breeds than in any other terrestrial species) seems to be controlled mainly by six genetic regions (CFA15.44226659, CFAX.106866624, CFA10.11440860, CFAX.86813164, CFA4.42351982, and CFA7.46842856) – with a few dozen other more minor genetic influences. “The signal on CFA15 corresponds to the location of IGF1 which encodes a growth factor previously described to control a significant proportion of size variation across dog breeds. The CFA10 signal corresponds to the location of HMGA2, a gene known to affect body size variation in humans and mice. Both HMGA2 and a locus corresponding to the CFA7 signal, SMAD2, have been previously associated with dog body size. In contrast, the signals on CFA4 and CFAX hits have not previously been associated with body size variation in dogs. Interestingly, the CFA4 signal contains (among other genes) the STC2 locus, a known growth inhibitor in mice. The two signals on the X chromosome lie in separate LD blocks that each contains dozens of genes.”

      http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1000451

      So, although such traits in dogs are controlled by fewer genetic regions, it seems quite clear that far more than just “4 possibilities” could be produced by a single breeding pair when it comes to most phenotypic traits – depending upon the combination of these genetic loci and how they control the expression of a given trait.

      Of course, “in all six regions, wolves are not highly polymorphic” – as would be expected since wolf morphology is fairly uniform (not having been bred to highlight unique morphologic features that could be isolated in relatively short order). Of course, there are additional allelic options, based on unique mutations, within modern dogs, as compared to the wolf…

      For example, the short stubby legs of Dachshunds, Basset Hounds, Corgis, and the like have an extra copy of a gene that codes for Fibroblast Growth Factor 4 (FGF4). This extra gene is a mutated retrogene. Neither the introns nor the upstream promoter sequences of the gene are present in the inserted retrogene. However all exons are present, with no alterations in the coding sequence, as well as the 3’ UTR and poly-A tail – characteristic of retrotransposition of processed mRNA. The lack of introns normally found in FGF4 genes causes the retrogene version to malfunction. In short, this malfunctioning retrogene results in the overproduction of FGF4 transcript. The “atypical expression” of the FGF4 transcript in the chondrocytes apparently causes the inappropriate activation of one or more of the fibroblast growth factor receptors – such as FGFR3. An activating mutation in FGFR3 is responsible for > 95% of achondroplasia cases, the most common form of dwarfism in humans, and 60–65% of hypochondroplasia cases, a human syndrome that is more similar in appearance to breed defining chondrodysplasia (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2748762/). In other words, this overproduction of FGF4 is thought to disturb the normal process of limb growth during fetal development, such as turning on key growth receptors at the wrong time, leading to short legs in dogs. What happens is that the development of long bones is curtailed due to calcification of growth plates, resulting in short legs with a curved appearance.

      This example illustrates the fact that dramatic phenotypic differences can be produced by gene dosage alterations – i.e., an increase or decrease in gene products. Mutations that cause an over or under production of gene products are not uncommon and can be realized in relatively short order – especially in larger populations.

      Remember, it is far far easier for mutations to cause a loss or disruption or even a gain of the same basic type of pre-established functionality vs. the evolution of entirely novel, qualitatively novel, functionality – which does not happen at all beyond very low levels of functional complexity.

      This is why such novel features in various breeds, such a dog breeds, or even “species” that were derived from the same ancestral gene pool, can be realized in such short order. They really have nothing truly new, qualitatively new, beyond very low levels of functional complexity – compared to what their original parents had. Almost all examples of the evolution of “new” functional traits or alleles are based on the disruption or loss of a pre-existing trait or functional system. And, those occasional examples of evolution where qualitatively novel functional systems are produced in observable time are all at very very low levels of functional complexity (requiring a minimum of no more than a few hundred specifically arranged amino acid residues).

      That is why I argue that the current phenotypic variety of breeds, such as dogs, is based on front-loaded genetic information with very little if any qualitatively novel traits evolving which were not based on the quantitative increase or decrease of expression of pre-existing genetic elements – something that can be achieved in very short order.

      I am again confused. Are you arguing for dogs derived from 2 wolves or not? If you take the genesis account literally which I understand you do, dogs are unclean and you must consider that they are therefore derived from the most severe genetic bottleneck possible.

      What I’m saying here is that it would be possible to produce all or nearly all the phenotypic diversity of modern dog breeds within a very short time starting with only two individuals. I’m not quite sure why you think longer periods of time would be required for selective breeding to produce essentially the same degree of phenotypic variety that we see today? Where is the limiting factor here?

      It would help your argument if you could point to an example of a reintroduction program where there was success with 2 genetically isolated animals. I certainly cannot find any.

      If you care to read the paper on reintroduction of wolfs into yellowstone

      http://www.ncbi.nlm.nih.gov/pubmed/17877715

      You will see they followed the standard practice built up based on long experience and reintroducing around 40 animals. [It is argued whether sustainable populations are around 30 or if 50 are needed)

      Which brings us back to our previous discussion about declining genomic quality over time. As already explained in some detail, this decline is due to the continual build-up of detrimental mutations in the gene pools of all slowly reproducing creatures far far faster than natural selection can get rid of them. The death rate required for natural selection to deal with this problem is simply far too high. That is why inbreeding within small groups of animals or people is such a big problem today. It enhances odds of the fixation of detrimental mutations within a population – resulting in a greater chance of genetic meltdown and extinction within a shorter time span. This is also why many modern dog pure-breeds suffer from far more genetic diseases than do hybrid dogs.

      There is also, of course, the problem of the dangers of living in the wild – of dealing with random accidents, injuries, sickness, disease, infertility, ext. Increasing the population size helps to alleviate these problems when trying to start a new colony.

      The experience with 4 avian species again shows that populations with low genome equivalents are subject to significant and life threatening inbreeding and loss of genetic diversity

      http://www.ncbi.nlm.nih.gov/pubmed/20825445

      2 genome equivalents is clearly in the unsustainable range according to all the current practical and theoretical models of population genetics.

      In modern times, yes. Thank you for highlighting my point. This was not the situation, however, when gene pools were much closer to their original creation and had not yet built up so many detrimental mutations…

      I really don’t know why you seem to be continually arguing for naturalistic mechanisms for scenarios around the miraculous global flood account. Can’t you accept that derivation of all populations from the ark is genetically untenable and accept it as miraculous. Creation science is intrinsically miraculous; turtles all the way down. Just accept it and don’t pretend it is some scientific hypothesis that can be tested by experiment. As prof Kent argues it is even worse because you not only try to argue a particular interpretation is scientifically valid but then pin your faith on your ability to argue the scientific validity. It’s a miracle. Move on to the consequences and you might not find it is so foundational.

      There is no need to invoke God to explain the phenotypic diversity of living things beyond His original programming of the parental population – His “front-loading” of the gene pools if you will. God did not need to step in and create novel alleles within wolves or dogs in order for the diversity of dog breeds to be realized in very short order via natural processes that have been in place since the beginning of life on this planet. It is simply your lack of understanding that makes you think that a subsequent Divine miracle, or an ongoing series of miracles of deliberate design, would have to have been required. What? would you really have me believe that God was the one who stepped in and deliberately created the retrovirus FGF4 gene for the “inappropriate activation” of FGFR3? so that modern dogs could have stumpy legs? I suppose God also causes achondroplasia in humans? Come on now…

      The same is true for the nature of the geologic / fossil records. No Divine miracle is required to explain most of their features from a Biblical perspective. Sure, there are still unanswered questions. However, the weight of evidence, science itself (true science that is), strongly supports the claims of the Bible. Faith in the reliability of the Bible as the true Word of God need not be blind or indistinguishable from wishful thinking…

      Sean Pitman
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        “There is no need to invoke God to explain the phenotypic diversity of living things beyond His original programming of the parental population – His “front-loading” of the gene pools if you will.” – Sean Pitman

        I clearly lack your gift. It must be wonderful to be always right even when I’m wrong.

        It seems that your position is that in creationism there are no miracles except when there are miracles. I can accept that. but lets consider the turtles.

        God created ex nihilo in 6 24hr contiguous days. We can of course define that as natural if we want.
        This life was totally unlike the carbon based life form we see today as there was no death so there is none of the normal concepts of ecology we understand today.

        He then miraculously introduced death associated with the many genes associated with cellular and organismal control of death (apoptosis and necrosis). Or maybe this was created by a alternative bad creator with similar power to the original good creator

        He then dispersed the animals terrestial from a boat in the middle east to the rest of the world over a period of a few thousand years, 500 year of which was an ice age with an ice sheet covering all of the northen and southern regions of the planet. Truly a miracle.

        He miraculously altered all concepts of genetics so that a population of 2 had enough genetic information and were so perfect (apart from the aforementioned introduction of death pathogens and immunity) that they could give the total diversity of the large number of species that exist now derived as they were from a few baramin that populated the ark.




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        • @pauluc:

          I clearly lack your gift. It must be wonderful to be always right even when I’m wrong.

          Don’t sell yourself short! You’re certainly no less “gifted” in this regard than I am. 😉

          It seems that your position is that in creationism there are no miracles except when there are miracles. I can accept that. but lets consider the turtles.

          The “God-did-it” hypothesis can actually explain anything and everything… and therefore nothing. It is therefore not a very useful or meaningful argument.

          On the other hand, the “God-only” hypothesis is useful in that it is testable in a potentially falsifiable manner. If it can be shown that some mindless force or process of nature could produce the phenomenon in question, the argument that only a God could do it is effectively falsified…

          God created ex nihilo in 6 24hr contiguous days. We can of course define that as natural if we want.

          There is no known natural process that could create in such a manner. Therefore, it is reasonable to argue that only a God or God-like being could create in such a manner.

          This life was totally unlike the carbon based life form we see today as there was no death so there is none of the normal concepts of ecology we understand today.

          There was no death for sentient creatures, true. However, there was death for plant-based life and other cellular life, such as bacteria and individual cells within the body, where such cells and organisms do not have a sense of self and are not able to appreciate suffering, pain, or the fear of death.

          It is true that such a world would have to be maintained by Divine intervention on a supernatural level in order to avoid decay over time via informational entropy. Certainly this type of maintenance would be truly miraculous from our perspective.

          He then miraculously introduced death associated with the many genes associated with cellular and organismal control of death (apoptosis and necrosis). Or maybe this was created by a alternative bad creator with similar power to the original good creator.

          Again, cellular death is not the same thing as the death of the animal that can appreciate pain and suffering. I’m sure there was cellular death, to include programmed apoptosis, before the Fall. There just was no death for sentient creatures before the Fall.

          Also, death for sentient creatures is not the result of a “miraculous” act on the part of God. It can be explained without the need to invoke God. All that has to happen is for God to stop working to maintain the quality of genetic information within living things and they will start to die quite naturally – from the natural inevitable build up of deleterious mutations that corrupt the underlying genetic code over time. By the time an average person reaches 60 years of age, each cell in his or her body carries approximately 60,000 mutations.

          Obviously, this results in aging and eventual death for the entire organism – not just on a cellular level. This decay process does not require the guidance of a Divine hand or any other form of deliberate intelligent design for that matter. Informational entropy is simply part of non-intelligent nature acting over time.

          He then dispersed the animals terrestial from a boat in the middle east to the rest of the world over a period of a few thousand years, 500 years of which was an ice age with an ice sheet covering all of the northen and southern regions of the planet. Truly a miracle.

          Right after the Flood the continents had yet to completely separate from each other. There were land bridges between them that would allow for animals to populate all the continents before they completely separated from each other. Continental drift was much more rapid in the early post-Flood years compared to today. This drift carried animals who had populated these continents long distances over time and also created isolated habitats around the globe. This contributed to unique specialization among different groups of animals that were once part of the very same gene pool.

          Also, ice sheets covering most of the northern and southern hemispheres would create a thin habitable band around the Earth’s equator and would dramatically lower ocean water levels, which would also aid in the rapid disbursement of animals around the Globe.

          There simply is no compelling need, therefore, to invoke the God-only hypothesis when it comes to explaining the disbursement of animals around the globe.

          He miraculously altered all concepts of genetics so that a population of 2 had enough genetic information and were so perfect (apart from the aforementioned introduction of death pathogens and immunity) that they could give the total diversity of the large number of species that exist now derived as they were from a few baramin that populated the ark.

          You have produced no examples of novel alleles or traits evolving, in observable time, beyond very very low levels of functional complexity. It just doesn’t happen and statistically is impossible to achieve, outside of deliberate design, this side of a practical eternity of time.

          Also, it is well known that novel alleles are not needed to get from just two individuals in a gene pool to a vast array of different phenotypes among the offspring. This is due to the polygenic nature of most traits in most plants and animals which can be selected along a long continuum of phenotypic options… along a “bell-shaped” curve. Of course, many new allelic variations have and do evolve all the time – quite rapidly in fact. However, the vast majority of these naturally evolved changes to pre-existing alleles are based on increasing or decreasing the expression of the very same trait. In other words, the evolved changes are functionally quantitative, not qualitative. Very few examples of the evolution of something qualitatively new, on a functional level, are known. And, among these, none are known that go beyond very very low levels of functional complexity.

          The only thing preventing the success of such a demonstrating (starting with just two individuals) is starting with a gene pool that is already damaged… starting with individuals that share the same or similar regions of damaged DNA. As you yourself point out, such damage within very closely-related individuals makes it far far more likely that their offspring will not be as viable. However, if you start with two individuals that have little or no damage within their own genes, they will produce healthy virile and vital offspring without any problem…

          Your problem is that you simply can’t imagine that modern gene pools are and have always been declining in informational quality since the Fall. It is truly “turtles all the way down”. There is no overall evolutionary progress when it comes to slowly reproducing creatures – like all mammals on the planet. Overall, there is only a gradual decline in genetic quality toward an eventual state of inevitable genetic meltdown and extinction.

          Neo-Darwinism simply has no rational answer for this fundamental problem that completely undermines the entire Darwinist perspective. Natural selection is not a very creative force, not at all beyond very low levels of functional complexity, and it is not a perfect maintaining force either. It does help to slow down the loss of genetic information, but it does not actually stop this loss completely. There is always a gradual build-up of detrimental mutations in each and every individual in every generation…

          This is devastating to the naturalistic perspective while being perfectly in line with the claims of the Bible…

          Sean Pitman
          http://www.DetectingDesign.com




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        • @Sean Pitman:

          You suggest

          “Don’t sell yourself short! You think you’re just as right in your opinions and that I’m clearly mistaken. You’re certainly no less “gifted” in this regard than I am.”

          No Sean this is really the core of the differences between you and me. It is not a matter of opinion but a matter of statistical probability. In almost all of what I have posted on this site I have reflected the evidence for the consensus view rather than my opinion.

          Dismiss me as kowtowing to authority if you will. I have faith in the process of hypothesis driven science and the community of scientists that seeks to arrive at objective truth by free and open communication of ideas by publication and peer review. In this process I continue to participate for I do think it is one of the most noble human endeavours.

          As a outsider to this process and as one who has never had formal training in science you uncritically accept the paranoid meme that says you must be somehow blessed by some scientific inner circle to have your papers accepted. You feel excluded but have you actually tried to participate?

          I accept in good faith the work of scientists and the derivative consensus view in most areas of science but like all good scientist understand it is always a tentative synthesis. I maintain a cynical attitude which unfortunately taints the way I view your claims. I nonetheless can appreciate the elegance of a solution to a conundrum and an hypothesis that has huge explanatory value while still accepting its tentative nature. I understand my limitations and have some inkling of the extent of the biomedical literature. I recognise expertise and am therefore happy to defer to the expertise of others with an appropriate track record.

          In contrast because of your religious views you do not accept the consensus view of scientists in a vast number of areas including geology, climatology and paleoclimatology, volcanology, oceanography, genetics, paleontology, cladistics, and molecular biology. In all these areas you imagine that you have more expertise and insight than the people who have dedicated their lives to the study of the content of these areas.

          In spite of the way you construct it I am not suggesting I am more righter than you and I have only ever suggested that you have some respect for the history of the current consensus view in science and a little more realism in your perception of mastery of these areas. You may view this as a contest and that you easily best some fool from the antipodes but in rejecting my appeals to the evidence and the orthodox consensus view in areas in which I have some expertise you are essentially claiming you know it all.

          [to save time I will acknowledge this space as containing some castigation from you or Bob Ryan such as “Gotta love the appeal to authority!!!”]

          Which brings me to the question of probabilities. Statistically who do you think is more likely to be right? 1] An MD from Southern California whose ambition in life seems to be to extinguish any open discussion of views that do not align with his own views and interpretation of most all of science. 2] The consensus view of many scientists who in good faith attempt to understand the world through a process of hypothesis testing and experimentation and open communication of that information and interpretation.




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        • @pauluc:

          It’s fine to have faith in the majority opinion of the experts. Such faith is rational and it gives one a sense of confidence when confronting those who hold opposing points of view. I suppose that is why you often use such condescending language and have such a paternalistic tone – because you are so very confident that a nobody MD from California couldn’t possibly be right while the vast majority of experts are so very very off base in their thinking on the topic of origins.

          That’s perfectly reasonable. The problem is, of course, that your opinions are therefore largely based on the opinion of others, not your own personal understanding of the issue in play.

          It’s fine to have faith that the majority know what they’re talking about while admitting that you do not, since most of the time you’d be correct – but not always. There have been many times when the majority of experts have been not only wrong, but painfully wrong. You would not be able to determine when the majority is wrong if you never learned to ever question the opinion of the majority and think for yourself for a change… to ask yourself why you agree with the majority besides the fact that the majority is usually right?

          I’ve been thinking about these concept and working on the various fundamental problems in play for almost 20 years now. You may not think I qualify as a “scientist”, but that’s basically irrelevant when it comes to answering my observations and questions. I’m sorry, but so far you haven’t produced must of anything to counter my basic arguments besides bald assertions, appeals to authority, occasionally misstating my position, and a great deal of bluster – like saying that you must respond to my “most egregious claims”, etc. None of that helps to substantively answer my questions or demonstrate where or how I’ve gone significantly off base…

          Sean Pitman
          http://www.DetectingDesign.com




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        • Sean

          Apropos of my good faith support of scientific expertise you suggest;

          “The problem is, of course, that your opinions are therefore largely based on the opinion of others, not your own personal understanding of the issue in play.”

          I am not sure this is really an accurate characterization since it is I not you who have done original research and published my observations on immunogenetics in the peer reviewed literature which you can very easily verify if you care to do so.

          As for my comment on your egregious claims. I was responding to this statement.

          “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.”

          In this you are essentially claiming that almost anyone who is an evolutionist is ignorant and doesnt know how mendelian inheritance occurs. If you really believe this, is it surprising if I express the view that you have no respect for expertise, knowledge, discipline or integrity in science.

          I am happy that you have spent 20 years in investigating these issues. I wish you continuing success I just ask that you take a little time in assessing your sources. In my experience places like ICR and CMI are less reliable than sources of information that do not start with the conclusion.

          I would suggest there are many of us who are followers of Christ and are prepared to accept the cost of discipleship associated with his claims but are scientists who believe we must honestly and transparently view the evidence.

          I appreciate you have clarified your model of the genetics of creation science. It is nascent and needs to be rigorously expanded and tested properly against the primary observations. Rather than simply using this site as an attack vehicle against those teachers you do not understand or agree with, you would make a real and significant contribution to the life of the church if you expanded your model of creation by running commentary on the freely accessible peer reviewed literature.

          Your comments on publications such as that in PLOS genetics paper I cited on dog evolution would help to develop the rigorous model of creationism that GRI suggest is lacking. Since we have only scratched the surface of dog genetics perhaps you could start with prospective commentary on genetics paper from the open access press; for example
          PLOS journal
          http://www.plos.org/publications/journals/
          BMC journals
          http://www.biomedcentral.com/journals

          This suggestion really comes from a comment by David Read on this site when we discussed the gene families and randomness in genomic structure. He suggested that every time he reads a scientific research publication he can see how it supports the biblical 6000/6/24 account of origins. I am not sure if you agree, but I think that is the only way in which a coherent model can be constructed.




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        • @pauluc:

          I am not sure this is really an accurate characterization since it is I not you who have done original research and published my observations on immunogenetics in the peer reviewed literature which you can very easily verify if you care to do so.

          Pardon me, but it seems like your expertise in immunogenetics hasn’t helped you much when it comes to understanding the huge phenotypic potential of small populations. You don’t seem to yet accept the fact that most traits are based on the interaction of many different genetic elements, not just two.

          Look, I’ve also published a few papers in my own field as well and contributed to the reclassification of certain forms of Hodgkin lymphoma in literature. So what? What does this have to do with understanding how evolution works? Hmmmm?

          If you want to know the answer to something beyond a mere faith in what the experts are telling you, you have to do some additional study outside of your own personal area of expertise… or perhaps even within your own personal area of expertise at times (when it comes to ideas you’ve never thought of before).

          It is just that I don’t have the same faith you seem to have in the opinions of the majority of scientists. I know that they can be and have been quite wrong on many occasions. And, when it comes to origins, it seems like they are indeed way off base.

          In this you are essentially claiming that almost anyone who is an evolutionist is ignorant and doesnt know how mendelian inheritance occurs. If you really believe this, is it surprising if I express the view that you have no respect for expertise, knowledge, discipline or integrity in science.

          What I’m saying is that most of Darwin’s own observations of examples of “evolution” can be largely if not entirely explained, ironically, by Mendelial variation and other forms of “front-loaded” information without the need to appeal to the novel evolution of new information – certainly not qualitatively new information beyond very very low levels of functional complexity. Such examples of “evolution in action” really aren’t based on any significant functional change to the underlying gene pool that was inherited from the original parent population. There really is nothing substantially new, qualitatively new, that has been evolved within the gene pool itself. And, modern neo-Darwinists have not caught on to this. They still persist in referring to Mendelian and other forms of phenotypic variation, which are not based on the gain of anything genetically new within the underlying gene pool, as true examples of Darwinian evolution. This claim is misleading at best…

          So far, none of your arguments seem to counter anything I’ve presented on this topic. You’ve seemed to continuously argue that traits are governed by only two genes, when in fact they are usually governed by many more. You haven’t acknowledge the phenotypic potential of a single pair of animals when in fact such potential is truly enormous. And, you haven’t acknowledge the steady genetic deterioration of the gene pools of slowly reproducing animals over time…

          Sean Pitman
          http://www.DetectingDesign.com




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  31. Pauluc,

    Your questions about conservation genetics are very insightful. I don’t understand how all these life forms were able to greatly increase in genetic diversity while simultaneously winding down and losing genetic information to mutations. Sean seems to insist that both processes happen simultaneously. I had the impression he has insisted all along that the former cannot overcome the latter. But I think you must be right: God had to intervene to alter the course of nature. However, we can probably test this empirically because there must be a signature of evidence available in the DNA. I’ll bet Sean can find the evidence for this.

    I’m also glad the predators (just 2 of most such species) in the ark had enough clean animals (14 of each such species) to eat during the deluge and in the months and years after they emerged from the ark that they didn’t wipe out the vast majority of animal species through predation. Maybe they all consumed manna while in the ark and during the first few months or years afterward. Perhaps Sean can find in the literature a gene for a single digestive enzyme that is common to all predatory animals, from the lowest invertebrate to the highest vertebrate. Now that would be amazing.

    Wait a minute–I remember once being told that SDA biologists like Art Chadwick believe that some animals survived on floating vegetation outside the ark. Now that would solve some of these very real problems! I wonder whether readers here would allow for this possibility. Multiple arks without walls, roof, and human caretakers.




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    • @Professor Kent:

      Your questions about conservation genetics are very insightful. I don’t understand how all these life forms were able to greatly increase in genetic diversity while simultaneously winding down and losing genetic information to mutations. Sean seems to insist that both processes happen simultaneously. I had the impression he has insisted all along that the former cannot overcome the latter.

      The former is caused by the latter…

      As already explained, “new” alleles are almost always produced by mutations that disrupt pre-established systems of function… as in the case of chondroplasias of dogs and humans – a product of mutated alleles that disrupt pre-existing functionality (and are therefore degenerative in nature).

      The vast majority of mutations that have a functional effect on the genome are known to be degenerative / detrimental. Also, most “new” forms of genetic diversity, based on novel mutations, only have quantitative effects on functionality, not qualitative effects. That is why they can be realized so rapidly. And, those relatively rare qualitative changes are always at very very low levels of functional complexity (which means that they can also be realized in relatively short periods of time).

      But I think you must be right: God had to intervene to alter the course of nature.

      You only say this because you do not understand the nature of functionally significant allelic mutations. There simply is no need to invoke intelligent design at all – much less a Divine intelligence.

      However, we can probably test this empirically because there must be a signature of evidence available in the DNA. I’ll bet Sean can find the evidence for this.

      There is empirical evidence and this evidence does in fact effectively falsify your suggestion that God had to have been involved with the production of novel alleles after the Fall or after the Flood. That’s simply not true.

      I’m also glad the predators (just 2 of most such species) in the ark had enough clean animals (14 of each such species) to eat during the deluge and in the months and years after they emerged from the ark that they didn’t wipe out the vast majority of animal species through predation. Maybe they all consumed manna while in the ark and during the first few months or years afterward.

      You know as well as I do that intelligent people can think of many ways to feed all kinds of animals for long periods of time. If God told Noah how to build the Ark, it is certainly reasonable that He told him how to care for and preserve the animals as well… by any number of possible means.

      Perhaps Sean can find in the literature a gene for a single digestive enzyme that is common to all predatory animals, from the lowest invertebrate to the highest vertebrate. Now that would be amazing.

      Obligate predators lack enzymes. Predator-specific digestive enzymes aren’t needed. The digestion of a vegetarian diet is more complex, requiring a greater diversity of enzymes compared to a meat-based diet. Of course, I’ve explained this to you before…

      Wait a minute–I remember once being told that SDA biologists like Art Chadwick believe that some animals survived on floating vegetation outside the ark. Now that would solve some of these very real problems! I wonder whether readers here would allow for this possibility. Multiple arks without walls, roof, and human caretakers.

      Art does not believe this. He thinks all land animals died, save those on the ark… just like the Bible says.

      Sean Pitman
      http://www.DetectingDesign.com




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  32. Sean

    Just trying to understand your model of life.

    1] The original creation between 6000-7000 BP was by divine fiat.
    2] only sentient creatured did not die in the original creation.
    3] Prokaryotic and eukaryotic cells contained the normal regulators of death and longevity.
    4] There was continuous and diven intervention preventing decay in biological information until the fall.
    5] In the time between the fall and the flood there was removal of the supernatural prevention of natural deterioration.
    6] At the time of the flood two animals had so much “front loaded” genetic “information” that they could generate a large population without inbreeding or loss of fitness.
    7] Over the last 4000 years there has been dramatic and life threatening accumulation of genetic defects
    8] At around 2000 BC the continental plates had not seperated and there were large ice caps and very low sea levels so animals could scroll across the ocean floors
    9] Somewhere beyond 2000BC the plates separated so we have the biogeography we see today.
    10] The diversification within species does not require new information.
    11] diversification of species is the same as phenotypic changes within species and does not require new genetic information.

    I see a few inconsistencies in this account.
    1] Was there really genetic degradation from the fall or from the flood? How does his impact the perfect pair model you have proposed.
    2] When did fast continental drift start and finish. You dont really seem to be allowing much time for the 10000 K pacific ocean to develop. 10K per year for seperation of Eurasia and america seem pretty fast.
    3] You use the dog model of phenotypic variation as a model of post flood diversification but claim there is no new mutations. Dog phenotypic variation is not at all speciation so you must have all the current species on the ark or you must believe that for example all canines species diversified by mechanisms that do not require new information.

    .




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    • @Pauluc:

      Just trying to understand your model of life.

      1] The original creation between 6000-7000 BP was by divine fiat.

      Yes, the original creation of this Earth as a place able to support complex life and then all living things on this planet took place within recent history (i.e., less than 10,000 years ago) – by Divine fiat.

      2] only sentient creatured did not die in the original creation.

      Yes. Obviously, if you take a bite out of an apple, cells die, are chewed up and digested. But no one cares because such cells are not sentient or “self-aware”.

      3] Prokaryotic and eukaryotic cells contained the normal regulators of death and longevity.

      Yes.

      4] There was continuous and diven intervention preventing decay in biological information until the fall.

      Yes.

      5] In the time between the fall and the flood there was removal of the supernatural prevention of natural deterioration.

      That’s right.

      6] At the time of the flood two animals had so much “front loaded” genetic “information” that they could generate a large population without inbreeding or loss of fitness.

      There obviously was inbreeding. It is just that such inbreeding (as in marrying one’s sister) wasn’t such a problem at this time since there weren’t as many detrimental mutations within the gene pool at that time. So, yes, a large population of fit as well as phenotypically diverse individuals could be produced starting with just two individuals.

      7] Over the last 4000 years there has been dramatic and life threatening accumulation of genetic defects

      The accumulation of detrimental mutations started at the Fall. However, this accumulation had not reached nearly the hazardous levels that are currently known by the time of the Flood.

      8] At around 2000 BC the continental plates had not seperated and there were large ice caps and very low sea levels so animals could scroll across the ocean floors

      The continental plates were broken up, for the first time, during the Flood and started their drift at that time. Right after the Flood, there were several hundred years when the entire world was warm and lush. The continents, while rapidly drifting apart, had not yet completely separated at all points. There were no ice caps or massive ice sheets yet as the first ice age had yet to be realized. After several hundred years, the first ice age struck suddenly and trapped millions of animals in a single season. It is for this reason that we still find frozen Mammoths and other post-Flood animals all around the Arctic circle today. The rapid increase of ice resulted in a significant decrease in ocean levels – also contributing to bridges between the separating continents. As the continents began to crash into each other, the energy used up in the process of creating huge mountain chains and ocean trenches slowed down their rate of drift.

      9] Somewhere beyond 2000BC the plates separated so we have the biogeography we see today.

      The biogeography we see today wasn’t realized immediately. It took some time for the continents to reach their current positions via drift.

      10] The diversification within species does not require new information.

      Very dramatic changes in phenotypic expression need not be based on the generation of new alleles at all – that’s correct. Of course, new mutations do affect alleles. However, as already noted, these effects are almost always quantitative effects, not qualitative. And, as you know, most functional mutations are detrimental. The relatively rare examples where something qualitatively new is actually produced by random mutations are always at very low levels of functional complexity. Because of these features, in combination, all that we see today as far as diversity within a species or even at the genus or family or even ordinal levels could be realized in a very short period of time.

      11] diversification of species is the same as phenotypic changes within species and does not require new genetic information.

      Not qualitatively new beyond very low levels of functional complexity. Again, there are no examples of qualitatively novel systems of function, based on any kind of underlying genetic mutation, being produced by RM/NS beyond very very low levels of functional complexity (i.e., requiring no more than a few hundred specifically arranged residues). If you want to call functionally detrimental mutations “new”, that’s fine. Just make sure and define the quality of the mutations and the resulting functions you’re talking about.

      I see a few inconsistencies in this account.

      1] Was there really genetic degradation from the fall or from the flood? How does his impact the perfect pair model you have proposed.

      From the Fall. The pairs at the Flood were not “perfect”. They were just a lot better than gene pools are today and therefore had far less odds of producing offspring that would be homozygous for detrimental genes.

      2] When did fast continental drift start and finish. You dont really seem to be allowing much time for the 10000 K pacific ocean to develop. 10K per year for seperation of Eurasia and america seem pretty fast.

      It was much faster right after the Flood. . . and has yet to finish. Continental drift is still taking place.

      3] You use the dog model of phenotypic variation as a model of post flood diversification but claim there is no new mutations. Dog phenotypic variation is not at all speciation so you must have all the current species on the ark or you must believe that for example all canines species diversified by mechanisms that do not require new information.

      Of course there are new mutations. New mutations happen all the time, in every individual in every generation. How many times have I pointed this out to you? Why then would you claim that I recognize no new mutations?

      I also think that creatures like dogs, wolves, foxes, coyotes, etc., are all part of the same original gene pool – the same original parents. Many phenotypic differences between these “species” are indeed based on novel mutations. It is just that these mutations did not produce qualitatively novel information/function beyond very very low levels of functional complexity.

      Sean Pitman
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        You are correct. I did inadvertently misstate your positiom

        I said

        “3] You use the dog model of phenotypic variation as a model of post flood diversification but claim there is no new mutations. Dog phenotypic variation is not at all speciation so you must have all the current species on the ark or you must believe that for example all canines species diversified by mechanisms that do not require new information.”

        You responded

        “Of course there are new mutations. New mutations happen all the time, in every individual in every generation. How many times have I pointed this out to you? Why then would you claim that I recognize no new mutations? ”

        “I also think that creatures like dogs, wolves, foxes, coyotes, etc., are all part of the same original gene pool – the same original parents. Many phenotypic differences between these “species” are indeed based on novel mutations. It is just that these mutations did not produce qualitatively novel information/function beyond very very low levels of functional complexity.”

        I did try to maintain your distinction between new mutations and new information although I think this is an unnecessarily opaque distinction that is not part of the peer reviewed genetics literature. I apologize in that I inadvertently suggested you do not recognize new mutations when in fact you do but then make a distinction between new mutations and new information. I seem to have failed to maintain that distinction. The point I was making was that you have often stated on this site and in relationship to Darwinian evolution your position that random mutations cannot generate new information or contribute to changes in phenotype. Now you seem to indicate that phenotypic changes in dogs (and I presume in all kinds represented by 2 animals) only occur by resorting multiple alleles in the original 2 founders but have qualified this somewhat in that you concede that you consider there may be minor mutation that do not have any significant functional contribution and do not contribute new information. I really do not understand; I have interpreted both you and David Read as saying there may be essentially information-less mutations but now you indicate some of them do have a little information or novelty. It seems you need to decide if there is new information or not. Beyond that as everyone recognizes novel changes may be neutral, beneficial or detrimental all to varying degrees based on circumstances. Is there novel information or not? If there is, no matter how small there is new information and even this minimal new information may still be fodder for selection and your position becomes, except in time frame, no different to the conventional view that sees variation (genetic variation) as the basis for natural selection and evolution.

        In terms of random mutation accumulation in dogs. Do you think the >2 millions SNP identified in dogs (actually canids) come from the founding pair of canids or were introduced by mutation over 4000 years? That is a new mutation rate per year of 500/year or approximately 500 per generation. The alternative is of 1 million nucleotide differences in each of the near perfect pairs. That means that in the 19000 genes in dogs there were on average 5000 nucleotide differences some 4000 years ago. An example of this in the sequence literature would be very helpful in testing your hypothesis. I say there is no example anywhere near this level of allelic variation within an individual but if you can give the URL for such alleles then i would concede I do not need to reject your hypothesis.

        Of course the SNP density in current day dogs is at around 1 per 1000 bases but in your model of 2 near perfect pairs you need more loci to account for more than 4 possibilities. You could account for more than 3 SNPs at a site by increasing the number of possible sites by gene duplications but you might have a novel solutions for which you can provide evidence.

        For details consult this freely available review.
        http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.0010058#s2
        or this less easily accessed paper
        http://www.ncbi.nlm.nih.gov/pubmed/22270221
        or the paper which I referenced before that gives the SNP data on dogs in comparison to other canids.
        http://www.ncbi.nlm.nih.gov/pubmed/16341006




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        • @pauluc:

          I did try to maintain your distinction between new mutations and new information although I think this is an unnecessarily opaque distinction that is not part of the peer reviewed genetics literature.

          That’s exactly right. Mainstream science has yet to draw this distinction. That is why mainstream science does not recognize or even discuss the statistical odds of the evolutionary mechanism (RM/NS) working at various levels of functional complexity. All levels of functional complexity are lumped together. It is simply assumed that if evolution can take place at any level that it can take place at all levels given enough time. No calculations are done to actually determine what the likely time would be to realize something qualitatively new at various levels of functional complexity – that higher levels of complexity would require exponentially greater periods of time to achieve.

          I’m not quite sure why these concepts are never discussed in mainstream literature? except perhaps because they so clearly undermine the entire concept of neo-Darwinism.

          I apologize in that I inadvertently suggested you do not recognize new mutations when in fact you do but then make a distinction between new mutations and new information. I seem to have failed to maintain that distinction.

          Indeed.

          The point I was making was that you have often stated on this site and in relationship to Darwinian evolution your position that random mutations cannot generate new information or contribute to changes in phenotype.

          Not true. Where did you get this idea? I’ve certainly never made such a statement. In fact, I’ve often given examples, to include in this very thread, in response to your own comments, of random mutations directly causing various phenotypic changes. I’ve specifically noted that these changes are most commonly qualitative in nature and usually degenerative. I’m not quite sure how you’ve been able to so consistently overlook these comments of mine?

          Now you seem to indicate that phenotypic changes in dogs (and I presume in all kinds represented by 2 animals) only occur by resorting multiple alleles in the original 2 founders but have qualified this somewhat in that you concede that you consider there may be minor mutation[s] that do not have any significant functional contribution and do not contribute new information. I really do not understand; I have interpreted both you and David Read as saying there may be essentially information-less mutations but now you indicate some of them do have a little information or novelty.

          I’ve consistently and repeatedly explained to you, in this thread and in many others, that many if not most random mutations have functional effects to one degree or another. They do affect the informational quality of the genome – of course! What is the nature of this affect?

          As repeatedly explained, the vast majority of functional mutations have a detrimental or degenerative effect on the genome. Those mutations that result in a survival advantage generally do so by producing quantitative changes in per-existing systems of function. Those relatively rare mutations that actually produce something that is truly qualitatively new, not already there within the ancestral gene pool, never so do beyond very very low levels of functional complexity.

          I’m not sure how many times I need to repeat myself here?

          It seems you need to decide if there is new information or not.

          Why would you think it an all or nothing situation? It’s not. There are levels of functional complexity. Lower levels are very easily realized, in short periods of time, by RM/NS. Higher levels are exponentially less likely to be realized in a given span of time.

          Beyond that as everyone recognizes novel changes may be neutral, beneficial or detrimental all to varying degrees based on circumstances. Is there novel information or not?

          Yes, but mostly quantitative in nature; rarely qualitative – and never beyond very low levels of functional complexity.

          If there is, no matter how small there is new information and even this minimal new information may still be fodder for selection and your position becomes, except in time frame, no different to the conventional view that sees variation (genetic variation) as the basis for natural selection and evolution.

          The difference is in the recognition of the functional quality of the mutations… and in the fact that novel information based on random mutations is not needed, not at all, before a vast array of phenotypic variations can be realized in short order – starting with a single breeding pair.

          In terms of random mutation accumulation in dogs. Do you think the >2 millions SNP identified in dogs (actually canids) come from the founding pair of canids or were introduced by mutation over 4000 years? That is a new mutation rate per year of 500/year or approximately 500 per generation.

          First off, genetic mutations started before the Flood at the Fall. The original post-Flood mating pair would very likely have had very different point mutations and therefore a higher SNP number to begin with to pass on to their offspring.

          Also, aren’t the >2 million SNPs simply part of the overall data base for canids? not necessarily representative of the average number of SNPs in a individual vs. individual comparison within or between breeds? or even species of canids? – as per the 2008 Lindblad-Toh et al. paper you cite from Nature? If so, large gross numbers of SNPs can be rapidly produced by larger populations in short order. Sure, the same article cites SNP densities of “1/900 base pairs (bp) between breeds and 1/1,500 bp within breeds… and 1/580 bp between dogs and wolves”, but aren’t these densities based on specific regions of the genome that tend to harbor SNPs? SNPs are classically clustered in a non-random pattern – strongly favoring recombination sites and the like. Also, “SNPs attract further mutations to their vicinity through heterozygote instability”.

          http://www.nature.com/nature/journal/v438/n7069/full/nature04338.html
          http://rspb.royalsocietypublishing.org/content/early/2010/01/08/rspb.2009.1757.full

          And, isn’t it true that the SNP rate, when taken as a comparison between any two individuals, is approximately double that of the mutation rate since the MRCA? due to the fact that random mutations rarely affect exactly the same site in different genomes? For example, say a pair of dogs has a litter of dogs, each with 100 random mutations. How many SNPs will there be, on average, between any two of the puppies in this F1 generation? Up to 200 SNPs per comparison – right? Consider also that the determination of SNPs is prone to significant lab errors that are rather difficult to compensate for.

          As far as the potential for a single breeding pair to produce a vast array of dog phenotypes in short order, consider watching a Nova documentary entitled, “Dogs Decoded”. Notice the part at about the 40 minute mark where foxes were bread for tameness. Very quickly, in just a handful of generations, this trait was significantly enhanced. Surprisingly, along with this trait phenotypic differences were also realized which were very similar to those realized in domesticated dogs.

          So, there you have it . . . starting with a very small population very significant phenotypic effects can be realized, based on pre-existing functional information, without the need for additional mutations . . .

          Sean Pitman
          http://www.DetectingDesign.com




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  33. Sean Pitman: The former [increased genetic diversity] is caused by the latter [loss of genetic information]…

    So…God created life with remarkable genetic mechanisms to ensure that living organisms 1) can rapidly diversify to overcome small population size and adapt to changing environmental conditions (I admire the foresight and loving care of this God), but also 2) collapse spectacularly because they eventually can no longer rapidly diversify and adapt to changing environmental conditions (I’m not so sure what to think of this God). If the latter is true, does this mean that God designed these life forms poorly, or that He simply wanted them one day to all die off? Surely you have some thoughts on WHY God designed all life forms to eventually crash.

    Which group do you suppose is proprammed to reach its termination point first: the fast-reproducing (short-lived) species, or the slow-reproducing (long-lived) species? When will all these genetic systems disintigrate to the point of total failure? You’re good at math and have a thorough understanding of genetic systems, so surely you have a good idea. This might give us a hint as to when Jesus returns; after all, the collapse can’t happen before His return, as Satan would be able to point out God’s utter failure in creating defective life forms.

    Furthermore, you have a thorough understanding of theology, so perhaps you could show us from scripture where we should have realized all along that the self-limiting genetic mechanisms of living creatures would offer testable falsifiable empirical evidence that God is real.

    Your theories become more fascinating the more elaborate they become.




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  34. Sean Pitman: Art does not believe this [the possibility that some animals survived on floating rafts of vegetation]. He thinks all land animals died, save those on the ark… just like the Bible says.

    When did he tell you this? I have a friend who says he got the idea from Chadwick (I’m not sure whether first-hand or second-hand).




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  35. Sean Pitman says

    “Pardon me, but it seems like your expertise in immunogenetics hasn’t helped you much when it comes to understanding the huge phenotypic potential of small populations. You don’t seem to yet accept the fact that most traits are based on the interaction of many different genetic elements, not just two.

    …………..observations of examples of “evolution” can be largely if not entirely explained, ironically, by Mendelial variation and other forms of “front-loaded” information without the need to appeal to the novel evolution of new information – certainly not qualitatively new information beyond very very low levels of functional complexity. Such examples of “evolution in action” really aren’t based on any significant functional change to the underlying gene pool that was inherited from the original parent population. There really is nothing substantially new, qualitatively new, that has been evolved within the gene pool itself. And, modern neo-Darwinists have not caught on to this. They still persist in referring to Mendelian and other forms of phenotypic variation, which are not based on the gain of anything genetically new within the underlying gene pool, as true examples of Darwinian evolution. This claim is misleading at best… ”

    1] That most phenotypic traits are polygenic is so blindingly obvious that no-one with a basic understanding of genetics would contest it.

    The problem is that in adopting your stance you are undermining your statistical arguments against the impossibility of evolution. Figures of 850 billion years is based on assumptions about sequential selection of genes. As you correctly observe if you select for phenotype then there is a wide selection of allelic forms in a single generation.

    2] I would think study of the most polymorphic system in the body (the MHC) is a suitable background to have some insight into questions on population size and allelic forms. For example there are some 60 allelic forms of HLA-B. I would have thought it obvious these allelic forms cannot all be found in a population of 2 and can only be seen in a larger population. The trans-species hypothesis is based around MHC genetics where it is proposed that large range of allelic forms are found in 2 populations are replicated in 2 populations because the range of polymorphism is carried along in the populations that becomes genetically separated. As we argued in our 1990 paper, allelic forms including retroviral insertions in the C4 region of the central MHC of chimps and humans with the A1 B8 DR3 haplotype are consistent with such a model.

    3] That a phenotypic trait can be influenced by multiple loci does nothing to increase the highly restricted possibilites at every locus contained in 2 genome equivalents. To argue anything beyond this is to appeal to miracles which you are of course quite welcome to do.




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    • @pauluc:

      1] That most phenotypic traits are polygenic is so blindingly obvious that no-one with a basic understanding of genetics would contest it.

      So, why did you act like you didn’t know what I was talking about when I was describing the vast phenotypic potential of a breeding pair?

      The problem is that in adopting your stance you are undermining your statistical arguments against the impossibility of evolution.

      How is that? Vast phenotypic potential is not based on the evolution of anything novel within the gene pool at all. Sure, novel mutations do happen all the time, but they aren’t needed or required for marked phenotypic diversity to occur via pre-existing genetic information.

      Figures of 850 billion years is based on assumptions about sequential selection of genes. As you correctly observe if you select for phenotype then there is a wide selection of allelic forms in a single generation.

      I’ve read and re-read this particular comment several times, but I’m still not sure what you’re try to say here? Perhaps you could explain it further?

      2] I would think study of the most polymorphic system in the body (the MHC) is a suitable background to have some insight into questions on population size and allelic forms. For example there are some 60 allelic forms of HLA-B.

      Actually, there are >1600 known allelic forms of HLA-B.

      http://bioinformatics.oxfordjournals.org/content/early/2011/02/07/bioinformatics.btr061.full.pdf

      I would have thought it obvious these allelic forms cannot all be found in a population of 2 and can only be seen in a larger population.

      Yes, that is obvious. These forms were produced by subsequent mutations in the offspring of the original parents.

      Of course, I was never talking about mutant allelic forms like this – which I would have thought was originally obvious and which I have repeatedly pointed out to you in this thread. I was and am talking about variability of phenotypic trait expression. Note, in this line, that MHC functionality is also polygenic.

      Again, the production of sequence differences between alleles happens all the time – more and more commonly as populations increase in size. However, the majority of these mutational differences are near neutral with respect to function with the vast majority of these only affecting the degree of functionality and the vast majority being detrimental or degenerative in nature to one degree or another. Qualitatively novel functionality, while relatively rare, is not realized beyond very very low levels of functional complexity.

      I’m not sure how many times I have to repeat this concept before you will stop mischaracterizing my position and start dealing with what I’m really talking about?

      3] That a phenotypic trait can be influenced by multiple loci does nothing to increase the highly restricted possibilites at every locus contained in 2 genome equivalents. To argue anything beyond this is to appeal to miracles which you are of course quite welcome to do.

      It doesn’t require intelligent design or a Divine miracle to rapidly produce mutated alleles for a particular site in a large population where the functional effects are either quantitative or at very low levels of qualitatively novel functionality. I’m really not sure why you’re even arguing this point? I don’t see how it is at all relevant to what I’ve been saying?

      Sean Pitman
      http://www.DetectingDesign.com




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  36. Professor Kent: When did he tell you this? I have a friend who says he got the idea from Chadwick (I’m not sure whether first-hand or second-hand).

    Okay, looks like my friend heard this, indeed, second-hand, and says that it came from a reliable source during a behind-closed-doors conversation. While EducateTruthers believe any such conversations must become public knowledge if found out about, I feel they are sacrosanct. My friend says he should not have let the cat out of the bag, and likewise I should not have closed the bag to keep the cat crawling about. My apologies to those involved in the conversation.

    Apparently, the notion has gained a lot of traction in private discussion, but it’s clear Sean Pitman would never allow for the possibility of any terrestrial animals surviving outside the ark. So all you faithful SDA academics out there who fear for your jobs, don’t ever breathe a word about this hypothesis. Your fate might resemble those poor critters outside of the ark. Don’t you dare Educate anything other than Truth.




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  37. Sean

    I am in 2 minds as to whether I should just stop thread or give it one more chance. As always I do it because I am concerned that readers here might give credence to your constructions which you insist are scientific rather than the faith positions which I think they are.

    1] Regarding polygenic traits you say;

    “So, why did you act like you didn’t know what I was talking about when I was describing the vast phenotypic potential of a breeding pair?”

    I was just hoping that what you had written was not really what you thought. I have questioned your position that a breeding pair has vast phenotypic potential which I think is unsustainable scientifically but is quite acceptable as a faith position based on a particular reading of the text.

    I have given you references to real studies with data that indicate that 2 animals is unquestionably a non-viable populations in any conservation breeding program which is the best we have in terms of replicating the ark scenario.
    .
    Further I have suggested that doing the math does not allow one to even conceive of vast phenotypic potential on the basis of allelic variation in a population of 2.

    You continue digging the hole by deprecating the role of new mutations and insisting that there is front loaded potential by a mechanism you cannot define in accepted genetic terms.

    “How is that? Vast phenotypic potential is not based on the evolution of anything novel within the gene pool at all. Sure, novel mutations do happen all the time, but they aren’t needed or required for marked phenotypic diversity to occur via pre-existing genetic information.”

    Regarding phenotypic selection and polygenic traits you say

    “I’ve read and re-read this particular comment several times, but I’m still not sure what you’re try to say here? Perhaps you could explain it further?”

    Having raised the issue of polygenic nature of phenotypic traits as an explanation of the vast potential I thought you would be familiar with some of the more foundational concepts in genetics. From your responses I once again seem to be in error. What is the conventional view.

    The current concept of a gene is of a sequence of DNA in the genome that codes for a protein and has associated regulatory elements and non-coding RNA. See for example the review by Gingeras http://www.ncbi.nlm.nih.gov/pubmed/17567989

    The organism at the level of the organelle cellular, organ, or organism is sustained by biochemical pathways and structures that rely on these genes.

    Depending on levels of redundancy loss of a gene may affect the function and result in a particular change in the organism which is recognized by observation grossly biochemically or microscopically. This is often called a trait as in sickle cell trait or phenotype where there is a particular shape of the red cells. Usually this there are multiple characteristics associated with this trait. For Sickle cell disease this is rapid clearance of the red cells from the blood and anaemia. Trouble with red cells in the circulation leading to blocked blood vessels and resistance to malaria infection of the red cells.

    Mendelian traits are those that map to a single gene locus and result in a phenotypic change. Sickle cell is one that maps to a gene coding for part of the haemoglobin molecule.

    Now production of red cells containing haemoglobin red cells is dependent on very many genes. From the genes such as eythropoietin that regulate amount of haemoglobin and red cells that are produced in erythroblasts and progeny cells in the bone marrow to the genes controlling the the proteins and carbohydated structure of the red cell membrane all are related to the red cell physiology and physical characteristics or phenotype.

    Now say a population of people move to the Himalayas or the Andes. They need more red cells. The response will be that those in the population that have the best ability to produce red cells will have better ability to carry oxygen in the presence of low oxygen tension and will have better fitness. This trait of high altitude fitness is unlikely to be a mendelian train but will be a polygenic trait. The initial measure of ability to carry oxygen will have something like a Gaussian distribution. If there is within the population multiple genes with some polymorphism or variability in function even through within that one gene it has minimal overall effect the selection will be on multiple such genes so that the fittest population with the high oxygen carrying phenotype will have a genotype that is has been selected for the phenotype. It is a not a selection of genes one at a time but a simultaneous selection. Allele frequency at multiple loci will be changes within a very short time. Now if one of the people in the population has a new mutation that has better function it will be quickly fixed in the population and carried along with a cluster of more or less useful genes. In other words selection integrated across a large number of genes. To argue about potential sequence space and absolute probabilities is a nonsense.

    This concept I would have thought was familiar to you as even Sanford in his book “Genetic entropy” does accept there is phenotypic rather than genotypic selection (see chapter 4 and his cute Princess and the nucleotide paradox).

    Current attempts to map diseases using genome wide arrays usually show that a disease process is polygenic. I will not go into the complexity of the reason for this in terms of founders and alternate genetic pathways to get to favourable phenotype.

    What Sean is arguing is that things like size and coat colour in Dogs that are clearly polygenic the cis interactions between mjultiple variable genes can compensate for a lack of polymorphism at any genetic locus imposed by a population size of 2.

    If we assume that dog size depends on products of pathways involving 5 genes [in fact this is vastly overestimating it as IGF-1 seems to be the predominant determinant]

    Then in a population of 2 there are maximum of 4 alleles at 20 loci. The possible genotypes assuming absolutely no genetic linkage are then 4^50 = 1024 compared to 20^5 = 3.2 million for a population of 20 with the same level of genetic heterogeneity and allelic variation.

    A population of 2 with complete heterogeneity over 5 loci is not what is seen in extant populations but allowing Seans assumption in any lottery I would take my chance with 3 millions rather than 1000 tickets.

    “Actually, there are >1600 known allelic forms of HLA-B.

    http://bioinformatics.oxfordjournals.org/content/early/2011/02/07/bioinformatics.btr061.full.pdf

    Thanks Sean, of course you know this is based on 4 digit typing which is the genotypic alleles and not the alleles that are serologically defined and correspond to protein sequence changes. As you know 4 digit typing is important in transplantation not because of the amino acid changes or an possible change in fitness or antigen binding by the alpha chain coded by that locus but because of the haplotype effect in that defining genetype predicts distant alleles and sequence variation in that haplotype.

    You then go on to totally confuse the difference between mutation, allelic forms, phenotypes and polygenic traits not least of all because of your private nomenclature and concepts.

    “Yes, that is obvious. These forms were produced by subsequent mutations in the offspring of the original parents.

    Of course, I was never talking about mutant allelic forms like this – which I would have thought was originally obvious and which I have repeatedly pointed out to you in this thread. I was and am talking about variability of phenotypic trait expression. Note, in this line, that MHC functionality is also polygenic.”

    What on earth are you talking about? you seem to be totally confusing a polygenic family and a polygenic trait. The MHC is not a phenotype or a function it is a region of 2 megabase or more contains a family of genes, likely of common origin, in tight linkage dysequilibrium and in which the different loci can be ascribed particular functions.

    HLA-B codes for the alpha chain of class I molecules. This encodes the CDR region of the molecule that is the site that can bind to specific 9-11 amino acid peptides that have a structurally complementary sequence to the class I alpha chain. The high levels of polymorphism at this locus determined the phenotype or what will bind to that molecule and be recognized by a CD8 or cytotoxic T cells. This is the phenotype that is subject to selection; the allele that can recognize a particular pathogen structure.
    Presence of the allele HLA*B57 has a clear survival advantage in HIV infection by recruiting particularly effective CD8 T cells that recognize that class I molecule. The HLA*B5701 haplotype as well as 5702 and 5703 and the related 5801 all have ability to create effective HIV specific CTL that determines the good responder phenotype not because of the associated changes outside the peptide binding groove or nucleotide variation elsewhere in the gene that defines the 4 digit specificity.

    Geneticist do not see any qualitative difference between allelic variation and mutation except in frequency within a population. There is absolutely no reason to conceptualize some distinction between changes in nucleotide sequence because of some imagined ancestory.

    It is up to you to provide a model and evidence if you wish to do so.

    “Again, the production of sequence differences between alleles happens all the time – more and more commonly as populations increase in size. However, the majority of these mutational differences are near neutral with respect to function with the vast majority of these only affecting the degree of functionality and the vast majority being detrimental or degenerative in nature to one degree or another. Qualitatively novel functionality, while relatively rare, is not realized beyond very very low levels of functional complexity.”

    “I’m not sure how many times I have to repeat this concept before you will stop mischaracterizing my position and start dealing with what I’m really talking about?”

    “It doesn’t require intelligent design or a Divine miracle to rapidly produce mutated alleles for a particular site in a large population where the functional effects are either quantitative or at very low levels of qualitatively novel functionality. I’m really not sure why you’re even arguing this point? I don’t see how it is at all relevant to what I’ve been saying?”

    I look forward to reading you PLOS one or PLOS genetics paper on the recognition and importance of mutations with “very very low levels of functional complexity”.




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    • @pauluc:

      mea Culpa. Numbers should be

      Then in a population of 2 there are maximum of 4 alleles at 5 loci. The possible genotypes assuming absolutely no genetic linkage are then 4^5 = 1024 compared to 20^5 = 3.2 million for a population of 20 with the same level of genetic heterogeneity and allelic variation.




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    • I have given you references to real studies with data that indicate that 2 animals is unquestionably a non-viable populations in any conservation breeding program which is the best we have in terms of replicating the ark scenario.

      Not only have modern breeds of dog been based on very limited numbers of breeding pairs, this experiment has been repeated with foxes (see nova video linked above).

      Beyond this, as already explained, your arguments are entirely based on gene pools that have built up large numbers of detrimental mutations. Mammalian gene pools, as with all other slowing producing creatures, are heading downhill. That is why the ancestral parental gene pool was much better off than it is today. You really have no rational basis to argue otherwise beyond your dedication to neo-Darwinism. The evidence of genetic deterioration far faster than natural selection can keep up with it is quite clear for all slowly reproducing creatures.

      Further I have suggested that doing the math does not allow one to even conceive of vast phenotypic potential on the basis of allelic variation in a population of 2.

      Oh really? I’ve yet to see you do much of any math. What math are you talking about that significantly limits the phenotypic trait potential of a breeding pair of wolves? – to a point where similar phenotypic diversity, on a practical level, could not be achieved without a basis in novel mutations?

      You continue digging the hole by deprecating the role of new mutations and insisting that there is front loaded potential by a mechanism you cannot define in accepted genetic terms.

      The role of new mutations is largely detrimental/degenerative – as you should know. I’ve listed examples of such in this same thread. Occasionally, of course, certain benefits do arise by novel mutations, but not beyond very very low levels of functional complexity – as I’ve also explained.

      Having raised the issue of polygenic nature of phenotypic traits as an explanation of the vast potential I thought you would be familiar with some of the more foundational concepts in genetics. From your responses I once again seem to be in error. What is the conventional view.

      The current concept of a gene is of a sequence of DNA in the genome that codes for a protein and has associated regulatory elements and non-coding RNA.

      Pretty good, except for the fact that the modern concept of a “gene” or functional genetic element has been expanded by the discovery that protein-coding genes do not contain the majority of functional information within the genome. “Non-coding genes” occupy the majority of the genome and control the “coding” genes as a blueprint dictates how the bricks and mortar are to be applied in the construction of a building.

      But anyway, I digress…

      The organism at the level of the organelle cellular, organ, or organism is sustained by biochemical pathways and structures that rely on these genes.

      Depending on levels of redundancy loss of a gene may affect the function and result in a particular change in the organism which is recognized by observation grossly biochemically or microscopically. This is often called a trait as in sickle cell trait or phenotype where there is a particular shape of the red cells. Usually this there are multiple characteristics associated with this trait. For Sickle cell disease this is rapid clearance of the red cells from the blood and anaemia. Trouble with red cells in the circulation leading to blocked blood vessels and resistance to malaria infection of the red cells.

      So far so good . . .

      Mendelian traits are those that map to a single gene locus and result in a phenotypic change. Sickle cell is one that maps to a gene coding for part of the haemoglobin molecule.

      Right . . .

      Now production of red cells containing haemoglobin red cells is dependent on very many genes. From the genes such as eythropoietin that regulate amount of haemoglobin and red cells that are produced in erythroblasts and progeny cells in the bone marrow to the genes controlling the proteins and carbohydated structure of the red cell membrane all are related to the red cell physiology and physical characteristics or phenotype.

      That’s right . . .

      Now say a population of people move to the Himalayas or the Andes. They need more red cells. The response will be that those in the population that have the best ability to produce red cells will have better ability to carry oxygen in the presence of low oxygen tension and will have better fitness. This trait of high altitude fitness is unlikely to be a mendelian train but will be a polygenic trait. The initial measure of ability to carry oxygen will have something like a Gaussian distribution. If there is within the population multiple genes with some polymorphism or variability in function even through within that one gene it has minimal overall effect the selection will be on multiple such genes so that the fittest population with the high oxygen carrying phenotype will have a genotype that is has been selected for the phenotype. It is a not a selection of genes one at a time but a simultaneous selection. Allele frequency at multiple loci will be changes within a very short time. Now if one of the people in the population has a new mutation that has better function it will be quickly fixed in the population and carried along with a cluster of more or less useful genes. In other words selection integrated across a large number of genes.

      Also true . . .

      To argue about potential sequence space and absolute probabilities is nonsense.

      How so? How do you determine the odds that any novel system of function, where all of the amino acid residues must work in a specific arrangement with each other, will be realized in a given span of time by random mutations? The fact is that you don’t make this determination at all. You don’t consider the math or the odds at all. You just assume that it happens without considering the level of functional complexity involved with finding novel beneficial sequences in sequence space.

      This concept I would have thought was familiar to you as even Sanford in his book “Genetic entropy” does accept there is phenotypic rather than genotypic selection (see chapter 4 and his cute Princess and the nucleotide paradox).

      Of course this concept is familiar to me. It is a correct concept. There is phenotypic selection that affects the underlying genotype. I’ve already gone into this before with you, if you will recall. Your problem is that you do not consider the level of functional complexity involved. Low-level systems can and do evolve all the time. However, as you consider higher and higher levels of qualitatively novel functional complexity, the evolvability of these higher level systems drops off – exponentially.

      What Sean is arguing is that things like size and coat colour in Dogs that are clearly polygenic the cis interactions between mjultiple variable genes can compensate for a lack of polymorphism at any genetic locus imposed by a population size of 2.

      That’s right.

      If we assume that dog size depends on products of pathways involving 5 genes [in fact this is vastly overestimating it as IGF-1 seems to be the predominant determinant], then in a population of 2 there are maximum of 4 alleles at 5 loci. The possible genotypes assuming absolutely no genetic linkage are then 4^5 = 1024 compared to 20^5 = 3.2 million for a population of 20 with the same level of genetic heterogeneity and allelic variation.

      A population of 2 with complete heterogeneity over 5 loci is not what is seen in extant populations; but allowing Sean’s assumption in any lottery I would take my chance with 3 millions rather than 1000 tickets.

      As already noted, size in dogs is primarily controlled by six genetic regions and dozens of genes with lesser influence (compared to humans were height is governed by >200 genes). The sequence space is 4^6 = 4096 based on just these six primary controls for size alone (not counting the dozens of other genes that are involved in more minor ways here). This seems like adequate control for this particular trait. How much more control over size one would want I don’t know?

      You seem to be totally confusing a polygenic family and a polygenic trait.

      How is that?

      The MHC is not a phenotype or a function. It is a region of 2 megabase or more contains a family of genes, likely of common origin, in tight linkage dysequilibrium and in which the different loci can be ascribed particular functions.

      The Major Histocompatibility Complex (MHC) is indeed a collection of different types of proteins that are collectively involved with appropriate immune system function – a polygenic trait. Are the different elements of the MHC complex individually selectable? Certainly . . .

      HLA-B codes for the alpha chain of class I molecules. This encodes the CDR region of the molecule that is the site that can bind to specific 9-11 amino acid peptides that have a structurally complementary sequence to the class I alpha chain. The high levels of polymorphism at this locus determined the phenotype or what will bind to that molecule and be recognized by a CD8 or cytotoxic T cells. This is the phenotype that is subject to selection; the allele that can recognize a particular pathogen structure.

      Yes . . .

      Presence of the allele HLA*B57 has a clear survival advantage in HIV infection by recruiting particularly effective CD8 T cells that recognize that class I molecule. The HLA*B5701 haplotype as well as 5702 and 5703 and the related 5801 all have ability to create effective HIV specific CTL that determines the good responder phenotype not because of the associated changes outside the peptide binding groove or nucleotide variation elsewhere in the gene that defines the 4 digit specificity.

      Right . . .

      Geneticist do not see any qualitative difference between allelic variation and mutation except in frequency within a population. There is absolutely no reason to conceptualize some distinction between changes in nucleotide sequence because of some imagined ancestory. It is up to you to provide a model and evidence if you wish to do so.

      Again, I’m not sure what you’re your main point is here? Of course mutations produce allelic variations! Where have I even suggested otherwise? In fact, some systems, especially immune systems, are based on the programmed production of genetic variations to produce a huge variety of antibodies (before non-self antigens are even encountered).

      It is just that random mutations do not produce qualitatively novel systems of function beyond very low levels of functional complexity is all. That’s the main point here. This is the point that you’re simply not addressing in any of your responses thus far.

      Also, what do any of your arguments have to do with my statement that the current phenotypic variety of animals is largely based on pre-programmed or “front-loaded” information? – that many current allelic options are detrimental or degenerative in nature? – or that there are no examples of qualitatively novel functionality beyond very low levels of functional complexity arising by RM/NS?

      I look forward to reading you PLOS one or PLOS genetics paper on the recognition and importance of mutations with “very very low levels of functional complexity”.

      I do not dispute the impact or even the importance of mutations with low-level functional effects. That’s not even in question here. Such mutational effects can and do happen – very commonly in fact in larger populations. That is why it doesn’t require long periods of time for such mutations to be realized. What cannot be explained by you or anyone else coming from a Neo-Darwinian perspective is the origin of qualitatively novel systems of function that require a minimum of more than 1000 specifically arranged amino acid residues.

      Sean Pitman
      http://www.DetectingDesign.com




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      • @Sean Pitman:
        I concede that I must be too dense to see that you have given an adequate explanation for the problem I think there is or that I have failed to adequately describe the problem. Either way maybe I can summarize your framework for canine ancestory.

        1] Wolves domestic dogs coyotes and jackals (genus canis) are derived from a single pair of animals roughly corresponding to the canidae family around 2000 BC according to a timeframe defined by the writings of EG White.
        http://www.ministrymagazine.org/archive/1984/April/ellen-g.-white-and-biblical-chronology

        2] Other members of this group including African Hunting Dogs, Jackal, Bush dog are also derived from this pair.

        3] The foxes of the genus vulpini are also derived from this pair.

        4] The racoon dog(Nyctereutes) and bat eared fox (Otocyn) are also derived from this pair.

        5] Other species within the suborder caniformia such as bear (ursidae) red pandas (alluridae) Skinks (Mephitidae) Badgers weasels and otters (mustelidae) racoons (procyonidae) are derived from other pairs of animals.

        6] All the genetic diversity in the canidae at present derive from this pair of animals.

        7] The highly polymorphic MHC genes (DLA or dog leukocyte antigens) are derived from this pair.

        8] The SNPs found in the derivative populations must be present in the original pair or derive from subsequent mutations.

        9] Since only 2 alleles can occur in any animal there can be only 4 alleles at any locus in the starting population.

        10] Only 4 SNPs defining alleles can be present in the original starting population. Additional SNP in any derivative population or species must have arisen during speciation.

        11] In the canine DLA there is significant polymorphism of amino acids in the peptide binding regions of class II alleles
        http://www.ncbi.nlm.nih.gov/pubmed/12366782
        http://www.ncbi.nlm.nih.gov/pubmed/12074709
        http://www.ncbi.nlm.nih.gov/pubmed/17445218

        12] as shown in tables 2, 4, and 6 of reference 1 above only 4 of the possible alleles can occur in the starting population. All the rest are new and novel changes in amino acid sequence.

        13] New mutations resulted in the new and novel functional peptide binding MHC molecules must have arisen post flood by mutation and cannot have been in the original population.

        14] The repertoire of peptide binding and breadth or immune responses was expanded by naturalistic random mutational events. Or there was miraculous intervention expanding the repertoire and ability to respond to new epitopes.

        I hope in these points I have not mischaracterized your position




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  38. Sean Pitman: Almost all examples of the evolution of “new” functional traits or alleles are based on the disruption or loss of a pre-existing trait or functional system. And, those occasional examples of evolution where qualitatively novel functional systems are produced in observable time are all at very very low levels of functional complexity (requiring a minimum of no more than a few hundred specifically arranged amino acid residues).

    Lymphostatin is a pernicious toxin made by enteropathogenic Escherichia coli, which colonizes the intestine of vertebrate animals. In humans, E. coli causes the majority of the 1 billion cases of diarrhea each year, resulting in 3-4 million deaths. This particular toxin is essential for bacterial adhesion, intestinal colonization, immunosuppression, and disruption of gut epithelial barrier function. It occurs in pathogenic strains of E. coli, but not in the harmless, non-pathogenic strains. It also shows the strongest statistical association with infectious diarrhea. The toxin itself is approximately 3,258 amino acid residues in length (or a few residues less). And this toxin is but one of a suite of virulence factors that work together to promote colonization of pathogenic bacteria within the intestine.

    Clostridium difficile toxins A and B are also nasty virulence factors that function similarly in enteropathogenesis. These toxins are approximately 2,772 and 2,430 amino acids, respectively. As for E. coli and lymphostatin, the pathogenecity of C. difficile and effectiveness of toxins A and B are modulated by additional virulence factors.

    If qualitatively novel functional systems cannot evolve beyond a few hundred specifically arranged amino acid residues, then where did these enormous toxins, and the other virulence factors that act in concert with them, come from? You have told us repeatedly that nothing beyond 1,000 fsaars (fairly specified amino acid residues) can evolve within trillions upon trillions of years. So did God create these highly virulent toxins to function as they do today in harming humans and other vertebrates, or did they evolve as qualitatively novel functional systems?




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    • @Professor Kent:

      Lymphostatin is a pernicious toxin made by enteropathogenic Escherichia coli, which colonizes the intestine of vertebrate animals. In humans, E. coli causes the majority of the 1 billion cases of diarrhea each year, resulting in 3-4 million deaths. This particular toxin is essential for bacterial adhesion, intestinal colonization, immunosuppression, and disruption of gut epithelial barrier function. It occurs in pathogenic strains of E. coli, but not in the harmless, non-pathogenic strains. It also shows the strongest statistical association with infectious diarrhea. The toxin itself is approximately 3,258 amino acid residues in length (or a few residues less). And this toxin is but one of a suite of virulence factors that work together to promote colonization of pathogenic bacteria within the intestine.

      The lymphostatin toxin consistent of three enzymatic motifs (a glucosyltransferase, a protease, and an aminotransferase motif). These motifs are not required to work together at the same time, but in sequence – as in an cascading-type enzymatic system. That means that there is little required specificity of their arrangement relative to each other. In other words, the lymphostatin toxin is not like a flagellar motility system where all the parts are required to be in a specific location at the same time in order for the motility function of the flagellar machine to work in a beneficial manner.

      Also, from what did the lymphostatin toxin evolve? Consider that the bacterial TTSS toxin injector system, which requires the services of 10 proteins and several thousand specifically arranged amino acid residues, is a truncated version of the flagellar motility system in bacteria. In other words, the TTSS system has been shown to have evolved from the fully formed bacterial flagellum. Its evolution is therefore based on a loss of parts from a pre-existing system. It is, of course, far far easier to lose parts than it is to gain parts to produce a functional system.

      Clostridium difficile toxins A and B are also nasty virulence factors that function similarly in enteropathogenesis. These toxins are approximately 2,772 and 2,430 amino acids, respectively. As for E. coli and lymphostatin, the pathogenecity of C. difficile and effectiveness of toxins A and B are modulated by additional virulence factors.

      C. diff toxins A and B are similar in form and function. They are also comprised of multiple motifs which are not required to work at the same time, but work in sequence – as with enzymatic cascades. For instance, there are 1) Domains for receptor binding, the first essential step in the process of cell entry. 2) After receptor-mediated endocytosis and membrane translocation, only the N-terminal domain of TcdB exits the endosome and gains access to substrates. 3) Once this occurs, TcdB glucosylates the GTPase RhoA and two other GTPases, Rac and Cdc42, via transfer of a sugar moiety to Thr-37 of the GTPase with UDP-glucose as a cosubstrate. The same thing happens with TcdA.

      In short, TcdA and TcdB act as glucosyltransferases, capable of inactivating small GTPases within the cell. This system functions in a sequential manner. It is therefore no more complex than its most complex individual part or functional element in the stepwise process. Also, you’ve not determined the likely minimum size for any of the domains in this cascading system. The current size is not the minimum size that would actually do the job.

      If qualitatively novel functional systems cannot evolve beyond a few hundred specifically arranged amino acid residues, then where did these enormous toxins, and the other virulence factors that act in concert with them, come from? You have told us repeatedly that nothing beyond 1,000 fsaars (fairly specified amino acid residues) can evolve within trillions upon trillions of years. So did God create these highly virulent toxins to function as they do today in harming humans and other vertebrates, or did they evolve as qualitatively novel functional systems?

      Beyond the fact that these toxins are not examples of “evolution in action” (at least not as far as I’m aware), they are not highly specified in their residue sequences nor do their current sizes reflect the minimum size requirement needed to produce their functionality. Also, you don’t know if these toxins are the result of a loss of functionality from some pre-existing system – as in the case of the TTSS toxin injector system.

      In other words, your examples fail to explain how RM/NS can likely find novel systems of function at higher levels of functional complexity in a reasonable amount of time . . .

      Sean Pitman
      http://www.DetectingDesign.com




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  39. Sean

    You have offered as support for your bold assertion that a a breeding pair has vast phenotypic potential you suggest

    “As far as the potential for a single breeding pair to produce a vast array of dog phenotypes in short order, consider watching a Nova documentary entitled, “Dogs Decoded”. Notice the part at about the 40 minute mark where foxes were bread for tameness. Very quickly, in just a handful of generations, this trait was significantly enhanced.”

    ……
    “So, there you have it . . . starting with a very small population very significant phenotypic effects can be realized, based on pre-existing functional information, without the need for additional mutations . . .”

    I am not sure if you just dont care about the veracity of the facts underpinning you statements or if you were aware of them and dont let them confuse you or just assumed that what you think cannot be wrong. From following this site over the last 3 years I think they are all equally probable.

    Simply googling the Russian fox domestication experiment you will find another video with some details

    The description of the experiment
    It was started by a researcher at the Novosibirsk Institute of Biology named Dr. Belyaev in the Soviet days, during which he had to keep it disguised as a fur farm since the Soviet administration perceived genetic studies like his as a sort of pseudoscience and did not permit it. Starting with a few hundred foxes obtained from Estonia, he selected the ones that were most friendly and most hostile toward humans for continued breeding.

    This wasn’t just capturing wild animals and trying to tame them, it was an attempt to artificially re-create the evolutionary process of domestication in few generations, a process which took thousands of years for other animals like that from wolves to dogs.

    Several hundred foxes!!
    several hundred is not a small number
    Several hundred is not a very small number
    Several hundred is not a breeding pair

    My point from the very beginning of this thread has been that a successful founding population of a breeding pair is a miracle. I have never contested that phenotypic variation can be selected from a population with variability at multiple loci. This is simply selective breeding whether natural or directed which was Darwins starting point for his theory of origins. What is the issue is that a breeding pair is not viable except by a miracles.

    To populate the world and generate a large number of related species from a breeding pair is a miracles.

    Look up authors Trut LN, Kukekova A on pubmed and look at this review of the experiment within context as publis

    http://www.ncbi.nlm.nih.gov/pubmed/19260016

    Gives the peer reviewed literature on the derivation of the domesticated foxes

    “Altogether several thousands foxes were tested at these fur farms. In the behavioral test, the experimenter approached the home cage, tried to open it and observed the expression of the response. This observational test was highly reproducible. According to its results about 10% of farm foxes displayed the responses of wild type very weakly or not at all (Fig. 3C). Such foxes (100 females and 30 males) were chosen from different farm bred populations as the initial parental generation for selection for tolerance of human or docility, then for tameability. The fox population was outbreeding.”

    Selection for a train from several thousand is not derivation from a breeding pair.
    100 females and 30 males is not derivation from a breeding pair.

    Why am I going on and on about this. I think like Prof Kent we must be honest with the scientific data. We all have faith in God and are happy to admit that the incarnation of God in Jesus is the core of Christianity and cannot be construed as anything but a miracle. If you feel compelled to a particular literal interpretation that cannot be logically supported except by miracles surely the honest thing to do is simply admit the miracles. Admittedly this may be construed as a God of the gaps approach but surely it is appropriate to have the courage of your convictions and honestly follow a literalistic hermaneutic wherever it may lead.




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    • @pauluc:

      This wasn’t just capturing wild animals and trying to tame them, it was an attempt to artificially re-create the evolutionary process of domestication in few generations, a process which took thousands of years for other animals like that from wolves to dogs.

      That’s right. It demonstrated a genetic basis for domestication as well as for a link with changes in physical appearance – similar to what is seen in domesticated dogs.

      Several hundred foxes!!
      several hundred is not a small number
      Several hundred is not a very small number
      Several hundred is not a breeding pair

      The experiment started with 130 foxes – 30
      male foxes and 100 vixens, most of them from a
      commercial fur farm in Estonia.

      http://www.hum.utah.edu/~bbenham/2510%20Spring%2009/Behavior%20Genetics/Farm-Fox%20Experiment.pdf

      While this isn’t as small as a single breeding pair by any means, it is still a pretty small population. There is no reason to believe that similar results could not be achieved with an even smaller population – even a single breeding pair given that there are numerous examples of single breeding pairs producing large viable populations (see below).

      My point from the very beginning of this thread has been that a successful founding population of a breeding pair is a miracle.

      Not true. There are many modern day examples of viable populations being produced from single breeding pairs.

      For example, The endangered Chatham Island Black Robin Petroica traversi was brought back from the brink of extinction starting with a single breeding pair. (http://www.birdlife.org/news/news/2002/10/690.html)

      The Isle Royale gray wolf population is a small population of wolves that inhabits an island in Lake Superior off the shore of Minnesota. The population was founded by a single breeding pair in 1950 (Peterson et al. 1998). Previous genetic research found population heterozygosity levels only half that observed in the mainland progenitor (Wayne et al. 1991).

      Populations of the Bald Eagle in North Carolina have increased from a single breeding pair in 1984 to over 70 breeding pairs in 2005. (http://www.basic.ncsu.edu/eaglecam/)

      The White Tern population on Oahu has increased from a single breeding pair in 1961 to approximately 250 pairs in 2002, a growth rate of 14% per year.

      The Ringneck Pheasant are a native of Asia and were imported to the United States in the 1880’s. It is thought that the escaping of a single breeding pair began the population of these birds in the U.S.

      The colony of African penguins (Simon’s Town) has grown to nearly 3,000 from a single breeding pair in 1982.

      The golden hamster is a similarly bottlenecked species, with the vast majority descended from a single litter found in the Syrian desert around 1930.

      Less extreme examples include the northern elephant seal, whose population fell to about 30 in the 1890s, but now number in the hundreds of thousands.

      I have never contested that phenotypic variation can be selected from a population with variability at multiple loci. This is simply selective breeding whether natural or directed which was Darwins starting point for his theory of origins. What is the issue is that a breeding pair is not viable except by a miracles.

      Oh please. If there are many modern day examples of the success of populations that were known to have begun from a single breeding pair, how is it at all unreasonable to suggest that a breeding pair with far less genomic damage to begin with could do the same thing?

      To populate the world and generate a large number of related species from a breeding pair is a miracle.

      How so? Where is the limiting factor?

      Sean Pitman
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        “How so? Where is the limiting factor?”

        I would not suggest that generation of a population of extreme homozygosity that depends on a continuing intervention program for survival is a population of “vast phenotypic potential”. In the absence of peer reviewed publication on this please just read the documents on the NZ conservation web site which I would consider the best source.

        http://www.doc.govt.nz/conservation/native-animals/birds/land-birds/black-robin/facts/

        Under the tab threats it reads

        “Predation

        By 1900, the introduction of rats and cats following human settlement had wiped out the birds from everywhere apart from Little Mangere Island. The accidental introduction of predators to the two islands where it presently survives is still a threat.

        Disease

        All black robins have the same weaknesses and strengths, stemming from the fact they have similar DNA. This means that a single disease could kill them. ”

        This is an artificial and fragile population that cannot survive in the wild without human intervention.

        Who intervened for the pairs from the ark. They either miraculously were protected by God along the way in some divine conservation program or had some magical properties conferred from the beginning that do not now exist. Either way I would call that a miracle.

        That you cannot see that population size matters is surprising for someone with a medical degree and I presume at least minimal accompanying training in genetics. If you do not believe what you learned then there is no hope I will effect any change in your view.




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        • @pauluc:

          I would not suggest that generation of a population of extreme homozygosity that depends on a continuing intervention program for survival is a population of “vast phenotypic potential”…

          Disease

          All black robins have the same weaknesses and strengths, stemming from the fact they have similar DNA. This means that a single disease could kill them. ”

          This is an artificial and fragile population that cannot survive in the wild without human intervention.

          You failed to mention the many other examples I gave you of single breeding pairs successfully reproducing in the wild – establishing healthy populations that have grown and survived over long periods of time without significant human intervention.

          Now, I will say, as I’ve originally said, that extreme population bottlenecks do indeed raise the risk for various diseases. Why is that? Because of the increased risk of expression of detrimental recessive traits and the lack of alleles that have evolved along with various infectious organisms that may attack a given population.

          For example, Europeans were resistant to many diseases that devastated the American Indians of the New World. This is because Europeans had evolved resistance to these diseases through repeated exposure (due to close association with domesticated animals) where these same diseases had not evolved in the New World because of a lack of close exposure to domestic animals.

          This was not the situation right after the Flood. Such diseases had not yet evolved to current levels of virulence and the gene pools of animals had not yet devolved to their current levels of degeneration.

          It is for this reason that the extremes of allelic variation that we see in some gene pools today simply wasn’t needed in order for a single breeding pair to produce a large, viable, healthy population of offspring. Even today with thousand of years of the build up of additional detrimental mutations such situations are not unheard of. I’ve given you numerous examples of something you said would be impossible.

          Who intervened for the pairs from the ark. They either miraculously were protected by God along the way in some divine conservation program or had some magical properties conferred from the beginning that do not now exist. Either way I would call that a miracle.

          As already noted, it is no miracle that their gene pools had far less detrimental/degenerative mutations than exist today in all slowly reproducing gene pools. It is no miracle that disease-causing organisms had not yet evolved their current level of virulence. It is no miracle that there are numerous modern day examples of single breeding pairs producing healthy populations in the wild – despite having inferior genetics compared to their ancestors.

          Where then is the basis for your argument?

          That you cannot see that population size matters is surprising for someone with a medical degree and I presume at least minimal accompanying training in genetics. If you do not believe what you learned then there is no hope I will effect any change in your view.

          You misrepresent me yet again.

          Where did I say that population size doesn’t matter? Hmmmm? I’ve said just the opposite many times in this very thread. Population size definitively matters. However, it didn’t matter nearly as much right after the Flood as it does today – for the reasons I’ve presented to you many times now.

          Your problem is that you reject the otherwise obvious reality of genetic deterioration over time for slowly reproducing animals. You also reject the obvious limitations to the creative potential of RM/NS. As far as I can tell, I see no other reason for your inability to recognize concept that a single breeding pair could easily have given rise to all the canids, and their significant allelic diversity, that we see today.

          I ask again, where is the limiting factor?

          Sean Pitman
          http://www.DetectingDesign.com




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  40. Sean Pitman: The lymphostatin toxin consistent of three enzymatic motifs…These motifs are not required to work together at the same time, but in sequence…It is therefore no more complex than its most complex individual part or functional element in the stepwise process. Also, you’ve not determined the likely minimum size for any of the domains in this cascading system. The current size is not the minimum size that would actually do the job…your examples fail to explain how RM/NS can likely find novel systems of function at higher levels of functional complexity in a reasonable amount of time . . .

    If you’re going to introduce sequentiality within a system as a criterion that conveniently skirts your 1000 amino acid limit for qualitatively novel systems of function, then you’ve changed the rules of your own game. Sequentiality is an attribute of all complex traits. You’re right that a trait is only the sum of its components, but natural selection can favor the origin of a qualitatitvely new trait only if it is acting on the trait itself, not its parts. If you’re going to stick with your fantastic claim, then you can’t disqualify any given “system” because the “system” is comprised of individual components. What kind of logic is this?

    All your Fsaar Side theory really claims is that a single mutation resulting in a >1000 amino acid change within a single motif of a single protein cannot result in a qualitatively new function in a single step or generation. No big deal. You’ve essentially admitted that your theory says nothing about the accumulation of smaller amino acid changes across multiple motifs and/or multiple proteins over multiple generations that collectively exceed a >1000 amino acid change in a system.

    Regardless whether the toxins I’ve described have components that act sequentially, these are very large systems that serve a pernicious role which seems highly unlikely to be a part of the original creation. These toxins most certainly constitute valid examples of complex, qualitatively new traits that have evolved.




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    • @Professor Kent:

      “The lymphostatin toxin consistent of three enzymatic motifs…These motifs are not required to work together at the same time, but in sequence.” – Sean Pitman

      If you’re going to introduce sequentiality within a system as a criterion that conveniently skirts your 1000 amino acid limit for qualitatively novel systems of function, then you’ve changed the rules of your own game.

      The rules have been the same all along. Do you not understand, after all this time, the concept of specificity? that systems where all residues must be specifically arranged relative to all of the other residues are at much higher levels of functional complexity compared to systems of similar size that do not have this specificity requirement?

      Do you really not think that I’ve dealt with your examples many many times before in discussions like this? that I’m not aware of vary large proteins and intricate enzymatic cascades? The function of such systems simply isn’t dependent upon the specific arrangement of all parts in 3D space.

      As I’ve explained to you before, at least a couple times now, these enzymatic systems are not like fully specified systems – such as the falgellar motility system or ATPsynthase where all of the proteins and amino acid residues must be specifically arranged in space for the system to work. The minimum size of sequence space needed to contain such systems is much much larger than the minimum size needed to contain non-specified systems.

      Sequentiality is an attribute of all complex traits… If you’re going to stick with your fantastic claim, then you can’t disqualify any given “system” because the “system” is comprised of individual components. What kind of logic is this?

      Specificity of part arrangement is not an attribute of all systems.

      All your Fsaar Side theory really claims is that a single mutation resulting in a >1000 amino acid change within a single motif of a single protein cannot result in a qualitatively new function in a single step or generation.

      Not true. No mutation or series of mutations of any kind or size over any period of time this size of a practical eternity of time can produce any qualitatively novel system of function that requires a minimum of 1000 specifically arranged amino acid residues… where all of the residues must have specifically coded positions relative to all the other residues in the system for the system to work.

      No such system has been observed to evolve. Your examples are not examples of observable evolution in action and they do not require a specific arrangement of all parts relative to all other parts within the system.

      Regardless whether the toxins I’ve described have components that act sequentially, these are very large systems that serve a pernicious role which seems highly unlikely to be a part of the original creation. These toxins most certainly constitute valid examples of complex, qualitatively new traits that have evolved.

      They are not examples of observed evolution and you have no idea from what they evolved? As already noted, fully specified systems at much higher levels of functional complexity have been observed to evolve, or rather devolve, from systems at even higher levels of functional complexity – like the TTSS toxin injector system devolving from the flagellar motility system.

      The potential evolution of most toxins, via RM/NS really isn’t as complex as you imagine. There are many other much more complex systems, such as the mechanism of the HIV virus (the cause of AIDS), that are much harder to explain without any origin in design – which then seems to have degenerated from its original purpose over time (as with the case of the TTSS system).

      Sean Pitman
      http://www.DetectingDesign.com




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  41. Sean Pitman: [On descendents from a single pair or litter] For example, The endangered Chatham Island Black Robin…the Bald Eagle in North Carolina…The White Tern population on Oahu….Ringneck Pheasant…imported to the United States…golden hamster…

    You’re overstating the relevance of these examples. We can rest assured that the breeding metapopulations of Bald Eagles in North Carolina and White Terns on Oahu, for example, had genetic input from individuals of other metapopulations joining them. Further, for every example that you can find of a species recovering from the genetic bottleneck of one pair, there are thousands of species reaching the same point that failed and became extinct.

    Anyone having a background in biology recognizes the validity of Pauluc’s concerns: genetic variation is HIGHLY CONSTRAINED with a starting point of two individuals, so much so that species extinction in nature becomes a high probability. Surely you can concede this. Genetic variability is critical for populations to persist in an ever-changing world.




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    • @Professor Kent:

      You’re overstating the relevance of these examples. We can rest assured that the breeding metapopulations of Bald Eagles in North Carolina and White Terns on Oahu, for example, had genetic input from individuals of other metapopulations joining them.

      Oh really? We can “rest assured” upon what basis? Are you equally confident for all of the cases I’ve presented? I suppose that Ringneck Pheasants just fly in from Asia on a regular basis?

      Further, for every example that you can find of a species recovering from the genetic bottleneck of one pair, there are thousands of species reaching the same point that failed and became extinct.

      I agree. Things are much more difficult now than they were right after the Flood. There are far more detrimental mutations in all gene pools and infectious elements are far more virulent.

      Anyone having a background in biology recognizes the validity of Pauluc’s concerns: genetic variation is HIGHLY CONSTRAINED with a starting point of two individuals, so much so that species extinction in nature becomes a high probability. Surely you can concede this. Genetic variability is critical for populations to persist in an ever-changing world.

      In this modern world, yes. Right after the Flood, no.

      Sean Pitman
      http://www.DetectingDesign.com




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  42. @ Sean Pitman – what happened to my post about insecticidal toxins, including the Make Catepillars Floppy (Mcf) toxin? Was it too difficult to explain within your 1000 fsaar threshold?

    This story is too remarkable to dismiss, so I’ll expand on it. Two genera of Gram-negative bacteria form symbiotic relationships with entemopathogenic (insect-eating) nematodes. The bacteria infect the gut of a juvenile nematode (a worm), which seeks out its prey: insect larvae within the soil. The nematode then penetrates the insect larvae, migrates to the hemocoel, and transfers the baceteria to the hemocoel where they can evade the insect’s immune response. The bacteria releases toxins to kill the insect, rendering the insect carcass a delightful nutrient soup for the bacteria to feast upon. The nematode then feasts on the bacteria and reproduces by laying eggs for three generations. Female nematodes of the fourth generation allow the larve to develop internally, which kills the mother (ouch!), but not until after the juveniles have acquired bacteria in their gut. Finally, the newly infectious juvenile nematodes exit the dead insect by the thousands. If you’ve read this far, you’ll surely agree with me that this entire predatory system orchestrated by a ton of gene products is PDD — pretty darned disgusting.

    And the story gets worse: one species of nematode with these bacteria appears to have acquired a taste for humans! I’ll spare you the details…

    So how did this horrific predatory symbiosis between nematode and bacteria come about? Did God create these organisms with this capacity? If not, and the system evolved, how complex is this evolved system?

    The insect prey itself has a complex humoral and cellular immune response by which it defends itself. To overcome this, the bacteria deploy a remarkably complex set of proteins to evade the insect host’s immune response. The bacteria then secrete a host of toxins and toxic secondary metabolites to destroy the insect. When the genome sequence of one of these bacterial species was published, it was found to encode more toxins than any other known bacterial genome.

    One highly unique toxin class in particular, the Makes Catepillars Floppy toxin (Mcf), has a size of close to 3,000 amino acids. The Mcf1 toxin contains one 900-amino acid region alone with no similarity to other proteins in the database. (Don’t you just love the name of this toxin?)

    Another toxin group produced by these bacteria, known as “toxin complexes,” has now been found to be widespread among bacteria, including those not associated with insects. The insecticidal toxin complex is comprised of four subunits, at least three of which must be present to cause toxicity. Collectively, the complexes exceed 9,000 amino acids (wow!)and show very limited homology to other known proteins. The four subunits vary somewhat among different bacteria, and achieve fixation within a species only when they confer an advantage in securing their specific nutritional needs through toxicity.

    Collectively, these massive proteins, plus numerous others I have not described, act in concert to kill animals. That’s what they do. If this is a qualitatively new function that the original bacteria in Eden lacked, then we need to think about how this highly complex killing trait evolved. If Sean wants to insist that the entire suite of toxins is no more complex than any one part, I think his argument fails. If he wants to insist that novel beneficial traits that exceed 1,000 amino acids cannot evolve within trillions upon trillions of years, I think he’s hitched himself to a very dubious argument (to put it politely).




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  43. Sean,

    Your insistence that dogs offer a representative case for rapid speciation falls short on many grounds.

    First, while you have claimed repeatedly that domestic dogs have evolved into multiple species, not a single mammalogist or taxonomist agrees with you, as I have pointed out. Actually, domestic dogs aren’t even considered to be a distinct species. They are considered but one of many subspecies of the gray wolf, Canis lupus. That’s right. They’re nothing more than a subspecies.

    Second, while you adroitly point out that most of the hundreds of breeds have evolved in the past 300 years, domestic dogs have been around since well before Christ–more than 2,000 years ago–and have yet to evolve into a distinct species, much less multiple species.

    Third, domesticated dogs show more behavioral and morphological variation than any other land mammal. In spite of this remarkable variation, they have yet to evolve into a distinct species, much less multiple species.

    Fourth, if the dogs have failed to speciate in 2,000+ years, this makes the argument that other major taxonomic groups could have evolved in the 4,000 years since the flood even less likely. I’m speaking, for example, of the 400 species of Plethodontid salamanders, 300 species of hummingbirds, 500 species of tyranid flycatchers, and 300 species of ovenbirds/woodcreepers, each of which presumably originated from a single pair of individuals just 4,000 years ago.

    Finally, I’m amused by what criteria you use to declare the multpiple breeds of dogs to be distinct species. You have cavalierly dismissed all recognized species concepts to suggest that fewer species exist today than professional taxonomists hold (which helps you counter the need for extreme rates of speciation required by the animal groups listed above). Instead, you cling to your own private criterion that species are defined as gene pools with qualitatively unique systems that require a minimum of at least 1,000 specifically arranged amino acid residues. Can you please give us examples of the unique systems in dogs that meet your criterion for species? You’ve also made the flabergasting suggestion that contemporary humans comprise more than one species. Again, what qualitatively unique systems differentiate the modern human species? You’ve certainly piqued my interest, Dr. Pitman.

    I’m afraid your arguments for more species or fewer species vary with whatever faith-based point you wish to make. I suggest you admit to your faith-based interpretations and find more consistency in your explanations of difficult-to-reconcile facts.




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    • @Professor Kent:

      Your insistence that dogs offer a representative case for rapid speciation falls short on many grounds.

      I never made this claim. What I said is that there are cases of plants and animals being classified as different “species” which have less genetic diversity than can be seen between different groups of modern humans and even dogs.

      First, while you have claimed repeatedly that domestic dogs have evolved into multiple species, not a single mammalogist or taxonomist agrees with you, as I have pointed out.

      Again, I’ve never made this claim. I’ve specifically claimed that most modern breeds of dog were developed within the last few hundred years.

      I’ve also noted that the species concept is based on subjective elements.

      Actually, domestic dogs aren’t even considered to be a distinct species. They are considered but one of many subspecies of the gray wolf, Canis lupus. That’s right. They’re nothing more than a subspecies.

      It depends who you’re reading. Some do indeed classify domestic dogs as distinct species compared to other canids… which only highlights my point as to the subjective nature of the species concept.

      Second, while you adroitly point out that most of the hundreds of breeds have evolved in the past 300 years, domestic dogs have been around since well before Christ–more than 2,000 years ago–and have yet to evolve into a distinct species, much less multiple species.

      Again, it depends upon who you’re talking to.

      Third, domesticated dogs show more behavioral and morphological variation than any other land mammal. In spite of this remarkable variation, they have yet to evolve into a distinct species, much less multiple species.

      Again, it depends upon who you’re talking to and your chosen definition of “species”.

      Fourth, if the dogs have failed to speciate in 2,000+ years, this makes the argument that other major taxonomic groups could have evolved in the 4,000 years since the flood even less likely. I’m speaking, for example, of the 400 species of Plethodontid salamanders, 300 species of hummingbirds, 500 species of tyranid flycatchers, and 300 species of ovenbirds/woodcreepers, each of which presumably originated from a single pair of individuals just 4,000 years ago.

      Again, it all depends upon how you choose to defined a “species” – which is quite different for different people.

      Sean Pitman
      http://www.DetectingDesign.com




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  44. Professor Kent:Actually, domestic dogs aren’t even considered to be a distinct species. They are considered but one of many subspecies of the gray wolf, Canis lupus. That’s right. They’re nothing more than a subspecies.

    Some authorities consider domestic dogs to be specifically distinct (Canis familiaris) rather than a subspecies of the wolf (Canis lupus familiaris). The vonHoldt et al. 2010 paper published in Nature, for example, lists it as a distinct species, yet shows an unresolved polytomy with the coyote and wolf in the phylograms of Fig. 1. The exact status doesn’t really matter. The point remains that domestic dogs as a group have not speciated. Genetic differentiation among the hundreds of different breeds remains very shallow.




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    • @Professor Kent:

      For years, the domestic dog was classified by scientists as a distinct species, Canis familiaris. However, many modern scientists have reclassified the domestic dog as Canis lupus familiaris, a subspecies of the wolf rather than a separate species.

      However, there is not universal agreement here. Some scientists still classify domesticated dogs as a distinct species. It all depends upon what criteria one chooses to use. The ability to interbreed and produce viable fertile offspring isn’t consistent. Neither are genetic Hamming distances consistent. Nothing is consistent or definitive when it comes to defining a “species” in modern science.

      Thank you again for highlighting my point for me.

      Sean Pitman
      http://www.DetectingDesign.com




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  45. Sean&#032Pitman: What I said is that there are cases of plants and animals being classified as different “species” which have less genetic diversity than can be seen between different groups of modern humans and even dogs.

    Such as? Cite some examples in which you are comparing apples with apples (the same DNA markers), not apples with oranges (different DNA markers). And while you’re doing your homework, consider coalescence theory to understand one factor that might influence genetic divergence.

    Sean&#032Pitman: Again, it all depends upon how you choose to defined a “species” – which is quite different for different people.

    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.

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




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    • @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
      http://www.DetectingDesign.com




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  46. Sean Pitman: This was not the situation right after the Flood. Such diseases had not yet evolved to current levels of virulence and the gene pools of animals had not yet devolved to their current levels of degeneration.

    How do you know this? If advanced predators like the poisonous snakes that struck down the Israelites in the desert had already evolved, surely a broad assortment of diseases had also evolved. On the flip side of the coin, immune responses to protect against disease are surely more evolved today than they were back then.




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    • @Professor Kent:

      You’re talking about the time of Moses, not Noah. As we’ve already discussed, the minimum degree of toxicity for a venom that would provide a selectable survival advantage would not require high levels of functional complexity and therefore could have been evolved in relatively short order.

      As far as evolved immunity, I agree. Exposure to modern pathogens has produced more evolved immunity than those in the past who were not exposed to such pathogens. I repeat, the story of the devastation of American Indians by Old World pathogens is a classic example of this.

      Sean Pitman
      http://www.DetectingDesign.com




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  47. Sean Pitman: Oh really? We can “rest assured” upon what basis? Are you equally confident for all of the cases I’ve presented? I suppose that Ringneck Pheasants just fly in from Asia on a regular basis?

    More bald eagles arrived in North Carolina from other locations in the southeast U.S.–just as the first pair did. More white terns arrived on Oahu from other locations in the Pacific Ocean–just as the first pair did. Humans released more ring-necked pheasants–lots more–in the U.S.

    Birds get around. You’ve assumed 100% natal philopatry. Look up “metapopulation” in Wikipedia.




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    • @Professor Kent:

      This is a reasonable argument for the White Terns on Oahu and perhaps even for the N. American ring-neck pheasants. However, it is a bit more difficult for bald eagles and several other known examples of populations surviving extreme bottlenecks.

      More bald eagles may indeed arrive in N. Carolina now days – true. However, when they were much more endangered during the time when the population in N. Carolina dropped to just one breeding pair, this situation doesn’t seem nearly as likely as a source of outside genetic input. The original single breeding pair did in fact survive and did produce an inbred population of Bald Eagles in this region that was most likely inbred for quite some time before outside influences could reasonably have been realized. Consider, in this line, that bald eagles are monogamous and remain faithful to each other until one of the pair dies.

      Various rabbit populations are known to have arisen from significant population bottlenecks.

      http://attic.areavoices.com/2012/03/17/hare-raising-times-on-duluths-park-point/

      The Brookfield herd of Wisent Bison stared from a single breeding pair in 1956. The only import after that time was a single full-sibling female to the breeding male. No animals have been added since.

      Anyway, there are numerous other such examples. And, while such inbreeding is no doubt problematic in today’s world, it is not impossible to achieve a viable population even today and was no doubt much easier when gene pools had far less detrimental mutations and when the environment was far less toxic.

      Sean Pitman
      http://www.DetectingDesign.com




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  48. Sean Pitman: Yes, I’m well aware of MCF toxins. Please refer to my comments regarding your other toxin examples. They apply here as well.

    Please explain how Mcf toxins and insecticidal toxin complexes fail your criteria. I’m calling your bluff.




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    • @Professor Kent:

      Please explain how Mcf toxins and insecticidal toxin complexes fail your criteria. I’m calling your bluff.

      As with some of the other toxins already described, the Mcf toxins have various domains that act in sequence, but do not require a specific arrangement relative to each other within the larger protein molecule. Also, the specificity of Mcf toxins is further reduced by the existence of RTX-like domains – which are based on large numbers of amino acid repeats ordered in tandem. Functions based on repetitive sequences have low minimum structural specificity requirements.

      Consider that for Mcf toxins to work they must first be transferred from the bacterium into the cells that the bacterium is attacking. This step requires a certain degree of specificity within one or more domains. It is interesting to note, in this regard, that the HrmA type 3 effector domain of the Mcf2 toxin (~350aa) is homologous to other HrmA toxins that are secreted by TTSS toxin injector systems. Once in the cells, the HrmA protein also helps the toxin to localize to the nucleus of the cell. Once in the nucleus, the HrmA sequence can induce plant cell death all by itself. And, as it turns out, HrmA, and sequences homologous to HrmA, are able to cause mammalian and insect cell death as well.

      Mcf1 proteins are a bit different, but the same principles apply. The N-terminal domain of Mcf1 proteins shows homology for a BH3 domain (in contrast to the HrmA N-terminal domain in Mcf2 toxins). The BID/BH3 sequence in other proteins that have this domain is pro-apoptotic – and cells treated with the N-terminal domain of Mcf1 in culture also show apoptotic nuclear morphology (DNA laddering, cleaved PARP, and active caspase-3). The mechanism of action is that Bid-like BH3-only proteins have the ability to bind to multi-domain pro-apoptotic members of Bax or Bak within cells. Apoptosis can be induced by BH3/BID-like sequences with ranges in size from 12aa to 200aa. The natural sequence is usually around 197aa in size.

      http://www.ebi.ac.uk/pdbe-srv/view/entry/2bid/summary
      http://www.faqs.org/patents/app/20080274956

      So, you see, the minimum size requirement for such toxins is rather minimal indeed. The additional size of the Mcf toxins in particular, to include numerous additional toxic domains, is just icing on the cake. These “bells and whistles”, so the speak, can be added in a stepwise manner of increasing toxicity over time without the need for a high degree of original complexity to achieve a selectable level of toxicity.

      As far as other active domains of Mcf toxins, they seem to have been concatenated, without the need for specificity of arrangement relative to the other domains of the Mcf toxins, from various sources. One of the domains of Mcf toxins (around 500aa worth) is similar to C. diff toxin B. As already noted, the Mcf1 toxin also has a C-terminus domain with homology to the RTX-toxin from A. pleuropneumoniae (not present in smaller Mcf2 toxin). Both Mcfs also have a second region with homology to RTX-toxin from V. vulnificus (~220aa of repetitive residue sequences as noted above).

      http://onlinelibrary.wiley.com/doi/10.1016/S0378-1097%2803%2900846-2/pdf

      So, you see, these toxins are not like flagallar motility systems, ATPsynthases, TTSS toxin injectors, and the like which require fully specificity of all their unique protein parts and fairly low sequence redundancy (within the underlying DNA/RNA) for their unique functions to be realized.

      Sean Pitman
      http://www.DetectingDesign.com




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  49. Sean Pitman: What I said is that there are cases of plants and animals being classified as different “species” which have less genetic diversity than can be seen between different groups of modern humans and even dogs.

    Such as? Cite some examples in which you are comparing apples with apples (the same DNA markers), not apples with oranges (different DNA markers). And while you’re doing your homework, consider coalescence theory to understand one factor that might influence genetic divergence.

    Sean Pitman: Again, it all depends upon how you choose to defined a “species” – which is quite different for different people.

    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.

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




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    • @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
      http://www.DetectingDesign.com




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  50. Sean you suggest

    “I agree. Things are much more difficult now than they were right after the Flood. There are far more detrimental mutations in all gene pools and infectious elements are far more virulent.”

    Anyone having a background in biology recognizes the validity of Pauluc’s concerns: genetic variation is HIGHLY CONSTRAINED with a starting point of two individuals, so much so that species extinction in nature becomes a high probability. Surely you can concede this. Genetic variability is critical for populations to persist in an ever-changing world.

    In this modern world, yes. Right after the Flood, no.”

    I am still worried you have not properly addressed the maths. Its not about the deleterious mutations though they are important it is about the gene pool.

    Lets do a thought experiment.

    I would like to create a new species of Dog that is totally unlike any of the previous extant species. Say like you want to recreate a Jackal.

    There are 4 options. 1] You can take a pair of Daschunds 2] you can take a pair of wolves 3] you can take one hundred pairs of Daschunds 4] You can take a 100 pairs of wolves.

    All the animals are maximally heterozygous and do not have any deleterious mutations.

    Which would you take?

    Based on what you have said so about genetic potential in a pair of animals it seems you would have no preference among these starting populations. All are equally able to be bred to the desired characteristics.

    Is that so? If you do you would likely disagree with every stock farmer in the country. Why so?




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    • @pauluc:

      Lets do a thought experiment.

      I would like to create a new species of Dog that is totally unlike any of the previous extant species. Say like you want to recreate a Jackal.

      There are 4 options. 1] You can take a pair of Daschunds 2] you can take a pair of wolves 3] you can take one hundred pairs of Daschunds 4] You can take a 100 pairs of wolves.

      All the animals are maximally heterozygous and do not have any deleterious mutations.

      Which would you take?

      By definition Daschunds have deleterious/degenerative mutations. As already described, their short stubby legs are based on the “atypical expression” of the FGF4 transcript in their chondrocytes – apparently causing the “inappropriate activation” of one or more of the fibroblast growth factor receptors – such as FGFR3.

      So, given the option, I would take the 100 pairs of genetically perfect wolves to start such an experiment… unless, of course, I had limited space to save as many basic gene pools as possible on a boat where all other animal gene pools outside of this boat are going to be destroyed. In such a situation I’d take the single pair of genetically perfect wolves… along with as many other pairs of unique animals that I could fit on the boat.

      Either way, starting with a genetically perfect gene pool, the evolution of novel alleles at lower levels of functional complexity can be rapidly realized as the population grows larger. The rate of generation of novel alleles as the population size increased would be able to keep up with many different environmental challenges what may arise – to include the co-evolution of pathogens.

      Based on what you have said so about genetic potential in a pair of animals it seems you would have no preference among these starting populations. All are equally able to be bred to the desired characteristics.

      Not true. A larger maximally diverse population has greater up-front odds of success when it comes to rapidly coping with novel environments. This does not mean, however, that the generation of an equivalent number of novel alleles over a relatively short period of time, starting with a single breeding pair, would be impossible or “miraculous”. That simply isn’t true. Once a large population has been realized from the original breeding pair, novel alleles can be realized very rapidly and acted on by natural selection as different environments are encountered.

      Is that so? If you do you would likely disagree with every stock farmer in the country. Why so?

      As already explained several times now, modern stock farmers are not starting with genetically perfect gene pools. They must deal with thousands of years of degenerative mutations that have built up in all slowly-reproducing gene pools.

      Sean Pitman
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        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?
        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.

        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.

        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

        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.

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

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

        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.

        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.

        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.

        10] You can of course invoke miracles. Indeed I think it is the only logically consistent conclusion given your premises.
        1] All species variation arose over 4000 years from an extremely bottle-necked population
        2] Mutations account for any variation not present in the original near perfect pair.
        3] These mutations cannot generate anything useful or novel that can contribute to the phenotypic development of breeds or species.

        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.




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        • @pauluc:

          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.

          Yes.

          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.

          Yep.

          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
          http://www.DetectingDesign.com




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  51. Sean you suggest

    “I agree. Things are much more difficult now than they were right after the Flood. There are far more detrimental mutations in all gene pools and infectious elements are far more virulent.”

    Anyone having a background in biology recognizes the validity of Pauluc’s concerns: genetic variation is HIGHLY CONSTRAINED with a starting point of two individuals, so much so that species extinction in nature becomes a high probability. Surely you can concede this. Genetic variability is critical for populations to persist in an ever-changing world.

    In this modern world, yes. Right after the Flood, no.”

    I am still worried you have not properly addressed the maths. Its not about the deleterious mutations though they are important it is about the gene pool.

    Lets do a thought experiment.

    I would like to create a new species of Dog that is totally unlike any of the previous extant species. Say like you want to recreate a Jackal.

    There are 4 options. 1] You can take a pair of Daschunds 2] you can take a pair of wolves 3] you can take one hundred pairs of Daschunds 4] You can take a 100 pairs of wolves.

    All the animals are maximally heterozygous and do not have any deleterious mutations.

    Which would you take?

    Based on what you have said so about genetic potential in a pair of animals it seems you would have no preference among these starting populations. All are equally able to be bred to the desired characteristics.

    Is that so? If you do you would likely disagree with every stock farmer in the country. Why so?




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    • @pauluc:

      Lets do a thought experiment.

      I would like to create a new species of Dog that is totally unlike any of the previous extant species. Say like you want to recreate a Jackal.

      There are 4 options. 1] You can take a pair of Daschunds 2] you can take a pair of wolves 3] you can take one hundred pairs of Daschunds 4] You can take a 100 pairs of wolves.

      All the animals are maximally heterozygous and do not have any deleterious mutations.

      Which would you take?

      By definition Daschunds have deleterious/degenerative mutations. As already described, their short stubby legs are based on the “atypical expression” of the FGF4 transcript in their chondrocytes – apparently causing the “inappropriate activation” of one or more of the fibroblast growth factor receptors – such as FGFR3.

      So, given the option, I would take the 100 pairs of genetically perfect wolves to start such an experiment… unless, of course, I had limited space to save as many basic gene pools as possible on a boat where all other animal gene pools outside of this boat are going to be destroyed. In such a situation I’d take the single pair of genetically perfect wolves… along with as many other pairs of unique animals that I could fit on the boat.

      Either way, starting with a genetically perfect gene pool, the evolution of novel alleles at lower levels of functional complexity can be rapidly realized as the population grows larger. The rate of generation of novel alleles as the population size increased would be able to keep up with many different environmental challenges what may arise – to include the co-evolution of pathogens.

      Based on what you have said so about genetic potential in a pair of animals it seems you would have no preference among these starting populations. All are equally able to be bred to the desired characteristics.

      Not true. A larger maximally diverse population has greater up-front odds of success when it comes to rapidly coping with novel environments. This does not mean, however, that the generation of an equivalent number of novel alleles over a relatively short period of time, starting with a single breeding pair, would be impossible or “miraculous”. That simply isn’t true. Once a large population has been realized from the original breeding pair, novel alleles can be realized very rapidly and acted on by natural selection as different environments are encountered.

      Is that so? If you do you would likely disagree with every stock farmer in the country. Why so?

      As already explained several times now, modern stock farmers are not starting with genetically perfect gene pools. They must deal with thousands of years of degenerative mutations that have built up in all slowly-reproducing gene pools.

      Sean Pitman
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        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?
        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.

        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.

        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

        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.

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

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

        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.

        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.

        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.

        10] You can of course invoke miracles. Indeed I think it is the only logically consistent conclusion given your premises.
        1] All species variation arose over 4000 years from an extremely bottle-necked population
        2] Mutations account for any variation not present in the original near perfect pair.
        3] These mutations cannot generate anything useful or novel that can contribute to the phenotypic development of breeds or species.

        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.




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        • @pauluc:

          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.

          Yes.

          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.

          Yep.

          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
          http://www.DetectingDesign.com




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  52. Sean

    “This does not mean, however, that the generation of an equivalent number of novel alleles over a relatively short period of time, starting with a single breeding pair, would be impossible or “miraculous”. That simply isn’t true. Once a large population has been realized from the original breeding pair, novel alleles can be realized very rapidly and acted on by natural selection as different environments are encountered.”

    Nice succinct description of Darwinian evolution to me.




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    • @pauluc:

      That’s right. Darwinian evolution does happen, commonly and very rapidly, at low levels of functional complexity. The limitation, of course, is when you start talking about higher and higher levels of functional complexity. The creative potential of Darwinian evolution stalls out, in an exponential manner, with each step up the ladder of functional complexity.

      This is the key error neo-Darwinists make. They do not recognize the limits of the Darwinian mechanism of RM/NS. They always think that a little more time can produce miracles at all levels of functional complexity. They do not recognize the exponential decay curve for the creative potential of the Darwinian mechanism at higher and higher levels of functional complexity.

      Sean Pitman
      http://www.DetectingDesign.com




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  53. Sean&#032Pitman: So, you see, the minimum size requirement for such toxins is rather minimal indeed.

    I don’t have the time to validate your explanations for why the minimal size requirements for the aformentioned toxins are “rather minimal indeed,” but I would like you to explain to me why the toxins are so massively large when smaller, more efficient versions should be favored by natural selection. Any mutant–and mutations, as you concede, are exceedingly important in generating diversity and adaptations–with a smaller, less metabolically expensive toxin or toxin complex should be favored. Why has this not happened? Why do these organisms synthesize and rely on such massive, bulky toxins?




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    • @Professor Kent:

      The obvious answer is that there is enhanced toxicity to a toxin that includes many toxic domains of various kinds. This results in a selective advantage to those who contain the multi-domain toxins that work by more than one mechanism to attack the prey.

      Of course, the real question is if the building of such a multi-domain toxin can be achieved in a selectably sequential manner where each small step is selectably advantageous. The answer to this question is yes. Pre-formed toxic domains can be fairly easily concatenated to each other in a selectably sequential manner without the need to invoke deliberate intelligence in the process. There are real-time observable examples of this sort of thing…

      Sean Pitman
      http://www.DetectingDesign.com




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  54. Sean

    “This does not mean, however, that the generation of an equivalent number of novel alleles over a relatively short period of time, starting with a single breeding pair, would be impossible or “miraculous”. That simply isn’t true. Once a large population has been realized from the original breeding pair, novel alleles can be realized very rapidly and acted on by natural selection as different environments are encountered.”

    Nice succinct description of Darwinian evolution to me.




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    • @pauluc:

      That’s right. Darwinian evolution does happen, commonly and very rapidly, at low levels of functional complexity. The limitation, of course, is when you start talking about higher and higher levels of functional complexity. The creative potential of Darwinian evolution stalls out, in an exponential manner, with each step up the ladder of functional complexity.

      This is the key error neo-Darwinists make. They do not recognize the limits of the Darwinian mechanism of RM/NS. They always think that a little more time can produce miracles at all levels of functional complexity. They do not recognize the exponential decay curve for the creative potential of the Darwinian mechanism at higher and higher levels of functional complexity.

      Sean Pitman
      http://www.DetectingDesign.com




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  55. Sean Pitman: The Ringneck Pheasant are a native of Asia and were imported to the United States in the 1880′s. It is thought that the escaping of a single breeding pair began the population of these birds in the U.S.

    Sean Pitman: I suppose that Ringneck Pheasants just fly in from Asia on a regular basis?

    FYI, ring-necked pheasants were first introduced to North America (New York) between 1730 and 1733, but failed to become established. The first successful release occurred during 1881-1882, when Judge O. N. Denny released some 100 pairs of Chinese ring-necks in Willamette Valley, Oregon. Other early introductions occurred in New York in 1877 and 1886–1891, Washington in 1883, Colorado in 1885, New Jersey in 1887, Georgia in 1888, California in 1889, Montana about 1895, Illinois in the 1890s, Massachusetts in 1897–1898, Pennsylvania in 1892–1895, California in 1889, Utah in 1890, and the Midwest about 1900. Numerous releases have continued since then.

    Sources (much superior to an internet search):

    Hill, D. A. and P. Robertson. 1988. The pheasant: ecology, management, and conservation. BSP Prof. Books, Oxford, UK.

    Lever, C. 1987. Naturalized birds of the world. John Wiley and Sons, Inc. New York.

    Long, J. L. 1981. Introduced birds of the world: the worldwide history, distribution, and influence of birds introduced to new environments. Universe Books, New York.

    Prince, H. H., P. Squibb, and G. Y. Belyea. 1988. Sichuans, pheasants of the future?-learning from past release programs. Pages 291-305 in Pheasants: symptoms of wildlife problems on agricultural lands. (Hallett, D. L., W. R. Edwards, and G. V. Burger, Eds.) N. Central Section of The Wildl. Soc. Bloomington, IN.




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  56. Sean Pitman: This is a reasonable argument for the White Terns on Oahu and perhaps even for the N. American ring-neck pheasants. However, it is a bit more difficult for bald eagles and several other known examples of populations surviving extreme bottlenecks.

    During the period in question, bald eagles bred in other southeastern states as well. You can rest assured that gene exchange occurred all up and down the Atlantic seaboard. Nestlings in Florida, for example, will fledge and disperse as far north as Canada, with some banded individuals recovered during the breeding season (i.e., presumed breeding) throughout the eastern seaboard–including North Carolina. No one has demonstrated that any bird species recognizes and remains within a state’s designated boundary.

    Yes, there was a genetic bottleneck of some 450 breeding pairs (900+ individuals) in the contiguous 48 states. We are, indeed, very fortunate they are still with us today.




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    • @Professor Kent:

      Perhaps, though far less likely for a specific area during general continental population bottlenecks.

      In any case, there are many other examples of extreme population bottlenecks where it is directly known that no outside genetic information was inserted into the population. Yet, the population remains viable and healthy… even starting with gene pools that have been subject to far greater numbers of deleterious mutations compared to the post-Flood era.

      Sean Pitman
      http://www.DetectingDesign.com




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  57. Sean Pitman: So, you see, the minimum size requirement for such toxins is rather minimal indeed.

    I don’t have the time to validate your explanations for why the minimal size requirements for the aformentioned toxins are “rather minimal indeed,” but I would like you to explain to me why the toxins are so massively large when smaller, more efficient versions should be favored by natural selection. Any mutant–and mutations, as you concede, are exceedingly important in generating diversity and adaptations–with a smaller, less metabolically expensive toxin or toxin complex should be favored. Why has this not happened? Why do these organisms synthesize and rely on such massive, bulky toxins?




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    • @Professor Kent:

      The obvious answer is that there is enhanced toxicity to a toxin that includes many toxic domains of various kinds. This results in a selective advantage to those who contain the multi-domain toxins that work by more than one mechanism to attack the prey.

      Of course, the real question is if the building of such a multi-domain toxin can be achieved in a selectably sequential manner where each small step is selectably advantageous. The answer to this question is yes. Pre-formed toxic domains can be fairly easily concatenated to each other in a selectably sequential manner without the need to invoke deliberate intelligence in the process. There are real-time observable examples of this sort of thing…

      Sean Pitman
      http://www.DetectingDesign.com




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  58. Sean,

    I’m glad to see you concede that profound adaptations involving qualitatively new traits–such as toxin systems–can indeed evolve via mutations and natural selection, regardless of how substantial the “fairly specified” specificity is. The remarkable, novel, unquestionably evolved lifestyles of parasitic and predatory animals amply illustrate this. I personally agree with you that God created the original lifeforms that have become parasites and predators (e.g., bacteria, nematodes, mosquitos, snakes).

    Your argument about 1,000 fsaars, however, still falls short of invoking God for two reasons that come to my mind:

    1. As some have suggested, the original life forms containing complex structures like flagellar motility systems, ATPsynthases, and TTSS toxin injectors could have arrived on our planet having evolved originally elsewhere in the universe. Your arguments of probability that require “trillions upon trillions” of years suffer when vast numbers of potential locations and vast numbers of replicating entities can be invoked. (Again, I agree with you on the basic faith-based premise that God, instead, created these life forms instantaneously.)

    2. I’m not convinced that, once the basic machinery is in place, mutations and natural selection cannot build indefinitely on existing systems. You argue that systems are winding down, but regardless of whether you are right, and whether the improvements cannot exceed 1000 fsaars, selection continues to refine and improve and create novel solutions to new challenges. We see evidence almost everywhere we look for the ongoing creativity of natural selection among both slow- and fast-reproducing life forms. The remarkable biodiversity that has evolved following the flood, with terrestrial animals in particular having become highly adapted to ever-changing niches, testifies to this.

    You could help me better understand your arguments for the limited creativity of RM/NS if you could describe some traits that, according to your theory, illustrate why it is impossible for the following transitions to occur because to do so would require >1,000 fsaars:

    – fishes to amphibians
    – amphibians to reptiles
    – reptiles to mammals

    In other words, what trait(s), precisely, would block the gradual evolution of a fish to an amphibian, an amphibian to a reptile, or a reptile to a mammal?




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    • @Professor Kent:

      Your argument about 1,000 fsaars, however, still falls short of invoking God for two reasons that come to my mind:

      1. As some have suggested, the original life forms containing complex structures like flagellar motility systems, ATPsynthases, and TTSS toxin injectors could have arrived on our planet having evolved originally elsewhere in the universe. Your arguments of probability that require “trillions upon trillions” of years suffer when vast numbers of potential locations and vast numbers of replicating entities can be invoked. (Again, I agree with you on the basic faith-based premise that God, instead, created these life forms instantaneously.)

      This argument is based on a failed understanding of the statistics involved. Even given an entire universe filled with planets similar to our own, each filled with bacteria to maximum capacity, no novel higher-level biological system is remotely likely to have evolved anywhere in the entire universe this side of a practical eternity of time – i.e., trillions upon trillions of years.

      2. I’m not convinced that, once the basic machinery is in place, mutations and natural selection cannot build indefinitely on existing systems. You argue that systems are winding down, but regardless of whether you are right, and whether the improvements cannot exceed 1000 fsaars, selection continues to refine and improve and create novel solutions to new challenges. We see evidence almost everywhere we look for the ongoing creativity of natural selection among both slow- and fast-reproducing life forms. The remarkable biodiversity that has evolved following the flood, with terrestrial animals in particular having become highly adapted to ever-changing niches, testifies to this.

      Darwinian-style evolution is indeed real and an amazing force of nature. When it works, it works quickly. It is just limited to very low levels of functional complexity is all. It simply cannot produce what neo-Darwinians claim for it.

      The reason you’re not convinced as to the limitations of RM/NS is because you do not understand the nature of protein or DNA sequence space, the distribution of potentially viable sequences within these spaces, or the odds of randomly coming across a qualitatively novel sequence at higher and higher levels of functional complexity within these sequence spaces. If you took the time to sit down and do the math, you’d quickly discover that the Darwinian mechanism has have clear limitations that definitively undermine neo-Darwinism.

      You could help me better understand your arguments for the limited creativity of RM/NS if you could describe some traits that, according to your theory, illustrate why it is impossible for the following transitions to occur because to do so would require >1,000 fsaars:

      – fishes to amphibians
      – amphibians to reptiles
      – reptiles to mammals

      In other words, what trait(s), precisely, would block the gradual evolution of a fish to an amphibian, an amphibian to a reptile, or a reptile to a mammal?

      Anything novel between these groups that requires a minimum of more than 1000 specifically arranged amino acid parts would qualify (or an equivalent number of codons of DNA) – like the middle ear with tympanic membrane and ear bone in amphibians as well as the amphibian ability to metamorphosize to the adult stage (vs. no such middle ears with in fish or the ability to metamorphosize legs, lungs, etc.), or the amniotic eggs of reptiles with a tough leathery shell (vs. the soft watery gel that surrounds the eggs of amphibians), or the hair and sweat glands of mammals (compared to a lack of such in reptiles), or the true flight feathers of birds with their interlocking Velcro-like features (compared to a lack of such in true reptiles).

      Some of these features might seem very close, morphologically, to certain structures within the proposed evolutionary pathways presented by neo-Darwinists. However, when one actually considers the underlying genetic programming that would be required to make the next morphologic step possible, it is well beyond what RM/NS could achieve in a reasonable amount of time.

      After all, if the pathways were really littered with such closely spaced steppingstones as evolutionists would have us believe, many of these proposed evolutionary steps, like in the evolution of the eye, could be reproduced in the laboratory. The fact is that the minimum number of specific genetic changes needed to realize the next morphologic step are far greater than evolutionists generally realize… or they don’t realize that just a few dozen specific mutational changes, which are not sequentially selectable, would require trillions of years for random mutations of any kind to realize.

      This is why such real time demonstrations have never been produced for such complex structures (like the eye or the flagellum, etc)… not even for the crossing of a single proposed evolutionary step between morphologic steps that are supposedly very tiny baby steps.

      Sean Pitman
      http://www.DetectingDesign.com




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  59. Professor Kent: We see evidence almost everywhere we look for the ongoing creativity of natural selection among both slow- and fast-reproducing life forms.

    For those who still question this very basic tenet of evolutionary biology/scientific creationism, which Dr. Pitman has aggressively supported with his arguments as of late, simply do a search at scholar.Google.com of “selection acting on.” You’ll find many thousands of publications documenting ongoing natural selection. Perhaps you’ll agree with Dr. Pitman that God himself created this fabulous evolutionary process so that life could better adapt to a sinful, ever-changing planet. (And how else could we possibly get millions of terrestrial animal species from the relative handful that survived inside the ark?)




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    • @Professor Kent:

      I’m not sure why you think it is news that random mutations happen and that novel allelic variations are often the result. There is no argument here among creationists. The argument is over the neo-Darwinist position that these changes can actually cross the line from very low levels to higher levels of functional complexity.

      That’s the real disagreement between creationists and evolutionists. Evolutionists do not recognize the limitations of the Darwinian mechanism. They do not recognize any point beyond which only an intelligent agent could step across the line.

      Sean Pitman
      http://www.DetectingDesign.com




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  60. Sean

    It is has been way too time consuming and life is too short to keep wade through the molasses that constitutes a dialog about science at this site.

    I wish you well and continue to hope that you will actually participate in science and grow knowledge rather than just rearranging the deck chairs in your own inimitable style. Even within the context of Adventist thought it would be very helpful if you could expand your ideas on the genetics of life over the last 4000 years with specificity. For sure the David Read model is incomprehensible beyond the confines of fringe Adventism.




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    • @pauluc:

      Thank you… and all the best to you in actually trying to think for yourself instead of simply relying on arguments from authority and your faith in conclusions of mainstream scientists – especially when it comes to the unlimited creative potential RM/NS beyond low levels of functional complexity.

      This is the primary error of mainstream science – that there is essentially no distinction between levels of functional complexity and evolutionary potential in mainstream literature. It is simply assumed that because Darwinian style evolution can and does commonly and rapidly happen at low levels of functional complexity that higher-levels of evolution are also evolvable given just a bit more time. This extrapolation is unsupported by either demonstration or statistical analysis. It is simply accepted, by mainstream science, on blind faith. The only support for this faith is a fundamentalist need for it to be true in order to prop up their naturalistic philosophy… their own naturalistic religion.

      Sean Pitman
      http://www.DetectingDesign.com




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  61. Sean Pitman: 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’m mildly surprised by your reticence to answer my questions. We both know that you have expertise that qualifies you to be a declared authority on most any discipline in science, including taxonomy and systematics (not to mention theology, history, and philosophy). I suggest you do some reading on your own, as I shouldn’t have to explain any of this to you. In the meanwhile, perhaps my primer will help you understand that systematics is a legitimate science based on very sound concepts and methodology, and that species delineation, while complex, has a sound method to what you imply is madness.

    The two primary approaches for delineating species using molecular (DNA) variation involve (1) genetic distance and (2) reciprocal monophyly. The latter is based on unique sequence variation, not amount of variation.

    For genetic distance (amount of variation), the amount of DNA base pair differences required for distinguishing between species and subspecies depends on DNA region (some regions evolve faster than others) and organism group (the same region in different groups can evolve at varying rates). I know that you would like a universal criterion, but you won’t get this unless you want to stick strictly with reciprocal monophyly–that’s about as universal as you’ll ever get, but it still has its limitations (e.g., incomplete lineage sorting and past introgressive hybridization).

    With regard to amount of DNA variation, here’s how it works. One simply examines variation among many taxa at various taxonomic ranks, including well-defined closely-related sympatric species (e.g., two frog species that look similar but despite living together rarely or never interbreed), and variation within population segments of those species. For certain mtDNA markers, for example, one may find that DNA differences above 5% exist among different genera, 1-2% exist among distinct species, and differences less than 1% correspond to subspecies. So, if one then wishes to discern whether two candidate populations–especially allopatric populations for which reproductive isolation cannot be discerned–are distinct species, one simply compares their genetic distance with that already established for different taxonomic ranks within the group. If frog A and frog B, for example, look virtually identical but differ by 2.9%, then one would conclude they are probably distinct species–indeed, these are cryptic species, as you recognize.

    There is nothing inherently wrong with this approach. It works.




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    • @Professor Kent:

      For certain mtDNA markers, for example, one may find that DNA differences above 5% exist among different genera, 1-2% exist among distinct species, and differences less than 1% correspond to subspecies.

      Are these percentages consistently and universally applied in all cases? Do you have a reference for these numbers and their universal application? If so, please do provide said reference regarding universally applied percentage of divergence for any mtDNA markers or other genetic regions…

      So, if one then wishes to discern whether two candidate populations–especially allopatric populations for which reproductive isolation cannot be discerned–are distinct species, one simply compares their genetic distance with that already established for different taxonomic ranks within the group. If frog A and frog B, for example, look virtually identical but differ by 2.9%, then one would conclude they are probably distinct species–indeed, these are cryptic species, as you recognize.

      Again, do you have a reference for your percentages for any region or kind of genetic sequence and their universal application in all cases?

      There is nothing inherently wrong with this approach. It works.

      Does it consistently work in all cases? Can it be universally applied without disagreement or contradiction? – the same definition for the degree of divergence of a specific genetic sequence defines all groups of plants or animals with this same degree of divergence as a different “species” group? If so, where is your reference to this effect?

      Sean Pitman
      http://www.DetectingDesign.com




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  62. Sean Pitman: 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 can’t help but smile when I read a remark like this.

    The simple reason why species concepts are varied, and delineation is inexact, is because biological variation is often continuously distributed, and is distributed in different ways among different traits and among different taxonomic groups. I don’t think you show sufficient understanding or appreciation of this. You simply wave your hands and dismiss most attempts to delineate taxonomic groups as inexact and, therefore, unscientific. I’ll elaborate more on this problem of variation.

    Speciation, as you recognize, occurs almost always in allopatry. The two populations exist under different selective regimes, which leads to change. Initially (immediately after the event that created allopatry, which we’ll call point A), everyone is agreed that a single species exists. Over time, if differences accumulate to a point where they become obvious enough (at point B), everyone agrees they’ve now evolved into two species. The differences we’re talking about can involve behavioral traits, ecological traits, morphological traits, molecular distances, and so forth. There’s a gray zone, however, between point A and point B in which disagreement can result. You need to recognize that the aforementioned traits diverge at different rates. In some cases, morphological traits will diverge faster than molecular traits; in such instances, the morphological species concept may be more appropriate than molecular differences for delineation. In other cases, molecular traits will diverge faster than morphological traits; in such cases, the phylogenetic species concept may be more appropriate for delineation. And while differences of opinion will often exist depending on which of these criteria are prioritized, practicioners very seldom quibble over differences beyond the boundary of two adjacent taxonomic ranks (i.e., they may argue whether two populations comprise the same subspecies or species, but will agree they both are within the same genus).

    Of course, allopatric populations can often merge again to become sympatric, and whether the two differentiated populations merge again into a single one or remain distinct will depend on how far they have become differentiated and whether reproductive isolating mechanisms can evolve to avoid hybridization.

    So, to summarize, the reason we have different species concepts, such as the biological (emphasizing reproductive isolation), morphological, ecological, and phylogenetic species concepts, is because these are all aspects of biological variation that can reflect differences in the gene pools of organisms. They don’t covary lock-in-step; instead, they vary independently of each other.

    In summary, as you well recognize, speciation can happen in a multitude of ways and involve a multitude of traits. Taxonomists and systematists recognize and acknowledge that, just as there are many ways to skin a cat, there are also many ways to explore and define differences among gene pools. I suggest you embrace this reality rather than besmirch it.




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    • @Professor Kent:

      The simple reason why species concepts are varied, and delineation is inexact, is because biological variation is often continuously distributed, and is distributed in different ways among different traits and among different taxonomic groups.

      That’s right. There’s a continuous spectrum of distribution – except when you’re talking about levels of functional complexity. Only here is there a distinct line between gene pools that is not dependent upon subjective interpretations as to where the line should be drawn between different “kinds” of plants or animals.

      I don’t think you show sufficient understanding or appreciation of this. You simply wave your hands and dismiss most attempts to delineate taxonomic groups as inexact and, therefore, unscientific.

      They fact is, as you admit, all of these definitions you cite take on a component of subjectivity as to exactly where the line of “speciation” should be drawn. It is not an exact science. It is more philosophy or art than science. Sure, there is a scientific component and even a component of reproducibility. However, these definitions also retain an arbitrary subjective element.

      I’ll elaborate more on this problem of variation.

      Speciation, as you recognize, occurs almost always in allopatry. The two populations exist under different selective regimes, which leads to change.

      Yep…

      Initially (immediately after the event that created allopatry, which we’ll call point A), everyone is agreed that a single species exists.

      Yep…

      Over time, if differences accumulate to a point where they become obvious enough (at point B), everyone agrees they’ve now evolved into two species.

      This isn’t quite true since the mechanism is still in question here. Certainly there are uniquely different kinds of gene pools that exist which are based on novel functionality at high levels of functional complexity – levels that cannot be produced by any mindless naturalistic mechanism.

      The differences we’re talking about can involve behavioral traits, ecological traits, morphological traits, molecular distances, and so forth.

      Right…

      There’s a gray zone, however, between point A and point B in which disagreement can result.

      Indeed! It is this “gray zone”, as you call it, that is part of the subjective nature of the definition of the “species” concept. It is not an exact science by any means. I’m glad you can actually admit this much.

      You need to recognize that the aforementioned traits diverge at different rates.

      Oh, I do recognize this concept. I totally agree with this point.

      In some cases, morphological traits will diverge faster than molecular traits; in such instances, the morphological species concept may be more appropriate than molecular differences for delineation.

      Not when it comes to dogs, ironically, where very different morphologic features are given different breed names, but are still considered to be part of the same species because of a lack of molecular divergence.

      You see the problem. Your “rules” cannot be, or at least are not, consistently applied in all cases. Again enters the subjective aspect of determining “species” groups.

      In other cases, molecular traits will diverge faster than morphological traits; in such cases, the phylogenetic species concept may be more appropriate for delineation.

      And here you have the “cryptic” species concept where the different groups of animals look and function in an identical manner. They can even interbreed with each other to produce viable and virile offspring. Yet, they are classified as different species without any regard to functionality – based only on some arbitrary cut-off for genetic divergence of a given genetic region or collection of regions… a cut-off for genetic distance that is also not consistently applied to all groups of plants or animals.

      And while differences of opinion will often exist depending on which of these criteria are prioritized, practicioners very seldom quibble over differences beyond the boundary of two adjacent taxonomic ranks (i.e., they may argue whether two populations comprise the same subspecies or species, but will agree they both are within the same genus).

      Not always true. And, even if this were the case, it doesn’t change the fact that the species concept itself is based on subjective arbitrarily chosen parameters – parameters that are debatable even among mainstream scientists on a case-by-case basis. That is because these parameters are not always consistently chosen or used in practice. They are not generally applied in a consistent universal manner.

      Of course, allopatric populations can often merge again to become sympatric, and whether the two differentiated populations merge again into a single one or remain distinct will depend on how far they have become differentiated and whether reproductive isolating mechanisms can evolve to avoid hybridization.

      True, but irrelevant to my point.

      So, to summarize, the reason we have different species concepts, such as the biological (emphasizing reproductive isolation), morphological, ecological, and phylogenetic species concepts, is because these are all aspects of biological variation that can reflect differences in the gene pools of organisms. They don’t covary lock-in-step; instead, they vary independently of each other.

      Which restates what I’ve been saying all along – that there is no universally applied species concept. The many methods used to defined “species” all have subjective elements that are arbitrarily applied and which are never universally applied in a consistent manner in all cases.

      In summary, as you well recognize, speciation can happen in a multitude of ways and involve a multitude of traits. Taxonomists and systematists recognize and acknowledge that, just as there are many ways to skin a cat, there are also many ways to explore and define differences among gene pools. I suggest you embrace this reality rather than besmirch it.

      I do embrace and affirm this reality. After all, it is this reality that makes the species concept so subjective and arbitrarily applied to various specific cases.

      Sean Pitman
      http://www.DetectingDesign.com




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  63. A couple of my edits took in the preceding comment, and a few did not show up. Now there are two summary statements. Oh well.

    I’ll add two more things:

    1 – Systematists appropriately acknowledge that their taxonomic arguments and reconstructions are simply hypotheses.

    2 – Most practicioners use more than one species concept (or operational definition) to argue the delineation of any given species boundaries. Clearly, the more concepts applied to the argument, the better. For Sean, it may merely be “depends upon which one among many potential definitions one chooses…,” but systematists are much more methodical and sophisticated than Sean would like for you to believe.




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    • @Professor Kent:

      Exactly. This is right in line with my comments that there is no single set species definition that can be consistently and universally applied. One is forced to pick and choose and combine various species concepts, with a component of human subjectivity thrown in, in order to define what is and what is not really a “species”.

      In contrast, my definition of a unique “kind” of gene pool, based on levels of functional complexity that are beyond the reach of any naturalistic mechanism, can be universally applied, in theory at least, without dependence upon human subjectivity.

      Sean Pitman
      http://www.DetectingDesign.com




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  64. Sean

    It is has been way too time consuming and life is too short to keep wade through the molasses that constitutes a dialog about science at this site.

    I wish you well and continue to hope that you will actually participate in science and grow knowledge rather than just rearranging the deck chairs in your own inimitable style. Even within the context of Adventist thought it would be very helpful if you could expand your ideas on the genetics of life over the last 4000 years with specificity. For sure the David Read model is incomprehensible beyond the confines of fringe Adventism.




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    • @pauluc:

      Thank you… and all the best to you in actually trying to think for yourself instead of simply relying on arguments from authority and your faith in conclusions of mainstream scientists – especially when it comes to the unlimited creative potential RM/NS beyond low levels of functional complexity.

      This is the primary error of mainstream science – that there is essentially no distinction between levels of functional complexity and evolutionary potential in mainstream literature. It is simply assumed that because Darwinian style evolution can and does commonly and rapidly happen at low levels of functional complexity that higher-levels of evolution are also evolvable given just a bit more time. This extrapolation is unsupported by either demonstration or statistical analysis. It is simply accepted, by mainstream science, on blind faith. The only support for this faith is a fundamentalist need for it to be true in order to prop up their naturalistic philosophy… their own naturalistic religion.

      Sean Pitman
      http://www.DetectingDesign.com




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  65. Sean Pitman: there is no single set species definition that can be consistently and universally applied. One is forced to pick and choose and combine various species concepts, with a component of human subjectivity thrown in, in order to define what is and what is not really a “species”.
    In contrast, my definition of a unique “kind” of gene pool, based on levels of functional complexity that are beyond the reach of any naturalistic mechanism, can be universally applied, in theory at least, without dependence upon human subjectivity.

    No, Sean, you are dead wrong, though I’m sure you will continue to argue otherwise.

    The key problem with your definition is that it lacks clarity and operational specificity. Here are just a few problems that come to mind without delving deep:

    1. Your definition assumes that two or more populations having functional differences are reproductively isolated, but fails to identify how different the differences must be–unless it’s your magical 1000 fsaars, in which case useful data are completely lacking for the vast majority of species. To illustrate this problem, try telling us exactly what functional differences exist among the following universally recognized sympatric species. Better yet, tell us the size of these differences (in fsaar or other relevant units).

    Small-mouthed bass, large-mouthed bass (fish)
    Tiger salamander, spotted salamander (amphibians)
    Golden eagle, bald eagle (birds)
    Deer mouse, cactus mouse (mammals)

    2. Your definition relies on the same criteria used in other species concepts or definitions. The functional differences that might exist could, for example, result from morphological differences (morphological species concept), ecological differences (ecological species concept), or behavioral differences (behavioral species concept). You haven’t introduced anything novel with your definition.

    3. Your definition fails to consider the relevance of functional differences to reproductive isolation and population divergence. It ignores polymorphisms, for example, which can result in dramatic functional differences among individuals within a single population, yet the functionally distinct genotypes do not emerge as distinct species. These polymorphisms can be maintained by frequency-dependent selection (you probably need to Google this) within a single population. Genetic polymorphisms in alternative mating tactics, for example, are widespread among animals. Consider the many species of fish which have multiple (as many as four) genetically-based alternative mating tactics. Some males (territorial males) take a long time to achieve a large size, but then set up and defend territories from other males, and mate many females that enter their territory. Other males (sneaker males) quickly mature at a small size and, resembling a female, they sneak into the territories of the territorial males and obtain fertilizations by cuckoldry. Functionally, these mating tactics are very, very different, yet they are maintained within a single gene pool by frequency-dependent selection. Another example of a genetic polymorphism would be the European cuckoo, in which some female lineages prefer to brood parasitize (lay eggs in nest of) one particular songbird species, and other female lineages prefer to brood parasitize other particular songbird species. Again, you’ve got a major functional difference resulting in multiple females gentes (lineages), but males cross-mate them to maintain the cuckoo as a single species. Genetic-based morphological polymorphisms are also abundant, such as within the snow goose. The white versus blue individuals, having very distinctive colors, result in significant thermoregularly differences, yet the two groups formerly considered distinct species maintain a single gene pool.

    4. Your definition overlooks subtle traits that may be non-functional, but which can still lead to reproductive isolation and population divergence. Consider the gray treefrog (Hyla versicolor) and Cope’s gray treefrog (Hyla chrysoscelis). These are two broadly sympatric cryptic species that look identical. The former is diploid and the latter is tetraploid. They can be distinguished by comparing their calls relative to body temperature (i.e., one must know the body temperature) and by examining the size of their red blood cells, which differs because of DNA content. Their gene pools are maintained separately because hybrids would be triploid and gamete production via meiosis would break down. Your definition would synonymize these two taxa unless–and I wish you good luck–you could identify functional differences.




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  66. To continue with problem #4 in the previous post, I should add that there are numerous polyploid species among plants and animals that have isolated gene pools not because of functional differences, but because of chromosomal constraints.

    Another problem with your definition is its limited ability to help us understand the speciation process. By focusing solely on identifying functional differences–which are exceedingly difficult to ascertain for many taxa because of the frequent need to examine traits functioning in the natural environment–we overlook a great deal of information more readily obtained from other traits, including molecular. Now that I think of it, by ignoring the molecular traits that are central to the phylogenetic and evolutionary species concepts, you might be completely unable to identify cryptic species.

    Yes, Sean, we would all love to identify a single universally-applicable species definition, but it’s simply not realistic. Don’t lull yourself into believing you can accomplish what thousands who have gone before you have failed to do. And don’t be so dogmatic about your correctness and the errant approach of everyone who disagrees with you.




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  67. Sean&#032Pitman: Thank you… and all the best to you in actually trying to think for yourself instead of simply relying on arguments from authority and your faith in conclusions of mainstream scientists

    I think you need to show more respect toward Pauluc and others. After all, you rely on the very same literature base that he does for your arguments–except you depart to a much greater degree than he does with anything that goes against your own faith-based beliefs in the authority and statements of ancient prophets and writers. It’s really quite humorous that you would chastize him for not thinking for himself because he rejects your thinking.

    Your smug, condescending attitude reflects very poorly on your Christian values.




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  68. Sean Pitman: Thank you… and all the best to you in actually trying to think for yourself instead of simply relying on arguments from authority and your faith in conclusions of mainstream scientists

    I think you need to show more respect toward Pauluc and others. After all, you rely on the very same literature base that he does for your arguments–except you depart to a much greater degree than he does with anything that goes against your own faith-based beliefs in the authority and statements of ancient prophets and writers. It’s really quite humorous that you would chastize him for not thinking for himself because he rejects your thinking.

    Your smug, condescending attitude reflects very poorly on your Christian values.




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  69. Sean Pitman: Are these percentages consistently and universally applied in all cases? Do you have a reference for these numbers and their universal application? If so, please do provide said reference regarding universally applied percentage of divergence for any mtDNA markers or other genetic regions…

    You’re not paying attention. I’ve already made clear that percentages used in delineating species will vary depending on the gene that is sequenced (genetic marker used), unit of measurement, and taxonomic group. There is no such thing as a universally applied percentage for delineating species, although Hey and Pinho (2012) make a valiant effort to derive one. If you want to learn more (which I seriously doubt since you’ve already decided what facts are true in advance), you can start with the following reference and check the papers cited within it:

    Hey, J. and C. Pinho. 2012. Population genetics and objectivity in species diagnosis. Evolution 66-5:1413-1429.

    But, of course, there’s little point in supplying you references because you and I both know that you won’t read them, as you can’t even access the vast majority of literature out there. And we both know that I’m not going to use my library access to do your work for you.




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  70. Sean Pitman: That’s right. There’s a continuous spectrum of distribution – except when you’re talking about levels of functional complexity. Only here is there a distinct line between gene pools that is not dependent upon subjective interpretations as to where the line should be drawn between different “kinds” of plants or animals.

    Oh sure, so “levels of functional complexity” are not continuously distributed? There’s a major gap–a bimodal distribution–for which you can objectively and correctly decipher what constitutes a population or subspecies versus a valid species? Where are the data for this claim? Can you cite a reference to back up this claim (I’ll most certainly look it up)? What is the precise measure for this magical criterion that you claim to be universally applicable? Do tell!

    Look Sean, you have indicated you have no desire to publish in appropriate journals your most profound syntheses regarding evolutionary theory. If you could convince me you truly have something at all valuable–or as revolutionary as your claims suggest–I’d happily write the paper for you and coauthor it with you as the first author. I know how to publish in mainstream science, and have the courage to do so.

    The problem is that it’s becoming increasingly clear that while you can dismiss everybody else’s science regarding taxonomy and systematics (and essentially every other discipline in science) and claim that your understanding, being informed by scripture, is far superior, you can’t convince anyone other than your non-scientist readers here that you have a firm grasp on what you make claims about.




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  71. Sean,

    Here is a paper you can actually access which also attempts to derive a universal criterion for species designation, in this case using the internal transcribed spacer 2 (ITS2) region of nuclear ribosomal DNA:

    http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0013102

    In table 1, you will see how sequence divergence within species varies among different groups of plants and animals.

    Of course, you’re going to declare the paper to be full of problems, but then again, the editors chose not to send it to you to review for one very obvious reason: they had no idea that you’re an authority on systematics.




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  72. Here are two more papers accessable on the web for readers to understand the approach I have outlined for using genetic distance to approximate taxonomic boundaries:

    http://www.bio.ulaval.ca/louisbernatchez/pdf/(206)%20Lara_MER_10.pdf
    (Cuban fish: 126 individuals, representing 217 taxonomically recognized species in 17 genera and 10 families)

    http://www.pnas.org/content/108/26/10602.full.pdf+html
    (North American fish: 752 species)

    Both of these papers deal with fish. They illustrate how genetic distance dervied from variation in base pair sequence of the cytochrome c oxidase subunit I (COI) varies within species, genera, and families. The results also suggest previously unrecognized cryptic diversity among the fish groups examined (i.e., more species exist than have previously been recognized).

    By rejecting conventional methods for delineating taxonomic boundaries, and using Sean Pitman’s very peculiar approach instead, the simple reality is that we would have no clue how to classify the vast majority of fish in the two studies. For most of the species studied, the only data available are geographic location (ecology), physical measurements (morphology), and base sequence for one or several genes (molecular). We lack data on any “levels of functional complexity” that might differ among the taxa. Sean insists his method is superior, but at its very best, it would be completely impractical for classifying these fish. The same can be said for most if not all protist, fungal, plant, and animal groups.

    Here is another accessible paper summarizing genetic distances in 643 species of North American birds using the same COI gene:

    http://www.bolinfonet.org/pdf/2007_-_Kerr_-_Comprehensive_DNA_barcode_coverage_of_North_American_birds.pdf

    While the natural history of individual species is much better understood among birds than fish, it would still be an impractical challenge to objectively identify Sean’s different “levels of functional complexity” to distinguish between most if not all sister and cryptic species. Establishing a comprehensive taxonomy would be impossible, which means Sean’s species concept is, in all practical terms, useless.




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  73. One particularly compelling conclusion from the three papers cited in the prior post is that the use of genetic distance shows a high level of agreement with other methods used for defining species boundaries (96%, Cuban fishes; 90%, North American fishes; 94%, North American birds).

    While Sean would like us to believe that species delineation is highly subjective and capricious, there is no question that taxonomists employing a diverse range of species concepts and methodologies can reach broad agreement. Reliance on a multitude of species concepts and methodologies is a strength of taxonomy, and not the weakness Sean would have us believe.




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    • @Professor Kent:

      All I asked you was if there was a single universally applicable and consistent definition of species? You’ve admitted that the answer to this question is no. There is no universal definition of a “species” group that is consistent in all cases.

      You also failed to provide a standardized genetic definition of a species group whereby a particular genetic distance in any one or any collection of genetic regions can be universally applied.

      Let me know if/when this situation changes…

      __________________

      Look, the main question in play here is if RM/NS can produce new “species” if the concept of a new species isn’t dependent upon changes in genetic functionality beyond very very low levels of functional complexity? The answer to this question is yes. If species are defined without regard to levels of genetic functionality, then new species can and will be evolved via RM/NS. However, if novel gene pools are defined by qualitatively novel systems of function beyond low levels of functional complexity, then such gene pools are separated beyond the powers of Darwinian mechanisms to explain – regardless of what taxonomic label you put on them. At this point, only intelligent design can explain the origin of such functionally novel gene pools…

      Now, you’ve admirably tried to come up with examples of evolution in action beyond low levels of functional complexity. Your problem is that you don’t yet seem to understand the concept of specificity. A level of functional complexity is defined not only by its minimum size requirement, but also by the minimum degree of specificity of arrangement of all of its parts relative to all the other parts within the system. Both of these elements are required when one is evaluating the level of functional complexity of a particular system.

      Sean Pitman
      http://www.DetectingDesign.com




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  74. Professor Kent,

    You wrote:

    The key problem with your definition is that it lacks clarity and operational specificity. Here are just a few problems that come to mind without delving deep:

    1. Your definition assumes that two or more populations having functional differences are reproductively isolated, but fails to identify how different the differences must be–unless it’s your magical 1000 fsaars, in which case useful data are completely lacking for the vast majority of species.

    When it comes to determining evolutionary potential, the differences between gene pools must be beyond the power of RM/NS (or any other mindless naturalistic mechanism) to explain – which is any qualitatively novel system of function that requires a minimum of more than 1000 specifically arranged residues to do a particular task.

    To illustrate this problem, try telling us exactly what functional differences exist among the following universally recognized sympatric species. Better yet, tell us the size of these differences (in fsaar or other relevant units).

    Small-mouthed bass, large-mouthed bass (fish)

    There are no significant gene pool differences here (functionally speaking) compared to the ancestral gene pool. Small and large mouth bass are derived from the very same ancestral gene pool – as are all of the other examples you list here.

    Tiger salamander, spotted salamander (amphibians)

    Golden eagle, bald eagle (birds)

    Deer mouse, cactus mouse (mammals)

    Same original gene pools without anything novel beyond very low levels of functional complexity . . .

    2. Your definition relies on the same criteria used in other species concepts or definitions. The functional differences that might exist could, for example, result from morphological differences (morphological species concept), ecological differences (ecological species concept), or behavioral differences (behavioral species concept). You haven’t introduced anything novel with your definition.

    Drawing a limit to what can be explained by RM/NS as far as the quality of genetic functionality is concerned is quite novel. Such a definition is fundamentally opposed to all of mainstream science regarding the topic of origins.

    3. Your definition fails to consider the relevance of functional differences to reproductive isolation and population divergence. It ignores polymorphisms, for example, which can result in dramatic functional differences among individuals within a single population, yet the functionally distinct genotypes do not emerge as distinct species. These polymorphisms can be maintained by frequency-dependent selection (you probably need to Google this) within a single population. Genetic polymorphisms in alternative mating tactics, for example, are widespread among animals. Consider the many species of fish which have multiple (as many as four) genetically-based alternative mating tactics. Some males (territorial males) take a long time to achieve a large size, but then set up and defend territories from other males, and mate many females that enter their territory. Other males (sneaker males) quickly mature at a small size and, resembling a female, they sneak into the territories of the territorial males and obtain fertilizations by cuckoldry. Functionally, these mating tactics are very, very different, yet they are maintained within a single gene pool by frequency-dependent selection. Another example of a genetic polymorphism would be the European cuckoo, in which some female lineages prefer to brood parasitize (lay eggs in nest of) one particular songbird species, and other female lineages prefer to brood parasitize other particular songbird species. Again, you’ve got a major functional difference resulting in multiple females gentes (lineages), but males cross-mate them to maintain the cuckoo as a single species. Genetic-based morphological polymorphisms are also abundant, such as within the snow goose. The white versus blue individuals, having very distinctive colors, result in significant thermoregularly differences, yet the two groups formerly considered distinct species maintain a single gene pool.

    I have no problem with this. Such phenotypic differences are not based on anything new within the gene pool that was not already there in the ancestral gene pool beyond very low levels of functional complexity. It’s like the white vs. the black peppered moth. Same gene pool with multiple phenotypic options programmed into it. What’s your point?

    4. Your definition overlooks subtle traits that may be non-functional, but which can still lead to reproductive isolation and population divergence. Consider the gray treefrog (Hyla versicolor) and Cope’s gray treefrog (Hyla chrysoscelis). These are two broadly sympatric cryptic species that look identical. The former is diploid and the latter is tetraploid. They can be distinguished by comparing their calls relative to body temperature (i.e., one must know the body temperature) and by examining the size of their red blood cells, which differs because of DNA content. Their gene pools are maintained separately because hybrids would be triploid and gamete production via meiosis would break down. Your definition would synonymize these two taxa unless–and I wish you good luck–you could identify functional differences.

    These frogs are also derived from the same gene pool and are not functionally unique beyond low levels of functional complexity. The same is true for donkeys and horses. They are derived from the very same gene pool and are not functionally unique beyond very low levels of functional complexity. Yet, their offspring (mules/hinnies) are almost universally sterile because of non-functional differences in chromosomal structure (chromosomal number, inversions, etc.) between the two gene pools.

    http://www.detectingdesign.com/donkeyshorsesmules.html

    You do understand that I do actually find value in mainstream methods of defining taxonomic groups of organisms? – right? It is just that these methods do not suggest limits to evolutionary potential whereas my definition does. That’s the key difference.

    Sean Pitman
    http://www.DetectingDesign.com




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  75. Sean Pitman: 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?

    Two species could potentially differ by a single mutation if the mutation happens to code for a reproductive isolating mechanism (consistent with the Biological Species Concept).




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  76. Sean Pitman: [Professor Kent asked]: In other words, what trait(s), precisely, would block the gradual evolution of a fish to an amphibian, an amphibian to a reptile, or a reptile to a mammal?

    Anything novel between these groups that requires a minimum of more than 1000 specifically arranged amino acid parts would qualify (or an equivalent number of codons of DNA) – like the middle ear with tympanic membrane and ear bone in amphibians as well as the amphibian ability to metamorphosize to the adult stage (vs. no such middle ears with in fish or the ability to metamorphosize legs, lungs, etc.), or the amniotic eggs of reptiles with a tough leathery shell (vs. the soft watery gel that surrounds the eggs of amphibians), or the hair and sweat glands of mammals (compared to a lack of such in reptiles), or the true flight feathers of birds with their interlocking Velcro-like features (compared to a lack of such in true reptiles).

    Thank you for giving some examples. I remember Geanna Dane once asking for these, but you didn’t answer then.

    Sean Pitman: Some of these features might seem very close, morphologically, to certain structures within the proposed evolutionary pathways presented by neo-Darwinists. However, when one actually considers the underlying genetic programming that would be required to make the next morphologic step possible, it is well beyond what RM/NS could achieve in a reasonable amount of time.

    I would like to believe you, but I am skeptical and do not see this as an essential argument to support our mutually shared, faith-based view that God created these major groups.

    Sean Pitman: After all, if the pathways were really littered with such closely spaced steppingstones as evolutionists would have us believe, many of these proposed evolutionary steps, like in the evolution of the eye, could be reproduced in the laboratory…This is why such real time demonstrations have never been produced for such complex structures (like the eye or the flagellum, etc)… not even for the crossing of a single proposed evolutionary step between morphologic steps that are supposedly very tiny baby steps.

    You should know better than to offer this argument. The window of time to observe “real time demonstrations” is highly limited–at most hundreds of years, from which you cannot infer evolutionary potential over millions of years. After all, you (and I) insist that the many remarkable adaptations of venomous animals and predators have evolved in a relatively short time frame. These include the massive toxin molecules I’ve described (often many different types within a single organism); the often massive venom glands and venom delivery structures (like fangs, spines, and stingers); and even entirely novel organs and organ systems like the infrared vision of snakes and bats. You insist that all of these traits–which are as substantial in qualitatively functional terms as virtually any other traits you’ve mentioned–could evolve by a sequence of small steps, yet none have not been demonstrated or observed in real time. Thus, your arguments against the major transitions between animal groups invalidates your own arguments of gradual changes resulting in poisonous and venomous animals and predators.

    Frankly, I think you have a very hard time selling your argument that the differences between major animal groups (e.g., amphibians to reptiles, reptiles to mammals) could not be accomplished by multiple smaller steps. And I think your argument rests largely on a faith-based assumption that it cannot happen.




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    • @Professor Kent:

      You should know better than to offer this argument. The window of time to observe “real time demonstrations” is highly limited–at most hundreds of years, from which you cannot infer evolutionary potential over millions of years.

      Upon what basis do the individual steps in the evolution of the flagellar motility system, for example, require millions of years? Where is the statistical basis for determining how long a particular evolutionary step, at a particular level of functional complexity, should be expected to take? – given high selective pressure?

      This is the problem with the claims of evolutionists. They aren’t really based on testable scientific theories when it comes to the proposed creative potential of the actual evolutionary mechanism. No one does the math or calculates the odds of success for anything qualitatively novel to evolve, within any given span of time, at various levels of functional complexity.

      This means, of course, that the proposal that RM/NS could and did do the job is based on just-so story telling and philosophical assumptions, not science.

      In other words, extrapolations from low-level examples to high-levels of evolution taking place in “millions of years” aren’t based on any actual scientific evidence or rational statistical analysis. Neo-Darwinism isn’t valid science. It’s as simple as that.

      After all, you (and I) insist that the many remarkable adaptations of venomous animals and predators have evolved in a relatively short time frame. These include the massive toxin molecules I’ve described (often many different types within a single organism); the often massive venom glands and venom delivery structures (like fangs, spines, and stingers); and even entirely novel organs and organ systems like the infrared vision of snakes and bats. You insist that all of these traits–which are as substantial in qualitatively functional terms as virtually any other traits you’ve mentioned–could evolve by a sequence of small steps, yet none have not been demonstrated or observed in real time. Thus, your arguments against the major transitions between animal groups invalidates your own arguments of gradual changes resulting in poisonous and venomous animals and predators.

      As I’ve already explained, venom isn’t very complex when it comes to minimum size and specificity requirements. Other features, while being more complex, are degenerative from higher levels of functional complexity – like the TTSS system devolving from the flagellar motility system. Also, one must consider that malevolent design may also have been employed in the creation of certain features of living things which could not have evolved (or devolved) via any mindless mechanism.

      Frankly, I think you have a very hard time selling your argument that the differences between major animal groups (e.g., amphibians to reptiles, reptiles to mammals) could not be accomplished by multiple smaller steps. And I think your argument rests largely on a faith-based assumption that it cannot happen.

      Like I said before, you simply do not understand the nature of sequence space and the vast genetic distances that are involved within sequence spaces when you start talking about qualitatively novel systems within different gene pools that require a minimum of more than 1000 specifically arranged residue parts. When you actually sit down and do some relevant statistical analysis, you will soon discover that the creativity of RM/NS is very limited to very low levels of functional complexity this side of trillions of years of time.

      Sean Pitman
      http://www.DetectingDesign.com




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  77. Sean Pitman: All I asked you was if there was a single universally applicable and consistent definition of species? You’ve admitted that the answer to this question is no. There is no universal definition of a “species” group that is consistent in all cases.
    You also failed to provide a standardized genetic definition of a species group whereby a particular genetic distance in any one or any collection of genetic regions can be universally applied.
    Let me know if/when this situation changes…

    All true; so what’s your point? Where’s the problem? There’s no universally agreed upon view of hermeneutics, theology, flood geology, Biblical archaeology, or fulfillment of prophetic history among Christians. Does plurality of views among Christians invalidate the basis or practical value of Christianity?

    I suggest you rethink your argument if you really think it supports your view that your own highly unorthodox definition of species is superior to those used successfully by mainstream scientists for many decades.




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    • @Professor Kent:

      My definition is not a new definition of “species”. My definition is a definition of qualitatively novel gene pools that contain functional systems that go well beyond the powers of any mindless naturalistic mechanism to explain.

      Various species definitions have their place and their utility. However, not one of these taxonomic definitions draws a distinct line that marks the limits of what the evolutionary mechanism of RM/NS can explain. My definition does mark the “edge of evolution” when it comes to explaining the origin of functionally novel gene pools.

      Sean Pitman
      http://www.DetectingDesign.com




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  78. Sean Pitman: [regarding Pitman’s species-recognizing criteria for distinguishing small mouth vs. large mouth bass; bald vs. golden eagles; tiger vs. spotted salamanders; deer vs. cactus mice] There are no significant gene pool differences here (functionally speaking) compared to the ancestral gene pool…Same original gene pools without anything novel beyond very
    low levels of functional complexity . . .

    Thank you for answering this question. It’s clear that your definition of species contrasts sharply with any notion of species that exists in mainstream science. Why do you insist on making your definition correspond to the species level? Why not a higher taxonomic group? Or a baramin? Frankly, you have a difficult time selling your ideas to others when you insist on using your own very peculiar and poorly articulated terminology.

    Sean Pitman: You do understand that I do actually find value in mainstream methods of defining taxonomic groups of organisms? – right? It is just that these methods do not suggest limits to evolutionary potential whereas my definition does. That’s the key difference.

    No; I’m surprised by this admission. Up to this point, I don’t see how your comments could possibly be construed as seeing value in mainstream methods of taxonomy.

    I’d say the problem is that you conflate the need to properly define species with your need to show limits to evolutionary potential. If you understood better the practice of taxonomy and its place in evolutionary theory as a tool merely for generating hypotheses about relationships, you’d recognize that the two goals (deciphering taxonomic relationships, including ancestor-descendent relationships, versus determining limits to RM/NS) are at completely different levels of analysis.

    I think you’re also conflicted in that you need to:

    1) explain substantial evolutionary diversification after the flood by simultaneously insisting

    a) substantial change can happen with remarkable genetic potential despite the very severe problems of genetic bottlenecking

    b) while minimizing realized biodiversity by use of a narrower species definition (i.e., to imply that much fewer than 400 species of a particular bird group restricted to the New World evolved in just a few thousand years)

    and

    2) show that only baby steps can happen as animals lurch forward with dramatic diversification even though the remarkable genetic potential for change has gradually but surely eroded, and continues to do so.

    You’re quite the expert at juggling a lot of seemingly incompatible notions. I commend you for your imagination, tenacity, and faith-based adherence to the claims of scripture.




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    • @Professor Kent:

      Thank you for answering this question. It’s clear that your definition of species contrasts sharply with any notion of species that exists in mainstream science.

      That is because, as already noted, my definition isn’t a species definition. My definition is a definition of the limits of the creative potential of RM/NS this side of trillions of years of time.

      Why do you insist on making your definition correspond to the species level?

      I don’t. The species concept, as I’ve already explained quite extensively in this and other threads, is almost entirely unrelated to the concept of levels of functional complexity and the limits that these levels place on potential evolutionary progress via the mechanism of RM/NS.

      Why not a higher taxonomic group? Or a baramin? Frankly, you have a difficult time selling your ideas to others when you insist on using your own very peculiar and poorly articulated terminology.

      If you’re trying to say that I’m in a distinctively minority position when it comes to the opinions of mainstream scientists, you’re obviously correct. If most accepted my ideas neo-Darwinism wouldn’t be nearly as popular an idea.

      No; I’m surprised by this admission. Up to this point, I don’t see how your comments could possibly be construed as seeing value in mainstream methods of taxonomy.

      That’s because this discussion isn’t about the value of mainstream taxonomy. It’s about the potential and limits of the evolutionary mechanism of RM/NS – which isn’t part of modern taxonomic classification systems.

      I’d say the problem is that you conflate the need to properly define species with your need to show limits to evolutionary potential.

      You’re the one who thinks I’m trying to redefine the species concept. I’m not. I’m only trying to defined the limits of the evolutionary mechanism – and to note that these limitations are not defined by any modern species concept.

      If you understood better the practice of taxonomy and its place in evolutionary theory as a tool merely for generating hypotheses about relationships, you’d recognize that the two goals (deciphering taxonomic relationships, including ancestor-descendent relationships, versus determining limits to RM/NS) are at completely different levels of analysis.

      Exactly – which is my main point here. I’m glad we’re in agreement on this key point.

      I think you’re also conflicted in that you need to:

      1) explain substantial evolutionary diversification after the flood by simultaneously insisting

      a) substantial change can happen with remarkable genetic potential despite the very severe problems of genetic bottlenecking

      Genetic bottlenecking is much more of a problem today than it was closer to Creation Week because of the substantial build-up of detrimental mutations in all slowly-reproducing gene pools – as already explained numerous times in this thread.

      b) while minimizing realized biodiversity by use of a narrower species definition (i.e., to imply that much fewer than 400 species of a particular bird group restricted to the New World evolved in just a few thousand years)

      Because modern species concepts are not related to the concept of levels of functional complexity, it is very easy to realize numerous “species” in a very short time via various forms of reproductive isolation and genetic changes at very low levels of functional complexity.

      and

      2) show that only baby steps can happen as animals lurch forward with dramatic diversification even though the remarkable genetic potential for change has gradually but surely eroded, and continues to do so.

      The potential for genetic change has not been eroded at all. Genetic mutations continue to affect all gene pools at a very rapid pace. It is just that the functional quality of slowly-reproducing gene pools has eroded over time in that there are far more detrimental mutations within all such genomes than there were right after the Flood.

      It is for this reason that all slowly-reproducing gene pools are headed for eventual genetic meltdown and extinction.

      You’re quite the expert at juggling a lot of seemingly incompatible notions. I commend you for your imagination, tenacity, and faith-based adherence to the claims of scripture.

      The various concepts I’ve presented to you regarding the potential and limits of RM/NS only seem incompatible to you because you’ve spent very little if any time considering what actually happens to this mechanism at various levels of functional complexity. Once you actually start to investigate the concept of levels of functional complexity and the nature of sequence space at various levels of functional complexity, things will start to come into focus for you too… and you’ll be able to move beyond your more or less empirically blind faith to a more rational understanding of the claims of the Bible regarding origins.

      Sean Pitman
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        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
        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.
        3] You allow for rapid development of phenotype and novel repurposing of proteins in the development of evenomation
        4] You claim some value for a limit of 1000fsaar but do not seem able to identify concrete examples of this during speciation.
        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
        http://www.ncbi.nlm.nih.gov/pubmed/19212409
        http://www.ncbi.nlm.nih.gov/pubmed/19718026
        http://www.ncbi.nlm.nih.gov/pubmed/21270892
        http://www.ncbi.nlm.nih.gov/pubmed/20448178

        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.
        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.

        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.

        The 29 genome project would be the place to start in defining the limits between for example rat vs mouse cat dog sloth armadillo little brown bat and fruit bat.

        http://www.ncbi.nlm.nih.gov/pubmed/21993624

        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.

        http://www.ncbi.nlm.nih.gov/pubmed/20981092

        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.

        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.




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        • @Pauluc:

          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
          http://www.ncbi.nlm.nih.gov/pubmed/19212409
          http://www.ncbi.nlm.nih.gov/pubmed/19718026
          http://www.ncbi.nlm.nih.gov/pubmed/21270892
          http://www.ncbi.nlm.nih.gov/pubmed/20448178

          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:

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

          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.

          http://www.ncbi.nlm.nih.gov/pubmed/20981092

          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
          http://www.DetectingDesign.com




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      • @Sean Pitman:
        Sean Pitman claims

        “The various concepts I’ve presented to you regarding the potential and limits of RM/NS only seem incompatible to you because you’ve spent very little if any time considering what actually happens to this mechanism at various levels of functional complexity. Once you actually start to investigate the concept of levels of functional complexity and the nature of sequence space at various levels of functional complexity, things will start to come into focus for you too… ”

        Sean I know it may seem to you that on these issues you alone have clarity of thought and knowledge that supercedes all other scientists who may disagree with you. But this is the perspective of all who are on a “mission from God”. I do think it a little arrogant to presume to know what precisely excercises the mind of Prof Kent or that the aspects of biology he investigates professionally does not at all address the issues you raise.

        I have read your ppt “All I Need is Time” and presume it an accurate portrayal of your perspective. To gain insight you suggest I should investigate

        1] The RM/NS mechanism at various levels of functional complexity.
        2] The nature of sequence space at various levels of functional complexity.

        I therefore did what any biologist would do did a pubmed search. Herein lies a problem.
        A pubmed search for”random mutation AND natural selection AND functional complexity” yeilded 5 references none particularly helpful.
        “protein evolution AND functional complexity” yields 424 publications with some fascinating papers few if any supporting your views on natural selection, sequence space and complexity. Papers on PDZ domain containing proteins is particularly relevant to your model of complexity. One in particularly I think you should address in your model.

        http://www.ncbi.nlm.nih.gov/pubmed/19738200

        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.

        Where I think scientists like Prof kent and myself and you seem to be at cross purposes is in our broad approach.

        You make an assumption that a certain aspect of science is impossible on theoretical grounds. You accept that theoretical model and construct increasing elaborate scenarios to preserve that model in the face of biological observations. We start with simple observation and construct models driven by the biological observations.

        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.
        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.




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        • @pauluc:

          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.

          http://www.detectingdesign.com/flagellum.html#Calculation

          Sean Pitman
          http://www.DetectingDesign.com




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  79. Sean Pitman: @Eddie:
    Is the Biological Species Concept universally applied? Unfortunately no. Also, reproductive isolation is not necessarily genetically based or obligatory. There are a great many examples of different “species” that can interbreed to produce viable and even virile offspring.

    Your remarks are so odd, coming from one whose definition is universally not applied.




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  80. Sean Pitman: In other words, extrapolations from low-level examples to high-levels of evolution taking place in “millions of years” aren’t based on any actual scientific evidence or rational statistical analysis. Neo-Darwinism isn’t valid science. It’s as simple as that.

    And you think that extrapolations based on math, suggesting that such changes are impossible, and therefore inferring only God could do it, is valid science as opposed to faith?

    Sean Pitman: Also, one must consider that malevolent design may also have been employed in the creature of certain features of living things which could not have evolved (or devolved) via any mindless mechanism.

    Wow. Could you please share some examples of God’s “malevolent design?”




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    • @Professor Kent:

      And you think that extrapolations based on math, suggesting that such changes are impossible, and therefore inferring only God could do it, is valid science as opposed to faith?

      The scientific basis for detecting the need to invoke intelligent design to explain any phenomenon is based on the known statistical limitations of what non-intelligent mechanisms are likely to be able to achieve. How else could you tell the difference between a naturally carved rock and a deliberately formed artifact – like an arrowhead or a highly symmetrical granite cube? – or a SETI radio signal?

      There is a scientific basis to detecting design that can be universally applied – even to information systems like that contained in the DNA of living things.

      Wow. Could you please share some examples of God’s “malevolent design?”

      God isn’t the only intelligent agent capable of intelligent action on this planet…

      Matthew 13:27-28

      Sean Pitman
      http://www.DetectingDesign.com




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  81. Sean Pitman: My definition is not a new definition of “species”. My definition is a definition of qualitatively novel gene pools that contain functional systems that go well beyond the powers of any mindless naturalistic mechanism to explain.

    This concession on your part comes as a bit of a surprise given the manner in which you contrasted existing species definitions with your definition (e.g., your comment on June 30, 2012 at 8:48 am). Nevertheless, I see you’ve made some progress in your thinking.

    Sean Pitman
    Various species definitions have their place and their utility. However, not one of these taxonomic definitions draws a distinct line that marks the limits of what the evolutionary mechanism of RM/NS can explain.

    Of course they don’t. No one has ever suggested they do. I encourage you to make up your mind: do you embrace (as you recently stated) or reject (as you’ve hinted all along) any utility of species definitions? If you’re going to continue criticizing existing species definitions, you should criticize them for what they actually address, not the attributes you seem to think they should address.

    Sean PitmanMy definition does mark the “edge of evolution” when it comes to explaining the origin of functionally novel gene pools.

    Your definition of what? You’ve represented it as the most suitable definition of a taxonomic entity, so what is its name if not a species? Personally, I think you’re trying to define the boundary between macroevolution and megaevolution–which is not at all a taxonomic unit.




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    • @Professor Kent:

      This concession on your part comes as a bit of a surprise given the manner in which you contrasted existing species definitions with your definition (e.g., your comment on June 30, 2012 at 8:48 am). Nevertheless, I see you’ve made some progress in your thinking.

      Many creationists think that no new species can evolve. Given the numerous modern definitions of the concept of “species”, none of which are based on levels of functional complexity, this common creationist argument is mistaken.

      That is why I draw a contrast between my definition of limitations to what can and cannot evolve via RM/NS and the modern concept of “species”. Also, my definition can be universally applied . . .

      Various species definitions have their place and their utility. However, not one of these taxonomic definitions draws a distinct line that marks the limits of what the evolutionary mechanism of RM/NS can explain. – Sean Pitman

      Of course they don’t. No one has ever suggested they do.

      Exactly my point. Practically no one in mainstream science recognizes any limitation to the creative potential of RM/NS based on levels of functional complexity.

      I encourage you to make up your mind: do you embrace (as you recently stated) or reject (as you’ve hinted all along) any utility of species definitions?

      Not when it comes to determining the potential and/or limits to the mechanism of RM/NS – no. The modern species concept simply is not useful here. And yet, this is the topic in play in this particular forum.

      If you’re going to continue criticizing existing species definitions, you should criticize them for what they actually address, not the attributes you seem to think they should address.

      Again, this forum is entirely about the potential and limits of RM/NS as an evolutionary mechanism. This forum is not about the various potential uses of taxonomy that are not related to the main topic of discussion.

      Your definition of what? You’ve represented it as the most suitable definition of a taxonomic entity, so what is its name if not a species? Personally, I think you’re trying to define the boundary between macroevolution and megaevolution–which is not at all a taxonomic unit.

      That’s right. Such boundaries are not part of any modern definitions of taxonomic classification. That’s my point here. My definition is unique in that it does specify the limitations of mindless naturalistic mechanisms when it comes to explaining qualitatively novel genetic elements in different gene pools beyond very low levels of functional complexity…

      Sean Pitman
      http://www.DetectingDesign.com




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  82. Sean Pitman: …and you’ll be able to move beyond your more or less empirically blind faith to a more rational understanding of the claims of the Bible regarding origins.

    Any reader here recognizes that the Bible makes relatively few claims regarding origins compared to those you make. The Bible claims God created all living life forms on this planet within a 6-day span. One can only infer that this event happened in the recent past; the Bible itself makes no such claims. Further, the Bible makes no claims about the creative limits of RM/NS (it says absolutely nothing about mutations or natural selection), the eventual demise of all slowly-reproducing animals, the distribution of life forms in the geologic column (the incontrovertible sequence from simple to complex) or explanations of it, the timing of glaciation events relative to the flood, the relative abundance of different radioisotopes, and so forth that form your elaborate construct which you call “reason” to believe God’s word regarding origins can be trusted.

    If you wish to put me down–hardly for the first time–for accepting Scripture’s claim(s) based on reliance on God’s word rather than all the other empirical claims you believe support your view, you’re certainly entitled to that. My belief in this regard is no different than that of the vast majority of faithful Christians prior to the first books that appeared in the creationist literature.

    Most readers here recognize that you derogate my faith and that of other like-minded SDA scientists not because we believe differently than you do regarding origins (many of us embrace young life creationism), but because we have arrived at our beliefs for different reasons. We’re amused that you insist your faith is superior and that ours is as useless as belief in the Tooth Fairy, Santa Claus, and the Flying Spaghetti Monster. Highly amused.




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    • @Professor Kent:

      Any reader here recognizes that the Bible makes relatively few claims regarding origins compared to those you make. The Bible claims God created all living life forms on this planet within a 6-day span. One can only infer that this event happened in the recent past; the Bible itself makes no such claims.

      While the Bible doesn’t list a specific date B.C.E for the creation week, the Bible is quite clear that it was in fact a recent historical event – i.e., within the last 10,000 years or so (certainly not millions of years ago).

      Further, the Bible makes no claims about the creative limits of RM/NS (it says absolutely nothing about mutations or natural selection), the eventual demise of all slowly-reproducing animals, the distribution of life forms in the geologic column (the incontrovertible sequence from simple to complex) or explanations of it, the timing of glaciation events relative to the flood, the relative abundance of different radioisotopes, and so forth that form your elaborate construct which you call “reason” to believe God’s word regarding origins can be trusted.

      The creation of all life within recent history via a 6-day creation week event, together with a Noachian Flood, necessitates the observation of certain features of living things if such a story is to be rationally credible. Also, the Bible does indeed describe the degeneration of vitality of living things and the wearing out of the planet over time.

      The Bible’s claims are consistent with the observed laws of informational entropy while mainstream science is inconsistent with these laws.

      If you wish to put me down–hardly for the first time–for accepting Scripture’s claim(s) based on reliance on God’s word rather than all the other empirical claims you believe support your view, you’re certainly entitled to that. My belief in this regard is no different than that of the vast majority of faithful Christians prior to the first books that appeared in the creationist literature.

      The weight of evidence shifts over time. As new evidence comes to light, it forces those who appreciate the empirical basis for faith to re-evaluate prior notions of truth. Those who refuse to do this, who will not evaluate their positions in light of new evidence, cannot be subject to potential falsification or any change of mind for any reason. These hold their positions blindly regardless of anything that may be presented. Many people in various faith traditions, to include many SDAs, are of this mindset – as are you.

      Your arguments tend to tear down a rational basis for faith for many people since you continually argue that the Bible must be accepted almost entirely on faith that is blind to empirical evidence – in the face of what you claim is the best science for the explanation of life on this planet. For many people, your faith position is irrational. I am one of those who, if I believed like you believe regarding the validity of mainstream science, would be forced to leave not only Adventism behind, but Christianity as well.

      Most readers here recognize that you derogate my faith and that of other like-minded SDA scientists not because we believe differently than you do regarding origins (many of us embrace young life creationism), but because we have arrived at our beliefs for different reasons. We’re amused that you insist your faith is superior and that ours is as useless as belief in the Tooth Fairy, Santa Claus, and the Flying Spaghetti Monster. Highly amused.

      Empirical evidence is no laughing matter. It is important to the faith position of many many people – a concept you seem to take lightly. So far, the current Adventist Church leadership recognizes the importance of providing an empirical basis for faith in the credibility of the claims of the Bible. If few were at all concerned along these lines, no one would care if any of our schools, like LSU in particular, promoted the scientific validity of neo-Darwinism or not…

      Sean Pitman
      http://www.DetectingDesign.com




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  83. Sean Pitman: The various concepts I’ve presented to you regarding the potential and limits of RM/NS only seem incompatible to you because you’ve spent very little if any time considering what actually happens to this mechanism at various levels of functional complexity. Once you actually start to investigate the concept of levels of functional complexity and the nature of sequence space at various levels of functional complexity, things will start to come into focus for you too… and you’ll be able to move beyond your more or less empirically blind faith to a more rational understanding of the claims of the Bible regarding origins.

    Why is it that so many geneticists arrive at a different conclusion? Is it because they spend less time investigating levels of functional complexity and sequence spacing than you do? Or because their conclusions are based on faith, unlike yours?




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    • @Eddie:

      Why is it that so many geneticists arrive at a different conclusion? Is it because they spend less time investigating levels of functional complexity and sequence spacing than you do? Or because their conclusions are based on faith, unlike yours?

      This is a difficult question, but it may have to do with the fact that most scientists are brought up from childhood indoctrinated in Darwinian thinking. They are never taught to question this untouchable doctrine. Beyond this, when one does think to question it, they experience heavy peer pressure to stop doing so – to the point of having their careers put in jeopardy.

      Regardless of the reasons, it is a fact that very few published papers even discuss the concept of levels of biological complexity – and none discuss the specific limitations that these levels place on the evolutionary mechanism of RM/NS when it comes to the average expected time needed to evolve anything novel at various levels.

      Sean Pitman
      http://www.DetectingDesign.com




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  84. Sean Pitman: Again, this forum is entirely about the potential and limits of RM/NS as an evolutionary mechanism. This forum is not about the various potential uses of taxonomy that are not related to the main topic of discussion.

    This is, of course, the Sean Pitman forum. It’s whatever you decide it should be–whatever educated truth is.

    Sean Pitman: the Bible does indeed describe the degeneration of vitality of living things and the wearing out of the planet over time. The Bible’s claims are consistent with the observed laws of informational entropy.

    Where are these claims? Human longevity declined, but where do we read that other life forms have degenerated? And how would the remarkable diversity we see today, which has come about subsequent to the extremely severe genetic bottleneck of the flood, be seen as degeneration?

    Sean Pitman: The weight of evidence shifts over time. As new evidence comes to light, it forces those who appreciate the empirical basis for faith to re-evaluate prior notions of truth. Those who refuse to do this, who will not evaluate their positions in light of new evidence, cannot be subject to potential falsification or any change of mind for any reason. These hold their positions blindly regardless of anything that may be presented. Many people in various faith traditions, to include many SDAs, are of this mindset – as are you.

    You have a remarkably dim view toward those who do not share your special talent in deducing all sorts of specific details that God neglected to share with us.




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  85. Sean Pitman: Your arguments tend to tear down a rational basis for faith for many people since you continually argue that the Bible must be accepted almost entirely on faith that is blind to empirical evidence – in the face of what you claim is the best science for the explanation of life on this planet.

    You remain as clueless as ever. I have never argued the Bible must be accepted almost entirely on faith that is blind to empirical evidence. I have simply stated, many times, that SDAs and most honest YLCs accept the origins account (and other miraculous claims in scripture that cannot be verified by science) largely on faith. Will you never stop denigrating faith?

    Sean Pitman: Empirical evidence is no laughing matter.

    What’s laughable is when one elevates their own reason and intelligence ahead of God’s sure word.




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    • @Professor Kent:

      The determination that the Bible is in fact the sure Word of God can be, and I think should be, based on reason and intelligence – The Bible itself advises us to use our God-given powers to think and reason to determine what is and isn’t true, based on the “weight of evidence”, among the many “Holy Books” or individuals who claim to contain or speak the words of God (Isaiah 1:18; 1 Peter 3:15; 1 John 4:1).

      “The human mind is endowed with power to discriminate between right and wrong. God designs that men shall not decide from impulse, but from weight of evidence… – Ellen G. White, Desire of Ages, p. 458

      Sean Pitman
      http://www.DetectingDesign.com




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  86. Sean Pitman: The determination that the Bible is in fact the sure Word of God can be, and I think should be, based on reason and intelligence

    No objection here whatsoever.

    Once accepted as the word of God, there are many claims in scripture beyond the purview of science that can only be accepted on faith (subject to appropriate interpretation), including a literal six-day creation week and a global flood (not to mention the floating axehead, virgin birth of Jesus, and resurrection of long-deceased human bodies). Seventh-day Adventists accept these claims on faith. And if these claims clearly contradict all available science (which the floating axehead, virgin birth, and resurrection of a deceased body most certainly do), Seventh-day Adventists do not then reject the Bible and Christianity in their entirety. Sean Pitman may, but true SDAs do not.




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    • @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
      http://www.DetectingDesign.com




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

    Ain’t gonna happen, Pauluc. And remarkably, no one seems to want to become famous by scooping Sean’s math.

    Pauluc: You [Sean Pitman] might like to also comment on your 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.

    Very fascinating problem! Seems someone could do some math on mutation rates over the 4,000-year time span.




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  88. Sean Pitman: Certainly all variation at lower levels of functional complexity could easily be realized in this period of time.

    This faith-based claim simply cannot be demonstrated.

    Sean Pitman: 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).

    You failed to indicate where the 1,000-fsaar gap would be. Where is the evidence these changes could not occur via gradual stepwise change? You’ve argued vociferously that all dog breeds could be derived from a single pair within 4,000 years (you’ve made a case for most occuring in 300 years), why couldn’t these closely-related apes evolve over millions of years?

    Sean Pitman: 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.

    Where are the 1,000-fsaar gaps?




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    • @Professor Kent:

      Again, the gap is not 1000aa for a 1000aa system. The 1000aa specified system is a system that is at a level of complexity that is unevolvable. The minimum gap distance, as explained to you several times before, is always smaller, much smaller, than the minimum size requirement for a specified system.

      There are many unique phenotypic differences between apes and humans, to include differences in the form and function of the brain, which require far more than 1000 specifically coded positions. The minimum gap distances produced by this level of functional complexity always less than 1000aa differences, but only a few dozen required differences are all that it takes to make a system unreachable via the evolutionary mechanism (explained further below).

      Sean Pitman
      http://www.DetectingDesign.com




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  89. Sean Pitman: [@ Pauluc] 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?

    Disregarding bacterial examples (which could have arrived from another galaxy), here are the examples Sean provided earlier to argue that transitions between major animal groups (e.g., amphibians to reptiles, reptiles to mammals or birds) would be impossible:

    Sean Pitman in a prior post: Anything novel between these groups that requires a minimum of more than 1000 specifically arranged amino acid parts would qualify (or an equivalent number of codons of DNA) – like the middle ear with tympanic membrane and ear bone in amphibians as well as the amphibian ability to metamorphosize to the adult stage (vs. no such middle ears with in fish or the ability to metamorphosize legs, lungs, etc.), or the amniotic eggs of reptiles with a tough leathery shell (vs. the soft watery gel that surrounds the eggs of amphibians), or the hair and sweat glands of mammals (compared to a lack of such in reptiles), or the true flight feathers of birds with their interlocking Velcro-like features (compared to a lack of such in true reptiles).

    I’d like to know how many specifically arranged amino acid parts would be necessary for each these traits. I see no reason why smaller baby steps can’t accomplish these transitions.

    Very dramatic mutations can result in entire supernumery limbs appearing out of place in both invertebrates and vertebrates, so I don’t see any difficulty with extra bones showing up in the ear.

    Regarding the evolution of hair, a prior study found chickens, lizards, and humans all possessed a similar set of genes that was involved in the production of alpha keratin. In chickens and lizards, the α-keratin produced was found in their claws, but in mammals it was used to produce hair.

    Speaking of the leathery eggs of reptiles, there are individual species which exhibit vivipary (live birth), ovovivipary (egg retained internally until birth), or ovipary (egg-laying) depending on where they live. And many embryologists no longer recognize these three categories, as there appears to be a continuum from live-bearing to egg-laying. Doesn’t seem to me the differences are all that insurmountable.




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    • @Professor Kent:

      I never said that all reptiles produce leathery eggs. What I said was that there are those that do and that this particular feature is a complex feature not found in amphibians.

      As far as the range of differences which you think are spaced closely enough for evolutionary mechanisms to realize, you simply do not understand the number of underlying genetic changes that would be required to cross between any one of your proposed steppingstones (see my response and references to your comment below).

      Sean Pitman
      http://www.DetectingDesign.com




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  90. Regarding the possible evolution of feathers in birds, information for producing feathers exists in the genes of the American Alligator, but the instructions are suppressed during embryological development, causing alligator hatchlings to produce only scales. Again, I don’t see a single huge step to go from featherless to feathered.

    When one considers the dramatic variation in feather types that exists today–from simple (single filament) to complex (with barbs and barbules), I don’t see a single 1,000-fsaar step as being necessary for this transition.




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    • @Professor Kent:

      Regarding the possible evolution of feathers in birds, information for producing feathers exists in the genes of the American Alligator, but the instructions are suppressed during embryological development, causing alligator hatchlings to produce only scales. Again, I don’t see a single huge step to go from featherless to feathered.

      Individual genes usually code for basic building blocks that can be used for very different purposes in different creatures. For example, humans and sea anemones share numerous genes, used for different purposes, that are not present in plants or animals that are supposedly much more closely “related” to the sea anemone.

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

      Regardless, the fact remains that flight feathers are complex structural systems that require far more than 1000 specifically coded residue positions where each position must be specifically coded relative to all the other positions in the system (involving many genes).

      Such a system could not have evolved from any gene pool where the original ancestors of that gene pool did not have the genetic code for a such a system. Such a complex system may be lost over time (as is the case with cave fish who have lost the ability to make eyes). However, such a system cannot be evolved via RM/NS.

      When one considers the dramatic variation in feather types that exists today–from simple (single filament) to complex (with barbs and barbules), I don’t see a single 1,000-fsaar step as being necessary for this transition.

      As I’ve explained to you numerous times before, the genetic distance between qualitatively novel systems that a require at least 1000 specifically arranged parts is never 1000aa differences. The Hamming distance is sequence space is always smaller, much smaller, than the minimum size/specificity requirement for the complex system.

      The Hamming distance need only be a few dozen required residues changes in order to be uncrossable by random mutations in what anyone would consider to be a reasonable amount of time.

      This is the same basic misunderstanding of the impact of the minimum likely gap distances that effectively block what might otherwise seem like small phenotypic steps between a proposed evolutionary “spectrum” of existing phenotypes… like the variation “spectrum” that exists between different types of eyes for example.

      The problem, of course, is that the gap distance between each one of the proposed steppingstones in such evolutionary sequences is far far too far for the evolutionary mechanism of RM/NS to actually cross.

      For further information on this topic, please refer to the following links:

      http://www.detectingdesign.com/flagellum.html#Calculation

      http://www.detectingdesign.com/humaneye.html#Nilsson

      http://sciencepolice2010.wordpress.com/2011/02/04/oh-what-a-tangled-web-he-weaves/

      Sean Pitman
      http://www.DetectingDesign.com




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  91. Adam, Eve, and sons and daughters of Noah

    Adam

    By analyzing the Y-chromosome DNA from males in all regions of the world, geneticist Spencer Wells has concluded that all humans alive today are patrilinealy descended from a single man who lived in Africa around 60,000 years ago.[2]

    http://news.nationalgeographic.com/news/2002/12/1212_021213_journeyofman.html

    Eve

    Calibrating the Mitochondrial Clock

    http://tinyurl.com/bmcv46b

    criticism of young age is premature

    http://creation.com/mitochondrial-eve-and-biblical-eve-are-looking-good-criticism-of-young-age-is-premature

    Sons of Noah?
    Global variation in copy number in the human genome

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2669898/?tool=pubmed

    Mitochondrial diversity within modern human populations
    Robert W. Carter
    Noah’s three “daughters”?
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1888801/
    The most recent common ancestor of all humanity lived just a few thousand years ago, according to a computer model of our family tree. Researchers have calculated that the mystery person, from whom everyone alive today is directly descended, probably lived around 1,500 BC in eastern Asia
    http://www.nature.com/news/2004/040927/full/news040927-10.html




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  92. Sean

    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.
    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.
    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.
    4] Most (80-90%) of the phenotypic differences seen between species has occurred by natural selection and genetic drift.
    5] Any differences due to RM/NS after selecting the front-loaded pair can only confer very very low level complexity.
    6] There is a barrier of 1000fsaar that limits any ability to generate anything novel and complex within this 80-90% of new mutations.

    Apropos of the recent paper

    http://www.ncbi.nlm.nih.gov/pubmed/22457641

    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 about genetics of feathers and the regulation of genes controlling feathered phenotype.




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    • @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
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        “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 may well be dense in not understanding your view of the primacy of mathematical modelling.

        We have had this discussion before apropos of the paper by ferrada on novel function in proteins.

        As I see it your modelling and statistics is largely based on the premise that functional sequence/s must derive denovo and that the probability of this is infinitely small is akin to questions surrounding abiogenesis. I do not have any knowledge of that and do not think it is a question worth asking. To me it must at this time be relegated to the realm of non-science as there is no obvious mechanism for testing it. A conclusion perhaps reinforced by the lack of any significant literature on this, a finding that you have articulated on this thread and attributed to the lack of insight by scientists.

        In terms of the reality of speciation and the associated functional change in existing sequences your statistical inferences premised as they are on assumptions about denovo production are not really helpful, at least in the mind of practising scientists.

        The reality is that we agree that speciation has occurred largely due to new mutational changes in your case you say accumulating within 4000 years.

        Now that is a question that can be addressed and will be addressed with rapid genomic sequencing and analysis. My predication is that there will be at the genomic level no essential qualitative difference in the process of genetic change for speciation/genetic diversity between subspecies like Neandertal and Denisova and between primates.
        If you disagree the onus is on you to provide the evidence within this or other mammalian groups to show that there is some qualitative barrier at the level of a “kind”. If you think there is a 1000fsaar limit then show where that would apply in primate phylogeny.




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  93. Sean
    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. 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.

    http://www.ncbi.nlm.nih.gov/pubmed/22412940
    Analysis of human accelerated DNA regions using archaic hominin genomes.

    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?

    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.




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    • @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
      http://www.DetectingDesign.com




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  94. Sean

    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.
    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.
    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.
    4] Most (80-90%) of the phenotypic differences seen between species has occurred by natural selection and genetic drift.
    5] Any differences due to RM/NS after selecting the front-loaded pair can only confer very very low level complexity.
    6] There is a barrier of 1000fsaar that limits any ability to generate anything novel and complex within this 80-90% of new mutations.

    Apropos of the recent paper

    http://www.ncbi.nlm.nih.gov/pubmed/22457641

    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 about genetics of feathers and the regulation of genes controlling feathered phenotype.




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    • @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
      http://www.DetectingDesign.com




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      • @Sean Pitman:

        “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 may well be dense in not understanding your view of the primacy of mathematical modelling.

        We have had this discussion before apropos of the paper by ferrada on novel function in proteins.

        As I see it your modelling and statistics is largely based on the premise that functional sequence/s must derive denovo and that the probability of this is infinitely small is akin to questions surrounding abiogenesis. I do not have any knowledge of that and do not think it is a question worth asking. To me it must at this time be relegated to the realm of non-science as there is no obvious mechanism for testing it. A conclusion perhaps reinforced by the lack of any significant literature on this, a finding that you have articulated on this thread and attributed to the lack of insight by scientists.

        In terms of the reality of speciation and the associated functional change in existing sequences your statistical inferences premised as they are on assumptions about denovo production are not really helpful, at least in the mind of practising scientists.

        The reality is that we agree that speciation has occurred largely due to new mutational changes in your case you say accumulating within 4000 years.

        Now that is a question that can be addressed and will be addressed with rapid genomic sequencing and analysis. My predication is that there will be at the genomic level no essential qualitative difference in the process of genetic change for speciation/genetic diversity between subspecies like Neandertal and Denisova and between primates.
        If you disagree the onus is on you to provide the evidence within this or other mammalian groups to show that there is some qualitative barrier at the level of a “kind”. If you think there is a 1000fsaar limit then show where that would apply in primate phylogeny.




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  95. Sean

    1] I’m afraid I am going to once again have to pass on your suggestion for wasting more time than I have in responding to your mantra about probability and complexity. Like accountants statistic is my servant not my master.
    I disagree with your bottom up approach of looking at data from some preconceived theoretical reality. You model sequence space as being the arbiter of reality and your basis for accepting it is an immovable faith position not an attempt to model real observations. I approach the reality of speciation in a top down fashion the same way as Darwin did; we have evidence for speciation (which you do seem to accept) but how did this happen at the genome and molecular and is there evidence of limitations?

    2] Your fixation on the front loading of genetic information ina a breeding pair seems impervious to logical or mathematical argument and you do not seem to be able to accept what any population geneticist would immediately see. 2 individuals is a gene puddle not a gene pool and arguments about evolution by allelic selection is completely unrealistic.

    3] I do not think you have actually read the references I have suggested as relevant to discussions on mechanisms of speciation. If you have, you seem to have read them as an apologist not as a scientist and see only what you want to see instead of reading the publication for what is the message of that publication.

    4] When I ask for an example of instances of 1000fsaar limitation in the human vs chimp comparisons I was, as a scientist, thinking perhaps you would give me a relevant response with some specificity including minimally a gene ID or base sequence ID so I can actually check what you are talking about.




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  96. Sean

    1] I’m afraid I am going to once again have to pass on your suggestion for wasting more time than I have in responding to your mantra about probability and complexity. Like accountants statistic is my servant not my master.
    I disagree with your bottom up approach of looking at data from some preconceived theoretical reality. You model sequence space as being the arbiter of reality and your basis for accepting it is an immovable faith position not an attempt to model real observations. I approach the reality of speciation in a top down fashion the same way as Darwin did; we have evidence for speciation (which you do seem to accept) but how did this happen at the genome and molecular and is there evidence of limitations?

    2] Your fixation on the front loading of genetic information ina a breeding pair seems impervious to logical or mathematical argument and you do not seem to be able to accept what any population geneticist would immediately see. 2 individuals is a gene puddle not a gene pool and arguments about evolution by allelic selection is completely unrealistic.

    3] I do not think you have actually read the references I have suggested as relevant to discussions on mechanisms of speciation. If you have, you seem to have read them as an apologist not as a scientist and see only what you want to see instead of reading the publication for what is the message of that publication.

    4] When I ask for an example of instances of 1000fsaar limitation in the human vs chimp comparisons I was, as a scientist, thinking perhaps you would give me a relevant response with some specificity including minimally a gene ID or base sequence ID so I can actually check what you are talking about.




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  97. Professor Kent: We see evidence almost everywhere we look for the ongoing creativity of natural selection among both slow- and fast-reproducing life forms.

    For those who still question this very basic tenet of evolutionary biology/scientific creationism, which Dr. Pitman has aggressively supported with his arguments as of late, simply do a search at scholar.Google.com of “selection acting on.” You’ll find many thousands of publications documenting ongoing natural selection. Perhaps you’ll agree with Dr. Pitman that God himself created this fabulous evolutionary process so that life could better adapt to a sinful, ever-changing planet. (And how else could we possibly get millions of terrestrial animal species from the relative handful that survived inside the ark?)




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    • @Professor Kent:

      I’m not sure why you think it is news that random mutations happen and that novel allelic variations are often the result. There is no argument here among creationists. The argument is over the neo-Darwinist position that these changes can actually cross the line from very low levels to higher levels of functional complexity.

      That’s the real disagreement between creationists and evolutionists. Evolutionists do not recognize the limitations of the Darwinian mechanism. They do not recognize any point beyond which only an intelligent agent could step across the line.

      Sean Pitman
      http://www.DetectingDesign.com




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