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Life Project Architecture

A point that Darwinists make is that anti-Darwinists have not developed any theory for the origins of species, and think that is a weakness. But for an IDer/creationist is not so difficult to have ideas about solutions of the problem of origins. I for one developed a proposal for a theory, and I will illustrate it here. I called it “LPA” (Life Project Architecture). See below its simple schema, where the x-axis is time and the y-axis the top-down intelligent causation:

LPA model for origins is cent percent design based. The role of natural selection, about the creation of biological information and complexity, is null. To grasp LPA one must entirely invert the reasoning of evolutionism. This means in the same time to assume a solid informatics engineering perspective and apply it to biology.

 

An axiom of Darwinism is the corporeal descent of all species from a simple unique corporeal common ancestor, by means of unintelligent processes. To pass to LPA this axiom has to be somehow inverted and becomes: abstract descent of all kinds from a unique complex abstract common archetype-kind, in the context of a global integrated project of life on Earth. While in Darwinism all the core stuff happens only at the corporeal level, in LPA it happens at the incorporeal level. The inversion of LPA compared to Darwinism not only substitutes non intelligent causes with intelligence but considers two layers upon the corporeal layer, the only one considered by materialist evolutionism. Darwinism is one-dimensional, LPA is three-dimensional.

 

This inversion of LPA vs. Darwinism (which in a sense is a restoration of truth) immediately removes the major absurdities and problems of evolutionism:

(1) Intelligence, able to create information and organization, substitutes chance and necessity, which are unable.

(2) The “less” comes from the “more” and not the opposite, as in evolutionism.

(3) The corporeal macroevolution, which is a real “engineering suicide”, is substituted with an abstract incorporeal derivation, done at a higher layer than the material one. The bodies have no more to materially and monstrously morph, with all the countless complications one can imagine.

(4) The Darwinian material common ancestor of minimal complexity becomes the immaterial template of the more complex being, from which all the simpler beings abstractly derive as sub-projects, when some major characteristics and architectural plans are changed.

(5) What is intelligent is created by intelligence. It is obvious that the unintelligent cannot produce the intelligent, as evolutionism pretends.

(6) The incapability of chance and necessity to create semiotic processing, sophisticated molecular machinery, CSI, correlated CSI, irreducible complexity, functional hierarchies, etc.

Who is the more complex living being that can pretend to be the “maximum project template” in LPA? Answer: man. Before this answer Darwinists object that man arose last in history, then cannot be first. In LPA man can well be the first in the order of design and last in the order of time. Conversely, bacteria, which are the simplest organisms, are last in the order of design and first in the time order. In fact, you can see in the middle of the schema, at the incorporeal layer, the possibility of a total scrambling between design order and time order. This is the flexibility that informatics shows so well. By the way, it is indeed the appearance over time from the simplest to the more complex species that caused the illusion of an evolution from simplicity to complexity, while instead it was simply a specific order of execution of a complexity already fully present from the beginning in the design incorporeal layer.

The LPA explains also all homologies, analogies and similarities between all living beings, at the genetic, morphological, functional and system levels, because LPA implements very strong “common design” “shared libraries” “high level integration” “software reuse” paradigms. In fact, in the schema, at the top level, you see the shared libraries (genotypic and phenotypic) strongly interrelated each other and in turn with the core design, by means of a tri-way bus/channel.

LPA entails three layers: archetypical, incorporeal and corporeal (on the left side of the schema). They are related in the informatics jargon (on the right side) to: design, installation and deployment, execution. The design phase deals with the “sources”, the installation phase deals with “executables” and the execution phase involves “processes” and outputs. Any computer programmer will recognize the standard iter of informatics engineering. LPA could quite well represent how an informatics or robotics engineer, in charge of developing a series of different robots, would organize the overall project, according to a high-level integrated vision. Warning: here I don’t affirm that living beings are simple robots. They are far higher and more complex than robots. But this, to greater reason, reinforces the ID argument, because this implies that their design and construction must be far more sophisticated than modern robotics.

The shift of the job from matter to abstractness, which greatly increases the flexibility, is a fundamental engineering principle, which LPA implements. The history of engineering and technology shows us that engineers have always strived to shift their job from matter to mind. Today engineers use high level abstract tools (CAE, CAD, CAM, etc.). No engineer would use directly low level Darwinian material evolution. Darwinism is a decrepit bankrupt way of thinking, unable to construct the least system. ID LPA is a modern and technologically sound way to construct complex systems.

Another point about LPA is that it agrees with engineering and in the same time is consistent with traditional cosmogony (when is correctly interpreted), according to which the manifestation of macrocosms and microcosms (which are analogous and share the same layering) is a top-down causation ID process that starts from archetypical principles, passes trough an intermediate incorporeal formation and finally concludes into the corporeal world. In LPA the teaching of tradition about creation and engineering meet. Not by chance or by my invention, rather because both describe complex constructions of intelligence. All sciences of construction necessarily share some basic principles that are universal. LPA meets such principles.

Also about the position of man in nature LPA is inverted respecting evolutionism because is “man-centric”. Here again tradition and engineering meet. In any traditional doctrine man is the “imago-Dei” “center of creation”, the hierarchically higher being who synthesizes in himself all others lower peripheral beings. Analogously, if an engineer wants to construct – say – a computer, he starts to think about the central processing unit, then he will develop the peripheral devices.

An important point is why I called the living beings as “kinds”, K0, K1, K2… in the LPA model. The high level design at the archetype layer doesn’t need to specify in advance and in details all the countless species, variants and races of a kind. These variants will differ from the parent kind only in some minor details, while kinds differ in major architectural body plan aspects. What is sufficient is to carefully design and insert into a set of main kinds the complex potentialities needed to generate their minor variants during reproduction of populations in history, by means of endogen and hexogen triggering signals or factors at run time. In few words, the biological “software” must be highly flexible and parametrized, scalable, allowing plasticity and micro-evolvability. I called “microevolution trees” the trees of variants for each kind K and I symbolized them with triangles inside the final corporeal layer. I believe it is sensible to identify the Ks to what in the classic taxonomy are families/kinds. Also most creationists agree on that. As example, Nathaniel T. Jeanson writes “reproductive compatibility identifies membership within a kind. Breeding experiments identify the classification rank of family (kingdom-phylum-class-order-family-genus-species) as roughly defining the boundaries of each kind”. This level is roughly the threshold below which microevolution trees begin.

What evidences support LPA? To my knowledge, the main biological data known so far – if you dismiss the evolutionist eyeglasses – fit well with LPA, because common design explains all things that Darwinian common descent seems to explain. With the difference that LPA has not the absurdities and contradictions that Darwinism has.

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62 Responses to Life Project Architecture

  1. Have the Darwinists developed a theory of the design of the species?

    The design of life has to be a top down process, but what the theory of evolution posits is a bottom-up process. No successful engineering project can begin at the bottom, that is, at the level of the individual part.

    I know. As a naïve engineer fresh out of college (many, many years ago), I began my first project, as simple as it was, without a plan in place. My supervisor sensed what I was doing and asked me if I knew what I was doing. Well, not really. (Imagine a very red face!)

    I see evolution much the same way. Does it know what it’s doing? Well, not really.

    It seems to me that the creation of a new body plan or the redesign of an existing one has to begin with an overview of the project plan. Evolution cannot start willy-nilly with the creation some tiny part without “knowing” how that part is going to be coordinated with many other tiny parts.

    Even if a number of tiny parts are created and by some miracle they form a sub-assembly, the problem has only moved up one level. How is the creation of some seemingly arbitrary sub-assembly going to be coordinated with any other sub-assembly that might have been created? And on to the next level of increasing complexity — assuming the imagined evolutionary process would get that far.

    An example of what I am talking about is the evolution of the eye. The eye in and of itself cannot see. It is part of a vision system consisting of many parts and sub-assemblies if you will, not the least of which in mammals is a brain to interpret the visual signals.

    Why is it that no one talks about the evolution of the vision system?

  2. Am I the only one who thinks this article is a bit too creationist in nature? This is supposed to be about intelligent design, so why borrow terms from creationism?

    Some problems with the LPA view:

    a. If I understand the LPA idea correctly, all species were designed at once. This is not only refuted by the fossil record, but also by molecular data.

    b. Furthermore, it entirely fails to explain why say, chimps and humans exclusively share some endogenous retroviruses, but humans and dogs do not share ERVs exclusively. Why is this the case?

    c. It also does not explain why crucial eukaryotic proteins share deep homology with prokaryotic counterparts – which is expected from front-loading but not from the LPA view.

  3. Why is it that no one talks about the evolution of the vision system?

    Because the evolutionists is out of touch with reality. If they were to actually try to build according to their science fictions, they would find that what (they think) works on paper is physically impossible.

    By focusing on as small a part as possible, they can ignore the hard part of a system’s component coordination and integration. They are completely oblivious to the fact that even the simplest component is part of a multi-component system. An “eye” consisting of single photo-sensitive molecule is of no value without the subsystem that integrates it with the behavior subsystem. The production of the photo-sensitive molecule requires another subsystem. That is three subsystems. Their brains are beginning to hurt. Better to just focus on the “eye” where everyone can see there is no problem for evolution to produce an “eye ball” from an “eye” just by adding a bit at a time. See, it’s just that easy. No advil required.

  4. Genomicus #2

    This [UD] is supposed to be about intelligent design, so why borrow terms from creationism?

    ID is a big tent.

    a. If I understand the LPA idea correctly, all species were designed at once. This is not only refuted by the fossil record, but also by molecular data.

    Fossil record is after the scrambling. I don’t see where molecular data refute LPA.

    b. Furthermore, it entirely fails to explain why say, chimps and humans exclusively share some endogenous retroviruses, but humans and dogs do not share ERVs exclusively. Why is this the case?
    c. It also does not explain why crucial eukaryotic proteins share deep homology with prokaryotic counterparts – which is expected from front-loading but not from the LPA view.

    Shared libraries and common design don’t imply that all must share all.

  5. Interesting OP, and some good thoughts worth thinking about.

    Just one thing I want to expand on a bit:

    A point that Darwinists make is that anti-Darwinists has not developed any theory for the origins of species, and think that is a weakness.

    Part of the difficulty comes with determining what the Darwinist objection is. In my experience, after pinning Darwinists down on what they mean by a theory of creation or origins, it turns out they are asking for a material mechanism. So rather than giving a long response with speculations about what a designer would or would not do, I prefer to point out that the very complaint they are making is misplaced.

    ID is not a mechanistic theory. It makes no more sense for me to develop a “theory” for a specific creative event in biology than it would for me to develop a mechanistic theory for how the iPod came about.

    How do designers create? Well, they have an idea, they research different materials, they draw upon various fields of knowledge and experience, they build prototypes, they tinker, they analyze, and ultimately come up with a finished design and an instruction set for building the item.

    We can have an interesting discussion about different design principles and design schemes; we can discuss other indicia of design found in biology. But ultimately these primarily just point back to the fact that something was designed, and only rarely give us insight into “how.”

    “How” is not a question ID necessarily has to answer. Purely mechanistic theories — evolution/Darwinism — are all about the “how.” They must propose a “how” or they fail as theories. Design is not about the “how” so much as it is about the purposiveness or the intentionality.

    Materialists can jump up and down and complain all they want about ID’s failure to provide a “how,” but that is not a failing of ID; it is just a failing of their materialistic expectations.

    —–

    All that said, if someone wants to go beyond ID itself and use the implications of design to propose possible design approaches to life, I think that is an interesting and valuable effort in its own right, as the OP shows. We should just keep in mind that for a design inference itself to be valid, it need not address the “how.”

  6. 6

    First, niwrad: what a great addition to ID resources! This needs to be pinned somewhere.

    Second: besides solving the same evolutionary issues that Darwinism cannot without employing absurdity (convergence, sudden appearance, lack of “junk” DNA, ORFan genes, stasis, etc.), have you thought much about how the LPA heuristic can be used to make more useful predictions or retrodictions?

    Because it looks to me like you’ve laid out the basic working premise for making significant ID-based “evolutionary” (in the general sense) predictions.

    Genomicus said:

    a. If I understand the LPA idea correctly, all species were designed at once. This is not only refuted by the fossil record, but also by molecular data.

    Designed “at once” doesn’t mean “implemented at once”. Indeed, certain organisms are required to exist for long periods of time before certain other organisms can be inserted because the environment must be conditioned in some way by the preceding organism. Otherwise, the following organisms cannot survive.

  7. ID is a big tent.

    But ID is not creationism. Why, then, use creationist terms? This only makes it seem like ID really is trying to further the creationist cause.

    Fossil record is after the scrambling.

    So you don’t accept the validity of dates obtained by radiometric dating? Why not?

    I don’t see where molecular data refutes LPA.

    See below on ERVs.

    Shared libraries and common design don’t imply that all must share all.

    This does not address the specific problems I outlined:

    a. Why will we never find an example of an ERV that is only shared between humans and dogs, while we often find ERVs that are shared between humans and chimps?
    To put this differently: if we find the same ERV in a dog and human, we can predict, based on common descent, that chimps will also have this ERV. But if we find an ERV shared between chimps and humans, we cannot predict we will find this ERV in dogs. Why is this the case, given the LPA model?

    b. The ID hypothesis of front-loading specifically predicts that key eukaryotic proteins will share deep homology with functional but unnecessary prokaryotic proteins (that is, proteins unnecessary to the survival of the prokaryotic cell plan). Thus, if we find a protein conserved throughout eukaryotes, we can predict that prokaryotes will have homologs of this protein. How does LPA account for this?

  8. William J. Murray:

    Designed “at once” doesn’t mean “implemented at once”. Indeed, certain organisms are required to exist for long periods of time before certain other organisms can be inserted because the environment must be conditioned in some way by the preceding organism. Otherwise, the following organisms cannot survive.

    See the figure in the OP. The taxa are implemented at once.

  9. Genomicus,

    Since I am one of the a dastardly Creationists that supports intelligent design arguments based on empirical data as a way to conduct a discourse with the evolutionist, allow me explain why I do not see the Creationist tone as inappropriate.

    In spite of the fact that I would prefer to stick with the empirical observables in the intelligent design vs. natural processes only discussion, the opponent, oft’ times, charges that there is no coherent, thoughtful attempt at an intelligent design mechanism put forth by anyone, anywhere, ever. The very fact that niwrad has put forth something that has obviously been given some consideration on his part, belies that canard. I do not expect his proposal to be acceptable to the opponents. It is not likely to be received with open arms by many on our side. However, the fact that it has been articulated is valuable.

    For myself, at first blush, I found it intriguing. It parallels much of my own thinking. I am glad niwrad has made the post. It may serve to help me crystallize some of my far more amorphous thoughts on the subject.

    Stephen

    PS. Eric, your point about the evolutionist’s real challenge- “Give me your answer to “How?” is right on point.

  10. niwrad,

    I see that Genomicus is taking something away from your schematic differently than I am. His is failing to understand that the time scale (at least not the same time scale) that is applicable to the corporeal layer is not applicable to the incorporeal and design layers.

    I trust I have understood your intentions correctly.

    An edit to the schematic may be in order so as to make that clear.

    Stephen

  11. William J Murray #6

    Thanks,
    your “how the LPA heuristic can be used to make more useful predictions?” is really a good question. I don’t know in details (I will think about). LPA is a general model. As you say, it, with its three main phases, decouples design and implementation by mean of an intermediate interface that gives flexibility. Anyway, the easy prediction of a strong design integration and flexibility, for example, is that molecular and also system similarities will be found again and again, likely also where now it is unthinkable.

  12. sterusjon #10

    Thanks,
    good note, you have understood my intentions correctly. Also if the time scale (x-axis) seems to apply to the entire surface of the Cartesian plane representing the LPA, the time scale in the two upper layers (archetypic and incorporeal – i.e. design and installation) somehow loses its meaning. In the analogy of informatics, the process time (or run time) is NOT the time of design and installation.

    Any schema is necessarily symbolic and defective respecting reality …

  13. niwrad,

    After posting my previous comment, it occurred to me that a good way to view the corporeal layer is as the execution of run-time code that is inherently time sequence dependent. While time is irrelevant to the design and incorporeal layers and the sequence of “events” is driven by the logistics of design. Not the time driven execution sequence.

    Stephen

  14. G:

    But ID is not creationism.

    Yet if Creation is true, ID is true. (However if Creation is false ID is not false)

  15. Niwrad:

    Warning: here I don’t affirm that living beings are simple robots. They are far higher and more complex than robots. But this, to greater reason, reinforces the ID argument, because this implies that their design and construction must be far more sophisticated than modern robotics.

    You say that living beings are not simple robots, but far higher, more complex and far more sophisticated than modern robots. But robots nonetheless?
    IOW is only the design process top-down, but are living beings themselves without top-down control; without agency?
    If not, where in LPA is the input of our own agency? Is the Designer doing everything?

  16. Eric Anderson #5

    Thanks,
    I largely agree with your comment.

  17. Box #16

    “Are living beings [...] without agency? If not, where in LPA is the input of our own agency? Is the Designer doing everything?”

    Living beings are different from robots because DO have agency. The “input of our own agency” is not illustrated in the LPA schema, because is metaphysical while LPA is cosmological. Of course “our own agency” comes directly from the Designer.

  18. I see that Genomicus is taking something away from your schematic differently than I am.

    You’re right, of course. I misread the figure. Nevertheless, my points a and b in #7 are relevant critiques of this view.

  19. Genomicus (7)

    To put this differently: if we find the same ERV in a dog and human, we can predict, based on common descent, that chimps will also have this ERV. But if we find an ERV shared between chimps and humans, we cannot predict we will find this ERV in dogs. Why is this the case, given the LPA model?

    And what if we’ve found the same ERV in basal primates and humans, but missing somewhere in-between primate evolution? To what extent are your predictions allowed to fail and still be used as evidence?

    If we do find an ERV in a basal mammal and human, but not other primates, will it falsify common descent? Or will it be absorbed with an ad-hoc explanation?

  20. And what if we’ve found the same ERV in basal primates and humans…

    What do you mean by “basal primates” exactly? Among primates, we would predict some phylogenetic incongruities of ERV sequences precisely because of lineage-specific sorting.

    If we do find an ERV in a basal mammal and human, but not other primates, will it falsify common descent?

    Yes.

  21. Some (inconsistencies) ERVs that don’t fit into the naturalistic evolutionary assumption of common descent:

    PTERV1 in chimpanzee, African great apes and old World monkeys but not in humans and asian apes (orangutan, siamang, and gibbon).
    http://www.sciencedaily.com/re.....174826.htm

    The Human Lineage Was Somehow “Purged” – Cornelius Hunter – April 2012
    Excerpt: Another such feature is the lack of endemic infectious retroviruses in humans. The problem is that these viruses are present in the other primates, and so according to evolutionists these viruses must be present in their common ancestor which, again according to evolution, would be an ancestor of humans as well.,, In other words, when evolution spontaneously created humans our DNA must have been “purged.” We got a do-over! Hilarious.
    http://darwins-god.blogspot.co.....-free.html

    More Counterpoints on ERVs – JonathanM – May 2011
    Excerpt: ‘In the absence of a feasible naturalistic mechanism to account for how evolution from a common ancestor could have occurred, how can we be so sure that it did occur? In such a case, one ought to reasonably expect there to be some quite spectacular evidence for common ancestry. Unfortunately for Darwinists, however, the evidence for common ancestry is paper thin on the ground.’
    http://www.evolutionnews.org/2.....46761.html

    Retroviruses and Common Descent: And Why I Don’t Buy It – September 2011
    Excerpt: If it is the case, as has been suggested by some, that these HERVs are an integral part of the functional genome, then one might expect to discover species-specific commonality and discontinuity. And this is indeed the case.
    http://www.uncommondescent.com.....nt-buy-it/

    moreover,,

    Refutation Of Endogenous Retrovirus – ERVs – Richard Sternberg, PhD Evolutionary Biology – video
    http://www.metacafe.com/watch/4094119
    Sternberg, R. v. & J. A. Shapiro (2005). How repeated retroelements format genome function. Cytogenet. Genome Res. 110: 108-116.

    Endogenous retroviruses regulate periimplantation placental growth and differentiation – 2006
    http://www.pnas.org/content/103/39/14390.abstract.

    Retrovirus in the Human Genome Is Active in Pluripotent Stem Cells – Jan. 23, 2013
    Excerpt: “What we’ve observed is that a group of endogenous retroviruses called HERV-H is extremely busy in human embryonic stem cells,” said Jeremy Luban, MD, the David L. Freelander Memorial Professor in HIV/AIDS Research, professor of molecular medicine and lead author of the study. “In fact, HERV-H is one of the most abundantly expressed genes in pluripotent stem cells and it isn’t found in any other cell types.
    http://www.sciencedaily.com/re.....133930.htm

    Transposable Elements Reveal a Stem Cell Specific Class of Long Noncoding RNAs – (Nov. 26, 2012)
    Excerpt: The study published by Rinn and Kelley finds a striking affinity for a class of hopping genes known as endogenous retroviruses, or ERVs, to land in lincRNAs. The study finds that ERVs are not only enriched in lincRNAs, but also often sit at the start of the gene in an orientation to promote transcription. Perhaps more intriguingly, lincRNAs containing an ERV family known as HERVH correlated with expression in stem cells relative to dozens of other tested tissues and cells. According to Rinn, “This strongly suggests that ERV transposition in the genome may have given rise to stem cell-specific lincRNAs. The observation that HERVHs landed at the start of dozens of lincRNAs was almost chilling; that this appears to impart a stem cell-specific expression pattern was simply stunning!”
    http://www.sciencedaily.com/re.....192838.htm

  22. PTERV1 in chimpanzee, African great apes and old World monkeys but not in humans and asian apes (orangutan, siamang, and gibbon).
    http://www.sciencedaily.com/re…..174826.htm

    I already answered that though:

    Among primates, we would predict some phylogenetic incongruities of ERV sequences precisely because of lineage-specific sorting.

    It’s predicted based on our understanding of population genetics.

    For all practical purposes, you’re spamming me with links. Choose one article you’d like to discuss that you think refutes my points.

  23. Genomicus

    Among primates, we would predict some phylogenetic incongruities of ERV sequences precisely because of lineage-specific sorting.

    To clarify, I’m referring to an ERV fixed at the root of a primate tree, but missing in only certain descendents.

    Conservation and loss of the ERV3 open reading frame in primates.
    http://www.ncbi.nlm.nih.gov/pubmed/15081124
    ERV3 sequences were amplified by PCR from genomic DNA of great ape and Old World primates but not from New World primates or gorilla, suggesting an integration event more than 30 million years ago with a subsequent loss in one species.

    Now to what extent is this incongruence permitted? If you can excuse it in primate lineages, what difference does it make to extend further down the tree? Where is the cut-off point for falsifiability, and what empirical criteria determines this?

    Additionally, as BA77 referred you to in his links, ERVs are found to play crucial roles in early development in the species in which they are present. How reasonable is it to conclude then, that they will be selected out of a population?

  24. Genomicus,

    Just seeking a clarification. In #18 did you intend to claim “points a and b in #7 are relevant critiques of this view” or “points b and c in #2 are relevant critiques of this view”?

    Not being hypercritical. Just don’t want to leave any confusion lying around on the table. Heaven knows, I make more than my share of slup ips.

    Stephen

    Stephen

  25. Hi Stephen,

    I see where the confusion lies. Points a and b in #7 are the same as b and c in number 2. My critique of the LPA model based on the fossil record appears to have been irrelevant and tangential. Thus, I am offering the following criticisms of the LPA view for analysis:

    a. Why will we never find an example of an ERV that is only shared between humans and dogs, while we often find ERVs that are shared between humans and chimps?
    To put this differently: if we find the same ERV in a dog and human, we can predict, based on common descent, that chimps will also have this ERV. But if we find an ERV shared between chimps and humans, we cannot predict we will find this ERV in dogs. Why is this the case, given the LPA model?

    b. The ID hypothesis of front-loading specifically predicts that key eukaryotic proteins will share deep homology with functional but unnecessary prokaryotic proteins (that is, proteins unnecessary to the survival of the prokaryotic cell plan). Thus, if we find a protein conserved throughout eukaryotes, we can predict that prokaryotes will have homologs of this protein. How does LPA account for this?

  26. Genomicus,

    Thanks for putting me on the straight and narrow.

    Also, thanks for you expansion of your two criticisms. That was helpful.

    I’ll have to chew on it for a bit.

    Stephen

  27. Genomicus:

    “It’s predicted based on our understanding of population genetics.”

    And exactly where are the population genetics equations published that predict these specific finding?

    Macroevolution, microevolution and chemistry: the devil is in the details – Dr. V. J. Torley – February 27, 2013
    Excerpt: Evolutionary biology has certainly been the subject of extensive mathematical theorizing. The overall name for this field is population genetics, or the study of allele frequency distribution and change under the influence of the four main evolutionary processes: natural selection, genetic drift, mutation and gene flow. Population genetics attempts to explain speciation within this framework.
    However, at the present time, there is no mathematical model – not even a “toy model” – showing that Darwin’s theory of macroevolution can even work, much less work within the time available. Darwinist mathematicians themselves have admitted as much.,,,
    We have seen that there’s currently no good theory that can serve as an adequate model for Darwinian macroevolution – even at a “holistic” level. As we saw, Professor Gregory Chaitin’s toy models don’t go down to the chemical level requested by Professor James Tour, but these models have failed to validate Darwin’s theory of evolution, or even show that it could work.
    At this point, there is an alternative line that (Nick) Matzke might want to take. He could claim that macroevolution is ultimately explicable in terms of bottom-level laws and physical processes, but that unfortunately, scientists haven’t discovered what they are yet. From a theoretical perspective, reductionism would then be true after all, and the chemical explanation of macroevolution demanded by Professor Tour could be given. From a practical standpoint, however, it would be impossible for scientists to provide such an explanation within the foreseeable future.
    If Matzke wishes to take this road, then he is tacitly admitting that scientists don’t yet know either the scientific laws (which are written in the language of mathematics) or the physical processes that ultimately explain and drive macroevolution. But if they don’t know either of these, then I would ask him: why should we believe that it actually occurs? After all, mathematics, scientific laws and observed processes are supposed to form the basis of all scientific explanation. If none of these provides support for Darwinian macroevolution, then why on earth should we accept it? Indeed, why does macroevolution belong in the province of science at all, if its scientific basis cannot be demonstrated?
    http://www.uncommondescent.com.....e-details/

    The next evolutionary synthesis: from Lamarck and Darwin to genomic variation and systems biology
    Excerpt: If more than about three genes (nature unspecified) underpin a phenotype, the mathematics of population genetics, while qualitatively analyzable, requires too many unknown parameters to make quantitatively testable predictions [6]. The inadequacy of this approach is demonstrated by illustrations of the molecular pathways that generates traits [7]: the network underpinning something as simple as growth may have forty or fifty participating proteins whose production involves perhaps twice as many DNA sequences, if one includes enhancers, splice variants etc. Theoretical genetics simply cannot handle this level of complexity, let alone analyse the effects of mutation..
    http://www.biosignaling.com/co.....X-9-30.pdf

    Oxford University Admits Darwinism’s Shaky Math Foundation – May 2011
    Excerpt: However, mathematical population geneticists mainly deny that natural selection leads to optimization of any useful kind. This fifty-year old schism is intellectually damaging in itself, and has prevented improvements in our concept of what fitness is. – On a 2011 Job Description for a Mathematician, at Oxford, to ‘fix’ the persistent mathematical problems with neo-Darwinism within two years.

    Peer-Reviewed Paper Concludes that Darwinism “Has Pretty Much Reached the End of Its Rope” – Jonathan M. – February , 2012
    Excerpt: Contrary to the Darwin lobby’s oft-repeated assertion that there are absolutely no weaknesses in Darwinian theory, the paper offers the concession that the modern synthesis has never provided an account of “how major forms of life evolved” — an omission that is not unsubstantial, to put it mildly.
    http://www.evolutionnews.org/2.....55941.html

    More from Ann Gauger on why humans didn’t happen the way Darwin said – July 2012
    Excerpt: Each of these new features probably required multiple mutations. Getting a feature that requires six neutral mutations is the limit of what bacteria can produce. For primates (e.g., monkeys, apes and humans) the limit is much more severe. Because of much smaller effective population sizes (an estimated ten thousand for humans instead of a billion for bacteria) and longer generation times (fifteen to twenty years per generation for humans vs. a thousand generations per year for bacteria), it would take a very long time for even a single beneficial mutation to appear and become fixed in a human population.
    You don’t have to take my word for it. In 2007, Durrett and Schmidt estimated in the journal Genetics that for a single mutation to occur in a nucleotide-binding site and be fixed in a primate lineage would require a waiting time of six million years. The same authors later estimated it would take 216 million years for the binding site to acquire two mutations, if the first mutation was neutral in its effect.
    Facing Facts
    But six million years is the entire time allotted for the transition from our last common ancestor with chimps to us according to the standard evolutionary timescale. Two hundred and sixteen million years takes us back to the Triassic, when the very first mammals appeared. One or two mutations simply aren’t sufficient to produce the necessary changes— sixteen anatomical features—in the time available. At most, a new binding site might affect the regulation of one or two genes.
    http://www.uncommondescent.com.....rwin-said/

    Why Evolution Is Misunderstood – P.J. Levi – March 4, 2013
    Excerpt: Consider the evolution of humans and chimps from a common ancestor, to which Coyne in his talk referred several times. Rather than offering evidence for such common ancestry, Coyne simply took it as a fact and then used it to support Darwinian selection. Yet the ubiquity of selection in creating these species makes little sense at the level of DNA — the very level at which heritable change (evolution) occurs. By current estimates, the genomes of these two species differ by at least 300 million nucleotides. Given the premise that humans and chimps shared a common ancestor 6 million years ago, such a degree of divergence can only be accounted for by an average of 25 nucleotide changes per year in each line of descent.
    For Coyne’s gradual version of the Darwinian mechanism to account for these differences, 25 new mutations would have to appear, conferring a reproductive advantage, and spread through each population every year. Yet even 25 advantageous substitutions per generation is unfathomable.
    http://www.evolutionnews.org/2.....69771.html

    Using Numerical Simulation to Test the Validity of Neo-Darwinian Theory – 2008
    Abstract: Evolutionary genetic theory has a series of apparent “fatal flaws” which are well known to population geneticists, but which have not been effectively communicated to other scientists or the public. These fatal flaws have been recognized by leaders in the field for many decades—based upon logic and mathematical formulations. However population geneticists have generally been very reluctant to openly acknowledge these theoretical problems, and a cloud of confusion has come to surround each issue.
    Numerical simulation provides a definitive tool for empirically testing the reality of these fatal flaws and can resolve the confusion. The program Mendel’s Accountant (Mendel) was developed for this purpose, and it is the first biologically-realistic forward-time population genetics numerical simulation program. This new program is a powerful research and teaching tool. When any reasonable set of biological parameters are used, Mendel provides overwhelming empirical evidence that all of the “fatal flaws” inherent in evolutionary genetic theory are real. This leaves evolutionary genetic theory effectively falsified—with a degree of certainty which should satisfy any reasonable and open-minded person.
    http://www.icr.org/i/pdf/techn.....Theory.pdf

  28. Genomicus #25

    a. Why will we never find an example of an ERV that is only shared between humans and dogs, while we often find ERVs that are shared between humans and chimps? To put this differently: if we find the same ERV in a dog and human, we can predict, based on common descent, that chimps will also have this ERV. But if we find an ERV shared between chimps and humans, we cannot predict we will find this ERV in dogs. Why is this the case, given the LPA model?

    LPA doesn’t exclude at all that at the corporeal run-time layer genomic material (also viruses, retroviruses, etc.) be exchanged (and eventually become ERVs or provirus and pass to offspring) between kinds (and their variants trees). It is possible that, at this layer, ERVs be shared between humans and chimps and not shared between humans and dogs (likely for complex reasons related to the proximity of humans and chimps just at the design level – after all, as body, chimps are the animals more similar to humans – nobody deny that).

    b. The ID hypothesis of front-loading specifically predicts that key eukaryotic proteins will share deep homology with functional but unnecessary prokaryotic proteins (that is, proteins unnecessary to the survival of the prokaryotic cell plan). Thus, if we find a protein conserved throughout eukaryotes, we can predict that prokaryotes will have homologs of this protein. How does LPA account for this?

    I see no principle reasons why, in LPA, prokaryotic cells cannot have, just at the design level, functional but unnecessary proteins shared with eukaryotic cells. After all, dormant software in informatics is everywhere.

  29. A point that Darwinists make is that anti-Darwinists has not developed any theory for the origins of species, and think that is a weakness.

    Even if ID has none were true, I think no theory would be a stronger position than having a false one.

  30. Genomicus,

    Eric has previously noted the evolutionist propensity for failure to note that the paradigm shift requires a shift in the thought process. In that vein, are you so fixated on the evolutionary explanations and how good you think they are that you are incapable of shifting your perspective and meeting the LPA proposal on its own terms? Have you deigned to put the shoe on the other foot and see how it fits, so to speak?

    Just askin’,
    Stephen

    PS. I’m still chewing in spite of the extraction of a wisdom tooth just yesterday. Really.

  31. A very interesting and thought provoking theory niward. You must have put a lot of thought into it.

    Here is an interesting thought, given the centrality of humans in this picture, this could also mean that the incorporeal design phase can be stretched back all the way to the initial fine-tuning of the big bang. Which means that the designing process deals with not only Earth-bound biological variables, but also with a much larger array of universal variables. But this would be off topic for now.

    I think the most mysterious part is the “how” of implementation. Is it possible that the library of information had a corporeal existence in the past as a unicellular organism that had all the information required to build all subsequent life forms? Such that the appearance of a major body plan is simply a matter of choosing which genes to express? Just a thought.

  32. Shogun #31

    Thanks,
    you ask:

    I think the most mysterious part is the “how” of implementation. Is it possible that the library of information had a corporeal existence in the past as a unicellular organism that had all the information required to build all subsequent life forms? Such that the appearance of a major body plan is simply a matter of choosing which genes to express?

    LPA is a stack of a three-layer top-down intelligent causation, which cause is the First Cause. This hierarchy cannot be stored simply in a flat one-layer body.

    In a sense this question is related to what I wrote in #17, to answer Box. IOW, agency/intelligence of beings (which always implies the higher layers of the LPA hierarchy) would be lost, if LPA is flattened to matter only.

  33. To clarify, I’m referring to an ERV fixed at the root of a primate tree, but missing in only certain descendents.

    Conservation and loss of the ERV3 open reading frame in primates.
    http://www.ncbi.nlm.nih.gov/pubmed/15081124
    ERV3 sequences were amplified by PCR from genomic DNA of great ape and Old World primates but not from New World primates or gorilla, suggesting an integration event more than 30 million years ago with a subsequent loss in one species.

    Now to what extent is this incongruence permitted? If you can excuse it in primate lineages, what difference does it make to extend further down the tree? Where is the cut-off point for falsifiability, and what empirical criteria determines this?

    The key phrase here is “with a subsequent loss in one species.” This is not an improbable event. Species lose genomic data relatively often.

    Now then, suppose we found a particular ERV sequence only in dogs and humans. This would be quite a significant find, because it would mean that those ERV sequences of all other mammalian species were independently lost. Unless the ERV sequence is deleterious in nature, this is a staggeringly improbable occurrence.

    The question, then, remains: why is it that we have not yet found an ERV sequence shared only between humans and dogs, or humans and cats, or cows and chimps? Etc. Think about it.

  34. Eric has previously noted the evolutionist propensity for failure to note that the paradigm shift requires a shift in the thought process.

    Since I’m an ID proponent, I’m quite adept at shifting into the ID perspective. Actually, I’m in the ID perspective virtually all of the time.

    In that vein, are you so fixated on the evolutionary explanations and how good you think they are that you are incapable of shifting your perspective and meeting the LPA proposal on its own terms?

    What exactly do you mean by “meeting the LPA proposal on its own terms”? The LPA view of life has been proposed; I’m bringing up biological data that seem to conflict with the LPA view. It is, of course, good to see that you all are actually beginning to think about and propose ID hypotheses (no disrespect intended, but I am slightly frustrated by the obsession with critiquing Darwinian evolution instead of proposing a testable ID hypothesis). However, in my humble opinion, this particular view (the LPA model) looks awfully ad hoc. Put differently, I am having difficulty thinking of any actual, hard predictions it might make (contrast this with, e.g., the front-loading hypothesis).

  35. Genomicus,

    To put this differently: if we find the same ERV in a dog and human, we can predict, based on common descent, that chimps will also have this ERV. But if we find an ERV shared between chimps and humans, we cannot predict we will find this ERV in dogs.

    From ancestral infectious retroviruses to bona fide cellular genes: role of the captured syncytins in placentation.
    http://www.ncbi.nlm.nih.gov/pubmed/22695103
    We focus on the recent discovery of genes derived from the envelope glycoprotein-encoding (env) genes of endogenous retroviruses that have been domesticated by mammals to carry out an essential function in placental development…

    Remarkably, the capture of syncytin or syncytin-like genes, sometimes as pairs, was found to have occurred independently from different endogenous retroviruses in diverse mammalian lineages such as primates–including humans–, muroids, leporids, carnivores, caviids, and ovis, between around 10 and 85 million years ago.

    Retroviruses push the envelope for mammalian placentation
    http://www.pnas.org/content/109/7/2184.short
    Domestication of the syncytin genes represents a dramatic example of convergent evolution via the cooption of a retroviral gene for a key biological function in reproductive biology. In fact, syncytin domestication from a retroviral envelope gene has been previously shown to have independently occurred at least seven times during mammalian evolution…

    Based on this data, certain cases of widespread and similar retroviral genes are attributed to convergent evolution.

    Interestingly, it seems these ERVs are ordered by usefulness in placental function, and not by common descent. This is a phenomenon predicted by common design.

  36. Based on this data, certain cases of widespread and similar retroviral genes are attributed to convergent evolution.

    Interestingly, it seems these ERVs are ordered by usefulness in placental function, and not by common descent. This is a phenomenon predicted by common design.

    However, the convergence isn’t at the sequence level. In other words, the ERV sequences aren’t located in the same genomic loci across different taxa. This is what matters here, and I probably should have clarified that earlier. When I say “an ERV sequence shared only between humans and dogs,” I mean an ERV sequence found in the same genomic location. Again, why don’t we see that?

  37. Genomicus,

    Sorry. Sometimes it is difficult to know/remember where everyone’ sympathies lie. Witness the recent antics of Chance Ratcliff. (Chance, I got a good laugh out of all of it. You have the caricature down pat. Very creative.)

    Now, I am confused in another way.

    The question, then, remains: why is it that we have not yet found an ERV sequence shared only between humans and dogs, or humans and cats, or cows and chimps? Etc. Think about it.

    I do not understand why you think the noted distribution of shared ERVs is at variance with what niwrad has proposed in LPA. I fail to see any reason that code incorporated into primates (for what reason we may not be able to discern but related to their primate-ness) would be expected or required to be included in dogs under LPA. What am I missing?

    Stephen

  38. The key phrase here is “with a subsequent loss in one species.” This is not an improbable event. Species lose genomic data relatively often.

    I believe there are similar studies showing loss in multiple species, I will have to dig up. Where is the cut-off point to where the probable becomes improbable? Does such criteria exist?

    The question, then, remains: why is it that we have not yet found an ERV sequence shared only between humans and dogs, or humans and cats, or cows and chimps? Etc.

    Well, I was speaking more of a sequence found in humans and lower mammals, but not any other primates, or not in other mammal orders in between. Or similar examples across taxa. As a general rule, I don’t think anyone predicts identical sequences found in only two morphologically or physiologically dissimilar species and none others.

  39. Lifespy: As a general rule, I don’t think anyone predicts identical sequences found in only two morphologically or physiologically dissimilar species and none others.

    Is convergence in echolocation ability in bats and whales an example? “our findings suggest that the high-frequency acoustic sensitivities and selectivities of bat and whale echolocation appear to rely on a common molecular design of prestin.”

  40. Box, yes, I was thinking about that case :) That’s why I said “as a general rule”

    Actually it probably depends on aspects of function. Whereas some ERV’s effect embryonic development, we might never expect to find identical sequences in any creatures that have different modes of reproduction. Yet sequences associated with more specialized function (like echolocation) we might expect to find in very dissimilar species that only have that specific function in common.

  41. Genomicus, You keep throwing around the word predict as if you have a scientific/mathematical basis for any of your ‘predictions’ for what we should find in the genome. i.e. Without any mathematical basis for any ‘predictions’ that you are making, you are just making up stories in my book!

    First, from mathematical and experimental work we can scientifically ‘predict’ that there has not been enough time on earth for neo-Darwinian processes to find even a single functional protein:

    Evolution vs. Functional Proteins – Doug Axe – Video
    http://www.metacafe.com/watch/4018222

    Doug Axe Knows His Work Better Than Steve Matheson
    Excerpt: Regardless of how the trials are performed, the answer ends up being at least half of the total number of password possibilities, which is the staggering figure of 10^77 (written out as 100, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000). Armed with this calculation, you should be very confident in your skepticism, because a 1 in 10^77 chance of success is, for all practical purposes, no chance of success. My experimentally based estimate of the rarity of functional proteins produced that same figure, making these likewise apparently beyond the reach of chance.
    http://www.evolutionnews.org/2.....35561.html

    Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact – Cornelius Hunter – July 2011
    Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude.
    http://darwins-god.blogspot.co.....d-not.html

    As well this severe limit includes changing an already existent protein into a slightly different function,,

    When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe
    Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied.
    http://www.biologicinstitute.o.....nt-collide

    But Hey Genomicus perhaps they missed something in their math and experimental work, so let’s go straight to empirical evidence and see what we find:

    Lenski’s Long Term Evolution Experiment – after 50,000 generations – which is equivalent to somewhere around 1,000,000 years of human evolution

    Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information – September 2011
    Excerpt: The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.
    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
    http://www.evolutionnews.org/2.....51051.html

    How about we see what happened when the ‘top five’ mutations from Lenski’s experiment were combined??? Surely now the Darwinian magic will start flowing!!!

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    Not even a single gene or protein, Genomicus, in 50,000 generations! Negative epistasis is extremely problematic to neo-Darwinism:

    The Real Barrier to Unguided Human Evolution – Ann Gauger – April 25, 2012
    Excerpt: Their results? They calculated it would take six million years for a single base change to match the target and spread throughout the population, and 216 million years to get both base changes necessary to complete the eight base binding site. Note that the entire time span for our evolution from the last common ancestor with chimps is estimated to be about six million years. Time enough for one mutation to occur and be fixed, by their account.
    To be sure, they did say that since there are some 20,000 genes that could be evolving simultaneously, the problem is not impossible. But they overlooked this point. Mutations occur at random and most of the time independently, but their effects are not independent. (Random) Mutations that benefit one trait (are shown to) inhibit another (Negative Epistasis).
    http://www.evolutionnews.org/2.....58951.html

    Tell you what, let’s just forget trying to observe evolution in the lab, let’s REALLY open the floodgates and let’s see what the almighty power of neo-Darwinian evolution can do with the ENTIRE WORLD at its disposal Genomicus.

    A review of The Edge of Evolution: The Search for the Limits of Darwinism
    The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have “invented” little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155).
    http://creation.com/review-mic.....-evolution

    “The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable.”
    - Michael Behe – The Edge of Evolution – page 146

    Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution
    “Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell–both ones we’ve discovered so far and ones we haven’t–at best extremely limited benefit, since no such process was able to do much of anything. It’s critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing–neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered–was of much use.”
    http://www.evolutionnews.org/2.....20071.html

    Now Genomicus, the experimental, empirical, and mathematical work all ‘predict’ that neo-Darwinian mechanisms are woefully inadequate to explain all the changes you want to attribute to it, For instance:

    From Jerry Coyne, More Table-Pounding, Hand-Waving – May 2012
    Excerpt: “More than 6 percent of genes found in humans simply aren’t found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps.”
    Jerry Coyne – ardent and ‘angry’ neo-Darwinist – professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics.

    Genomicus, instead of just insisting that neo-Darwinian processes fixed all those 1400 ORFan genes (ERV’s or whatever), and weaving ‘just so’ stories for hours on in to placate you desire for Darwinism to be true, please show me the exact math, experimental, and empirical, work that what you are insisting is true for neo-Darwinism is even possible in the real world,, so that you may be considered scientific in then first place instead of just another dogmatist!

    supplemental notes:

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.
    PDF – article
    http://eebweb.arizona.edu/nach.....l_2010.pdf

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.

  42. Genomicus, You keep throwing around the word predict as if you have a scientific/mathematical basis for any of your ‘predictions’ for what we should find in the genome. i.e. Without any mathematical basis for any ‘predictions’ that you are making, you are just making up stories in my book!

    First, from mathematical and experimental work we can scientifically ‘predict’ that there has not been enough time on earth for neo-Darwinian processes to find even a single functional protein:

    Evolution vs. Functional Proteins – Doug Axe – Video
    http://www.metacafe.com/watch/4018222

    Doug Axe Knows His Work Better Than Steve Matheson
    Excerpt: Regardless of how the trials are performed, the answer ends up being at least half of the total number of password possibilities, which is the staggering figure of 10^77 (written out as 100, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000, 000). Armed with this calculation, you should be very confident in your skepticism, because a 1 in 10^77 chance of success is, for all practical purposes, no chance of success. My experimentally based estimate of the rarity of functional proteins produced that same figure, making these likewise apparently beyond the reach of chance.
    http://www.evolutionnews.org/2.....35561.html

    Proteins Did Not Evolve Even According to the Evolutionist’s Own Calculations but so What, Evolution is a Fact – Cornelius Hunter – July 2011
    Excerpt: For instance, in one case evolutionists concluded that the number of evolutionary experiments required to evolve their protein (actually it was to evolve only part of a protein and only part of its function) is 10^70 (a one with 70 zeros following it). Yet elsewhere evolutionists computed that the maximum number of evolutionary experiments possible is only 10^43. Even here, giving the evolutionists every advantage, evolution falls short by 27 orders of magnitude.
    http://darwins-god.blogspot.co.....d-not.html

    As well this severe limit includes changing an already existent protein into a slightly different function,,

    When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe
    Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied.
    http://www.biologicinstitute.o.....nt-collide

    But Hey Genomicus perhaps they missed something in their math and experimental work, so let’s go straight to empirical evidence and see what we find:

    Lenski’s Long Term Evolution Experiment – after 50,000 generations – which is equivalent to somewhere around 1,000,000 years of human evolution

    Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information – September 2011
    Excerpt: The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski’s research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT.
    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)
    http://www.evolutionnews.org/2.....51051.html

    How about we see what happened when the ‘top five’ mutations from Lenski’s experiment were combined??? Surely now the Darwinian magic will start flowing!!!

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    Not even a single gene or protein, Genomicus, in 50,000 generations! Negative epistasis is extremely problematic to neo-Darwinism:

    The Real Barrier to Unguided Human Evolution – Ann Gauger – April 25, 2012
    Excerpt: Their results? They calculated it would take six million years for a single base change to match the target and spread throughout the population, and 216 million years to get both base changes necessary to complete the eight base binding site. Note that the entire time span for our evolution from the last common ancestor with chimps is estimated to be about six million years. Time enough for one mutation to occur and be fixed, by their account.
    To be sure, they did say that since there are some 20,000 genes that could be evolving simultaneously, the problem is not impossible. But they overlooked this point. Mutations occur at random and most of the time independently, but their effects are not independent. (Random) Mutations that benefit one trait (are shown to) inhibit another (Negative Epistasis).
    http://www.evolutionnews.org/2.....58951.html

    Tell you what, let’s just forget trying to observe evolution in the lab, let’s REALLY open the floodgates and let’s see what the almighty power of neo-Darwinian evolution can do with the ENTIRE WORLD at its disposal Genomicus.

    A review of The Edge of Evolution: The Search for the Limits of Darwinism
    The numbers of Plasmodium and HIV in the last 50 years greatly exceeds the total number of mammals since their supposed evolutionary origin (several hundred million years ago), yet little has been achieved by evolution. This suggests that mammals could have “invented” little in their time frame. Behe: ‘Our experience with HIV gives good reason to think that Darwinism doesn’t do much—even with billions of years and all the cells in that world at its disposal’ (p. 155).
    http://creation.com/review-mic.....-evolution

    “The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable.”
    - Michael Behe – The Edge of Evolution – page 146

    Michael Behe, The Edge of Evolution, pg. 162 Swine Flu, Viruses, and the Edge of Evolution
    “Indeed, the work on malaria and AIDS demonstrates that after all possible unintelligent processes in the cell–both ones we’ve discovered so far and ones we haven’t–at best extremely limited benefit, since no such process was able to do much of anything. It’s critical to notice that no artificial limitations were placed on the kinds of mutations or processes the microorganisms could undergo in nature. Nothing–neither point mutation, deletion, insertion, gene duplication, transposition, genome duplication, self-organization nor any other process yet undiscovered–was of much use.”
    http://www.evolutionnews.org/2.....20071.html

    Now Genomicus, the experimental, empirical, and mathematical work all ‘predict’ that neo-Darwinian mechanisms are woefully inadequate to explain all the changes you want to attribute to it, For instance:

    From Jerry Coyne, More Table-Pounding, Hand-Waving – May 2012
    Excerpt: “More than 6 percent of genes found in humans simply aren’t found in any form in chimpanzees. There are over fourteen hundred novel genes expressed in humans but not in chimps.”
    Jerry Coyne – ardent and ‘angry’ neo-Darwinist – professor at the University of Chicago in the department of ecology and evolution for twenty years. He specializes in evolutionary genetics.

    Genomicus, instead of just insisting that neo-Darwinian processes fixed all those 1400 ORFan genes (ERV’s or whatever), and weaving ‘just so’ stories for hours on in to placate you desire for Darwinism to be true, please show me the exact math, experimental, and empirical, work that what you are insisting is true for neo-Darwinism is even possible in the real world,, so that you may be considered scientific in then first place instead of just another dogmatist!

    supplemental notes:

    Experimental Evolution in Fruit Flies (35 years of trying to force fruit flies to evolve in the laboratory fails, spectacularly) – October 2010
    Excerpt: “Despite decades of sustained selection in relatively small, sexually reproducing laboratory populations, selection did not lead to the fixation of newly arising unconditionally advantageous alleles.,,, “This research really upends the dominant paradigm about how species evolve,” said ecology and evolutionary biology professor Anthony Long, the primary investigator.

    Response to John Wise – October 2010
    Excerpt: A technique called “saturation mutagenesis”1,2 has been used to produce every possible developmental mutation in fruit flies (Drosophila melanogaster),3,4,5 roundworms (Caenorhabditis elegans),6,7 and zebrafish (Danio rerio),8,9,10 and the same technique is now being applied to mice (Mus musculus).11,12 None of the evidence from these and numerous other studies of developmental mutations supports the neo-Darwinian dogma that DNA mutations can lead to new organs or body plans–because none of the observed developmental mutations benefit the organism.

  43. I predict more links.

  44. lifespy, you put up some interesting links on ORFans earlier that I was going to take a closer look at when I got the time,,, I can’t seem to locate them now,, do you happen to still have them handy?

  45. Excuse my mispell,,, lifepsy

  46. BA77,

    Hmm, we were talking about them in the thread from the other day. Is this what you meant?

    http://www.uncommondescent.com.....ent-449371

  47. Yes Lifepsy, and this one down a bit from that,,

    How Can There Be Orphan Genes? 2012 Ken Weiss – Professor of Anthropology and Genetics

    by the way thanks for the expansion, and links, on the ERV discussion

  48. niwrad:

    LPA doesn’t exclude at all that at the corporeal run-time layer genomic material (also viruses, retroviruses, etc.) be exchanged (and eventually become ERVs or provirus and pass to offspring) between kinds (and their variants trees). It is possible that, at this layer, ERVs be shared between humans and chimps and not shared between humans and dogs (likely for complex reasons related to the proximity of humans and chimps just at the design level – after all, as body, chimps are the animals more similar to humans – nobody deny that).

    I’m not quite sure I’m following you. Are you saying that the reason we don’t find any instances of ERV sequences shared only between humans and dogs (but not chimps) is because of “complex reasons related to the proximity of humans and chimps just at the design level”? Yet this seems to me be ad hoc. What precisely is it in the LPA model that excludes the possibility of the designers implementing ERVs in two different organisms?

    I see no principle reasons why, in LPA, prokaryotic cells cannot have, just at the design level, functional but unnecessary proteins shared with eukaryotic cells. After all, dormant software in informatics is everywhere.

    Sure, but it’s not predicted by the LPA model, while it is predicted from front-loading. Thus, front-loading appears to me to be a superior ID hypothesis. In other words, the LPA model – like Darwinian evolution – must explain this pattern through ad hoc adjustments.

  49. sterusjon:

    I do not understand why you think the noted distribution of shared ERVs is at variance with what niwrad has proposed in LPA. I fail to see any reason that code incorporated into primates (for what reason we may not be able to discern but related to their primate-ness) would be expected or required to be included in dogs under LPA. What am I missing?

    This is not the problem I’m seeing. The problem is that the pattern of ERV distribution fits with what we’d predict from common descent but does not fit with the LPA model.

    If common descent was true, then if an ERV sequence is shared between dogs and humans, we would predict that the vast majority of other mammals would also have this ERV sequence in the same genomic region. This is indeed what we see. On the other hand, the LPA model does not make this prediction, and can only explain this pattern with ad hoc formulations.

    There are other problems I am seeing with the LPA model at the molecular level (beyond the very real problem that it may not make any real predictions), which I might detail in an article on my website. Maybe.

  50. So Genomicus, it doesn’t bother you in the least when the math, experimental, and empirical, evidence ‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life??? And since you deny the relevance of math, experiment, and empirics any relevance to forming a basis for neo-Darwinism, please tell me exactly why you consider yourself to be ‘scientific’ in such rampant story telling on ERV’s or anything else in the genome?

  51. More on ERV’s

    The Nucleotide Sequence of Koala (Phascolarctos cinereus) Retrovirus: a Novel Type C Endogenous Virus Related to Gibbon Ape Leukemia Virus
    http://jvi.asm.org/content/74/9/4264.short
    KoRV (Koala retrovirus) paradoxically clusters with gibbon ape leukemia virus (GALV). The strong similarity between GALV and KoRV suggests that these viruses are closely related and that recent cross-host transmission has occurred.

    ^^^Koala and Gibbon HGT

    Interclass Transmission and Phyletic Host Tracking in Murine Leukemia Virus-Related Retroviruses
    http://jvi.asm.org/content/73/3/2442.short
    ..two recent instances of transmission of zoonotic infections between distantly related host organisms were identified. One, from mammals to birds, has led to a rapid adaptive radiation into other avian hosts. The other, between placental and marsupial mammals, involves viruses clustering with recently described porcine retroviruses

    Multiple Groups of Endogenous Betaretroviruses in Mice, Rats, and Other Mammals
    http://jvi.asm.org/content/78/11/5784.short
    We propose a model whereby betaretroviruses have been evolving within the genomes of murid rodents for at least the last 20 million years and, subsequent to (or concomitant with) the global spread of their murid hosts, have occasionally been transmitted to other species.

    ^^^Mice Bat HGT

    Divergent Patterns of Recent Retroviral Integrations in the Human and Chimpanzee Genomes: Probable Transmissions between Other Primates and Chimpanzees
    http://jvi.asm.org/content/80/3/1367.short
    We screened both the human genome (version hg16) and the chimpanzee genome (version PanTro1) for ERVs and conducted a phylogenetic analysis of recent integrations. We found a number of recent integrations within both genomes. They segregated into four groups. Two larger gammaretrovirus-like groups (PtG1 and PtG2) occurred in chimpanzees but not in humans. The PtG sequences were most similar to two baboon ERVs and a macaque sequence but neither to other chimpanzee ERVs nor to any human gammaretrovirus-like ERVs. The pattern was consistent with cross-species transfer via predation. This appears to be an example of horizontal transfer of retroviruses with occasional fixation in the germ line.

    Porcine endogenous retrovirus integration sites in the human genome: features in common with those of murine leukemia virus.
    http://www.ncbi.nlm.nih.gov/pubmed/16928752
    All these results show similarities between PERV and murine leukemia virus integration site selection, suggesting that gammaretroviruses have a common pattern of integration and that the mechanisms of target site selection within a retrovirus genus might be similar.

    ^^^ ERV sites not random

    The distribution of endogenous chicken retrovirus sequences in the DNA of galliform birds does not coincide with avian phylogenetic relationships.
    http://www.ncbi.nlm.nih.gov/pubmed/225036
    Domestic chickens carry the genome of the endogenous retrovirus RAV-O as DNA sequences integrated into host chromosomes transmitted through the germ line…. No fragments with sequences related to chicken retroviruses were found, however, in digests of DNA prepared from Sonnerat’s, Ceylonese and Green Junglefowl, from two other Pheasant genera (Chrysolophus and Lophura), or from one Quail genus (Coturnix). Thus the DNA of three Junglefowl species closely related to Gallus gallus lacked RAV-O sequences while the DNA of more distantly related Phasianus species showed significant homology. These results show that RAV-O-related sequences have not diverged together with the normal host genes during the evolution of the Phasianidae. Although RAV-O sequences are endogenous in all domestic chickens and Red Junglefowl studied thus far, it appears that the RAV-O genome has been introduced relatively recently into the germ line of Gallus gallus, following speciation but before domestication, and independently of the related sequences found in members of the genus Phasianus.

    ^^ERV missing in multiple closely related bird species

    Retroviral diversity and distribution in vertebrates.
    http://www.ncbi.nlm.nih.gov/pu.....00m,isrctn

    We used the PCR to screen for the presence of endogenous retroviruses within the genomes of 18 vertebrate orders across eight classes, concentrating on reptilian, amphibian, and piscine hosts….
    There was also some indication that viruses isolated from individual vertebrate classes tended to cluster together in phylogenetic reconstructions. This implies that the horizontal transmission of at least some retroviruses, between some vertebrate classes, occurs relatively infrequently.

    ^^ERV’s shared among distant taxa – HGT

  52. BA77:

    So Genomicus, it doesn’t bother you in the least when the math, experimental, and empirical, evidence ‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life???

    You forgot to include all the links that would allegedly make the argument that you only claim to make.

    1) Math…‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life

    So?

    2) experimental evidence ‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life

    How so?

    3) empirical, evidence ‘predicts’ that neo-Darwinism is woefully inadequate to explain the staggering levels of integrated complexity we are finding in life?

    How do empirical observations “predict” anyth8ing at all?

    It seems to me that you don’t know what you’re talking about.

  53. Genomicus

    In other words, the ERV sequences aren’t located in the same genomic loci across different taxa. This is what matters

    If you’re suggesting ERVs found in similar loci is indicative of common descent, there are many studies suggesting non-random and preferential positioning of retrovirus sequences. This kind of data refutes the claims of re-used ERV sites having to be an ‘amazing coincidence’ if not by common descent.

    Perpetually mobile footprints of ancient infections in human genome
    http://www.sciencedirect.com/s.....9398004785

    Although not available for HERVs at this point, the results for other retroelements demonstrate that transcriptionally active genome regions might be preferred targets for retrovirus integration and that the site selection during retroposition can be influenced by many factors

    A good example of retroelement–host interaction gives the study of de novo insertions of Ty1 and Ty3 yeast retrotransposons that are analogues of endogenous retroviruses. Most of the integration sites were found clustered upstream of the genes transcribed by RNA polymerase III.

    There were identified `hot spots’ containing integration sites used up to 280 times more frequently than predicted mathematically. A recent study of the de novo retroviral integration demonstrated also preference for scaffold- or matrix-attachment regions (S/MARs) flanked by DNA with high bending potential.

    Integration specificity of the hobo element of Drosophila melanogaster is dependent on sequences flanking the integration site
    http://link.springer.com/artic.....3712619487

    We analyzed the integration specificity of the hobo transposable element of Drosophila melanogaster. Our results indicate that hobo is similar to other transposable elements in that it can integrate into a large number of sites, but that some sites are preferred over others, with a few sites acting as integration hot spots.

    Large-scale discovery of insertion hotspots and preferential integration sites of human transposed elements
    http://nar.oxfordjournals.org/...../1515.full

    We first discovered that most TEs insert within specific ‘hotspots’ along the targeted TE… Finally, we performed a global assessment to determine the extent to which young TEs tend to nest within older transposed elements and identified a 4-fold higher tendency of TEs to insert into existing TEs than to insert within non-TE intergenic regions. Our analysis demonstrates that TEs are highly biased to insert within certain TEs, in specific orientations and within specific targeted TE positions. TE nesting events also reveal new characteristics of the molecular mechanisms underlying transposition.

    Retroviral DNA Integration: ASLV, HIV, and MLV Show Distinct Target Site Preferences

    http://www.plosbiology.org/art.....io.0020234

    Chromosomal regions rich in expressed genes were favored for HIV integration, but these regions were found to be interleaved with unfavorable regions at CpG islands. MLV vectors showed a strong bias in favor of integration near transcription start sites, as reported previously. ASLV vectors showed only a weak preference for active genes and no preference for transcription start regions.
    Thus, each of the three retroviruses studied showed unique integration site preferences, suggesting that virus-specific binding of integration complexes to chromatin features likely guides site selection.

    Integration of retroviral vectors
    http://www.sciencedirect.com/science/article
    /pii/S095279151200129X

    Several members of the retrovirus family show distinct pattern for preferential integration into the host genome. Despite many years of investigation, precise mechanisms of target site selection and the fundamental interplay of viral integrase and host cell proteins are still unknown.

  54. Genomicus #48

    “Sure, but it [functional but unnecessary proteins] is not predicted by the LPA model, while it is predicted from front-loading. Thus, front-loading appears to me to be a superior ID hypothesis. In other words, the LPA model – like Darwinian evolution – must explain this pattern through ad hoc adjustments.”

    In my short description of the LPA model (1345 words, it’s a blog after all) I didn’t include that “prediction” because it was implicit. LPA is a cent percent informatics based model and it was absolutely trivial to waste words to say that in informatics there are “functional but unnecessary subroutines”, exactly as to say there are bits.

    I think that LPA has the pros of your macroevolutionary front-loading but has not the cons.

    Likely here is the point, our disagreement is that, despite of we are two IDers, you believe in corporeal macroevolution while I don’t.

  55. Mung???

    How do empirical observations “predict” anyth8ing at all?

    It seems to me that you don’t know what you’re talking about.

    and yet I had cited @ 42:

    “The immediate, most important implication is that complexes with more than two different binding sites-ones that require three or more proteins-are beyond the edge of evolution, past what is biologically reasonable to expect Darwinian evolution to have accomplished in all of life in all of the billion-year history of the world. The reasoning is straightforward. The odds of getting two independent things right are the multiple of the odds of getting each right by itself. So, other things being equal, the likelihood of developing two binding sites in a protein complex would be the square of the probability for getting one: a double CCC, 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the world in the last 4 billion years, so the odds are against a single event of this variety in the history of life. It is biologically unreasonable.”
    - Michael Behe – The Edge of Evolution – page 146

    Did Dr. Behe make a ‘prediction’ about what we should expect to find from the empirical evidence or not?

    ,,, And why this irrational antagonism towards me from you on this and the other thread? This irrationality is uncharacteristic of you.

  56. lifepsy, thanks for the links. ,,, It is one thing to just proclaim something to be true as Darwinists continually do, it is quite another to empirically back it up.

  57. lifepsy you may be interested in this video clip, where Ian Juby interviews Dr. Jean Lightner and they clearly lay out, for the layman, what the ERV argument is and exactly why the ERV argument from Darwinists is now falsified:

    ERV’s – Dumb DNA design? – Ian Juby – February 2013 – video
    http://www.youtube.com/watch?f.....dC4#t=768s

  58. Just the interview portion with Dr. Lightner is here:

    The definitive response on ERV’s and Creation, with Dr. Jean Lightner
    http://www.youtube.com/watch?v=feHYEgzaGkY

  59. thanks BA77, that is a good interview.

  60. Shogun #31

    Here is an interesting thought, given the centrality of humans in this picture, this could also mean that the incorporeal design phase can be stretched back all the way to the initial fine-tuning of the big bang. Which means that the designing process deals with not only Earth-bound biological variables, but also with a much larger array of universal variables.

    That’s true, and worth of future investigations. Sure the shared libraries must contain also what you call “a much larger array of universal variables”.

  61. I can certainly understand the idea of there being a grand ‘construction’ project in mind for which smaller, support systems must first be implemented. And certainly, in the case of human beings, some of those preliminary steps would have to be taken and allowed to progress to a sufficient level. I’m thinking of things like oxygen levels, food sources, etc.

    I’ll try and have a better think about this and see if I can justify the immense time involved. But it does seem to me that, inherent in your model, is a not all-powerful designer, i.e. one that could not just ‘create’ the whole living biosphere in one go. I’m just trying to get my head around what kind of tools the designer used and/or had available and/or was capable of using. Getting a handle on the design implementation techniques would help explain some of the data we see in the fossils, the genomes, the observed morphology and the bio-geographic distribution of species.

    But interesting!

  62. Johnathan M. Have you ever rebutted this take on your ERV articles? It was shown to me 2 days ago. Thank you in advance.

    http://www.evolutionarymodel.com/evolutionnews.htm

    David Buzulak (Evolution Myth on Facebook)

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