Common descent: Ann Gauger’s response to Vincent Torley

_{News
June 10, 2016

Human evolution, News

2}_{Categories
Human evolution
News}

Share: Facebook; Twitter/X; LinkedIn; Flipboard; Print; Email

Well, I must say I didn’t expect to be honored by a 7500 word broadside by philosopher Dr. Vincent Torley, assisted by Dr. Josh Swamidass, Assistant Professor at Washington University. I guess they must have a lot of spare time. The reason for the post at Uncommon Descent? Both hold common descent to be absolutely, incontrovertibly, obviously true, and they apparently wish I would fall into line and stop embarrassing them by doubting common descent. They wish I would give up my “peculiar kind of intellectual obstinacy.”

The argument is in the end all about common descent. (There are a few accusations of poor reasoning, obscuring the issue, and even a little bad faith along the way.) Look, intelligent design is not wedded to common descent. Neither is it wedded to a denial of common descent. Intelligent design states that there is evidence of design in the universe. I think we are in agreement on this point. In terms of biology, how the designer instantiated that design is still subject to debate, based on the strength of the evidence for each position.

As a biologist, I see evidence on both sides of the debate. The evidence is equivocal — hence the fact that ID advocates take different positions on the subject. Yet common descent — the idea that organisms descend from one or a few common ancestors — is treated like a sacred cow by many scientists, and even, it appears, by some philosophers. Indignation arises that anyone would doubt it, would even have questions. Scientists take common descent as axiomatic, and accept evidence that is itself interpreted through a lens of common descent as proof of common descent. As a consequence, any evidence against common descent meets opposition and is explained away.More.

Background: Vincent Torley: Evidence for common descent: here

Comments

Torley you do know those sequences are not protein coding don't you? And you do know that is why I commented on that fact and why I also referenced Dr. Hunter's paper refuting the just so story from Darwinists and Theistic evolutionists of how those sequences supposedly magically and 'randomly' became functional don't you? Moreover, It is disingenuous of you to ignore my main observation which focused on the extreme rarity of protein folds and yet the recent finding of a huge percentage of 'Dark' proteins with no known structural homologs. That finding, regardless of what I consider to be hoodwinked gene sequence comparisons that overlook several problems, is devastating to the gradualistic scenario. re-reference:
Unexpected features of the dark proteome – Oct. 2015 Excerpt: We surveyed the “dark” proteome–that is, regions of proteins never observed by experimental structure determination and inaccessible to homology modeling. For 546,000 Swiss-Prot proteins, we found that 44–54% of the proteome in eukaryotes and viruses was dark, compared with only ~14% in archaea and bacteria. Surprisingly, most of the dark proteome could not be accounted for by conventional explanations, such as intrinsic disorder or transmembrane regions. Nearly half of the dark proteome comprised dark proteins, in which the entire sequence lacked similarity to any known structure. Dark proteins fulfill a wide variety of functions, http://www.pnas.org/content/early/2015/11/16/1508380112 Orphan enzymes could be an unexplored reservoir of new drug targets. – 2006 Excerpt: Despite the immense progress of genomics, and the current availability of several hundreds of thousands of amino acid sequences, >39% of well-defined enzyme activities (as represented by enzyme commission, EC, numbers) are not associated with any sequence. http://www.ncbi.nlm.nih.gov/pubmed/16580971
bornagain77_{June 13, 2016
June
06
Jun
13
13
2016
08:19 AM
8
08
19
AM
PDT}

bornagain77, In response to your post #66 about ORFan genes, you might like to have a look at Glenn Williamson's latest post, demolishing Dr. Tomkins' claims about these genes: https://roohif.wordpress.com/2016/06/13/jeff-tomkins-orphan-genes-mind-the-gap/ "Drum Roll, Please. Who would have thunk it? These human genes which supposedly had no evolutionary history have corresponding sequence in the chimpanzee genome which is – on average – about 95.41% identical." I'd say Dr. Tomkins has some explaining to do.vjtorley_{June 13, 2016
June
06
Jun
13
13
2016
08:06 AM
8
08
06
AM
PDT}

aap's arguments against theistic evolution are based on emotion rather than reason:
...[T]he truth is evolutionary common descent is a death cult. It only progresses through the immeasurable pain and death of trillions of creatures and this continues today. The TE god is a god of death, not life. Their Jesus is a mild mannered compassionate philosopher doctor during office hours and a sadistic torturous murderer the rest of the day and night who loves to invent new diseases to inflict on his disposable creatures. Is that a JESUS you can worship?
1. Dembski's book, The End of Christianity, has shown how belief in common descent is perfectly compatible with the belief (held by many Christians) that animal suffering was caused by the Fall, provided you are willing to accept the possibility of retrospective causation. 2. In any case, we don't know how much animals suffer, and how many (if any) have a sense of "self." Without an "I" who suffers, there is no-one whom suffering can be ascribed to. 3. Nor do we know whether God has, in His goodness, prepared an after-life (not Heaven, but some kind of happy hereafter) for sentient creatures. If He has, then the transient sufferings of this world are unimportant by comparison.vjtorley_{June 13, 2016
June
06
Jun
13
13
2016
08:00 AM
8
08
00
AM
PDT}

In further reflection of the inability of Darwinian processes to create new protein folds:
Estimating the prevalence of protein sequences adopting functional enzyme folds: Doug Axe: Excerpt: The prevalence of low-level function in four such experiments indicates that roughly one in 10^64 signature-consistent sequences forms a working domain. Combined with the estimated prevalence of plausible hydropathic patterns (for any fold) and of relevant folds for particular functions, this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences. http://www.toriah.org/articles/axe-2004.pdf Dan S. Tawfik Group – The New View of Proteins – Tyler Hampton – 2016 Excerpt: Their sober conclusion is that “point mutation alone is incapable of evolving systems with substantially new protein folds.” http://inference-review.com/article/the-new-view-of-proteins
Although new protein folds are extremely prohibitive for Darwinian processes to account for, (optimistic low end of 1 in 10^12), most all Darwinists and Theistic Evolutionists (such as Prof Swamidass, Torley, and gpuccio), hold that there are really no new protein folds, or exceeding few protein folds, required for the supposed transition from an ape-like create to a human. This recent paper calls that Darwinian presumption into question.
Unexpected features of the dark proteome – Oct. 2015 Excerpt: We surveyed the “dark” proteome–that is, regions of proteins never observed by experimental structure determination and inaccessible to homology modeling. For 546,000 Swiss-Prot proteins, we found that 44–54% of the proteome in eukaryotes and viruses was dark, compared with only ~14% in archaea and bacteria. Surprisingly, most of the dark proteome could not be accounted for by conventional explanations, such as intrinsic disorder or transmembrane regions. Nearly half of the dark proteome comprised dark proteins, in which the entire sequence lacked similarity to any known structure. Dark proteins fulfill a wide variety of functions, http://www.pnas.org/content/early/2015/11/16/1508380112 methods of tertiary protein structure determination http://www.proteinstructures.com/Experimental/experimental-methods.html ter·ti·ar·y struc·ture the overall three-dimensional structure resulting from folding and covalent cross-linking of a protein or polynucleotide molecule.
and this:
Orphan enzymes could be an unexplored reservoir of new drug targets. - 2006 Excerpt: Despite the immense progress of genomics, and the current availability of several hundreds of thousands of amino acid sequences, >39% of well-defined enzyme activities (as represented by enzyme commission, EC, numbers) are not associated with any sequence. http://www.ncbi.nlm.nih.gov/pubmed/16580971
As well, although Darwinists and Theistic evolutionists have tried to 'explain away' the large percentage of ORFan genes being found in all genomes that are being sequenced by appealing to supposedly 'junk' DNA sequences that are similar to the ORFan sequence, (with no actual demonstration of how a supposedly non-functional 'junk' sequence can suddenly become functional),
Mechanisms and dynamics of orphan gene emergence in insect genomes - January 2013 Excerpt: Orphans are an enigmatic portion of the genome since their origin and function are mostly unknown and they typically make up 10 to 30% of all genes in a genome. http://gbe.oxfordjournals.org/content/early/2013/01/24/gbe.evt009.full.pdf+html Is the Origin of New Genes “Basically a Solved Problem”? - Cornelius Hunter - Sept. 11, 2014 Excerpt: If you read the headlines, you would have the impression that the problem is well in hand. For instance, super-star science writer Carl Zimmer wrote in the New York Times earlier this year that “researchers have documented the step-by-step process by which a new gene can come into existence.” Case closed right? Well not quite. In fact, not even close. What Zimmer tells his readers is a “step-by-step process” is what scientists affectionately refer to as a cartoon. In fact, here it is:,,, ,,,This evolutionary narrative is certainly not “basically a solved problem.” In fact, what evolutionists have are high claims of the spontaneous evolution of incredibly complex structures, not because of the evidence, but in spite of the evidence. So what gives evolutionist’s their confidence? It is not that they understand how such genes could have evolved, but that the genes must have evolved because solo genes are observed over and over: "Several studies have by now also shown that de novo emerged transcripts and proteins can assume a function within the organism. All of this provided solid evidence that de novo gene birth was indeed possible.",,, Does any of this mean that the de novo genes evolved from random mutations as the evolutionists claim? Of course not.,,, Only a few years ago they agreed that such evolution of new genes would be impossible. Now they have been forced to adopt it because the evidence unambiguously reveals solo genes, and evolutionists dogmatically insist that everything must have spontaneously evolved.,, http://darwins-god.blogspot.com/2014/09/is-origin-of-new-genes-basically-solved.html
Although Darwinists (and theistic evolutionists) unsuccessfully tried to sweep this huge problem under the rug, this ORFan gene problem simply is not so easily dismissed by Darwinists as this recent paper by Tomkins highlights
Genetic Gap Widens Between Humans and Chimps by Jeffrey P. Tomkins, Ph.D. - January 21, 2016 Excerpt: In yet another recent research report, scientists describe 634 orphan genes in humans and 780 in chimpanzees.1 In other words, we now have a new set of 1,307 genes that are completely different between humans and chimpanzees. In fact, the chimp-specific genes are not found in any other supposed chimp ancestor—like macaque, an extant monkey. They are unique to the chimps just like the human orphan genes are unique to humans. Darwinian evolution did not predict this remarkable discovery. Essentially exposing evolution's weakness in explaining orphan genes, the researchers say, "For the past 20 years scientists have puzzled over a strange-yet-ubiquitous genomic phenomenon; in every genome there are sets of genes which are unique to that particular species i.e. lacking homologues [similar counterparts] in any other species."1 Another interesting fact about these newly discovered orphan genes is that they represent just a subset of the genes unique to chimp or human. The researchers only analyzed genes expressed in liver, heart, brain, and testes. Many other bodily tissues still need to be examined. In addition, the team only analyzed genes that were spliced, meaning complex genes that have coding and non-coding regions, with the coding regions being snipped out of the RNA transcript after they are copied from the DNA. Many other genes in the genome are not spliced and were not included in this study. Needless to say, the numerous gene differences that scientists discovered between humans and chimps cannot be accounted for by Darwin's theory of common ancestry. http://www.icr.org/article/genetic-gap-widens-between-humans-chimps
Needless to say, Darwinian evolution did not 'predict' any of this.bornagain77_{June 13, 2016
June
06
Jun
13
13
2016
06:45 AM
6
06
45
AM
PDT}

Hi HeKs, Thanks for your reply. Please do not apologise for referencing your background as a programmer as DNA is a code (and that is very clear now to anyone who studies it) that is far more complex than any code any human has designed. So understanding DNA as a code from that perspective is entirely relevant. Completely agree with what you say and the analogy. The reason those 3 questions are important is because they speak to what I think you are trying to ask yourself. I expect the commonly given answers would be something like: 1) Why is it a genetic remnant? Ans: it is non-functional, and, see (2) 2) How do you know it is a genetic remnant? Ans: it is non-functional, and a duplication of a functional gene (high sequence homology but “broken”) 3) How do you know any assigned function is the result of [corrected word] exaptation? Ans: because anything that differs from the original gene (see 2) is an adapted function and not original. There are multiple problems with such answers: 1)Not currently knowing a function does not equal non-functional. Second to this, the evidence is growing that a number of alleged “pseudogenes” are in fact sequences with different function than traditionally thought. E.g. do not have traditional promotor sites, stop codon usage, usual flanking sequences etc so we have decided they must not be functional and have used CD as evidence (!) to assume they must have originated from functional genes first 2) See flaw with (1); again, how do you know it is a duplication of a working gene? Homology does not mean that it is, only it must be under methodological naturalism. Now imagine a scenario where a designer is making increasingly complex organisms. The more complex ones require greater regulation of genes than the more simple ones, perhaps. Therefore you need more complex code and new regulatory information to control the other genes. Pseudogenes in the literature and constant new research keeps identifying regulatory roles for pseudogenes. I could cite many examples but the trend is that actually these are not traditional genes but encode RNA regulatory molecules with function. There is a chance that these are therefore not duplications but intentional. Now this statement only applies under the design paradigm – under the naturalistic paradigm the only way they could arise would be through a duplication of a similar sequence and then RM into a regulatory RNA role. But that is self-propelling the naturalistic viewpoint and not therefore proof of CD. Further to this, we know that a Toyota Yaris hybrid looks more similar to a Toyota Yaris than it does to a Toyota Avensis. We would expect more similarities between those. Similarly, a human looks phenotypically (not just outward appearance but on anatomy and physiology settings) more like a chimp than a chicken therefore is it any surprise that if they shared a common designer that designer would use the same type of regulation between the two organisms and therefore these two organisms are more likely to share these apparent pseudogenes? 3) Again this is where the “evidence” presented is self-fulfilling and circular. To arrive to exaptation you must assume a role that once existed (assume CD to do this) but now no longer exists. This is because it “looks like” another gene that is functional. If a designer decides to use similar sequences in regulatory function (rather than as a protein-encoding gene) to existing genes, how do you know that is a duplication event? Of course this is just one example of b-hemoglobin and I am making my own assumptions here. But it demonstrates the circular thinking and reasoning and self-fulfilment of CD (CD in the sense of chimps share a CA with humans). It also highlights the inability for many people who hold to this to view the simple explanation of how design can explain some of these phenomenon. Granted, other observations are harder to explain by design than perhaps such an example as discussed in this post, but the point remains that design can explain quite rationally many of these observations. It is merely a choice to ignore this explanation as it relies on design rather than naturalistic means – which is ultimately what this argument boils down to. Not evidence nor even conception; rather your starting assumptions on supernatural designers or everything must fall into the naturalistic category. With regards to your slightly different note this was on the Opossum thread and in response to a point I made about so much junk. Given that ~80% of the genome is transcribed, and that 100% of the genome is copied in mitosis, I find it difficult to believe that if an organism could get away with less of a genome (10-fold less if junk figures are to be believed) that this would not be of an advantage. That is a lot of transcription and copying that is required for no gain. I am not sure where this evidence about fitness cost comes from.Dr JDD_{June 13, 2016
June
06
Jun
13
13
2016
05:54 AM
5
05
54
AM
PDT}

If virtually unlimited 'plasticity of form' for an entire organism that is built with over a billion-trillion protein molecules total is supposedly undeniably true, (as is currently held by Atheistic Darwinists and by Theistic Evolutionists such as Prof Swamidass who toe the Darwinian line), then virtually unlimited 'plasticity of form' should be that much more undeniably true for single proteins themselves. Yet proteins themselves are severely constrained in their 'plasticity of form'. In trying to get an enzyme to switch functions, Dr. Ann Gauger and Dr. Axe found severe constraints with the Darwinian scenario:
"Shared Evolutionary History or Shared Design?" Ann Gauger January 1, 2015 Excerpt: In an evolutionary scenario, to get an enzyme to switch functions the first step is to make a spare copy that can be mutated without destroying a function the cell needs. Second, the cell has to overproduce the mutating enzyme, because any newly emerging enzyme will be very bad at the job at first. To compensate there will need to be lots of enzyme around. Third, there is the problem of finding the right combination of mutations by random search. Taken together, since we found no enzyme that was within one mutation of cooption, the total number of mutations needed is at least four: one for duplication, one for over-production, and two or more single base changes. The waiting time required to achieve four mutations is 1015 years. That's longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations. http://www.evolutionnews.org/2015/01/happy_new_year092291.html
Along that same line, Dr. Gauger also comments that to the extent that proteins do evolve then 'the enzyme already has to be arranged to carry out the innovative function'.
New Article in BIO-Complexity Addresses the Problem of Biological Innovation - Ann Gauger - January 4, 2016 Excerpt: Next he, (Doug Axe), tested whether an already existing character with some weak similarity to the target could be evolved by mutation and selection to a proficient version of the target character. Once again, the answer was no. However, if the starting character was only six mutations away from optimization, it improved rapidly upon mutation and selection.,,, Our conclusion? Unless the starting protein already exists as a functional fold of the right design, the protein's activity cannot be optimized to wild-type levels. In other words, you'll never get an innovation optimized, even with a pre-existing low level of the desired activity if the innovation is not already present in substantial form. By that I mean that the enzyme already has to be arranged to carry out the innovative function -- its structure has to be of the right kind. Natural selection cannot create innovation, and it can't even optimize pre-existing weak functions that are not of the right design to begin with. http://www.evolutionnews.org/2016/01/new_article_in102051.html
You don't have to take Dr. Gauger's word for it, you can also look at the excellent experimental work of Dan S. Tawfik's Group.
Dan S. Tawfik Group - The New View of Proteins - Tyler Hampton - 2016 Excerpt: To the extent that Tawfik’s selection experiments were successful, it is because mutations were localized and contextualized. Mutation had a key but confined role. If evolution proceeded, the prevailing architecture of the active sites and protein shapes nonetheless remains intact. Changes were not to central structures, but to peripheral loops. A great deal of flexibility was discovered. Still, it is hard to see how any of this could build proteins—that is, in the sense of building their fundamental shapes, or scaffolds; and build proteins in terms of explaining the key catalytic strategies of each active site. Even in the impressive demonstration of a transition through nine orders of magnitude, in which a full exchange of a promiscuous activity for the primary activity was seen, the overall geometry of the protein was unchanged, and, although substrates had changed, the fundamental active site strategy stayed the same. ,,, “Modern neo-Darwinism and neutral evolutionary treatments,” remark Leonard Bogarad and Michael Deem, “fail to explain satisfactorily the generation of the diversity of life found on our planet.” It is not that they did not evolve, they say, but that “... most theoretical treatments of evolution consider only the limited point-mutation events that form the basis of these theories.” Their sober conclusion is that “point mutation alone is incapable of evolving systems with substantially new protein folds.”60,,, “In fact, to our knowledge,” Tawfik and Tóth-Petróczy write, “no macromutations ... that gave birth to novel proteins have yet been identified.”69 The emerging picture, once luminous, has settled to gray. It is not clear how natural selection can operate in the origin of folds or active site architecture (of proteins). It is equally unclear how either micromutations or macromutations could repeatedly and reliably lead to large evolutionary transitions. What remains is a deep, tantalizing, perhaps immovable mystery. http://inference-review.com/article/the-new-view-of-proteins
Thus, since proteins themselves are severely constrained in their ability to evolve a new 'form', then why in blue blazes should anyone believe that an entire organism consisting of over a billion-trillion protein molecules should be any less constrained in its plasticity than the protein molecule itself is? Here is a supplemental quote from Dr. Gauger on the often overlooked, but crucially important, issue of 'context dependency':
"Why Proteins Aren't Easily Recombined, Part 2" - Ann Gauger - May 2012 Excerpt: "So we have context-dependent effects on protein function at the level of primary sequence, secondary structure, and tertiary (domain-level) structure. This does not bode well for successful, random recombination of bits of sequence into functional, stable protein folds, or even for domain-level recombinations where significant interaction is required." http://www.biologicinstitute.org/post/23170843182/why-proteins-arent-easily-recombined-part-2
bornagain77_{June 13, 2016
June
06
Jun
13
13
2016
04:59 AM
4
04
59
AM
PDT}

Dr. Joshua Swamidass #47 “I will point out too, that I have said repeatedly that there are good reasons for rejecting CD. In particular, there are good and dignified reasons for rejecting CD for theological reasons. This is what Todd Woods does, and I respect that.” TE would fit in well with most philosophical theology in which an individual is free to create and make the image of a god according to their own personal, scientific or philosophical perspective. Deism is a perfectly legitimate TE theology. One of humanities obsessions is to attempt to create a god in our own image, after our likeness or preference. This has been the source of religions down through history. Most today prefer the absentee father kind of god which TE certainly provides. If there has to be a god, that is the kind of god they prefer over a god who would actually interfere with their life or hold them accountable, or, bring his judgement. The theistic god of evolution is certainly comfortable enough to fit in pretty well with most religious, mystic views of a god: native religion, Hinduism, Buddhism, Bahai, humanism, liberal theology in many churches, etc. TE is a new gnostic version of god conjured up from the “superior” insights of the great theological and philosophical minds of the past 100 years who know god better than those simple early Christians. To put it mildly, TE really doesn’t fit in with the GOD of the Bible, with JESUS and His FATHER and HOLY SPIRIT of Truth. Christian theology isn’t a philosophical theology that springs from human imagination or reason, but a Word - Logos based, CHRIST centered, HOLY SPIRIT revealed faith. Through faith in CHRIST and through the ministry of GOD’S SPIRIT alone an individual can receive and grow in their understanding of the grace and truth of GOD and His Word, but cannot approach GOD and His Word by human reason alone. It is a faith that little children can perceive, but learned theologians and philosophers stumble over, even in the institutional church (1 Corinthians 1: 18-31). The Apostle Peter wrote: “Above all, you must understand that no prophecy of Scripture came about by the prophet’s own interpretation. For prophecy never had its origin in the will of man, but men spoke from GOD as they carried along by the HOLY SPIRIT.” 2 Peter 1:20,21 The Apostle Paul through the same HOLY SPIRIT stated: “The Church is built on the foundation of the apostles and prophets, with CHRIST JESUS Himself as the chief cornerstone.” Ephesians 2:20 TE fails as a Christian theology because it isn’t based on CHRIST or the testimony of the HOLY SPIRIT through the prophets and apostles. It is a theology based on faith in the assured results of methodological naturalism; faith in human reason alone. As JESUS said to the Sadducees of His generation: “You are in error because you do not know the Scriptures or the power of GOD.” (Matthew 22:29) The heart and center of the Christian faith is the profession that JESUS, Was, Is, and Always will be GOD’S SON, One with the FATHER and the SPIRIT. JESUS is the Word- Logos (information) through which all things have been created, and brought into being (John 1, Colossians 1). To hold to TE, and some forms of ID, would be to believe that their Jesus is the Creator of all diseases, mutational deformities, violence, pain, and death. They further believe that he has pronounced that all of these realities in our world today are very good; that he was and is pleased with his evolutionary common descent world. The one who confronted the religious leaders of his generation for being hypocritical would be the master hypocrite. He shows up on the scene for a few brief years, claims to be compassionate and heals a few people of their suffering, while for at least a few hundred million years he has enjoyed the spectacle of all of the suffering caused by his deadly process. Contrary to the lavish praise that most TE’s heap on evolution for its ability to produce the incredible marvels of life today, the truth is evolutionary common descent is a death cult. It only progresses through the immeasurable pain and death of trillions of creatures and this continues today. The TE god is a god of death, not life. Their Jesus is a mild mannered compassionate philosopher doctor during office hours and a sadistic torturous murderer the rest of the day and night who loves to invent new diseases to inflict on his disposable creatures. Is that a JESUS you can worship? The real JESUS, weeps over this fallen world of ours, and His true followers weep with Him. Anyone who has come to know JESUS, through the testimony of His HOLY SPIRIT in His Word given through His prophets and apostles, will understand that JESUS is not the god of TE. TE: a theology “yes”, Christian “no”. Dr. Swamidass #47 “On the scientific front, looking at evidence, I (and the rest of the mainstream scientific community) contend that the case for CD is rock solid. So I am doing too things here. Scientifically, “recent” evolutionary history (e.g. the last 50M years of mammalian evolution) the evidence points in one direction unambiguously to CD.” Within the definition of science that the mainstream scientific community operates under, his statement here is a true statement. If you hold to methodological naturalism, that everything in our world has to have its cause and origin in material alone, then the case for CD is rock solid. There is simply no other materialistic explanation for life on earth besides CD. All data has to be forced into a CD mold because it is the only possible naturalistic explanation. The reality that: 1) CD is mathematically impossible, 2) they cannot demonstrate the creation of any new life form or organ through genetic mutations, 3) all of observable science bears testimony that life only comes from life, and that kinds of life only reproduce after their kind, 4) many aspects of life are irreducibly complex, not only in their function but in the genetic computerized specified information that is involved, etc. These observable and experimental realities are all irrelevant to them, because they don’t fit in with their assumptions. Life exists and there is some morphological or genetic commonality amongst different kinds of life and therefore CD is true. Within their closed naturalistic circle there is nothing else that can account for life. They are very close minded when it comes to GOD having anything to do with reality or life. Creationists and IDers are often accused of implying that scientists are hiding some massive conspiracy about the truth about evolution. There is absolutely no need for a conspiracy of scientists because their naturalistic presuppositions have limited their options to evolutionary CD. Human reason based on belief in nature alone, which isn’t the conclusion of modern science but their starting premise, has predetermined that CD has to be true, and, therefore all of the evidence has to fit in. Any scientist that suggests otherwise deserves to be tar and feathered and run out of town, or at least the university. For all of you ID advocates out there, don’t ever expect that the mainstream scientific community will ever tolerate the possibility of an intelligent designer having anything to do with either the cosmos or life, that is not a possibility that their assumptions allow for. To allow for an ID alternative they would have to change their basic understanding of science to a pursuit of truth, instead of the pursuit of a naturalistic explanation. What if there is no naturalistic explanation for life on earth? That is the testimony of the HOLY SPIRIT: “In the beginning GOD”! He is the Beginning and the End, and I believe we are much closer to the end than the beginning. Amen, come LORD JESUS! “It’s a battlefield brother, not a recreation room. It’s fighten, not a game.””aap_{June 13, 2016
June
06
Jun
13
13
2016
12:34 AM
12
12
34
AM
PDT}

Dr JDD @56
Let’s look at the b-hemoglobin pseudogene then, or hbbp1. You say that this is a generic “remnant of evolution” but again as per my previous post this is completely circular. 1) why is it a genetic remnant? 2) how do you know it is a genetic remnant? 3) how do you know any assigned function is the result of exaltation? I’m genuinely interested to know the answers to these questions.
These are the same kinds of questions I've been trying to get some kind of answer to for the past few days (week?)... Well, answers apart from the obvious, which is that Methodological Naturalism is used as a guiding principle and so purposelessness is assumed until definitively proven otherwise. I don't mean to annoyingly keep referencing my background as a programmer (among other things), but that is the perspective that I look at this issue from, and I think quite rightly, since DNA is widely recognized as software by people on both sides of this issue. Also, the fact that I'm specifically a UI programmer, for the most part, may give me a particularly applicable perspective, since my work requires me to split my attention between the underlying functional requirements in the code and the constraints presented by the various physical media on which it will display. The reason I bring up this background yet again is because, over the last several days, I've repeatedly seen smug declarations about the presence of copious amounts of evidence that only make sense on the hypothesis of naturalistic common descent and are not explicable on a pure design hypothesis. And what is the nature of this evidence? Well, it seems to be things like the presence of similar or identical code in sections of DNA that are not observed to execute and which are, for this reason, assumed to be purposeless junk, and the presence of different function from similar DNA sequences at the same or similar locations, or the fact that greater amounts of sequence divergence is observed in organisms believed to be more distantly related than in ones believed to be more closely related. When I see claims that these sorts of things don't make sense on a pure design hypothesis, the first thing that occurs to me is that either the people making such claims have no experience with software development, or else they are so trained to assume the truth of natural explanations over artificial ones that they completely fail to realize that these types of things are not only consistent with a software design hypothesis, but they are actually expected on it. In my opinion, all one needs to do to make sense of all of this data is conceive of life, in its entirety, as one big software application instantiated in 3D. On an only slightly different note, here's a question I'd like to know the answer to. Someone on another thread (can't remember who) said it was believed that carrying around a whole bunch of DNA that is currently assumed to be junk has little or no fitness cost on an organism. Does anyone know if that's correct?HeKS_{June 12, 2016
June
06
Jun
12
12
2016
11:43 PM
11
11
43
PM
PDT}

We also know today that whale evolution is nonsense and Dr. Warner exposed that Dr. Grinirich added artistic license to his fossil finds. So it is Kenneth Miller who was being ignorant.Andre_{June 12, 2016
June
06
Jun
12
12
2016
09:13 PM
9
09
13
PM
PDT}

Dr Torley On The evidence Duane Gish won... we know today what Kenneth Miller cited as transitional fossils were in fact not. Duane has never lost a debate on Darwinian evolution against any Darwinist.Andre_{June 12, 2016
June
06
Jun
12
12
2016
09:07 PM
9
09
07
PM
PDT}

Andre writes:
When someone tells you you’re Gish Galloping you can absolutely consider it a compliment. Dwayne Gish has never lost a debate against a Darwinist...
Sorry, but that's just not true. First of all, it's Duane Gish, and second, he died in 2013. Third, Gish did indeed lose spectacularly to Darwinist Kenneth Miller in a debate that took place in Tampa, Florida, on March 21, 1982. The following is an excerpt from the article, "Creation-Evolution Debates: Who's Winning Them Now?" by Frederick Edwords, in the Creation Evolution Journal, Issue 8 (Spring 1982), pp. 35-36:
But now Miller was facing Gish (whom he had faced only once before). Gish used the usual creationist debate arguments, particularly those linking the gaps in the fossil record and the absence of transitional fossils. Miller focused again on the theories of the worldwide flood and the young earth. He also predicted that Gish would not defend his model, and this prediction came true. Miller presented quotes from Henry Morris's writings that declared creationism to be a science and quotes from Gish's writing that said creationism was not science. After this he suggested that maybe the next debate should feature Morris arguing with Gish on this point until it is settled. After attacking creationism, Miller defended evolution. He answered Gish's arguments against Archaeopteryx and Ichthyostega being transitional fossils. He then quoted from Gish's paper on the mammal-like reptiles and showed how it contained rudimentary errors (such as misrepresenting the position of the middle-ear bones in reptiles and in saying that the columella connects the eardrum to the tympanum when actually the eardrum is the tympanum). Finally, he showed how the probability calculations against evolution used by Gish were based on faulty premises. The audience appeared surprised that Gish had made so many mistakes in his speaking and writing. Since Miller had presented a slide series on Triceratops, showing how it evolved from Monoclonius which evolved from Protoceratops, Dr. Gish argued that Monoclonius did not show any incipient horns that were precursors to the horns on Triceratops. He declared that Dr. Miller's slide was in error. But Miller rebutted by reading word-for-word from a leading text on the evolution of this dinosaur. The text even used Gish's words, "incipient horns," declaring their existence, complete with illustrations. Miller then handed this material to Gish and suggested that he study up before the next debate, causing the audience to roar with laughter. Dr. Gish used a humorous caricature drawing of a cow evolving from a whale; Dr. Miller came back with solid data supporting the evolution of whales from land mammals. There were other thrusts and parries, but, by the time the question-and-answer period came, Gish was rather quiet. He even made a stab at supporting "progressive creation," the position that the creator "created" on a number of occasions over billions of years. But Miller quoted Henry Morris on the evils of "progressive creation" and jokingly told Gish that he would inform Dr. Morris of this compromise and get Gish into trouble when he went home.
vjtorley_{June 12, 2016
June
06
Jun
12
12
2016
03:56 PM
3
03
56
PM
PDT}

Prof. Swamidass: You wrote:
Let’s recap… 1. A paper was published claiming that VTG1 has homology to DNA in humans in the exact right place in Chr1. The exact p-values were not reported. 2. Ann Gauger doubts CD, and disputed the statistical quality of that match. She asserted that perhaps the match was not really there, and just a statistical illusion. 3. I, however, trust that CD is a helpful framework in biology, that has a very good track record of PREDICTING patterns in biology. I supposed that the statistical match between VTG1 and this region was probably high. So now, we have two hypothesis: there (#3) is or (#2) is not a good statistical match between VTG1 and the correct region in the human genome. Now we can ALL test this for ourselves to see what hypothesis the data indicates is justified. Of course, this is not “proof.” Science, rather is about making rigorous explanations, and CD explains this data. An independent party has done just this, demonstrating that I was right and that Ann was wrong.
Point-by-point: (1) Entirely correct. (2) Ann Gauger doesn't "doubt" CD; rather, she is an agnostic. In her latest post at EvolNews she demonstrates that supposed match, and doesn't feel it matches the "claims" the authors make. I tend to agree with her. (More on this later) Now, I haven't followed the entirety of this conversation, but, I don't think Ann was "predicting" anything. (3) You again, and again, fail to distinguish between "common ancestry" and "common descent." It would be silly for someone to claim that new "types" are mad entirely "de novo." The entire idea, actually, is silly. Why would a designer 'design' that way if various organisms were meant to interact with one another. (Philosophically, more could be said about this; but we leave it to the one side). Naturally, there will be similarities. These similarities, however, do NOT prove "common descent," but, rather, only "common ancestry." The entire revolution in modern physics revolves around moving away from the continuous fields of classical theory, and embracing the discrete fields of quantum theory. Common descent implies a continuous, gradual evolution of sorts. We don't know this to have happened. We ONLY see "discrete" differences. The human and chicken versions of this gene are only slightly similar. There are huge differences between the two of them--at least as far as I can see based on Gauger's latest post. Your whole point in all of this is trivial. It has no bearing on any kind of discussion of Darwinian evolution versus Intelligent Design. The fact that most of those who take the ID position accept common descent as you seem to understand it makes this point exactly. Finally, who is this "independent party"? Are you referring to vjtorley? He is entitled to his opinion; but it is no more than opinion. Years ago, I had a go-round with an "expert" in BLAST searches. I told him that the vpu protein of HIV reminded me quite a bit of the influenza A (or was it B, matters not really). He did one BLAST sequence match after another, and told me I didn't know anything, and that there was no way that the two were related. I said that if you replaced the hydrophobic (or was it hydrophilic) portion of the vpu with the Influenza A virus, that the HIV would likely reproduce. He said again, no way. However, it turned out that experimenters had performed this exact experiment, and that, indeed, the Influenza A virus worked just fine. IOW, so much for BLAST matching, and experts who do it.PaV_{June 12, 2016
June
06
Jun
12
12
2016
03:09 PM
3
03
09
PM
PDT}

gpuccio: If you take a Chevy truck chasis used for their large sized trucks, and then turn it into a Suburban, which is basically a SUV, they share "common ancestry," but not "common descent." The axles will be the same. Much of the electrical system will be the same. The engine may be the same. But the exterior and interior design will be entirely different.PaV_{June 12, 2016
June
06
Jun
12
12
2016
02:30 PM
2
02
30
PM
PDT}

Let's look at the b-hemoglobin pseudogene then, or hbbp1. You say that this is a generic "remnant of evolution" but again as per my previous post this is completely circular. 1) why is it a genetic remnant? 2) how do you know it is a genetic remnant? 3) how do you know any assigned function is the result of exaltation? I'm genuinely interested to know the answers to these questions.Dr JDD_{June 12, 2016
June
06
Jun
12
12
2016
01:47 PM
1
01
47
PM
PDT}

Prof. S. Joshua Swamidass @48, Thank you. I always prefer to make people smile. Nevertheless, it seems that most evolutionary predictions that I've seen over time are abandoned when "surprising" evidence to the contrary emerges. I have no ideological or theological qualms with the concept of evolution. The primary problem is that mutation is an inadequate mechanism within the time frame given (not to mention that a mutation in only one organism won't persist as I'm sure you know), and that TOE has pushed out other paradigms by incorporating or rationalizing any other approach to the data. While your statistical analysis is commendable, perhaps even irrefutable, I think there are a lot of assumptions built into your approach. Let me explain. Let's consider the genome of dogs. Imagine every variety from Chihuahuas to Great Danes. Now let's say that dogs are sadly hit with some deadly virus that leaves only a tiny percentage of their varieties alive: Chihuahuas, Poodles, Greyhounds, and Great Danes. Not knowing about this event, what would your statistical analysis tell you about the evolution of these four (what would be subsequently be considered different) species? What if the genomes of all animals at one time had as much diversity as that of dogs? Would your statistical analysis be able to detect this? Let's consider bacteria, specifically the wide variety of gut bacteria. As you know, bacteria are the most adapted (or evolved) organisms on the planet, and that the prevalence of the varieties of gut bacteria vary depending on their location within their host's gut, and their host's diet. Let's assume that there's an efficient method for these bacteria to transfer certain genes to their hosts, helping their hosts adapt to changing environmental conditions. How would your statistical analysis be able to detect the source of these genes to gut bacteria? Finally, the most important factor is scientific validation by direct observation. This is why I wonder whether you've ever tried to validate the similarities (and differences!) in DNA by simulating evolution. The easiest way that I can think of is through using proportionately high levels of ionizing radiation on bacterial populations, although I've just read that there might be an alternative: https://www.sciencedaily.com/releases/2016/06/160609134243.htm Although evolutionary biologists were (once again) surprised at what they found, what unpublished predictions would you be willing to make regarding these bacteria? Regards, -QQuerius_{June 12, 2016
June
06
Jun
12
12
2016
01:18 PM
1
01
18
PM
PDT}

BA When someone tells you you're Gish Galloping you can absolutely consider it a compliment. Dwayne Gish has never lost a debate against a Darwinist... Keep it coming...Andre_{June 12, 2016
June
06
Jun
12
12
2016
12:31 PM
12
12
31
PM
PDT}

Swamidass: I have a history of demonstrating that I am not BSing when I say there is evidence that proves a bad arguments false ...
Yes, you have a history indeed.
Swamidass: (on SETI vs. ID methodology): Of the top of my head, I can come up with about five material differences.
&
Swamidass: So let me start with the ID work I found highest quality in this genre. This is is a paper published by Behe in 2004 (…) As a trained computational biologist, I spent 15 minutes reading the paper, about 2 hours thinking about it, and identified two clear errors.
In both cases you are simply BSing. You don’t point out those "five material differences", nor do you point out those “two clear errors” by Behe. It's all just part of your attempt to blow smoke.Origenes_{June 12, 2016
June
06
Jun
12
12
2016
11:37 AM
11
11
37
AM
PDT}

I consider your post a compliment. Despite your blatant ad hominem, my posts stand on their own merit. And I will leave it to the unbiased reader to decide who is being 'scientific' and who is 'blowing smoke'.bornagain77_{June 12, 2016
June
06
Jun
12
12
2016
11:16 AM
11
11
16
AM
PDT}

@50 BornAgain77 With all sincerity and fondness, I must complement you in your suberb ability to Gish Gallop (http://rationalwiki.org/wiki/Gish_Gallop). Your posts are great examples of "Proof by Verbosity," and you are at a master at this. You repeat several false and misleading arguments in quick sequence, quoting others rather than explaining actual data. You, sir, are amazingly effective at your intended goal: blowing so much smoke that casual readers are effectively blinded from the truth. Congratulations. To be clear, every argument you raise is false, and is easily demonstrated to be false using the evidence. In fact, many of the papers you quote actually expose the your arguments as false. I have a history of demonstrating that I am not BSing when I say there is evidence that proves a bad arguments false (look at my comments on prior VJ posts). I just refuse to do so when people are GIsh Galloping, even when one does so as expertly as do you. Those of us that care about evidence, I am sure, will just ignore you from here out. I hope you consider learning science some day. It is really amazing, and much more beautiful than an awkward gallop.Prof. S. Joshua Swamidass_{June 12, 2016
June
06
Jun
12
12
2016
09:38 AM
9
09
38
AM
PDT}

As to this claim:
"You are in the middle of a case study in a successful prediction of evolution. It absolutely does make predictions."
Except when Darwinian evolution does not make successful predictions, then it is merely 'explained away' as 'a striking example of convergent evolution between these clades at the molecular level."
The octopus genome and the evolution of cephalopod neural and morphological novelties – August 13, 2015 Excerpt: the independent expansions and nervous system enrichment of protocadherins in coleoid cephalopods and vertebrates offers a striking example of convergent evolution between these clades at the molecular level. http://www.nature.com/nature/journal/v524/n7564/full/nature14668.html
Contrary to what Prof. S. Joshua Swamidass prefers to believe, and besides Darwinian evolution being a unfalsifiable pseudo-science (posts 40-43), the list of fundamentally failed predictions of Darwinian evolution is rather long: First a little background as to 'predictive power's' rank in science. Predictive power, although impressive, actually ranks below falsifiability as to determining whether a theory is 'scientific' or not.
"In so far as a scientific statement speaks about reality, it must be falsifiable; and in so far as it is not falsifiable, it does not speak about reality." Karl Popper - The Two Fundamental Problems of the Theory of Knowledge (2014 edition), Routledge Dubitable Darwin? Why Some Smart, Nonreligious People Doubt the Theory of Evolution By John Horgan on July 6, 2010 Excerpt: Early in his career, the philosopher Karl Popper ,, called evolution via natural selection "almost a tautology" and "not a testable scientific theory but a metaphysical research program." Attacked for these criticisms, Popper took them back (in approx 1978). But when I interviewed him in 1992, he blurted out that he still found Darwin's theory dissatisfying. "One ought to look for alternatives!" Popper exclaimed, banging his kitchen table. http://blogs.scientificamerican.com/cross-check/dubitable-darwin-why-some-smart-nonreligious-people-doubt-the-theory-of-evolution/
Unlike Popper, philosopher of science Imre Lakatos tipped toed around the fact that Darwinism does not have rigid mathematical falsification criteria to test against, as other overarching theories of science have, in order to potentially falsify it,,,
A Philosophical Question...Does Evolution have a Hard Core ? Some Concluding Food for Thought In my research on the demarcation problem, I have noticed philosophers of science attempting to balance (usually unconsciously) a consistent demarcation criteria against the disruptive effects that its application might have with regard to the academic status quo (and evolution in particular)… Few philosophers of science will even touch such matters, but (perhaps unintentionally) Imre Lakatos does offer us a peek at how one might go about balancing these schizophrenic demands (in Motterlini1999: 24) “Let us call the first school militant positivism; you will understand why later on. The problem of this school was to find certain demarcation criteria similar to those I have outlined, but these also had to satisfy certain boundary conditions, as a mathematician would say. I am referring to a definite set of people to which most scientists as well as Popper and Carnap would belong. These people think that there are goodies and baddies among scientific theories, and once you have defined a demarcation criterion. you should divide all your theories between the two groups. You would end up. for example, with a goodies list including Copernicus’s (Theory1), Galileo’s (T2), Kepler’s (T3), Newton’s (T4) … and Einstein’s (T5), along with (but this is just my supposition) Darwin’s (T6). Let me just anticipate that nobody to date has yet found a demarcation criterion according to which Darwin can be described as scientific, but this is exactly what we are looking for.” So basically, the demarcation problem is a fun game philosophers enjoy playing, but when they realize the implications regarding the theory of evolution, they quickly back off… http://www.samizdat.qc.ca/cosmos/philo/hardcore_pg.htm
Lakatos, although he tipped toed around the failure of Darwinism to have a rigid demarcation criteria, he was brave enough to state that a good scientific theory will make successful predictions in science and a bad scientific theory will generate ‘epicycle theories’ to cover up embarrassing failed predictions:
“In degenerating programmes, however, theories are fabricated only in order to accommodate known facts” – Imre Lakatos (November 9, 1922 – February 2, 1974) a philosopher of mathematics and science, , quote as stated in 1973 LSE Scientific Method Lecture
And that is exactly what we find with Darwinian evolution. Dr. Hunter comments,,
"When their expectations turn out to be false, evolutionists respond by adding more epicycles to their theory that the species arose spontaneously from chance events. But that doesn’t mean the science has confirmed evolution as Velasco suggests. True, evolutionists have remained steadfast in their certainty, but that says more about evolutionists than about the empirical science." ~ Cornelius Hunter Here’s That Algae Study That Decouples Phylogeny and Competition - June 17, 2014 Excerpt: "With each new absurdity another new complicated just-so story is woven into evolutionary theory. As Lakatos explained, some theories simply are not falsifiable. But as a result they sacrifice realism and parsimony." - Cornelius Hunter http://darwins-god.blogspot.com/2014/06/heres-that-algae-study-that-decouples.html
And following in Lakatos footsteps, Dr. Hunter has compiled a list of some of the major false predictions generated by evolutionary theory. False predictions that are fundamental to evolutionary theory, i.e. go to the ‘core’ of the theory, and falsify it from the inside out as it were.
Darwin's (failed) Predictions - Cornelius G. Hunter - 2015 This paper evaluates 23 fundamental (false) predictions of evolutionary theory from a wide range of different categories. The paper begins with a brief introduction to the nature of scientific predictions, and typical concerns evolutionists raise against investigating predictions of evolution. The paper next presents the individual predictions in seven categories: early evolution, evolutionary causes, molecular evolution, common descent, evolutionary phylogenies, evolutionary pathways, and behavior. Finally the conclusion summarizes these various predictions, their implications for evolution’s capacity to explain phenomena, and how they bear on evolutionist’s claims about their theory. *Introduction Why investigate evolution’s false predictions? Responses to common objections *Early evolution predictions The DNA code is not unique The cell’s fundamental molecules are universal *Evolutionary causes predictions Mutations are not adaptive Embryology and common descent Competition is greatest between neighbors *Molecular evolution predictions Protein evolution Histone proteins cannot tolerate much change The molecular clock keeps evolutionary time *Common descent predictions The pentadactyl pattern and common descent Serological tests reveal evolutionary relationships Biology is not lineage specific Similar species share similar genes MicroRNA *Evolutionary phylogenies predictions Genomic features are not sporadically distributed Gene and host phylogenies are congruent Gene phylogenies are congruent The species should form an evolutionary tree *Evolutionary pathways predictions Complex structures evolved from simpler structures Structures do not evolve before there is a need for them Functionally unconstrained DNA is not conserved Nature does not make leaps *Behavior Altruism Cell death *Conclusions What false predictions tell us about evolution https://sites.google.com/site/darwinspredictions/home Why investigate evolution’s false predictions? Excerpt: The predictions examined in this paper were selected according to several criteria. They cover a wide spectrum of evolutionary theory and are fundamental to the theory, reflecting major tenets of evolutionary thought. They were widely held by the consensus rather than reflecting one viewpoint of several competing viewpoints. Each prediction was a natural and fundamental expectation of the theory of evolution, and constituted mainstream evolutionary science. Furthermore, the selected predictions are not vague but rather are specific and can be objectively evaluated. They have been tested and evaluated and the outcome is not controversial or in question. And finally the predictions have implications for evolution’s (in)capacity to explain phenomena, as discussed in the conclusions. https://sites.google.com/site/darwinspredictions/why-investigate-evolution-s-false-predictions
of supplemental note to the Darwinian prediction that genes are supposedly not suppose to be that similar or even in the same order in supposedly widely divergent species:
Kangaroo genes close to humans Excerpt: Australia's kangaroos are genetically similar to humans,,, "There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order," ,,,"We thought they'd be completely scrambled, but they're not. There is great chunks of the human genome which is sitting right there in the kangaroo genome," http://www.reuters.com/article/science%20News/idUSTRE4AH1P020081118
bornagain77_{June 12, 2016
June
06
Jun
12
12
2016
08:43 AM
8
08
43
AM
PDT}

A word about exapation and homology. Exaptation is the use of one structure (e.g. a stretch of DNA) for different purpose than it was used in evolutionary history. Just proving that the remnants of a pseudogene (e.g. b-hemoglobin or VTG1) might have a new function (in gene regulation or as a non-functional lncRNA) does not in any way invalidate CD. Asserting function in the pseudogenes does not validate design either. In addition to showing function you have to demonstrate that the POSITION (the synteny) in the genome right there is necessary. That is the specific signature here we are focusing on. Not just homology, but also synteny. Now, regarding exaptation and homology for distantly related sequences, there is a relationship. It turns out for very distantly related sequences (like VTG1 and the human DNA match), homology is more likely to be preserved where there is some evolutionary history of function (e.g. exaptation). This is an explicit part of some mathematical models. The more function, the more exaptation, the more preservation of the original sequence. This is important, because (in these distantly related sequence) we do expect to occasionally encounter new functions and for this to be where they homology is strongest. This is exactly predicted by CD and neutral theory. While this is consistent with design, the POSITION in the genome is not precisely predicted by design, unless we include some form of common ancestry too. This is why scientists think the evidence for CD is so solid. This (of course) is just one line of evidence. The correlation between de novo mutation and divergence is also predicted by CD, and not explained by design. That should be the next type of evidence to look closely at.Prof. S. Joshua Swamidass_{June 12, 2016
June
06
Jun
12
12
2016
08:29 AM
8
08
29
AM
PDT}

@44 "Great point! The theory of evolution can explain everything, but successfully predicts nothing." I had to smile when I read this. You are in the middle of a case study in a successful prediction of evolution. It absolutely does make predictions. Let's recap... 1. A paper was published claiming that VTG1 has homology to DNA in humans in the exact right place in Chr1. The exact p-values were not reported. 2. Ann Gauger doubts CD, and disputed the statistical quality of that match. She asserted that perhaps the match was not really there, and just a statistical illusion. 3. I, however, trust that CD is a helpful framework in biology, that has a very good track record of PREDICTING patterns in biology. I supposed that the statistical match between VTG1 and this region was probably high. So now, we have two hypothesis: there (#3) is or (#2) is not a good statistical match between VTG1 and the correct region in the human genome. Now we can ALL test this for ourselves to see what hypothesis the data indicates is justified. Of course, this is not "proof." Science, rather is about making rigorous explanations, and CD explains this data. An independent party has done just this, demonstrating that I was right and that Ann was wrong. https://roohif.wordpress.com/2016/06/11/where-did-that-guy-get-his-data-from/ HERE IS THE RECIPE FOR YOU TO TRY TOO... a) Get the VTG1 sequence from here: http://www.ncbi.nlm.nih.gov/gene/424547 http://www.ncbi.nlm.nih.gov/nuccore/NC_006095.4?report=fasta&from=18694448&to=18737086 b) Paste sequence into blastn website (default parameters, https://blast.ncbi.nlm.nih.gov/Blast.cgi). Choose to search against human…and you get this top hit.. Homo sapiens chromosome 1, alternate assembly CHM1_1.1 291 1.613e+06 9% 5e-74 75% NC_018912.2 To be clear, you might get a slightly different result if you use different parameters. The e-value of 5e-74 is not exactly a p-value, but has some close correspondence to it, close enough to be interpreted in a "similar" way. c) Now, we can also visualize this using the UCSC genome browser BLAT search. Just paste the VTG1 sequence into BLAT (https://genome.ucsc.edu/cgi-bin/hgBlat?command=start). Click the first hit, then zoom out far enough to see ETLD1 and check the tracts as required. I did this to get this image here: https://genome.ucsc.edu/cgi-bin/hgTracks?db=hg38&lastVirtModeType=default&lastVirtModeExtraState=&virtModeType=default&virtMode=0&nonVirtPosition=&position=chr1%3A78659897-78919796&hgsid=497817261_89LABjkhtaZ9Vn8cDAIDVganAACJ http://swami.wustl.edu/hgt_genome_680f_62a4d0 (if the first one doesn’t work use this). A couple things to note. (1) the sequence is right where we expect it to be, (2) in my image, I plotted the match alongside transcript levels. The VTG1 match is not expressed nearly at all (because it is not likely functional) while the two flanking genes (see bar graphs) are expressed in a large number of tissues at a high level. THE SAME PROCESS CAN BE REPEATED (minus blat) USING THE WHOLE INTERGENEC REGION. Gotta go now, but I will post this recipe later. Depending on the exact parameters, I get 8 to 24 matches accross the region. Here is the summary of the matches in one run... Length 278bp, identity 71% Length 248bp, identity 73% Length 288bp, identity 70% Length 278bp, identity 75% Length 483bp, identity 74% Length 390bp, identity 74% Length 321bp, identity 68% So this gives us an overall alignment of 2286 base pairs with an overall similarity (weighted) of about 72.3%. Much better than 150bp with 50% similarity that Ann reports. Also, all with very very high statistical significance. Now, for those of you that now want to claim that this is all a lncRNA. A few points. From a CD point of view, "exaptation" allows this to be functional. It does not to be non-functional to be evidence for CD. That is just a red herring. Moreover, this is little (no?) evidence that this actually is a lncRNA. I reread the Tomkins paper that claims this and see no strong evidence (just wild speculation) that the original vtg fragment actually is a lncRNA. As for the whole region? He does not even try to claim it is all a lncRNA. So, for two reasons, that lncRNA theory really is entirely irrelevant here. Now, if you really do care about evidence as you claim, do the experiment yourself, and see if CD makes predictions. It does, and they are usually correct. ===EXTRA CREDIT: SYNTENY=== @26 Ann.. We can also ask, does the VTG1 sequence match to the right place in the human genome with the highest similarity? Does it match next to the ETLD1 gene? HINT: Just as we would predict with CD, it does match there. And it does so in the right direction too. This becomes obvious when you use the BLAT search in the UCSC browser, and zoom out to see the surrounding genes: PGTFR and ETLD1. You can also just click the link I gave you there to see it. Btw, Ann, I give you credit for acknowledging publicly that this is a good match. I respect your willingness to change your mind, especially in public like that.Prof. S. Joshua Swamidass_{June 12, 2016
June
06
Jun
12
12
2016
08:04 AM
8
08
04
AM
PDT}

Hello All, VJ asked me to contribute a few comments. I have a small break today, and decided to use it to participate. I do have one request. Please be kind and respectful. Disagree with me, of course, but please give me reason to gladly spend my time with you. I'll post a few comments. First regarding infighting and terminology. @6 terminology Some have expressed concern with the term "common descent". This has come up before. I will say, as a scientist, that there are several nearly equivalent terms that are acceptable in this conversation: common descent common ancestry common descent with designed modification common ancestry with designed modification To be clear, this conversation does not even concern "universal" common descent. We are talking, usually, in the more restricted sense of common ancestry of man, mammals, or vertebrates. If you don't like one term, and feel the use to another from this list, that is entirely fine by me. I will also point out (at some risk) that this notion of "common ancestry" is the historically most consistent definition of evolution. This is why Behe considers himself, correctly, a theistic evolutionist. I know that "evolution" is a bad word for many in the ID community, so I understand if you reject evolution but accept CD. @5 @4 about infighting "I think that we the ID community need to demonstrate to the rest of science that we are an evidence driven people, not a position driven people." "I agree. A healthy exchange is good. Lets discover together what the evidence is really telling us. I thought Ann did a very good job defending her position and agree Dr Hunter has surfaced some very good points." This is significant and important. I want to affirm it. Right now, there is a perception that ID is only concerned with attacking people outside the ID camp, without really grappling with evidence internally. This is why internal debate (even with me as an outside observer) is healthy and valuable. If you demonstrate to the scientific world you can come to and evidence based consensus about things like, for example. common descent, it enables to take you more seriously about other things. @4 @5 about Hunter "That said, I recently watched Dr. Hunter put out a compelling case against common descent." I disagree with this strongly. Every point that Hunter has raised is clearly wrong on an evidentiary basis. Dead wrong, often accusatory, and also what appears to be deceptive. The only reason his specific arguments are not being answered by me is because (1) he has refused to publicly conceded a point in where was clearly demonstrated to be wrong, and (2) he has not even attempted to answer VJ's 13 questions. If you think Hunter has made a solid case, ask him why he is unwilling to answer VJ's questions. Why is he is unable/unwilling to answer an careful and honest critique from a member of the ID community? Instead of engaging, he moved on to another long list of inaccurate and false claims about the evidence. In particular, I find it galling that he seems to argue that there is "absolutely no evidence" for common descent. This is a truly absurd claim. Even Ann acknowledges that at least some evidence exists for CD, even though she ultimately seems to reject it. I would love to entertain a real conversation with Hunter, but until he answers VJ and can acknowledge the clear evidence for CD that he himself uncovered, I dispute the notion that he has made a compelling case against CD. ================= For those that just do not like CD, despite the evidence. I will point out too, that I have said repeatedly that there are good reasons for rejecting CD. In particular, there are good and dignified reasons for rejecting CD for theological reasons. This is what Todd Woods does, and I respect that. On the scientific front, looking at evidence, I (and the rest of the mainstream scientific community) contend that the case for CD is rock solid. So I am doing too things here. Scientifically, "recent" evolutionary history (e.g. the last 50M years of mammalian evolution) the evidence points in one direction unambiguously to CD. More remote evolutionary history (e.g. microbial evolution) is less clear, primarily because the genomic signature degrades substantially past about 100mya.Prof. S. Joshua Swamidass_{June 12, 2016
June
06
Jun
12
12
2016
07:43 AM
7
07
43
AM
PDT}

Mung @10
The scientific evidence? Because I’d really like to know the Biblical evidence against the proposition that chickens and porcupines share a common ancestor.
The biblical evidence against said idea is that chickens would have been created on day 5 according to their kind while porcupines would have been created on day 6 according to their kind.
Were both chickens and porcupines on the ark? How do you decide what “kind” a chicken belongs to and what “kind” a porcupine belongs to? How do you decide which “kinds” survived the flood?
Since the Bible doesn't tell us what the original kinds were, we have to try and figure that out using genetics. This necessarily involves a lot of assumptions and interpretation, so nothing is for certain. Research in baraminology is ongoing. All of the "kinds" would have survived the flood unless some of them had already gone extinct before the flood and therefore would not have been on the ark. Of course, most IDers do not believe in a global flood so I'm not sure why you would bring this up here.tjguy_{June 12, 2016
June
06
Jun
12
12
2016
07:40 AM
7
07
40
AM
PDT}

Dr Hunter is mentioned a few times in this thread, who, in relation to the "truth" of common descent (which Dr Torley appears to hold as scientifically dogmatic), disagrees with Professor Dennis Venema, and to whom Dr Ann Gauger also refers to, as "weak evidence for common descent." Dr Hunter writes: ----------------------------------------------- "In spite of these problems with his argument, Venema is enthusiastic about this evidence. In fact his enthusiasm leads to the fallacy of affirming the consequent, as he equates shared synteny (genes with similar positioning in the genomes of different species) with common descent": 'This evidence increases our confidence that we are indeed looking at regions with shared synteny: in other words, a region in two present-day species that was once a region in the genome of their common ancestral population.' "That is a fallacy. Ignoring the problems discussed above for the moment, even if evolution did make a hard prediction of shared synteny, and even if it was universally observed, that would not prove evolution. In that case, you would have a confirmed prediction. That is good, but it is not equivalent to a finding of evolution. Venema violates this scientific fundamental when he defines shared synteny as 'a region in two present-day species that was once a region in the genome of their common ancestral population.' Unfortunately, affirming the consequent is not uncommon in the evolution literature." http://darwins-god.blogspot.co.uk/2016/06/biologos-and-vitellogenin-genes.html?m=1 -------------------------------------------------- "I am the way, and the truth and the life" (Jn 14:6). Not in this case when it comes to common descent, Lord!mw_{June 12, 2016
June
06
Jun
12
12
2016
05:58 AM
5
05
58
AM
PDT}

bornagain77,
The genetic similarity argument for common ancestry highlights the unfalsifiable nature of Darwinian theory. If genetic similarity between supposedly closely related species, as their reasoning goes, is suppose to be undeniable proof for the hypothesis of common ancestry, then finding highly similar sequences in widely divergent species should serve as a falsification for that hypothesis. Yet highly similar sequences in widely divergent species are not allowed to falsify the common ancestry hypothesis. Darwinists and Theistic Evolutionists, whether intentionally or not, invoke ‘convergent evolution’ to ‘explain away’ highly similar sequences in widely divergent species.
Great point! The theory of evolution can explain everything, but successfully predicts nothing. HeKS, Considering the similarity between software and DNA, another problem is that not only does one need an effective mechanism for the program to be able to evolve, but the programming language and the operating system must also have evolved somehow before there was any survival advantage. This leaves massively improbable "luck" as the mechanism, for which the age of the universe is a ridiculously insufficient amount of time. But don't worry. Some scientists can draw on the limitless probabilities available from the Multiverse, each one of which also needs to be able to instantly spawn trillions of the Many Worlds needed to avoid the interpretation problems materialists have with the demonstrated ability for human observation being able to collapse the wave functions in quantum mechanics. All we need is an infinity of infinities, more properly called "a miracle." Parsimony need not apply. And when this Miraculous Mutation (TM) finally appears in an organism, all that needs to happen is for the *identical* Miraculous Mutation to appear within thousands of other organisms at the same time to ensure that this amazing trait is able to survive within the genome. But, hey. We have plenty of time. No wonder Thick Python and Professor Swamidrass don't seem to be eager to accept the challenge of demonstrating their assertions using a huge, rapidly reproducing population of non-motile bacteria subjected to enough ionizing radiation to simulate millions of years of mutagenic impact to finally produce a mutated bacteria with flagella, cilia, legs, propellers, teensy jet engines, or whatever to make them motile! This is called "science" in contrast to imaginative extrapolation, interpretation, and speculation. -QQuerius_{June 11, 2016
June
06
Jun
11
11
2016
10:58 PM
10
10
58
PM
PDT}

bFast @39
Dr. JDD (29) First, most humans don’t have any of these alleles. However the population does. The mutational hot spot theory would only be a reasonable explanation if “hot spots” didn’t mean “hot zones”, but it would require specific hot mutational points. If not, then the fact that the alignment of these mutations (relative to the gene’s start) would rarely match.
Not necessarily. For example, what if you had functional elements in both chimps and humans that relied on dependencies that were prone to degradation or wholesale loss? If that were the case, all of the similarities would be due to function but the current disease outcome in both species would be a result of malfunction of a shared system due to breakage in dependencies that are prone to failure. I'm a web UI programmer and I've been talking recently in the 'consider the opossum' thread about how programming design patterns should impact on assumptions about junk DNA and common descent. I think that in order to make sense of DNA from a design standpoint, one needs to consider DNA from the dual perspective of software programming and structural engineering. I have no expertise whatsoever in the latter, but I know from personal experience that physical systems tend to have consistent break points, or pathways of least resistance to system failure. This system over here tends to have this element fail after X amount of time. That system over there tends to have another element fail after a certain amount of time. In programming you don't typically have blocks of code that are prone to breaking down in the sense of the language somehow getting corrupted, but you can sometimes have blocks of code that are prone to failing because they rely on external resources that might be unreliable. Take care, HeKSHeKS_{June 11, 2016
June
06
Jun
11
11
2016
07:58 PM
7
07
58
PM
PDT}

And as should be needless to say, if your materialistic theory cannot explain the 'form' of an organism in the first place, then any materialistic theory that purports to explain the transformation of form in all organisms on earth is, to put it mildly, severely misguided in its theoretical foundation. Moreover, this failure of materialistic explanations to explain 'form' happens at a very foundational level. “Random” Darwinian explanations cannot even explain how a protein finds it final folded form, much less how an entire organism achieves its final form:
Physicists Discover Quantum Law of Protein Folding – February 22, 2011 Quantum mechanics finally explains why protein folding depends on temperature in such a strange way. Excerpt: First, a little background on protein folding. Proteins are long chains of amino acids that become biologically active only when they fold into specific, highly complex shapes. The puzzle is how proteins do this so quickly when they have so many possible configurations to choose from. To put this in perspective, a relatively small protein of only 100 amino acids can take some 10^100 different configurations. If it tried these shapes at the rate of 100 billion a second, it would take longer than the age of the universe to find the correct one. Just how these molecules do the job in nanoseconds, nobody knows.,,, Today, Luo and Lo say these curves can be easily explained if the process of folding is a quantum affair. By conventional thinking, a chain of amino acids can only change from one shape to another by mechanically passing though various shapes in between. But Luo and Lo say that if this process were a quantum one, the shape could change by quantum transition, meaning that the protein could ‘jump’ from one shape to another without necessarily forming the shapes in between.,,, Their astonishing result is that this quantum transition model fits the folding curves of 15 different proteins and even explains the difference in folding and unfolding rates of the same proteins. That's a significant breakthrough. Luo and Lo's equations amount to the first universal laws of protein folding. That’s the equivalent in biology to something like the thermodynamic laws in physics. http://www.technologyreview.com/view/423087/physicists-discover-quantum-law-of-protein/
Of related note to 'quantum' proteins: Quantum Mechanics is completely antagonistic to the 'bottom up' materialistic foundation that Darwinian evolution is built upon:
Jim Al-Khalili, at the 2:30 minute mark of the following video states, ",,and Physicists and Chemists have had a long time to try and get use to it (Quantum Mechanics). Biologists, on the other hand have got off lightly in my view. They are very happy with their balls and sticks models of molecules. The balls are the atoms. The sticks are the bonds between the atoms. And when they can't build them physically in the lab nowadays they have very powerful computers that will simulate a huge molecule.,, It doesn't really require much in the way of quantum mechanics in the way to explain it." At the 6:52 minute mark of the video, Jim Al-Khalili goes on to state: “To paraphrase, (Erwin Schrödinger in his book “What Is Life”), he says at the molecular level living organisms have a certain order. A structure to them that’s very different from the random thermodynamic jostling of atoms and molecules in inanimate matter of the same complexity. In fact, living matter seems to behave in its order and its structure just like inanimate cooled down to near absolute zero. Where quantum effects play a very important role. There is something special about the structure, about the order, inside a living cell. So Schrodinger speculated that maybe quantum mechanics plays a role in life”. Jim Al-Khalili – Quantum biology – video https://www.youtube.com/watch?v=zOzCkeTPR3Q
Here is a bit closer look at the falsification of Darwinian evolution by Quantum Mechanics:
Molecular Biology - 19th Century Materialism meets 21st Century Quantum Mechanics - video https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1141908409155424/?type=2&theater Looking beyond space and time to cope with quantum theory – 29 October 2012 Excerpt: “Our result gives weight to the idea that quantum correlations somehow arise from outside spacetime, in the sense that no story in space and time can describe them,” http://www.quantumlah.org/highlight/121029_hidden_influences.php Physicists find extreme violation of local realism in quantum hypergraph states - Lisa Zyga - March 4, 2016 Excerpt: Many quantum technologies rely on quantum states that violate local realism, which means that they either violate locality (such as when entangled particles influence each other from far away) or realism (the assumption that quantum states have well-defined properties, independent of measurement), or possibly both. Violation of local realism is one of the many counterintuitive, yet experimentally supported, characteristics of the quantum world. Determining whether or not multiparticle quantum states violate local realism can be challenging. Now in a new paper, physicists have shown that a large family of multiparticle quantum states called hypergraph states violates local realism in many ways. The results suggest that these states may serve as useful resources for quantum technologies, such as quantum computers and detecting gravitational waves.,,, The physicists also showed that the greater the number of particles in a quantum hypergraph state, the more strongly it violates local realism, with the strength increasing exponentially with the number of particles. In addition, even if a quantum hypergraph state loses one of its particles, it continues to violate local realism. This robustness to particle loss is in stark contrast to other types of quantum states, which no longer violate local realism if they lose a particle. This property is particularly appealing for applications, since it might allow for more noise in experiments. Per physorg
Moreover, it is important to learn that ‘non-local’, beyond space and time, quantum entanglement (A. Aspect, A. Zeilinger, etc..) can be used as a ‘quantum information channel’,,,
Quantum Entanglement and Information Quantum entanglement is a physical resource, like energy, associated with the peculiar nonclassical correlations that are possible between separated quantum systems. Entanglement can be measured, transformed, and purified. A pair of quantum systems in an entangled state can be used as a quantum information channel to perform computational and cryptographic tasks that are impossible for classical systems. The general study of the information-processing capabilities of quantum systems is the subject of quantum information theory. http://plato.stanford.edu/entries/qt-entangle/
Besides providing direct empirical falsification of neo-Darwinian claims that say information is emergent from a material basis, the implication of finding 'non-local', beyond space and time, and ‘conserved’ quantum information/entaglement in molecular biology on such a massive scale, in every DNA and protein molecule, is fairly, and pleasantly, obvious. That pleasant implication, or course, being the fact that we now have direct physical evidence of a transcendent component to our being that is strongly suggestive to the fact that we do indeed have an eternal soul that lives beyond the death of our material bodies.
Scientific (physical) evidence that we do indeed have an eternal soul - video https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1116313858381546/?type=2&theater Does Quantum Biology Support A Quantum Soul? – Stuart Hameroff - video https://www.youtube.com/watch?v=iIyEjh6ef_8
Verse and Music:
Mark 8:36 What good is it for someone to gain the whole world, yet forfeit their soul? Metallica & San Francisco Symphony Orchestra - Nothing Else Matters http://www.youtube.com/watch?v=ziThYl6B2vw
bornagain77_{June 11, 2016
June
06
Jun
11
11
2016
07:38 PM
7
07
38
PM
PDT}

"Shared Evolutionary History or Shared Design?" - Ann Gauger - January 1, 2015 Excerpt: The waiting time required to achieve four mutations is 10^15 years. That's longer than the age of the universe. The real waiting time is likely to be much greater, since the two most likely candidate enzymes failed to be coopted by double mutations. http://www.evolutionnews.org/2015/01/happy_new_year092291.html Is There Enough Time For Humans to have Evolved from Apes? Dr. Ann Gauger Answers - video http://www.youtube.com/watch?v=KN7NwKYUXOs
Dr. Sanford's work agrees with Gauger and Axe's empirical work, as this paper from BioMed shows:
The waiting time problem in a model hominin population – 2015 Sep 17 John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,, Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information. While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man. It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/
Here are several more peer reviewed papers by Dr. Sanford and company, on population genetics, falsifying Darwinian evolution from numerous different angles:
Genetic Entropy – peer reviewed references http://www.geneticentropy.org/#!properties/ctzx
Moreover, even as bad as the preceding is for 'bottom up' Darwinian explanations, it was still falsely presumed in the preceding papers by Drs. Gauger, Axe, and Sanford, that changes to DNA can explain transformations in form, or 'body-plan morphogenesis' as Dr. Stephen Meyer calls it. Yet, Darwinists and Theistic Evolutionists have no hard evidence whatsoever that changes to DNA will lead to fundamentally new transformations in form:
“Any transition of form is pure fantasy. There is no demonstration of it.” Douglas Axe – co-author of Science & Human Origins – video http://www.youtube.com/watch?v=XxMmLakH2LQ 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. http://www.evolutionnews.org/2010/10/response_to_john_wise038811.html
Dr. Stephen Meyer puts the insurmountable problem for Darwinian explanations of 'form' like this:
‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body-plan. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ Stephen Meyer - Functional Proteins and Information for Body Plans - video https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1140536289292636/?type=2&theater
That the 'form' of a organism is not reducible to material particulars, as is presupposed by both Darwinists and Theistic Evolutionists, is made clear by the two following examples:
What Do Organisms Mean? Stephen L. Talbott - Winter 2011 Excerpt: Harvard biologist Richard Lewontin once described how you can excise the developing limb bud from an amphibian embryo, shake the cells loose from each other, allow them to reaggregate into a random lump, and then replace the lump in the embryo. A normal leg develops. Somehow the form of the limb as a whole is the ruling factor, redefining the parts according to the larger pattern. Lewontin went on to remark: "Unlike a machine whose totality is created by the juxtaposition of bits and pieces with different functions and properties, the bits and pieces of a developing organism seem to come into existence as a consequence of their spatial position at critical moments in the embryo’s development. Such an object is less like a machine than it is like a language whose elements... take unique meaning from their context.[3]",,, http://www.thenewatlantis.com/publications/what-do-organisms-mean "Last year I had a fair chunk of my nose removed in skin cancer surgery (Mohs). The surgeon took flesh from a nearby area to fill in the large hole he’d made. The pictures of it were scary. But in the healing process the replanted cells somehow ‘knew’ how to take a different shape appropriate for the new location so that the nose now looks remarkably natural. The doctor said he could take only half the credit because the cells somehow know how to change form for a different location (though they presumably still follow the same DNA code) . — I’m getting the feeling that we’ve been nearly as reductionist in the 20-21st century as Darwin and his peers were when they viewed cells as little blobs of jelly." leodp - UD blogger
bornagain77_{June 11, 2016
June
06
Jun
11
11
2016
07:36 PM
7
07
36
PM
PDT}

"In so far as a scientific statement speaks about reality, it must be falsifiable; and in so far as it is not falsifiable, it does not speak about reality." Karl Popper - The Two Fundamental Problems of the Theory of Knowledge (2014 edition), Routledge
The genetic similarity argument for common ancestry highlights the unfalsifiable nature of Darwinian theory. If genetic similarity between supposedly closely related species, as their reasoning goes, is suppose to be undeniable proof for the hypothesis of common ancestry, then finding highly similar sequences in widely divergent species should serve as a falsification for that hypothesis. Yet highly similar sequences in widely divergent species are not allowed to falsify the common ancestry hypothesis. Darwinists and Theistic Evolutionists, whether intentionally or not, invoke 'convergent evolution' to 'explain away' highly similar sequences in widely divergent species.
Darwinism Versus the Octopus: An Evolutionary Dilemma - Eric Metaxas - September 08, 2015 Excerpt: What’s the difference between evolutionary theory and an octopus? Well, one is a slippery, color-changing escape artist that can get out of any tough situation and the other is an aquatic invertebrate.,,, The key to this uncanny intelligence is the octopus’ so-called “alien” nervous system, brain, and eyes. But these features are not alien to the animal kingdom at all. In fact, they’re quite common in higher vertebrates. The octopus genome shares key similarities with ours, including the development of high-powered brains and “camera eyes” with a cornea, lens, and retina. Now here’s the problem for evolution: according to Neo-Darwinists, we’re not related to octopi—at least not within the last several hundred million years. That means all of these genes, complex structures, and incredible capabilities came about twice. The researchers who sequenced the octopus genome call this “a striking example of convergent evolution,” or the supposed tendency of unrelated creatures to develop the same traits in response to environmental pressures. Isn’t that just a fancy way of saying a miracle happened twice? But the octopus isn’t the only such miracle. “Convergent evolution” is all over nature, from powered flight evolving three times to each continent having its own version of the anteater. Think about that. As one delightfully un-self-conscious “Science Today” cover put it, convergent evolution is “nature discover[ing] the same design over and over.” Well, good for nature! But as Luskin argues, there’s a better explanation for a tentacled mollusk having a mammal’s brain and human eyes. And that explanation is common design by an intelligent Engineer. And like all good engineers, this this one reused some of His best designs. Now that explanation isn’t going to satisfy Darwinian naturalists. And they’ll probably keep on invoking “convergent evolution” when faced with impossible coincidences in nature. But hopefully knowing a more straightforward explanation leaves you forearmed—or should I said “eight-armed”? http://www.christianheadlines.com/columnists/breakpoint/darwinism-versus-the-octopus-an-evolutionary-dilemma.html
Here are a few more examples of 'convergent evolution':
Newly Discovered Convergent Genetic Evolution Between Bird and Human Vocalization Poses a Severe Challenge to Common Ancestry - Casey Luskin - December 15, 2014 Excerpt: "We've known for many years that the singing behavior of birds is similar to speech in humans -- not identical, but similar -,,, "But we didn't know whether or not those features were the same because the genes were also the same." "Now scientists do know, and the answer is yes -- birds and humans use essentially the same genes to speak.",,, "there is a consistent set of just over 50 genes,,," "These changes were not found in the brains of birds that do not have vocal learning and of non-human primates that do not speak," So certain birds and humans use the same genes for vocalization -- but those genetic abilities are absent in non-human primates and birds without vocal learning? If not derived from a common ancestor, as they clearly were not, how did the genes get there? This kind of extreme convergent genetic evolution points strongly to intelligent design. http://www.evolutionnews.org/2014/12/newly_discovere092041.html First Decoded Marsupial Genome Reveals "Junk DNA" Surprise - 2007 Excerpt: In particular, the study highlights the genetic differences between marsupials such as opossums and kangaroos and placental mammals like humans, mice, and dogs. ,,, The researchers were surprised to find that placental and marsupial mammals have largely the same set of genes for making proteins. Instead, much of the difference lies in the controls that turn genes on and off. http://news.nationalgeographic.com/news/2007/05/070510-opossum-dna.html
When both the supporting evidence and the falsifying evidence count as evidential support for your hypothesis, it is a sure sign you are dealing with a pseudo-science instead of a proper science. Although examples of Darwinists adding 'epicycles' to their theory in order to protect it from falsification abound (Cornelius Hunter: 2015), the primary reason why Darwinian evolution is more properly thought of as a pseudo-science instead of a proper science is because Darwinian evolution has no rigid mathematical basis like other overarching physical theories of science do. A rigid mathematical basis to test against in order to potentially falsify it (in fact, in so far as math can be applied to Darwinian claims, mathematics constantly shows us that Darwinian evolution is astronomically unlikely),,
“On the other hand, I disagree that Darwin’s theory is as `solid as any explanation in science.; Disagree? I regard the claim as preposterous. Quantum electrodynamics is accurate to thirteen or so decimal places; so, too, general relativity. A leaf trembling in the wrong way would suffice to shatter either theory. What can Darwinian theory offer in comparison?” - Berlinski, D., “A Scientific Scandal?: David Berlinski & Critics,” Commentary, July 8, 2003 Darwinian Evolution is a Unfalsifiable Pseudo-Science - Mathematics – video https://www.facebook.com/philip.cunningham.73/videos/vb.100000088262100/1132659110080354/?type=2&theater
Moreover, in all of this talk about genetic similarity, there is one VERY important point that seems to be completely lost on Darwinists (and apparently completely lost on Theistic Evolutionists too)! That very important point is that to say that organism A and B are similar and that you have a theory that can explain the similarities is to say nothing at all. Because similarities don't need an explanation. What needs an explanation are the differences that produced the changes not the similarities that tell us nothing.
“If the overall biology of the animals tells you that they are very different, and the genetics tells you that they are nearly identical, it follows that the genetic comparison is telling you something relatively trivial about the overall biology.” Jonathan Marks – evolutionary biologist/anthropologist at the University of North Carolina – 1993 http://www.evolutionnews.org/2014/08/evolution_used089441.html Doug Axe on What Seduces Us in the “Darwinian Story” - video Quote: “I've recognized that people find something seductive about the evolutionary story. And that is, if you can point out similarities between things then people find it at least intriguing the idea that there can be transitions that go from A to B, because you see the similarities. And the similarities are certainly suggestive. A key take home for me that I would like people to get from reading the book, (Human Origins), is that Darwinists really need to confront not the similarities, but the differences. To say that A and B are similar and that you have a theory that can explain the similarities is to say nothing at all. Because similarities don't really need an explanation. What needs explanation is the differences in all these transitions of going from A to B. So that is the key focus for us. In all of these substantial transitions of form, there are not only similarities , they are there, but there are differences. Can Darwinism explain the differences? If I can get people to think about that, to realize how hard it is for Darwinism to explain even really, really modest differences”,,, https://www.youtube.com/watch?v=pnFs5D-vvnI
And when one tries to explain the differences that produced the changes, instead of just focusing on the similarities which tell us next to nothing important scientifically as to how transformation of form is even remotely possible, then one soon realizes that Darwinian explanations are grossly inadequate:
Thou Shalt Not Put Evolutionary Theory to a Test – Douglas Axe – July 18, 2012 Excerpt: McBride criticizes me for not mentioning genetic drift in my discussion of human origins, apparently without realizing that the result of Durrett and Schmidt rules drift out. Each and every specific genetic change needed to produce humans from apes would have to have conferred a significant selective advantage in order for humans to have appeared in the available time. Any aspect of the transition that requires two or more mutations to act in combination in order to increase fitness would take way too long (>100 million years). My challenge to McBride, and everyone else who believes the evolutionary story of human origins, is not to provide the list of mutations that did the trick, but rather a list of mutations that can do it. Otherwise they’re in the position of insisting that something is a scientific fact without having the faintest idea how it even could be. That’s just not what scientists should be doing. Doug Axe PhD. http://www.evolutionnews.org/2012/07/thou_shalt_not062351.html 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://biologicinstitute.org/2011/04/16/when-theory-and-experiment-collide/
bornagain77_{June 11, 2016
June
06
Jun
11
11
2016
07:35 PM
7
07
35
PM
PDT}

Prev 1 … 5 6 7 8 9 Next

You must be logged in to post a comment.

Leave a Reply