The receipts of the Darwinian pathway to the blood clotting cascade?

 Has Russell Doolittle Provided an Evolutionary Explanation of the Blood Clotting Cascade?

Jonathan McLatchie

In two previous articles (here and here ), I reviewed the process of vertebrate blood clotting and summarized why it cannot readily be explained by naturalistic unguided processes, such as those proposed by neo-Darwinian evolutionary theory. In this final installment, with the foregoing challenges in mind, let us inspect Russell Doolittle’s paper on the evolution of vertebrate blood clotting1 to determine to what extent his analysis assuages these concerns. Since Doolittle has also published a book dealing with this subject2, in which he elaborates on the arguments expressed in the paper in more detail, I occasionally will refer to things said in the book as well.

Do Gene Duplications Explain Vertebrate Blood Clotting?

Doolittle contends that “Many of the proteins involved [in coagulation] are clearly related to one another by gene duplications, and in the past, sequence-based phylogenies have offered insights into the relative order in which certain factors appeared.”3 But sequence similarity does not necessarily imply common ancestry (due to the possibility of common design) and common ancestry does not necessarily imply a stepwise evolutionary pathway. Michael Behe explains this point:

Although useful for determining lines of descent… comparing sequences cannot show how a complex biochemical system achieved its function—the question that most concerns us in this book. By way of analogy, the instruction manuals for two different models of computer put out by the same company might have many identical words, sentences, and even paragraphs, suggesting a common ancestry (perhaps the same author wrote both manuals), but comparing the sequences of letters in the instruction manuals will never tell us if a computer can be produced step-by-step starting from a typewriter… Like the sequence analysts, I believe the evidence strongly supports common descent. But the root question remains unanswered: What has caused complex systems to form?4

This aside, however, Doolittle’s proposed mechanism runs into the problem enumerated above — namely, that duplicating a gene coding for one of the blood clotting factors would lead to that factor becoming over-expressed, disrupting the cascade’s delicate balance and leading to excessive clotting. This difficulty is nowhere even acknowledged in Doolittle’s paper, let alone addressed.

Doolittle raises a valid concern: “The question may be asked, how can new factors be introduced into an existing pathway?” Good question. How does Doolittle respond? He writes, “It was long ago suggested that in the case of clotting pathways, new factors that are the products of gene duplications could easily be sandwiched into the middle of pathways where they initially were only performing the same operation as the original gene product. Only a few amino acid replacements were likely needed to broaden the proteolytic specificity to the point where the duplicon could itself activate the other surviving gene product.”5 In support of this thesis, Doolittle notes that “all of the vitamin-K dependent proteases (prothrombin, factors VII, IX, and X, and protein C) cleave after arginine residues in the same general regions of their homologous substrates.”6 This, again, however, runs into the problem described above — namely, that gene duplication events would be likely to upset the delicate balance of the system, increasing the risk of thrombosis. Such duplicate genes are thus unlikely to be preserved by selection. Moreover, a few specific amino acid replacements in animals such as vertebrates (assuming none of them are beneficial until all have arisen) are unlikely to happen on a realistic timescale. As has been much discussed at Evolution News in the past, and in the academic literature, evolution depends on prohibitively long times to attain and fix multiple co-dependent mutations, where none of them confer a fitness benefit until all have arisen.7,8,9,10,11,12 Doolittle gives a time window for the emergence of the coagulation cascade of approximately fifty to a hundred million years, since fibrin clots have never been detected in any protochordate (i.e., organisms lacking a backbone but possessing a notochord at some stage during development) though it has been identified in the earliest vertebrates — that is, jawless fish. Thus, he argues, blood clotting must have arisen between the emergence of protochordates and jawless fish. As he writes in his book, 

Because fibrin clots have never been observed in our nearest non-vertebrate relatives, the protochordates, we must accept that the clotting system was assembled in the relatively brief interval since protochordates diverged from the lineage leading to vertebrates and the appearance of creatures like the hagfish and lamprey. In years, the available time is estimated to have been 50 to 100 million.13

Given that it is highly probable that each step in the evolution of coagulation would require multiple co-dependent mutations (since each proenzyme would have to evolve in a coordinated way with its activating enzyme), this time window appears to be quite brief. Compounding this is the fact that the mutations in the evolving gene duplicate would need to occur in a coordinated way with its own activating enzyme to ensure that the new factor is active only when needed.

Simpler Blood Clotting Systems in Jawless Fish

There are two extant genera of jawless fish — hagfish (pictured above) and lamprey. Doolittle predicts, from an evolutionary framework, that jawless vertebrates would have a simpler blood clotting cascade than the human system described above. Doolittle limits the scope of his analysis to the lamprey, for which there was better genomic data than for hagfish. Doolittle’s research has revealed that lampreys lack both factor IX and factor VIII.14,15 It may thus be concluded that factors IX and VIII are not essential, at least in the jawless vertebrates. Why are jawless vertebrates not hemophilic, unlike humans who lack these factors? Without knowing more about how coagulation works in jawless vertebrates, it is impossible to say for sure. Clearly, there are other differences as well — since apparently there are two factor X genes in lamprey. Is it possible that one of those is functioning as a factor IX gene? There are also three factors VII. Unfortunately, the precise mechanisms of coagulation in lampreys have yet to be elucidated. Given that humans who are deficient in factors IX or VIII suffer from hemophilia, this provides an indirect justification for believing that there are, quite probably, compensating mechanisms in lampreys that have yet to be uncovered.

Failing to Address Behe’s Argument

A crucial point is that, even if Doolittle’s entirely evolutionary scheme were correct, it would not even address — much less refute — Behe’s original thesis about the blood clotting cascade. In Darwin’s Black Box, Behe only argued that the common pathway is irreducibly complex — he does not give an assessment of whether the intrinsic pathway (to which these factors IX and VIII, missing in jawless fish, belong) or the extrinsic pathway are irreducibly complex as well.16 To summarize, in Darwin’s Black Box, Michael Behe only argued for irreducible complexity of the common pathway — i.e., the pathway after the convergence of the extrinsic and intrinsic initiation pathways, or what Behe calls the components “after the fork.” Behe made this very explicit in his book, where he wrote:

Leaving aside the system before the fork in the pathway, where some details are less well known, the blood-clotting system fits the definition of irreducible complexity.17

The system “before the fork in the pathway” is the intrinsic and extrinsic initiation pathways highlighted by Doolittle. But Behe explicitly leaves this part of the system “aside” and does not argue it is irreducibly complex. Thus, even if Doolittle’s arguments held merit, they would still not refute, even address, the portion of the pathway that Behe argues is irreducibly complex.

Regarding the systems “after the fork,” to my knowledge, there are no vertebrates with a functional coagulation system that lack thrombin, fibrinogen, factor X, or factor V. Clearly, there also has to be some way of activating factor V in response to tissue damage. Thus, to be conservative, blood coagulation must require a minimum of five parts (and probably more) – the very components which Behe argues comprise the irreducibly compelx portion of the blood clotting cascade. Behe’s argument has not been refuted. This same mistake was made in response to Behe by Kenneth Miller, as has been previously noted at Evolution News by Casey Luskin.

Co-Option of Thrombin / Fibrinogen

Doolittle concedes that “it seems unlikely that thrombin and fibrinogen would appear simultaneously,” and posits that “one already existed with an alternative function.”18 He suggests that “fibrinogen may have had a role in cell-cell interactions, a property of many proteins with fibrinogen-related domains.”19 Doolittle postulates that “a more likely scenario, however, is that thrombin had an early role in agglutinating thrombocytes by proteolyzing cell surface proteins, something it is known to do today, attacking a set of G-protein-coupled receptors called PAR proteins.”20 On this hypothesis, “a tissue factor would become exposed during the course of injury, activating prothrombin that would then clump cells which were the ancient ancestors of mammalian platelets. A GLA domain could have helped to keep thrombin localized on the surface of the thrombocytes.”21 The emergence of fibrinogen “would allow thrombin to broaden its attack, generating a more durable clot composed of fibrin. Duplications of the prothrombin gene would lead to the appearance of factors VII, X, and eventually IX.”22

Such a scenario, however, presents a number of problems. One is acknowledged by Doolittle himself: “Besides the GLA domain, thrombin has two kringle domains, usually thought to have an affinity for fibrin. The kinds of domains that interact with tissue factor, however, are the EGF domains found in factors VII, X, and IX.”23 He, therefore, has to postulate that “there was much domain shuffling in the early stages and that thrombin originally had EGF domains, or no peripheral domains at all.”24 Second, he makes no attempt to estimate how durable a clot composed of nothing more than clumped cells would be — though, if the initial flow rate was relatively low, this issue could be less of a concern. Finally, a duplication of a prothrombin gene would result in a second prothrombin gene. Doolittle makes no attempt to determine how difficult it would be for factors VII, X and IX to arise from a duplicated prothrombin gene (and evolve in a coordinated way with their corresponding activating enzymes), nor how the overexpression problem described above may be overcome.

Doolittle’s Four Stage Scenario

In his book, Doolittle proposes four stages in the evolution of vertebrate blood clotting, based on the presence or absence of coagulation factors in various animals.

The first stage, according to Doolittle, “existed in the last common ancestor of jawless and jawed vertebrates and was characterized by the presence of only six different proteins, three of which are vitamin K-dependent proteases.”26 These six proteins included tissue factor, factor VII, factor X, factor V, prothrombin and fibrinogen. The second stage, Doolittle suggests, involved the emergence of factors VIII and IX prior to the evolution of jawed fish. The third stage was characterized by the acquisition of prekallikrein and factor XII. A duplication of the gene coding for prekallikrein, resulting in the origins of factor XI, led, according to Doolittle’s scenario, to the fourth stage.

Notice that even the primitive system that constitutes stage one contains all of the four components that Behe claimed to comprise the irreducibly complex system — that is, thrombin, fibrinogen, factor X and factor V — in addition to tissue factor and factor VII (key components of the extrinsic pathway, required for initiating coagulation in response to tissue damage). Behe’s hypothesis predicts that every coagulation system will contain these four proteins (or equivalents), in addition to there being some way of activating factor V in response to tissue damage. This is preciselywhat the data show. The only aspect of the coagulation cascade that emerged subsequent to the origins of coagulation itself, then, so far as can be told by the data, are the components that make up the intrinsic pathway. That the intrinsic pathway is redundant is not particularly surprising, since there only needs to be one mechanism by which factor V is activated. Adding the intrinsic pathway is certainly helpful, though not necessarily essential. The intrinsic pathway serves to amplify the coagulation response initiated by the extrinsic pathway, and provides additional layers of activation and enzyme generation. Again, Behe’s fundamental thesis about irreducible complexity of the blood clotting cascade has not been refuted or even touched by Doolittle’s arguments.

But perhaps the most damning problem confronting Doolittle’s proposed scenario is that his analysis entirely ignores all of the clotting inhibitors (such as antithrombin, protein C, and protein S) that prevent excessive clot formation, as well as those factors that dismantle clots (as he himself acknowledges27). And this even though he correctly notes elsewhere that “this suppression of activity is very important; there is enough prothrombin in one milliliter of plasma to clot all the fibrinogen in the whole body if the prothrombin were all converted to thrombin.”28 Thus, the emergence of the pathway for coagulation along the lines suggested by Doolittle would likely result in runaway thrombosis without the simultaneous advent of inhibitors.

A Formidable Challenge 

In summary, the coagulation cascade presents a formidable challenge to evolutionary theory. While Doolittle is to be commended for his work in attempting to provide an evolutionary account for coagulation, the failure of those attempts underscores the difficulty of the problem. They simply do not address the issues at the heart of Behe’s argument in Darwin’s Black Box, which remains untouched by Doolittle’s thesis.

Notes

Doolittle RF. Step-by-step evolution of vertebrate blood coagulation. Cold Spring Harb Symp Quant Biol. 2009;74:35-40.

Doolittle RF. The Evolution of Vertebrate Blood Clotting. University Science Books 2013.

Doolittle RF. Step-by-step evolution of vertebrate blood coagulation. Cold Spring Harb Symp Quant Biol. 2009;74:35-40.

Behe, Michael J. (1996). Darwin’s Black Box: The Biochemical Challenge to Evolution. Free Press, kindle.

Ibid.

Doolittle RF. Step-by-step evolution of vertebrate blood coagulation. Cold Spring Harb Symp Quant Biol. 2009;74:35-40.

Hössjer O, Bechly G, Gauger A. On the waiting time until coordinated mutations get fixed in regulatory sequences. J Theor Biol. 2021 Sep 7;524:110657.

Sanford J, Brewer W, Smith F, Baumgardner J. The waiting time problem in a model hominin population. Theor Biol Med Model. 2015 Sep 17;12:18.

Durrett R, Schmidt D. Waiting for two mutations: with applications to regulatory sequence evolution and the limits of Darwinian evolution. Genetics. 2008 Nov;180(3):1501-9. Erratum in: Genetics. 2009 Feb;181(2):819-20; author reply 821-2.

Behe MJ, The Edge of Evolution: The Search for the Limits of Darwinism. Free Press 2007.

Behe MJ, Snoke DW. Simulating evolution by gene duplication of protein features that require multiple amino acid residues. Protein Sci.2004 Oct;13(10):2651-64. doi: 10.1110/ps.04802904. Epub 2004 Aug 31. PMID: 15340163; PMCID: PMC2286568.

Axe DD. The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations. Bio-Complexity2010.

Doolittle RF. The Evolution of Vertebrate Blood Clotting. University Science Books 2013, 184.

Doolittle RF, Jiang Y, Nand J. Genomic evidence for a simpler clotting scheme in jawless vertebrates. J Mol Evol. 2008 Feb;66(2):185-96. doi: 10.1007/s00239-008-9074-8.

Doolittle RF. Bioinformatic Characterization of Genes and Proteins Involved in Blood Clotting in Lampreys. J Mol Evol. 2015 Oct;81(3-4):121-30.

Behe, Michael J. Darwin’s Black Box: The Biochemical Challenge to Evolution. Free Press 1996, kindle.

Ibid.

Doolittle RF. Step-by-step evolution of vertebrate blood coagulation. Cold Spring Harb Symp Quant Biol. 2009;74:35-40.

Ibid.

Ibid.

Ibid.

Ibid.

Ibid.

Ibid.

Ibid., 185.

Ibid.

Doolittle RF. The Evolution of Vertebrate Blood Clotting. University Science Books 2013, 196.

Ibid., 17.

Man continues to be a wolf to his fellow man.

 

From one infallible bishop to another?

 

On your talking dog.

 

Christendom's genius for explaining away obvious logic

 1Corinthians ch.15:27NIV"For he “has put everything under his feet.” c Now when it says that “everything” has been put under him, it is CLEAR that this does not include God himself, who put everything under Christ. "

The word of JEHOVAH is addressed to the wise, those who know that humility and logic are necessary prerequisites to clear thinking. It ought to be clear that the God who put everything under Christ feet is not his equal or that one who always had everything under his feet would not need anyone else's authorisation to wield that authority ,and yet some apparently loose a grasp of basic logic when it comes examining the bible. The most plain manifestation of this malaise for me is failure to grasp the concept of supremacy.

Supremacy according to Merriam Webster:: the quality or state of being supreme

especially : a position of unquestioned authority, dominance, or influence

2:ultimate authority or power.

So Supremacy excludes equality. The two concepts are mutually exclusive one who is equal to even one other than himself is not supreme/ does not possess supremacy, our Brother Paul might say that this should be clear.

But the trinity doctrine causes brain damage especially that part of the brain responsible for our grasp of basic logic.

Luke ch.1:32NIV"He will be great and will be called the Son of the MOST HIGH. The LORD God will give him the throne of his father David," (we'll bypass the Trinitarian style proof of David's Godhood) Note that the God and Father of Jesus Christ is Supreme.

He is both the greatest person and the greatest God. This totally excludes there being any other person or God being his equal by definition. Yet Trinitarians ignore what ought to be clear and claim that the God of Jesus is not the most high God and that in fact there are three distinct entities that are a least equal to him . Indeed as I have pointed out the trinity doctrine blinds its adherents to a clear identification of the MOST HIGH God JEHOVAH If the trinity is true there is no most high God.

On replicating the primeval chaos in the lab

 

On secular occultism.

 J. P. Moreland on the Contradictions of Scientism

J P Moreland

Are the hard sciences the only source of truth about reality? On a classic episode of ID the Future, host Michael Keas begins a conversation with philosopher J. P. Moreland about Moreland’s book Scientism and Secularism: Learning to Respond to a Dangerous Ideology. As Moreland explains, scientism is the belief that only the hard sciences can provide any reliably true knowledge. It’s a claim that also gets applied to other disciplines outside science as well, suggesting that claims of reality in any field of human knowledge cannot be known one way or another. “It’s in the drinking water,” Moreland says, but it’s also self-refuting, and therefore irrational — and very damaging besides. Moreland gives examples. This is Part 1 of a conversation. Download the podcast or listen to it here.

The machine code of life?

 

Speaking of ID some more

 An Intriguing Conversation with Casey Luskin About Intelligent Design

David Klinghoffer

Ha, well this is a new frontier for intelligent design. Live Life in Motion is a podcast with Sam Kleckley about personal fitness, sponsored by, among other fine products, Rebel Rabbit, which I had not heard of. Sam shares enthusiastically that Rebel Rabbit is a cannabis-infused soda drink that comes in two strengths, billed as a healthier alternative to alcohol. Which it may well be! It’s news to me that there was such a thing. Anyway, Sam is also a thoughtful and curious individual who put aside his accustomed subjects and had on our geologist colleague Casey Luskin for an hour to talk about ID — everything, and I mean everything, about ID — biology, cosmology, education, and more. They had a great conversation, really quite charming, made more intriguing by the fact that Sam is evidently a searcher, uncertain, as he says, about what he believes about god or gods. Find the podcast on Apple (here) or Spotify (here). God bless the curious and the open-minded.

Seafaring simians?

 Fossil Friday: Did Monkeys Raft Four Times Across the Atlantic?

Gunter Bechly

A few years ago, I published an article at Evolution News titled “Rafting Stormy Waters” (Bechly 2018), which discussed the various highly implausible events of oceanic dispersal with vegetation rafts to explain the biogeographic patterns of living animals. This includes the dispersal of monkeys from Africa to South America that implied a 60-day voyage of 1,400 km across the Eocene early Atlantic Ocean (Gabbatiss 2016).

Now, a new fossil find has made this problem much worse. Marivaux et al. (2023) describe in the journal PNAS a new primate genus from the Paleogene of Western Amazon and provide a new phylogenetic analysis of the earliest fossil Neotropical monkeys. This phylogenetic study shows that three genera of fossil monkeys, all known by fossil teeth from the Early Oligocene of South America, are not related to living New World monkeys (Platyrrhini), but are nested in three distinct African clades respectively: Ashaninkacebus is nested within the Eosimiidae clade (Marivaux et al. 2023), Perupithecus is nested within the Oligopithecidae clade (Bond et al. 2015), and Ucayalipithecus is nested within the Parapithecidae clade (Seiffert et al. 2020). This implies three independent Eocene colonization events of South America by rafting from Africa, additional to the dispersal of platyrrhine monkeys, and additional to the dispersal of caviomorph rodents.

Beyond Ridiculous

Did viable populations of monkeys really raft successfully four times across the Atlantic Ocean from Africa to South America? Seriously? One such event is already a stretch, but four times is beyond ridiculous. If such events happened so often with unlikely passengers like monkeys, why don’t we find many more cases of similar Neotropic-Afrotropic relationships in much more likely candidates such as reptiles or insects, which could far more easily survive long transoceanic rafts? Not to mention the simple fact that in the whole history of human seafaring we have never observed rafting vertebrates in the middle of the ocean and only observed rafting dispersal events in cases of relatively close islands and even there only with reptiles. Longrich (2021) called this an “incredible ocean crossing” which “beat odds that make Powerball lotteries seem like a safe bet.” Something is clearly wrong here, and I mean way off. But evolutionary biology has a cheap cop out that was made explicit by Nobel laureate George Wald (1954):

Given so much time, the [nearly] “impossible” becomes possible, the “possible” becomes probable, and the “probable” becomes virtually “certain.”

It does not require that one be a Darwin doubter to recognize that this hardly qualifies as good science, as shown, for example, in this highly recommended article by Lu (2021) from an AI perspective. Time is not the hero of the plot when actual improbabilities and probabilistic resources are ignored or glossed over with fancy storytelling according to the unspoken dogma of evolutionary biology: It must have been possible because it happened. After all, God forbid if we were to consider explanations beyond blind naturalistic mechanisms.

References

Bechly G 2018. Rafting Stormy Waters: When Biogeography Contradicts Common Ancestry. Evolution News June 27, 2018. https://evolutionnews.org/2018/06/rafting-stormy-waters-when-biogeography-contradicts-common-ancestry/

Bond M, Tejedor MF, Campbell KE Jr, Chornogubsky L, Novo N & Goin F 2015. Eocene primates of South America and the African origins of New World monkeys. Nature 520(7548), 538–541. DOI: https://doi.org/10.1038/nature14120

Gabbatiss J 2016. The monkeys that sailed across the Atlantic to South America. BBC January 26, 2016. https://web.archive.org/web/20160127084123/http://www.bbc.com/earth/story/20160126-the-monkeys-that-sailed-across-the-atlantic-to-south-america

Longrich NR 2021. One incredible ocean crossing may have made human evolution possible. The Conversation April 29, 2021. https://theconversation.com/one-incredible-ocean-crossing-may-have-made-human-evolution-possible-157479

Lu CP 2021. Infinite Dilemma 1: Not Enough Time. Towards Data Science February 3, 2021. https://towardsdatascience.com/neo-darwinistic-concepts-of-chance-and-time-through-the-lens-of-ai-2eee4d5c2bd6

Marivaux L, Negri FR, Antoine P-O et al. 2023. An eosimiid primate of South Asian affinities in the Paleogene of Western Amazonia and the origin of New World monkeys. PNAS 120(28):e2301338120. DOI: https://doi.org/10.1073/pnas.2301338120 (PDF: https://hal.science/hal-04153825/document)

Seiffert ER, Tejedor MF, Fleagle JG, Novo NM, Cornejo FM, Bond M, de Vries M & Campbell KE Jr 2020. A parapithecid stem anthropoid of African origin in the Paleogene of South America. Science 368(6487), 194–197. DOI: https://doi.org/10.1126/science.aba1135

Wald G 1954. The Origin of Life. Scientific American 191, 45–53. https://www.scientificamerican.com/article/the-origin-of-life/

Yet another revolution eating its own?

 

James Tour throws down the guantlet?

 

Why the lab is not a window on the prebiotic earth.

 Hands-On Chemistry Can’t Simulate Prebiotic Earth

Andrew McDiarmid

When scientists claim they have simulated early Earth chemistry to create life from non-life, are they being honest? A new episode of ID the Future is the fourth and final installment in a series of conversations between philosopher of science Dr. Stephen Meyer, author of Signature in the Cell: DNA and the Evidence for Intelligent Design, and Dr. James Tour, a world-renowned synthetic organic chemist at Rice University. Dr. Tour has recently been engaged in a series of back-and-forth responses to attacks on his work from YouTuber “Professor” Dave Farina. This has given Tour a new opportunity to critique experts in the field of abiogenesis and allows an interested public to better evaluate both sides of the argument.

In Part 4, Meyer and Tour evaluate the work of chemist Bruce Lipshutz; specifically his work designing surfactant molecules that enable amide/peptide bonds. By itself, Lipshutz’s work developing synthetic techniques for doing chemistry in water is interesting and has value. But for those tempted to think that his work validates chemical evolutionary theories of the origin of life, Tour has bad news. Peptides don’t form in aqueous environments like water. A realistic prebiotic environment would not be capable of producing the reactions necessary to form proteins. And Lipshutz acknowledges this. In their conversation, Tour and Meyer discuss how Lipshutz applies hands-on chemistry that bears no resemblance to the likely conditions of a prebiotic Earth. If anything, the work of Lipshutz and others in origin of life research is actually simulating the need for intelligent agency to move simple chemicals in a life-friendly direction. Says Meyer, “Even the modest movement they get towards life seems to be intelligently designed at each step of the way, and even the vocabulary will sometimes reveal that: ribozyme engineer, designer surfactants. Very curious!”

Download the podcast or listen to it here.

The conditionalist/annihilationist position is not a kook position? Pros and cons.

 

Common design on the march?

 From Winston Ewert, New Peer-Reviewed Paper on Dependency Graph Model

Brian Miller

Winston Ewert has published a new paper in the journal BIO-Complexity expanding on his previous research related to the pattern of similarities between species. He further demonstrated how the distribution of similarities fits his dependency graph model better than the standard common ancestry model. The paper can be downloaded here. I described the superior explanatory power of Ewert’s model here. His original BIO-Complexity paper is here.

The Dawkins Test

One of the central predictions of evolutionary theory is that similarities between species should consistently point to the same evolutionary tree based on the premise of common ancestry. The branching points in the tree should correspond to the common ancestor of a group of organisms (e.g., mammals) that first acquired all the traits common to that group (e.g., glands to produce milk and three bones in the inner ear). 

Richard Dawkins stated that a reliable test of the design hypothesis for life is whether similarities are highly inconsistent with a single tree. Data collected over the past several decades has demonstrated that the distribution of similarities is far more inconsistent with common ancestry than any evolutionist imagined, so the intelligent design framework has passed the Dawkins test. Casey Luskin cited numerous studies detailing the inconsistencies here.

This data undermines evolutionary theory at its core. Nearly all the arguments for the grand evolutionary narratives (e.g., transformation of fish into humans) rest on the assumption that similarities reliably point to common ancestry. In many groups, the high level of inconsistency of similarities with any evolutionary tree demonstrates that this foundational assumption is false. 

Particularly problematic, the places where evolutionists most require reliable data is where the data is most inconsistent. For instance, a central icon of evolution is the “whale series” consisting of fossils that purportedly illustrate a land mammal incrementally transforming into a fully aquatic mammal. The animals in the series are not believed to have directly descend from or evolved into each other, but their similarities are interpreted as their having descended from animals that are part of an ancestor-descendent series encompassing the land-sea transition. 

The challenge is that the rescaled consistency index (RCI) for aquatic mammals and their purported ancestors is 0.24. An RCI value of 1.0 corresponds to perfect consistency of all traits with one evolutionary tree, and a value of 0.0 corresponds to traits that are randomly distributed. An RCI value significantly lower than 0.5 indicates that similarities are so inconsistent with the assumption of common ancestry that arguments for evolution based on similarities, such as with the whale series, become highly suspect. As another key example, the RCI for primates and their purported relatives is 0.29, so claims related to the evolution of humans resting on similarities in fossils also carry little weight. 

Dependency Graph Model

In contrast, the pattern of similarities fits design-based models, as I previously described here. To summarize, human engineers use design modules, such as engines, in different creations to meet common goals. Likewise, similarities between species are often not consistent with an evolutionary tree, but they appear implemented in different creatures for a common purpose. Ewert’s framework is the first to identify modules based on proteins. 

In Ewert’s first paper, he identified modules as sets of proteins from distinct families. Some modules are dependent on smaller modules, and the smaller modules are at times used by multiple larger modules (Figure 1). Ewert demonstrated quantitatively that the protein data far better fits the dependency graph model than common ancestry. 

Figure 1. Part of a dependency graph for proteins in the Ensemble database from Ewert (2018), Figure 12. Circles represent modules, which are sets of proteins. An arrow represents a dependency relationship between two modules. The head of the arrow points to a set of proteins contained in the module connected to the arrow’s tail. The tail module also contains other proteins and possibly other modules. The protein data could be forced into a tree, but the interrelationships inconsistent with that tree would be lost. 

Application to Protein Sequences

In Ewert’s recently published article, he did not identify modules as sets of distinct proteins. Instead, he focused on variations in the protein prestin between a variety of mammal species including those capable of echolocation. The protein plays a critical role in mammal hearing by serving as a motor protein in the outer hair cells. The versions of the protein supporting echolocating bats, whales, and dolphins show the same amino acid alterations compared to the versions in mammals lacking echolocation. The pattern of alterations is not simple. Different pairs of mammals share similar amino acid alterations. Constructed evolutionary trees for mammals based on common ancestry lose this information while Ewert’s model highlights it. 

To visualize the interrelationships, Ewert created a program called AminoGraph that identifies modules as specific amino acid alterations from an archetypal sequence that is a representative version of the protein. One module depends on another if it includes the latter’s alterations plus additional alterations. The program takes as input amino acid sequences for the same protein in different species, and it creates from this data the most consistent graph of module dependences. 

The program displays sets of sequences that are not related as each input sequence directly linking to the archetypal sequence (Figure 2a). It displays data that best fits a common ancestry model as a standard evolutionary tree (Figure 2b), and it displays data that corresponds to modules with complex interrelationships as a dependency graph (Figure 2c). Ewert tested the program on simulated data corresponding to unrelated sequences, sequences connected by common ancestry, and sequences connected through a specific dependency graph. In each case, the program properly identified the correct structure and accurately identified most of the modules and their interrelationships, thus confirming the reliability of the program.

Figure 2. Comparison of different graphs generated by AminoGraph. The grey circles represent the archetypal sequences. The black circles represent the input sequences. The blue circles represent modules. If the data best fits the common ancestry model, the modules represent the common ancestors of sequences pointing to them, and the archetypal sequence represents the common ancestor of all the sequences. 

Results for Prestin Protein

Ewert ran AminoGraph on the sequences of prestin proteins from species of echolocating bats, bats without echolocation, echolocating whales, whales without echolocation, and other mammals without echolocation. The generated dependency graph revealed a key insight into how the prestin proteins were modified to respond to the high sound frequencies generated in echolocation. The reengineering in each echolocating mammal employed some combination of two modules labeled Echolocation A and Echolocation B (Figure 3). 

Figure 3. Dependency graph of prestin proteins from different mammals generated by AminoGraph. The prestin molecules in echolocating aquatic mammals and bats used module Echolocation A, module Echolocation B, or both. 

Future Research

This result naturally leads to research into the effects of amino acid modifications. The design framework predicts that alterations coordinate in each module to support echolocation in a way that best serves the needs of the species that employ it. Another expectation is that the prestin modules must coordinate with other modules for echolocation to function at a level that would benefit its possessor. This prediction appears consistent with the numerous similarities between echolocating mammals in both their genetics (here, here) and their overarching design logic (here, here).

In contrast, the standard evolutionary framework provides no insight into how echolocation is implemented in different mammals. The commonly accepted evolutionary tree requires echolocation to have evolved independently three times as illustrated in Ewert (2023), Figure 1. Yet the maximum possible time for the evolution of a fully aquatic mammal or a bat is insufficient for more than two coordinated mutations to appear. Any evolutionary scenario for echolocation would require far more than two coordinated mutations (here,here), so evolution fails to explain this trait’s origin even once, let alone multiple times. 

Ewert’s model could be applied to several other proteins in echolocation and in other biological systems to gain similar insights. It represents a valuable tool in the developing theory of biological design, which should eventually supplant phylogenetic analyses.  

The blood clotting cascade is irreducibly complex in any language.

 The Incredible Design of Vertebrate Blood Clotting

Jonathan McLacthie

  Recently, a commenter on the Center for Science and Culture’s Facebook page asked about a paper by the late biochemist Russell F. Doolittle (1931-2019)1 in relation to Michael Behe’s claim, defended in Darwin’s Black Box2 (and in the video below), that the blood clotting cascade is irreducibly complex. Doolittle claims to show “Step-by-step evolution of vertebrate blood coagulation.” However, in a series of three articles I will respond to this claim. First, I will provide a brief description of the blood clotting cascade, for the purpose of bringing readers unfamiliar with the pathway up to speed. Second, I will discuss why vertebrate coagulation is considered to be an irreducibly complex system that poses a significant challenge to evolutionary explanations. Third and finally, I will summarize the key points of the Doolittle paper and offer an evaluation of whether it calls Behe’s argument into question. Since Doolittle has also published a book dealing with this subject3, in which he elaborates on the arguments expressed in the paper in more detail, I will occasionally refer to things said in the book as well. 

The Formation of the Platelet Plug

Blood clotting, also known as coagulation, is a complex physiological process that plays a crucial role in maintaining the integrity of the circulatory system. It involves a series of intricate molecular and cellular interactions that result in the formation of a clot at the site of injury within a blood vessel. This process prevents excessive bleeding while promoting wound healing.

Upon injury, platelets adhere to the exposed collagen fibers in the damaged area.4 The platelets then undergo a conformational change and release various substances stored within their granules, which promote further platelet activation and attract more platelets to the site of injury, forming a plug over the hole. Activated platelets bind together, forming aggregates or clumps, reinforcing the platelet plug and creating a temporary seal over the injured area. This seal is a short-term solution, however, and is not strong enough to hold for long. As blood continues to flow through the injured vessel, it can dislodge the loosely adhering platelets. Thus, the formation of this platelet plug (and the injury itself) initiates the coagulation cascade.

The Fibrin Gel

The coagulation pathway involves many different components, which can be difficult to keep track of. For ease of following the description that follows, I recommend referring to the figure below, which depicts aspects of the human coagulation system. An arrow from one component to another indicates that the former activates the latter. A barred line signifies inhibition of one protein by another

Vertebrate blood coagulation is best understood by focusing first on the ultimate objective of the cascade, which is the formation of a fibrin gel that reinforces the initial platelet plug, thereby strengthening the clot. The clot itself is made of fibers composed of the protein fibrin, which circulates in an inactive form (fibrinogen) in the blood plasma5,6 , shown in the figure below.

Fibrinogen is comprised of three pairs of polypeptide chains, known as Aα, Bβ, and γ chains, which are held together by disulfide bonds. Fibrinogen becomes activated when another protein, called thrombin, cleaves specific peptide bonds in the fibrinogen molecule, specifically near the N-terminus of the Aα and Bβ chains.7 This cleavage removes small peptide fragments called fibrinopeptides A and B, respectively, from the fibrinogen molecule, resulting in a similar protein with remarkably different functions referred to as fibrin. The cleavage of fibrinopeptides exposes new binding sites on the fibrin molecule, allowing the individual fibrin molecules to polymerize into a clot.8 The fibrin molecules further aggregate and form a mesh-like network, which is stabilized by the enzyme factor XIIIa.9 Factor XIIIa catalyzes the crosslinking of fibrin molecules through the formation of covalent bonds between specific amino acid residues, creating a stable fibrin clot. The resulting fibrin clot, together with the platelets, provides a physical barrier at the site of injury, preventing further blood loss. It also serves as a scaffold for other components of the clotting process, which aggregate on the fibrin network to form a stable blood clot.

If the pathway consisted only of fibrinogen and thrombin, thrombin would constantly cleave fibrinogen, and the consequence would be uncontrolled and excessive clotting throughout the bloodstream. To avoid this, it is essential that the process be carefully regulated. Blood clotting involves the use of proenzymes, which are enzymes that are retained in an inactive state and need to be converted into active enzymes through specific cleavage by proteases such as thrombin.

Thrombin itself exists in an inactive form, prothrombin. To convert prothrombin into active thrombin, another enzyme (factor Xa), along with its cofactor (factor Va), assembles on the surface of platelets or other phospholipid membranes to form the prothrombinase complex.10 This complex provides the platform for the subsequent activation of prothrombin. The conversion of prothrombin to thrombin, mediated by the prothrombinase complex, occurs (as with fibrinogen) through a proteolytic cleavage of prothrombin at specific sites. Curiously, factor V also exists in an inactive state, but is cleaved and activated (to form factor Va) by thrombin itself (a small trace of which circulates in the bloodstream due to a low rate of cleavage of prothrombin by factor Xa).11 Once activated, factor Va plays a critical role in the amplification of the coagulation process by enhancing the activity of factor X and promoting the production of more thrombin. This makes the coagulation cascade autocatalytic, since the activation of clotting factors leads to the activation of more of the same proteins.

Factor Xa also exists in an inactive form, factor X. Factor X may be activated by two different pathways: the extrinsic and intrinsic pathway. In the extrinsic pathway, so-named because it is triggered by the external factors, tissue factor (also known as factor III) is released.12 Tissue factor forms a complex with factor VII, leading to the activation of factor X. The first step of the intrinsic pathway, so-named because all of the components required for its initiation and progression are present within the blood itself, involves the activation of factor XII (also called Hageman factor) by contact with negatively charged surfaces, such as exposed collagen at the site of injury.13 Activated factor XII then activates factor XI, which, in turn, activates factor IX. Activated factor IX (IXa) forms a complex with its cofactor, factor VIIIa, on a phospholipid surface. This complex, along with calcium ions, is called the tenase complex or intrinsic tenase.14,15 The tenase complex plays a crucial role in amplifying the clotting process by cleaving, and thereby activating, factor X.

Preventing Excess Clotting

To prevent excess clotting and ensure that the clotting cascade remains localized to the site of injury, there are several regulatory mechanisms.16 Antithrombin III (ATIII) is a natural anticoagulant that inhibits the activity of thrombin and several other coagulation factors, including factor Xa and factor IXa. It achieves its anticoagulant effects through a mechanism called “serpin” inhibition.17 Serpins (serine protease inhibitors) are a class of proteins that regulate the activity of proteases, including those involved in blood clotting. ATIII binds to Thrombin’s active site, effectively blocking its ability to cleave fibrinogen into fibrin. By inhibiting thrombin, antithrombin III indirectly helps regulate the activation of factor V and thereby prevents excessive clotting.18

Thrombin not only activates factor V but also activates protein C, which, in the presence of its cofactor protein S, inactivates factor Va (activated form of factor V).19 Protein C cleaves factor Va at specific sites, rendering it less active and inhibiting its procoagulant properties. This negative feedback loop helps to limit and regulate the clotting process. Tissue factor pathway inhibitor (TFPI) is a protein that directly inhibits the activity of factor Xa and the factor VIIa-tissue factor complex.20 By inhibiting these factors, TFPI also indirectly prevents excessive activation of factor V and, thereby, of thrombin.

Clot Retraction and Dissolution

After the clot is formed, it undergoes retraction, which involves the contraction of fibrin by platelets within the clot, resulting in the clot becoming denser.21 This process helps to reduce the size of the clot and brings the edges of the wound closer together. Eventually, as the wound heals, the clot needs to be dissolved to restore normal blood flow. Plasmin, a proteolytic enzyme, breaks down the fibrin meshwork into soluble fragments, leading to the dissolution of the clot.22 Plasmin is generated from plasminogen by tissue plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-Pa), among other molecules.

The Role of Vitamin K

Several of the proteins discussed here depend upon vitamin K for their synthesis — these are prothrombin, factors VII, IX, and X, as well as proteins C and S (i.e., the anticoagulant proteins that serve to inhibit excessive clot formation). Vitamin K is essential for the post-translational modification of these clotting factors. Without adequate vitamin K, these proteins cannot undergo the necessary chemical changes, which would impair their ability to function properly in the coagulation process. For this reason, deficiency in vitamin K can lead to a bleeding disorder known as vitamin K deficiency bleeding, or coagulopathy.

Summary

In summary, vertebrate blood clotting is an incredible, tightly regulated, multi-component cascade that intuitively points to intelligent design. This is in view of its goal-directedness towards its final end, which is producing a successful clot. In a second article in this series, I will discuss why unguided evolutionary explanations are implausible in accounting for the origins of the coagulation pathway

Notes

Doolittle RF. Step-by-step evolution of vertebrate blood coagulation. Cold Spring Harb Symp Quant Biol. 2009;74:35-40.

Behe, MJ. Darwin’s Black Box: The Biochemical Challenge to Evolution. Free Press 1996.

Doolittle RF. The Evolution of Vertebrate Blood Clotting. University Science Books 2013.

Periayah MH, Halim AS, Mat Saad AZ. Mechanism Action of Platelets and Crucial Blood Coagulation Pathways in Hemostasis. Int J Hematol Oncol Stem Cell Res. 2017 Oct 1;11(4):319-327.

Kattula S, Byrnes JR, Wolberg AS. Fibrinogen and Fibrin in Hemostasis and Thrombosis. Arterioscler Thromb Vasc Biol. 2017 Mar;37(3):e13-e21.

Pieters M, Wolberg AS. Fibrinogen and fibrin: An illustrated review. Res Pract Thromb Haemost. 2019 Mar 4;3(2):161-172.

Greenberg CS, Miraglia CC, Rickles FR, Shuman MA. Cleavage of blood coagulation factor XIII and fibrinogen by thrombin during in vitro clotting. J Clin Invest. 1985 May;75(5):1463-70.

Weisel JW, Litvinov RI. Fibrin Formation, Structure and Properties. Subcell Biochem. 2017;82:405-456. doi: 10.1007/978-3-319-49674-0_13.

Lorand L. Factor XIII and the clotting of fibrinogen: from basic research to medicine. J Thromb Haemost. 2005 Jul;3(7):1337-48.

Krishnaswamy S. The transition of prothrombin to thrombin. J Thromb Haemost. 2013 Jun;11 Suppl 1(0 1):265-76.

Keller FG, Ortel TL, Quinn-Allen MA, Kane WH. Thrombin-catalyzed activation of recombinant human factor V. Biochemistry. 1995 Mar 28;34(12):4118-24.

Mackman N, Tilley RE, Key NS. Role of the extrinsic pathway of blood coagulation in hemostasis and thrombosis. Arterioscler Thromb Vasc Biol. 2007 Aug;27(8):1687-93.

Grover SP, Mackman N. Intrinsic Pathway of Coagulation and Thrombosis. Arterioscler Thromb Vasc Biol. 2019 Mar;39(3):331-338.

Autin L, Miteva MA, Lee WH, Mertens K, Radtke KP, Villoutreix BO. Molecular models of the procoagulant factor VIIIa-factor IXa complex. J Thromb Haemost. 2005 Sep;3(9):2044-56.

Childers KC, Peters SC, Lollar P, Spencer HT, Doering CB, Spiegel PC. SAXS analysis of the intrinsic tenase complex bound to a lipid nanodisc highlights intermolecular contacts between factors VIIIa/IXa. Blood Adv. 2022 Jun 14;6(11):3240-3254.

Dahlbäck B. Blood coagulation and its regulation by anticoagulant pathways: genetic pathogenesis of bleeding and thrombotic diseases. J Intern Med. 2005 Mar;257(3):209-23.

Sanrattana W, Maas C, de Maat S. SERPINs-From Trap to Treatment. Front Med (Lausanne). 2019 Feb 12;6:25.

van Boven HH, Lane DA. Antithrombin and its inherited deficiency states. Semin Hematol. 1997 Jul;34(3):188-204.

Kalafatis M, Mann KG. Role of the membrane in the inactivation of factor Va by activated protein C. J Biol Chem. 1993 Dec 25;268(36):27246-57. PMID: 8262965.

Wood JP, Ellery PE, Maroney SA, Mast AE. Biology of tissue factor pathway inhibitor. Blood. 2014 May 8;123(19):2934-43.

Tucker KL, Sage T, Gibbins JM. Clot retraction. Methods Mol Biol. 2012;788:101-7.

Alkjaersig N, Fletcher AP, Sherry S. The mechanism of clot dissolution by plasmin. J Clin Invest. 1959 Jul;38(7):1086-95. 

The riot act

There will be no anonymous commenting on this site period.

Against Roman XXV

 Roman I.e. the essence of a human is, for some thinkers, a "rational animal," essences are not concrete objects, they do not have extension. Our bodies delimit our power and perception which is exactly what makes it our body.

AservantofJEHOVAH:our bodies if fully functional are instantiations of the ideal they are the source of our potential that is why we ought to take care of them.That is why we ought to view our healthy bodies as gifts from a benevolent God.

Roman:if God is has a 'body' i.e. extension, yet that does not delimit any of his perception or power, what is it bordering (btw it's impossible for something to have a border without it being bound by that border in some what), if you're saying his "essence" I don't know what that means if that essence does not include his power and perception

AservantofJEHOVAH:JEHOVAH is defined by his body not limited by it once more you have fallen in to the trap of imposing human type insecurities on JEHOVAH JEHOVAH'S body is the source of his limitless potential and the means to actualise it just as our created bodies are the source of our potential and the means to activate that potential actually borders can be empowering by including what is essential and excluding what is not.

Against Roman XXIV

 Roman:Btw, if your point is simply to deny Pantheism, i.e. God is distinct from creation, such that he does not exist literally everywhere, I agree with that, but that does not necessitate some kind of "body."

AervantofJEHOVAH:Prior potential as a effective first cause demands a living body where an Infinite store of potential energy under the complete control of a omniscient mind can reside. Energy can neither be created nor destroyed only converted from form to form anything else is magic/mysticism.

Roman:When we use literal (non metaphorical) language, even if we are using it analogically, if there is not analogue to what words actually refer in our own univocal sense, then we are speaking nonsense.

The analogies derived from creation are going to be limited in there ability to describe JEHOVAH and his work as long as they don't involve the embrace of logical contradictions they ought not to be dismissed out of hand.

Roman:if I say God is a fortress that's a metaphor, when I say God gets angry it's literal but of analogy, i.e. we can not make a one to one connection between our anger and his, but we can understand what it means in terms of certain features of our emotional life.

O.K

This is why I am harping on what langauge means, I don't want to speak nonsense about God, and I frankly think that the almost entire theistic tradition of saying God is incorporeal is based on the incompatibility with corporeality and being unlimited. So My issue here is largely the inconsistency of language ... i.e. being "bordered, but not bounded" the vague use of telekenisis and appeals to quantum entanglement which is nothing like telekenisis, the unintelligable notion of a bordered essence, as though essence were a physical extended thing. And the contradiction of saying one person has a body, yet that body does not delimit that person in anyway in terms of their actions and perceptions, nor is it logically prior to the person such that the person 'depends' on it in some way.

AservantofJEHOVAH:If you truly want to think sensibly about any topic you need to remove your ego from the equation. I for one presume that I and my interlocutors are probably going to walk away thinking the same thing about the given topic after the exchange as before it. I use the word essence to refer to those qualities that make JEHOVAH worthy of absolute worship as these are instantiated in the real world.

JEHOVAH'S Concrete form is the source of his potential and enables him to actualise his potential over distance. Quantum entanglement is called spooky action over distance so it does have one similarity to telekinesis as you pointed out scientists don't know how it works but it is evidence from creation that the ability to immediately produce effects over distance is not an impossibility even within the creation. Why then be dismissive about the possibility of our creator having some more superior means of actualising potential over distance in a controlled way.

Against Roman XXIII

Roman:. This wasn't a lifelong position of mine, and it's not charitable of you to assume I've only taken a "shallow reading."

AservantofJEHOVAH: My assessment was based on your answers on your answers and I must say that your response here has done little to change my mind.

Roman:2. What does bordered mean if not bounded?

If what is bordered is mobile then it is not bounded. Bounded suggest limits as to reach JEHOVAH Has no limits re:the reach of his power . Although his having a form that embodies his essence.

3. I know what quantum entanglement is, but as you know I’m sure quantum entanglement involves is not anything like telekinesis, but it’s rather the physical entanglement of particles at a distance, modelled mechanically and which is not really understood by science. But it is not usually described as a kind of unmediated causation. If telekinesis in the actual sense existed in the world, i.e. a person could access and have control over say, a brick, just as much as he could access and control his body, and his body did not act as a center of perception such that it limited it, and his existence didn’t depend on the functioning of various body parts, then I have no idea what it means to say he has a body.

His telekinesis is not magical it is a result of the actualisation of potential energy stored in his form which is projected from said form over distance from nothing nothing comes his form has the tech to convert potential energy into actual energy and make a controlled projection over distance. I hope that you are not saying that you thought that my use of quantum entanglement as analogue was any thing more that that

4. What do you mean by “essence?” Generally an essence is an abstract set of essential properties, not something which can be described as having a border, so my ‘body’ is not my essence, every particle in my body will be different in about 10 or 15 years yet I will be the same person, I will also be the same person if I happened to be anointed and was resurrected in a non-physical state. So generally, God’s essence is thought to be his omnipotence/omniscience etc etc … Other than that, I don’t know what you mean by essence.

An abstraction that does not describe a reality or possible reality is nothing but projection there is a concrete form that enables the actualisation of JEHOVAH'S Limitless potential  JEHOVAH is sage and not mage.

As I have pointed out this body which is the reservoir of his infinite potential is unlike anything in the creation so to compare your created body which receives all its potential from outside with JEHOVAH'S Uncreated body which which is  self-existent is an exercise in futility 

5. What makes my body my body is my direct access to it and it being a necessary condition of me, i.e., if you cut off my finger it is no longer part of my body, because I do not have direct access to it, i.e. it’s not just my mind that can move it, I have to “pick it up,” my body also is what my consciousness depends on as it’s center of perception and power … it’s not my “essence.”

Again your body is created JEHOVAH'S is Uncreated so his body is simply not subject to any kind of change his body is a necessary substrate to his essence Just as is the case with every other concrete reality.

Roman6. According to contemporary physics space and time are not mere abstractions in that they would exist independent of human conceptualization. So, gravity is not a concrete reality, but it’s not an “abstraction” either, or if it IS an abstraction, you’re using the term in a way that it’s not usually used. 

Abstract realities are realities they are not imaginary you seem to think that my saying that something is an abstraction means that it is not real. time and space are neither cause nor effect they are just values necessary to describe/evaluate concrete realities i.e causes and effects.

Human conceptualisations are not most important ones.

7. If I am bound by my body, I can exert power outside my body by use of my body. If God is bordered but that body, but not dependent on in for perception or power in anyway, or dependent on it in anyway, and it does not bound anything, then what is it bordering? His essence? What does that mean? Essence is an attributive concept.

JEHOVAH can actualise the potential energy stored in his body over distance. His body is the store of that potential and the means by which that potential is actualised in a precisely controlled way comparisons between the only cause that is not itself an effect and any created reality are limited in their usefulness

All the first cause arguments for JEHOVAH depend on the existence of prior potential of causes to produce effects only a cause with a store of infinite potential energy under its absolute control Can account for the existence of creation. Unless we are appealing to magic this entails a living body of some kind under the control of mind.

Left and right demystif

 

A bare bones take on design in biology?

 

On the one God and his only Son.

 

Hardwired for music?

 The Human Mind Is Wired for Music: How Did That Come About?

Eric Hedin

The appreciation of the human mind for music knows no limits. A quick look at a list of the most watched YouTube videos shows that 90 percent of the top thirty are songs, with total views for each ranging from 3 billion to 13 billion.1 Most of us can correctly remember melodies and lyrics learned in childhood, even years after last having heard them. While speaking words effectively communicates information, we seldom remember even a short speech verbatim. It seems that the human mind is wired for music.

What’s the evidence for design in the linkage between mind and music? We could start by observing that from an evolutionary perspective, music is not something we grew up with ancestrally. Beyond the calls and trills of birds, nature as we know it provides few sounds that resemble even the simple melodies of children’s nursery songs. Is our ability to appreciate music akin to our ability to comprehend mathematics? Again, from an evolutionary standpoint, human mathematical ability far exceeds any adaptation we might have from needing to count the number of ducks in the pond.

Benefits for the Soul

The benefits of music for the human soul and its effects on our emotions are well-documented.

Music is ubiquitous across human cultures — as a source of affective and pleasurable experience, moving us both physically and emotionally…2

Music has a bewitching power when it comes to our thoughts and emotions….The psychology of music has been recognized and studied since ancient times, with Plato theorizing that different styles of music stirred different emotions in listeners.3

Plato’s thoughts on music are confirmed by recent scientific studies. UC Berkeley researchers studying 2500 people from the United States and China have identified 13 different emotions evoked by music, from amusement to annoyance, and sadness to triumph.4

More than just stimulating emotions, music’s influence on us extends to deeper levels as well. 

The use of music in the realm of medicine is impressively far-reaching. It’s been known to assist in therapy and healing for a wide range of illnesses and conditions.5

Music therapy can minister to people with mental health issues and help to regulate moods and reduce stress.

Is the connection between mind and music limited to humans?

One context in which music therapy may be used to enhance animal welfare is to alleviate stress in domestic environments.6

Testimony to Human Exceptionalism?

However, a survey of the effects of varieties of music on different animals reveals inconsistent results. This may indicate that animal minds perceive and process musical sounds categorically unlike humans. Rats, however, do respond positively to Mozart.7

Is there anything inherent in nature that could suggest the connection between music and mind? Music is based on vibrations at varying frequencies, and vibrations are pervasive in nature. Most natural frequencies exist at levels far beyond the range of human hearing and occur apart from sound waves. All atoms have electrons that orbit with varying frequencies, exemplified by the hydrogen atom in its ground state for which the electron orbits about 6.57×1015 times per second, in the range of visible light frequencies (an electromagnetic wave), or approximately a trillion times higher than the frequency of sound waves humans can hear.

Planets orbit around the sun with much lower frequencies, approximately one billionth of an orbit per second, corresponding to a frequency about a trillion times lower than the frequency range of human hearing. The rotation rates of collapsed cores of massive stars, known as pulsars, include many millisecond pulsars, whose rotation frequency would be audible in the frequency range of human speech, if converted into a sound wave. 

Design in Hearing

Whale song” also occurs within the range of human hearing but went unnoticed by humans until its discovery in 1967 by marine biologist Roger Payne.8

The whale song is considered one of the most complex non-human forms of communication created by any species in the animal kingdom. The whale song carries a predictable melodic tone and the notes are repeated over and over again like a chorus.9

In our discussion of the connection between music and mind, the biocomplexities of our auditory senses certainly play a key role and the documented evidence for design in hearing is profound. Our deep emotional and aesthetic appreciation for music adds to the argument that we are more than unguided outcomes of natural forces that evolved the ability to hear because it imparted to us a survival advantage. Attempting to reduce our love for music — the mystery of music — to an evolutionary adaptation has a dissonant edge to discerning ears.

On Darwinism's dependency on engineerless engineering.

 Dr. Glicksman: How Life Leverages the Laws of Nature

Andrew McDiarmid

Left to their own devices, the natural result of physics and chemistry is death, not life. So how are we still breathing? On this ID the Future, host Eric Anderson concludes his conversation with physician Howard Glicksman about some of the remarkable engineering challenges that have to be solved to produce and maintain living organisms such as ourselves. Glicksman is co-author with systems engineer Steve Laufmann of the recent book Your Designed Body, an exploration of the extraordinary system of systems that encompasses thousands of ingenious and interdependent engineering solutions to keep us alive and ticking. In the “just so” stories of the Darwinian narrative, these engineering solutions simply evolved. They emerged and got conserved. Voila! But it takes more than the laws of nature to keep us from dying. 

In Part 1, Glicksman discussed how two laws of nature — diffusion and osmosis — must be innovated by living systems to avoid cell death. In this episode, Glicksman provides another example: how we regulate the flow of water and blood through our bodies without the excess leakage or shrinkage that can lead to cell death. The protein albumin is crucial. Along with helping to transport minerals and hormones, albumin vitally maintains blood volume by regulating the water flow in and out of the capillaries. How does our liver know how to make albumin, or how much of it to make? Can a gradual Darwinian process be credited with these essential innovations? Or do they bear hallmarks of design? Dr. Glicksman explains this remarkable system, just one of many engineering feats our bodies perform every day to keep us alive. Download the podcast or listen to it here.

Continuing to rethink the unrethinkable?