Friday 20 September 2024
Thursday 19 September 2024
Tuesday 17 September 2024
Monday 16 September 2024
Saturday 14 September 2024
The fossil record vs. The dinosaur to bird narrative.
Fossil Friday: More Evidence That “Feathered Dinosaurs” Were Secondarily Flightless Birds
in one of my recent Fossil Friday articles (Bechly 2024) I elaborated on the neoflightless hypothesis by paleo-ornithologist Alan Feduccia, who convincingly argues that all those feathered bipedal “dinosaurs” are in fact not related to theropod dinosaurs at all but rather represent secondarily flightless birds. I also discussed new evidence that strongly supports this view. Indeed, Agnolin et al. (2019) already commented in their study on the dinosaur-bird transition:
In a ground-breaking proposal, Xu et al. (2011) hypothesized that Archaeopteryx was more nearly related to deinonychosaurians than to birds and that deinonychosaurs become secondarily flightless, a hypothesis previously envisaged by Paul (2002). This hypothesis was supported by a variety of more recent analyses (Godefroit et al., 2013a; Xu et al., 2015; Hu et al., 2018).
Yet Another Discovery
After my article was published (Bechly 2024), I stumbled upon yet another discovery that may lend additional support to Feduccia’s hypothesis:
Just about a decade ago, Godefroit et al. (2013b) described a new supposed theropod dinosaur from the Middle-Late Jurassic Tiaojishan Formation of Liaoning in China. With an estimated age of 160 million years it is 10 million years older than the famous Archaeopteryx. They named the new species Eosinopteryx brevipenna, because of its reduced plumage. The single known specimen (an artist’s depiction of the living animal is above, or see here for the fossil) represents a very well-preserved fossil and almost complete skeleton, which allowed scientists to identify the new taxon as a close relative of the feathered dinosaur Anchiornis.
But this generated a problem: the new dinosaur appeared to be nested deeply in the tree of feathered dinosaurs, so that its reduced plumage cannot be a primitive state but has to be a secondary reduction from a more complete set of feathers. Furthermore, the bone structures of the shoulder articulation showed that the animal was not capable of flapping its arms or wings. This is even more perplexing, as this case of reduced flight adaptations predates the famous missing link Archaeopteryx. Consequently, the press release to the new study (University of Southampton 2013) announced that this fossil “challenges bird evolution theory” and suggested “that the origin of flight was much more complex than previously thought.” The lead author, Dr. Gareth Dyke from the University of Southampton, is quoted with this remarkable admission: “This discovery sheds further doubt on the theory that the famous fossil Archaeopteryx — or “first bird” as it is sometimes referred to — was pivotal in the evolution of modern birds.”
Challenged by Other Evolutionists
Don’t hold your breath, though, waiting for textbooks to be updated accordingly, because this confounding result was quickly challenged by other evolutionist scientists. They claimed that the distinct features of Eosinopteryx could rather be based on variability of the plumage and incomplete preservation of the tail, so that it could even represent the very same species as Anchiornis huxleyi (Pei et al. 2017, Hu et al. 2018, Agnolin et al. 2019). But these studies partly disagreed on certain crucial issues, such as the question of whether the shorter tail in Eosinopteryx is complete and diagnostic (Pei et al. 2017) or not (Hu et al. 2018, Agnolin et al. 2019). Moreover, other experts had recorded further diagnostic differences between the skeletons of two taxa, such as anteriorly convex pubic shafts that are present in Anchiornis but absent in Eosinopteryx (Foth & Rauhut 2017), or the length and shape of the prefrontal and maxillary processes (Guo et al. 2018). Also the cladistic studies by Lefèvre et al. (2014), Guo et al. (2018), Hu et al. (2018), and Pei et al. (2020) did not recover Eosinopteryx as closest relative of Anchiornis, or even rejected the monophyly of Anchiornithidae. One could almost get the impression that the desire to explain away inconvenient results may have guided the interpretations of those scientists, who denied the distinctness of Eosinopteryx.
There are clearly open questions and it definitely looks like the common dino-to-bird narrative has been massively oversold to the public and represents a theory with numerous holes and problems.
References
Agnolin FL, Motta MJ, Brissón Egli F, Lo Coco G & Novas FE 2019. Paravian Phylogeny and the Dinosaur-Bird Transition: An Overview. Frontiers in Earth Science 6: 252, 1–28. DOI: https://doi.org/10.3389/feart.2018.00252
Bechly G 2024. Fossil Friday: New Study Confirms “Feathered Dinosaurs” Were Secondarily Flightless Birds. Evolution News April 5, 2024. https://evolutionnews.org/2024/04/fossil-friday-new-study-confirms-feathered-dinosaurs-were-secondarily-flightless-birds/
Foth C & Rauhut OWM 2017. Re-evaluation of the Haarlem Archaeopteryx and the radiation of maniraptoran theropod dinosaurs. BMC Evolutionary Biology 17: 236, 1–16. DOI: https://doi.org/10.1186/s12862-017-1076-y
Godefroit P, Cau A, Dong-Yu H, Escuillié F, Wenhao W & Dyke G 2013a. A Jurassic avialan dinosaur from China resolves the early phylogenetic history of birds. Nature 498(7454), 359–362. DOI: https://doi.org/10.1038/nature12168
Godefroit P, Demuynck H, Dyke G, Hu D, Escuillié F & Claeys P 2013b. Reduced plumage and flight ability of a new Jurassic paravian theropod from China. Nature Communications 4(1): 1394, 1–5. DOI: https://doi.org/10.1038/ncomms2389
Guo X, Xu L & Jia S 2018. Morphological and Phylogenetic Study Based on New Materials of Anchiornis huxleyi (Dinosauria, Theropoda) from Jianchang, Western Liaoning, China. Acta Geologica Sinica – English Edition 92(1), 1–15. DOI: https://doi.org/10.1111/1755-6724.13491
Hu D, Clarke JA, Eliason CM, Qiu R, Li Q, Shawkey MD, Zhao C, D’Alba L, Jiang J & Xu X 2018. A bony-crested Jurassic dinosaur with evidence of iridescent plumage highlights complexity in early paravian evolution. Nature Communications 9(1): 217, 1–12. DOI: https://doi.org/10.1038/s41467-017-02515-y
Lefèvre U, Hu D, Escuillié FO, Dyke G & Godefroit P 2014. A new long-tailed basal bird from the Lower Cretaceous of north-eastern China. Biological Journal of the Linnean Society 113(3), 790–804. DOI: https://doi.org/10.1111/bij.12343
Paul GS 2002. Dinosaurs of the Air: The Evolution and Loss of Flight in Dinosaurs and Birds. The John Hopkins University Press, Baltimore (MD), 472 pp.
Pei R, Li Q, Meng Q, Norell MA & Gao K-Q 2017. New Specimens of Anchiornis huxleyi (Theropoda: Paraves) from the Late Jurassic of Northeastern China. Bulletin of the American Museum of Natural History 411, 1–67. DOI: https://doi.org/10.1206/0003-0090-411.1.1
Pei R, Pittman M, Goloboff PA, Dececchi TA, Habib MB, Kaye TG, Larsson HCE, Norell MA, Brusatte SL & Xu X 2020. Potential for Powered Flight Neared by Most Close Avialan Relatives, but Few Crossed Its Thresholds. Current Biology 30(20), 4033–4046.e8. DOI: https://doi.org/10.1016/j.cub.2020.06.105
University of Southampton 2013. Discovery of ‘Bird-Dinosaur’ Eosinopteryx Challenges Bird Evolution Theory. SciTechDaily January 24, 2013. https://scitechdaily.com/discovery-of-bird-dinosaur-eosinopteryx-challenges-bird-evolution-theory/
Xu X, You H, Du K & Han F 2011. An Archaeopteryx-like theropod from China and the origin of Avialae. Nature 475(7357), 465–470. DOI: https://doi.org/10.1038/nature10288
Xu X, Zheng X, Sullivan C, Wang X, Xing L, Wang Y, Zhang X, O’Connor JK, Zhang F & Pan Y 2015. A bizarre Jurassic maniraptoran theropod with preserved evidence of membranous wings. Nature 521(7550), 70–73. DOI: https://doi.org/10.1038/nature14423
Our fingers point to design?
The Formation of Our Digits Points to a Process with Foresight
Have you ever wondered how our fingers and toes form during embryonic development? Our digits are, in fact, sculpted from a paddle-like structure in the embryo through the process of apoptosis — that is, programmed cell death. During early development, the hands and feet begin as solid, webbed structures. Through carefully controlled apoptosis, the tissue between them is eliminated, facilitating the separation of the digits. As one paper put it, “the role of apoptosis can be compared with the work of a stone sculptor who shapes stone by progressively chipping off small fragments of material from a crude block, eventually creating a form.”1 Apoptosis, of course, serves other important biological functions as well — such as eliminating old, damaged, or infected cells.
When cells die as a consequence of acute injury, they tend to swell and burst, releasing their contents into the surrounding tissue. This is known as necrosis, and it can result in an inflammatory response that can be damaging to the cells around them. Death by apoptosis, by contrast, is much cleaner. During apoptosis, the cytoskeleton breaks down and the nuclear envelope disassembles, and the genetic material is broken down into smaller fragments. The surface of the cell is modified such that it attracts macrophages that phagocytose (engulf) the cell before its contents can spill out into the environment and cause damage.
The process of apoptosis is tightly regulated by genetic and biochemical signals, ensuring that the correct number of cells die in the right areas. But how could such a developmental process involving programmed cell death evolve in a gradual, incremental fashion without any awareness of where the target is? This presents a significant obstacle to unguided evolutionary mechanisms. Here, I will give a brief overview of how this remarkable process is regulated and controlled.
Initiation of Apoptosis
The zones of undifferentiated cells between what will become the digits are called interdigital mesenchyme. It is here that apoptosis is initiated by signaling molecules. For example, bone morphogenetic proteins (BMPs) are secreted signaling molecules that are critical for inducing apoptosis in the cells of the interdigital spaces.2 Indeed, knocking out BMP molecules has been shown to result in webbed feet in chickens.3 BMPs are upregulated in the regions between the forming digits, resulting in cellular death and tissue regression.
These BMPs bind to receptors on the surface of target cells in the developing limb bud.4 This, in turn, activates intracellular SMAD proteins, which translocate to the nucleus and regulate the expression of pro-apoptotic and anti-apoptotic genes.5 For instance, pro-apoptotic genes such as Bax and Bak (discussed later) are upregulated. Anti-apoptotic genes, such as Bcl-2, are also downregulated. This facilitates cell death in areas where tissue needs to be removed.
The activity of BMPs is regulated by antagonists, such as Noggin, which binds directly to BMPs, forming a complex that inhibits them from interacting with their receptors. This ensures that apoptosis only occurs in the interdigital spaces, while preserving the cells that will form the digits.6
Executioner Caspases
A family of proteases called caspases comprise the molecular machinery responsible for apoptosis.7,8 These proteases are initially produced as inactive precursors known as procaspases. In response to apoptosis-inducing signals, they are activated. Executioner caspases are responsible for dismantling essential cellular proteins — these are themselves cleaved (and thereby activated) by initiator caspases. One executioner caspase targets for destruction the lamin proteins that comprise the nuclear lamina, resulting in its disintegration.9 This facilitates the entry of the nucleases into the nucleus where they degrade the cell’s DNA. Other targets of executioner caspases include the cytoskeleton10 and other critical cellular proteins.
Execution of the Death Program: The Intrinsic Pathway
There are two ways in which the cell’s death program can be initiated — the extrinsic and intrinsic pathways. The extrinsic pathway is initiated by external signals through the binding of ligands to death receptors on the cell surface. The intrinsic pathway is triggered by signals from within the cell itself. Since the intrinsic pathway is associated with digit formation, it will be my focus here.
In nucleated animal cells, inactive procaspases roam, waiting for a signal to activate the death program and kill the cell. Unsurprisingly, then, the activity of caspases must be very carefully controlled. This presents another conundrum for their origins — how could they arise without a mechanism in hand for holding them in check until required?
The Bcl2 family of proteins is responsible for regulating caspase activation.11 Some of these proteins promote activation of caspases and apoptosis, while others negatively regulate these processes. Two essential proteins for promoting cell death are Bax and Bak.12 These proteins trigger the release of cytochrome c from the mitochondria. Other Bcl2-family proteins sequester apoptosis by inhibiting Bax and Bak from releasing cytochrome c.13 Critical to a cell’s survival is the balance between the activities of the pro-apoptosis and anti-apoptosis Bcl2-family members.
Image credit: David Goodsell, CC BY 3.0 https://creativecommons.org/licenses/by/3.0, via Wikimedia Commons
Upon release of cytochrome c from the mitochondria, the cytochrome c molecules bind to Apaf-1 (apoptotic protease activating factor 1).14 Apaf-1 has a specific region called the WD40 repeat domain that interacts with cytochrome c.15,16This binding induces a conformational change in Apaf-1, which allows it to oligomerize. The Apaf-1 monomers thus assemble into a large heptameric complex called the apoptosome (shown in the figure above). This wheel-like structure serves as a scaffold for further recruitment of procaspase-9 molecules.17 Within the apoptosome, the proximity of multiple procaspase-9 molecules results in their autocleavage and activation.18 This induces a caspase cascade (involving the activation of downstream effector caspases, such as caspase-3 and caspased-7), ultimately resulting in programmed cell death.19
The Need for Foresight
We began by comparing the role of apoptosis in digit formation to a stone sculptor, chipping off tiny fragments from a block with a view towards ultimately creating a form. Of course, an actual stone sculptor has a vision of the final form — the ability to visualize a distant outcome. Conversely, a feature of natural selection is that it lacks foresight, or any awareness of complex end goals. How can a mindless evolutionary process select for a process of carefully regulated programmed cell death during development, without knowledge of the target? It would seem that any process capable of producing this mechanism would have to possess intelligence and foresight — characteristics uniquely associated with a conscious mind.
Notes
Suzanne M, Steller H. Shaping organisms with apoptosis. Cell Death Differ. 2013 May;20(5):669-75.
Storm EE, Kingsley DM. GDF5 coordinates bone and joint formation during digit development. Dev Biol. 1999 May 1;209(1):11-27.
Zou H, Niswander L. Requirement for BMP signaling in interdigital apoptosis and scale formation. Science. 1996 May 3;272(5262):738-41. doi: 10.1126/science.272.5262.738. PMID: 8614838.
Ovchinnikov DA, Selever J, Wang Y, Chen YT, Mishina Y, Martin JF, Behringer RR. BMP receptor type IA in limb bud mesenchyme regulates distal outgrowth and patterning. Dev Biol. 2006 Jul 1;295(1):103-15.
Gomez-Puerto MC, Iyengar PV, García de Vinuesa A, Ten Dijke P, Sanchez-Duffhues G. Bone morphogenetic protein receptor signal transduction in human disease. J Pathol. 2019 Jan;247(1):9-20.
Guha U, Gomes WA, Kobayashi T, Pestell RG, Kessler JA. In vivo evidence that BMP signaling is necessary for apoptosis in the mouse limb. Dev Biol. 2002 Sep 1;249(1):108-20.
McIlwain DR, Berger T, Mak TW. Caspase functions in cell death and disease. Cold Spring Harb Perspect Biol. 2013 Apr 1;5(4):a008656. Erratum in: Cold Spring Harb Perspect Biol. 2015 Apr 01;7(4):a026716..
Cohen GM. Caspases: the executioners of apoptosis. Biochem J. 1997 Aug 15;326 ( Pt 1)(Pt 1):1-16.
Gheyas R, Menko AS. The involvement of caspases in the process of nuclear removal during lens fiber cell differentiation. Cell Death Discov. 2023 Oct 21;9(1):386.
Vakifahmetoglu-Norberg H, Norberg E, Perdomo AB, Olsson M, Ciccosanti F, Orrenius S, Fimia GM, Piacentini M, Zhivotovsky B. Caspase-2 promotes cytoskeleton protein degradation during apoptotic cell death. Cell Death Dis. 2013 Dec 5;4(12):e940.Kale J, Osterlund EJ, Andrews DW. BCL-2 family proteins: changing partners in the dance towards death. Cell Death Differ.2018 Jan;25(1):65-80.
Westphal D, Kluck RM, Dewson G. Building blocks of the apoptotic pore: how Bax and Bak are activated and oligomerize during apoptosis. Cell Death Differ. 2014 Feb;21(2):196-205.
Dlugosz PJ, Billen LP, Annis MG, Zhu W, Zhang Z, Lin J, Leber B, Andrews DW. Bcl-2 changes conformation to inhibit Bax oligomerization. EMBO J. 2006 Jun 7;25(11):2287-96.
Kim HE, Du F, Fang M, Wang X. Formation of apoptosome is initiated by cytochrome c-induced dATP hydrolysis and subsequent nucleotide exchange on Apaf-1. Proc Natl Acad Sci U S A. 2005 Dec 6;102(49):17545-50.
Hu Y, Ding L, Spencer DM, Núñez G. WD-40 repeat region regulates Apaf-1 self-association and procaspase-9 activation. J Biol Chem. 1998 Dec 11;273(50):33489-94.
Shalaeva DN, Dibrova DV, Galperin MY, Mulkidjanian AY. Modeling of interaction between cytochrome c and the WD domains of Apaf-1: bifurcated salt bridges underlying apoptosome assembly. Biol Direct. 2015 May 27;10:29.
Yuan S, Yu X, Topf M, Ludtke SJ, Wang X, Akey CW. Structure of an apoptosome-procaspase-9 CARD complex. Structure. 2010 May 12;18(5):571-83.
Li Y, Zhou M, Hu Q, Bai XC, Huang W, Scheres SH, Shi Y. Mechanistic insights into caspase-9 activation by the structure of the apoptosome holoenzyme. Proc Natl Acad Sci U S A. 2017 Feb 14;114(7):1542-1547.
Li P, Nijhawan D, Budihardjo I, Srinivasula SM, Ahmad M, Alnemri ES, Wang X. Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascade. Cell. 1997 Nov 14;91(4):479-89.
Wednesday 11 September 2024
Tuesday 10 September 2024
Small volume /Big tech?
Intelligent Design — In Miniature
A recent research award from the European Research Council supports the study of some of the world’s tiniest vertebrates, hoping to unravel what is considered the mystery of animal miniaturization. Small vertebrates may be a thousand times larger than single-cell organisms, but they occupy a region of parameter space that presents uniquely fascinating properties.
Within a single cell, the multitude of interacting organelles are basically large, complex molecules with specific structures allowing them to carry out particular functions. Interactions proceed along the lines of biochemistry. At the size scale of insects, spiders, and small vertebrates, multicellular components form the functioning structure of the living organism. At such miniature size scales formidable engineering challenges are encountered, appreciated within the field of micro-robotics.
Among the contenders for the smallest vertebrates are flea toads.
Just seven millimetres long, flea toads are among the smallest vertebrates on Earth. Despite their diminutive size, their organs and functions hardly differ from animals a thousand times larger. While examples of extreme miniaturisation abound in nature, just how these creatures get so small remains a scientific mystery.
Serious Engineering Challenges
Is it easier to construct a micro-robot or a macro-scale robot? From an engineering point of view, the smaller size scale introduces serious challenges.
Over the past years, the field of miniaturized robotics has rapidly expanded with many research groups contributing to the numerous challenges inherent to this field….However, despite all efforts and many available soft materials and innovative technologies, a fully autonomous system-engineered miniaturized robot (SEMR) of any practical relevance has not been developed yet….A careful examination of current SEMRs that are physically, mechanically, and electrically engineered shows that they fall short in many ways concerning miniaturization, full-scale integration, and self-sufficiency.
Physics principles concerning the mechanical properties of a system change appreciably with increasing miniaturization. Designing a functioning miniaturized system involves more difficulties than simply scaling down the physical size of every component.
As the systems become smaller, the relative forces that act on the system change dramatically, and the robots experience an increase in friction and adhesion. At the same time, weight and inertia gradually become irrelevant. Changes in fluid mechanics and stochastic motion challenge fundamental engineering notions of how mechanical elements move and interact. These physical effects form a crucial factor in designing and operating robots on a small scale.
Ingenious Solutions to Miniaturization
Tiny living creatures abound, demonstrating ingenious solutions to miniaturization that surpass human technological skills. A short list of the challenges that engineers face in trying to make robots the size small-scale life is given below, and includes adequate power, “intelligence,” and sensor-feedback-control mechanisms.3
“One of the challenges in designing capable SEMRs [system-engineered miniaturized robots] is the limited power budget, as existing propulsion methods require significant power, and the energy-storage systems (ESSs) are extremely difficult to downscale into the submillimeter range.”
“However, with miniaturization of the robot’s size, it is also clear that robots lose the ability of on-board intelligence and become limited in functionalities.”
“Current SEMRs have no energy on-board and lack any continuous feedback-controlled sensing, actuation, data processing, and communication.”
Observing a tiny spider that built its web in the corner of a window in my house was what set me to thinking about the amazing design in miniature creatures. Although this little critter had taken up its residence on the inside of the window, I let it alone out of fascination. I had to look closely to even see the spider, barely a millimeter or two in size. And yet it had woven this little web stretching several centimeters across the corner of the windowsill. For comparison, this would be like me using rope to construct a web the size of a football field.
This little arachnid warrior had managed to capture prey in its web (several of their remains could be seen) and presumably nourished itself thereby. Think about the capabilities packed into this tiny creature. It’s mobile and autonomous. It can see its surroundings and make decisions based on that sensory input regarding where to make its web. It manufactures and dispenses the finest web strands — not randomly, but with a specific type of design that can trap other small bugs. It can immobilize its prey and appropriately consume it. It metabolizes its food to generate sufficient energy for mobility, web production, and sensory processing. And it can presumably reproduce itself multifold (although my forbearance with its existence in my house may not extend to cover this circumstance!)
An Advancing Discipline
Even though micro-robotics is an advancing discipline, all the efforts of specialists in this field have not come close to manufacturing anything with the capabilities of this one little spider. The smallest spiders discovered on Earth measure only about 0.4 mm across, perhaps five times smaller than my little window dweller. Packing the many sophisticated capabilities of a spider into such a miniscule package speaks of the highest level of engineering design.
Notes
Vineeth Kumar Bandari and Oliver G. Schmidt, “System-Engineered Miniaturized Robots: From Structure to Intelligence,” Adv. Intell. Syst. 2021, 3, 2000284.
Vineeth Kumar Bandari and Oliver G. Schmidt, “System-Engineered Miniaturized Robots: From Structure to Intelligence,” Adv. Intell. Syst. 2021, 3, 2000284.
Vineeth Kumar Bandari and Oliver G. Schmidt, “System-Engineered Miniaturized Robots: From Structure to Intelligence,” Adv. Intell. Syst. 2021, 3, 2000284.
Monday 9 September 2024
Sunday 8 September 2024
Second Samuel chapter one New World translation study bible.
After Saul’s death, when David had returned from defeating* the A·malʹek·ites, David stayed at Zikʹlag+ for two days. 2 On the third day, a man came from the camp of Saul with his garments ripped apart and dirt on his head. When he approached David, he fell down to the ground and prostrated himself.
3 David asked him: “Where are you coming from?” He replied: “I have escaped from the camp of Israel.” 4 David asked him: “How did things turn out? Please tell me.” To this he said: “The people have fled from the battle and many have fallen and died. Even Saul and his son Jonʹa·than have died.”+ 5 Then David asked the young man who brought him the news: “How do you know that Saul and his son Jonʹa·than are dead?” 6 The young man replied: “By chance I was on Mount Gil·boʹa,+ and there was Saul supporting himself on his spear, and the chariots and horsemen had caught up with him.+ 7 When he turned around and saw me, he called me, and I said, ‘Here I am!’ 8 He asked me, ‘Who are you?’ I replied, ‘I am an A·malʹek·ite.’+ 9 Then he said, ‘Please stand over me and put me to death, for I am in great agony, but I am still alive.’* 10 So I stood over him and put him to death,+ for I knew that he could not survive after he had fallen down wounded. Then I took the crown* that was on his head and the bracelet that was on his arm, and I brought them here to my lord.”
11 At this David took hold of his garments and ripped them apart, and so did all the men who were with him. 12 And they wailed and wept and fasted+ until evening for Saul, for his son Jonʹa·than, for the people of Jehovah, and for the house of Israel,+ because they had fallen by the sword.
13 David asked the young man who brought him the news: “Where are you from?” He said: “I am the son of a foreign resident, an A·malʹek·ite.” 14 Then David said to him: “Why did you not fear to lift your hand to do away with the anointed of Jehovah?”+ 15 With that David called one of the young men and said: “Step forward and strike him.” So he struck him down, and he died.+ 16 David said to him: “Your blood is on your own head, because your own mouth testified against you by saying, ‘I myself put the anointed of Jehovah to death.’”+
17 Then David chanted this dirge* over Saul and his son Jonʹa·than+ 18 and said that the people of Judah should be taught the dirge called “The Bow,” which is written in the book of Jaʹshar:+
19 “The beauty, O Israel, lies slain upon your high places.+
How the mighty have fallen!
20 Do not tell it in Gath;+
Do not announce it in the streets of Ashʹke·lon,
Or the daughters of the Phi·lisʹtines will rejoice,
Or the daughters of the uncircumcised men will exult.
21 You mountains of Gil·boʹa,+
May there be no dew or rain upon you,
Nor fields producing holy contributions,+
Because there the shield of mighty ones was defiled,
The shield of Saul is no longer anointed with oil.
22 From the blood of the slain, from the fat of mighty ones,
The bow of Jonʹa·than did not turn back,+
And the sword of Saul would not return without success.+
23 Saul and Jonʹa·than,+ beloved and cherished* during their life,
And in death they were not separated.+
Swifter than the eagles they were,+
Mightier than the lions.+
24 O daughters of Israel, weep over Saul,
Who clothed you in scarlet and finery,
Who put gold ornaments upon your clothing.
25 How the mighty have fallen in battle!
Jonʹa·than lies slain upon your high places!+
26 I am distressed over you, my brother Jonʹa·than;
You were very dear to me.+
More wonderful was your love to me than the love of women.+
27 How the mighty have fallen
And the weapons of war have perished!”
Saturday 7 September 2024
The case for uncommon descent?
Fitness Landscapes Demonstrate Perfection in Vertebrate Limbs Resulted from Intelligent Design
In two previous articles (here, here), I summarized Stuart Burgess’s new paper (“Universal optimal design in the vertebrate limb pattern and lessons for bioinspired design”) that demonstrates common features of vertebrate limbs are better explained by design than by common ancestry, and I explained how embryological studies further support the design hypothesis. Here, I will detail how the conclusion of design is also bolstered by studies of evolutionary fitness landscapes.
Tutorial on Fitness Landscapes
A common metaphor for visualizing evolution is a fitness landscape (here, here, here), which is a three-dimensional plot of the fitness of an organism as a function of variables associated with different traits such as hair color, the shape and length of bones, and the efficiency of digesting toxins. The number of variables can be very large, so the values of all the variables are projected onto the x and y axes of the graph. These axes could also represent individuals’ genetic sequences. The z-axis corresponds to an individual’s fitness, which is commonly understood as the probability that it will produce offspring (Figure 1).
Figure 1. Evolutionary Fitness Landscape. The x and y axes represent the values of all trait variables for individuals in a population. The z-axis represents the fitness of an individual as measured by the probability of producing offspring. Populations tend to move uphill as represented by the white arrow-tipped line leading from point (1) to point (2). The path from (1) to (2) could represent an animal’s hair changing from dark grey to white or a fish transforming into an amphibian. © Thomas Shafee, CC BY 4.0, via Wikimedia Commons.
An individual represents a single point on the landscape, a population represents a cluster of points on the landscape, and the genetic variation in the population corresponds to the area or spread of the cluster. The variation can increase through individuals accumulating mutations. The population tends to move uphill since larger z corresponds to individuals producing more offspring (Figure 2).
Figure 2. Population trajectory on a static fitness landscape. Each dot represents an individual in the population. Within the population, the variation in traits represents the area the dots cover. If the fitness landscape does not change, the population typically moves to the top of the nearest fitness peak and then stops. Refresh this webpage to see the animation. © Randy Olson and Bjørn Østman, CC BY-SA 3.0, via Wikimedia Commons
A dynamic landscape will reshape if environmental conditions change, or individual organisms interact with each other in such a way as to alter their reproductive success (Figure 3). In practice, many peaks will remain relatively fixed since they correspond to the operation of traits in any environment an organism might encounter. If a population reaches the top of a static peak, it could remain trapped there for a period or indefinitely
Figure 3. Population trajectory on a dynamic fitness landscape. The fitness landscape changes with time, so the trajectory of the population also changes. For instance, in rainy seasons finches’ beaks could become thinner and longer, while in dry seasons they could become thicker and shorter. Refresh this webpage to see the animation. © Randy Olson and Bjørn Østman, CC BY-SA 3.0, via Wikimedia Commons
The extent to which a population can traverse a landscape depends on whether the landscape is smooth or rugged. A smooth landscape contains relatively few peaks with gently rising paths connecting the base of one peak to the summit of another (Figures 1 and 4d). An organism could potentially traverse significant distances along such a landscape, resulting in large evolutionary change. In contrast, a rugged landscape contains a multitude of sharp peaks (Figure 4f). Populations will tend to spend most of their time trapped on a local peak, so evolutionary change will be largely confined to minor modifications to existing traits.
The extent to which a landscape is smooth or rugged depends significantly on whether mutations interact additively (Figure 4a) or epistatically (Figure 4c). If they interact additively, the fitness change of two mutations roughly corresponds to the fitness changes of each individual mutation added together. If they interact epistatically, the fitness change from two mutations might be negative (i.e., detrimental) even if the fitness change from each individual mutation is positive (i.e., beneficial). Additive interactions lead to smooth landscapes supporting evolutionary change while epistatic interactions lead to rugged landscapes greatly limiting evolutionary change.
Figure 4. Relationship between mutation interactions and fitness landscapes. The top figures represent the fitness for different combinations of two versions of two genes. Genes a and b are the original genes. Gene A is a mutated version of gene a, and gene B is a mutated version of gene b. a) Mutation interactions are additive, so the fitness change from both mutations is approximately the sum of the fitness change from each individual mutation added together. b) Mutation interactions are partially additive and partially epistatic since the fitness of aB is greater ab, and AB is greater than aB, but Ab is not greater than ab. c) Mutation interactions are epistatic since AB’s fitness is less than aB’s and Ba’s fitness. d) Fitness landscape for additive interactions is a smooth peak. e) Fitness landscape for partially additive and partially epistatic interactions is partially rugged. f) Fitness landscape for epistatic interactions is highly rugged. © Thomas Shafee, CC BY 4.0, via Wikimedia Commons
Assessing the Evidence
Empirical studies and theoretical analyses consistently demonstrate that the fitness landscapes associated with complex traits are highly rugged. For instance, paleobiologist Graham J. Slater (2022) in his article “Topographically distinct adaptive landscapes for teeth, skeletons, and size explain the adaptive radiation of Carnivora (Mammalia)” analyzed the landscape for carnivores based on 16 trait variables. He concluded that the fitness landscape is rugged with multiple fitness peaks:
I found evidence of an early partitioning of mandibulo-dental morphological variation in Carnivora (Mammalia) that occurs on an adaptive landscape with multiple peaks, consistent with classic ideas about adaptive radiation.…The dietary adaptive landscape estimated from the first two mandibulodental PC axes by the PhylogeneticEM algorithm contains 21 peaks that are distinct from the ancestral regime.
The ruggedness of landscapes associating with the mechanical design of anatomical structures is further supported by studies on the use of evolutionary algorithms to assist improving robotic designs. Doncieux et al. (2011) observe in their article “Evolutionary Robotics: Exploring New Horizons”:
The difficulty of a problem often arises with the complexity of the fitness landscape: while a smooth, convex fitness landscape with no noise will be quite easy to deal with, most of the problems from the real world often comes with multimodal, noisy fitness landscapes that feature neutrality regions. The direct consequence is that search may often get stalled, would it be at the very beginning of the algorithm execution (i.e. a boostrap problem) or during the course of evolution (i.e. premature convergence), with no hint on how to escape a local optimum or on how to direct the search within a region where all neighboring candidate solutions are equally rewarded.
The ruggedness appears even more extreme for landscapes based on genetic sequences. Visser and Krug (2014) summarize in their paper “Empirical fitness landscapes and the predictability of evolution” how mutational studies demonstrate that fitness landscapes are rugged even for genetic changes confined to small sections of DNA:
At the small genomic scales considered so far, it is observed that sign epistasis is common, which reduces the number of accessible mutational pathways and leads to rugged landscapes with multiple fitness peaks.
Only a limited number of paths are accessible, and those paths require series of mutations that either do not increase the fitness (aka neutral mutations) or reduce it.
The Implications
The technical literature from paleobiology, robotics, and genetics uniformly concludes that fitness landscapes are generally highly rugged even when only a small portion of relevant variables are studied. The ruggedness and constraints on viable paths is only believed by evolutionary theorists to increase with the number of contributing variables and interactions, and the landscape in sequence space for vertebrate limbs represents a set of variables and interactions of enormous size.
These observations present two dire challenges to undirected evolutionary models considering Burgess’s study. First, the vast number of suboptimal local peaks in the fitness landscape precludes any possibility of an evolutionary search ever discovering the perfection of design consistently seen in vertebrates and in other taxa. Second, the constraints on viable paths require a portion of any trajectory along the landscape to include multiple specific neutral and harmful mutations. Yet the timescales required for obtaining coordinated neutral and deleterious mutations is prohibitively long (here, here).
Compounding the challenge, the fitness landscape is only rugged in regions near existing limb designs. The landscape between these regions represent vast seas of nonviable intermediates (here, here, here, here). The only plausible explanation for the perfection of design observed in vertebrate limbs is that a mind engineered them, for only a mind can choose highly optimized solutions out of a sea of possibilities.
Friday 6 September 2024
Thursday 5 September 2024
Homology by design?
Developmental Biology of Vertebrate Skeletons Shows Similarities are Better Explained by Design
In an article yesterday, I reported on Stuart Burgess’s new paper in the journal Bioinspiration & Biomimetics, “Universal optimal design in the vertebrate limb pattern and lessons for bioinspired design.” He demonstrates that the common features of vertebrate limbs are better explained by design than by common ancestry. He explains how the limbs are engineered around the triple-hinged layout because that layout is the best for allowing diverse complex motions. He also details how the instantiation of that layout in each vertebrate group (e.g., birds) is optimally designed for the group’s environment and behaviors. Here, I will describe how embryological studies further undermine evolutionary explanations for the limbs’ similarities and, by extension, support Burgess’s conclusion.
Evolutionary Predictions
Evolutionists assume that the traits they classify as homologous share similarities due to their having evolved from a common ancestor. For instance, the forelimb of a mammal is similar in many ways to the wing of a bird. The forelimb of each is believed to have evolved from the forelimb of a common ancestor that possessed the same similarities. Evolutionists predicted that homologous traits should share similar developmental pathways — the specific steps of cell migration and differentiation that form the trait as an egg develops into an offspring.
Manfred D. Laubichler is a distinguished theoretical biologist and historian of science. In his article “Homology in Development and the Development of the Homology Concept,” he summarizes this expectation:
The core assumption of the biological homology concept is that homologues are the units of phenotypic evolution. As such they are individuated quasi-autonomous parts of an organism that share certain elements and variational properties. Therefore, if two characters are to be homologous, they can only differ in those aspects of their structure that are not subject to shared developmental constraints. The role of developmental mechanisms is to guarantee the identity of two structures since they limit the variational properties of quasi-autonomous units
In other words, the differences between homologous traits in different species result from the ways their common ancestor’s developmental pathway was free to change, and the similarities between their traits correspond to the ways the pathway could not change. In the context of vertebrates, homologous limbs should result from highly similar developmental pathways since the three-hinged layout was maintained in most of the ancestors due to developmental and operational constraints.
Failure of the Prediction
Yet the embryological evidence demonstrates that this central prediction is false. Evolutionary biologists Tatsuya Hirasawa and Shigeru Kuratani detail in their article “Evolution of the vertebrate skeleton: morphology, embryology, and development” how homologous bones often develop from different developmental pathways supported by different genes:
Historical continuities of skeletal elements as step-wise morphological changes along a phylogenic lineage are inferable from detailed comparative analyses. However, within these continuities, discontinuities of genetic and developmental bases arise in which morphologically homologous bones are produced through different developmental processes.
The differences can include homologous bones originating in different regions of the embryos in different types of cells, and they can employ very different cell migration, cell differentiation, and genetic mechanisms and pathways. The authors explain how this discovery conflicts with evolutionary expectations:
A similar reductionist argument was once widespread with a vague expectation in the dawn of evolutionary developmental biology; namely, that morphologically homologous structures should be patterned through certain unchanged infrastructures, like function of evolutionarily conserved sets of regulatory genes or gene regulatory networks.
Implications
Other research has identified many additional differences in vertebrate limb development (here, here). The same holds true for the entire body plans of different vertebrate groups. These often-dramatic differences in both developmental pathways and their genetic bases severely challenge the claim that homologous limbs can be explained by common ancestry.
As an analogy, two versions of Microsoft Windows look very similar, and their programming and the computers that run them are also very similar. The similarities in both the operating systems’ appearance and the underlying software and hardware suggest that one operating system served as the basis for the other or they share a common ancestral source. In contrast, Microsoft Windows and Mac OS also look very similar, but their programming and the computers that run them are very different. Their similarity in appearance is not the result of common ancestry but of a software engineer choosing to design one similarly to the other.
In the same way, two vertebrate limbs might look similar, but the similarity can result from fundamentally different developmental pathways supported by different sets of genes. Consequently, the similarity is best explained by a mind choosing to craft them based on the same general design pattern. Other common design patterns in biology have been discussed in recent articles by biologist Emily Reeves and science journalist David Coppedge (here, here), further illustrating how the design framework is essential to advancing what we understand of the higher-level organization of living systems.
Tuesday 3 September 2024
A world finetuned for science?
Plate Tectonics and Scientific Discovery
you haven’t seen it, you should read Casey Luskin’s detailed Summary of a recent study arguing for the importance of plate tectonics for advanced life. The basic conclusions of the study are that plate tectonics is important for advanced life in multiple ways and that planets with plate tectonics are very rare. This comports with what Jay Richards and I wrote in The Privileged Planet: How Our Place in the Cosmos Is Designed for Discovery, out now in an expanded 20th-anniversary edition, and what my former colleagues Donald Brownlee and Peter Ward wrote in Rare Earth almost a quarter century ago. But here, I would like to focus on those aspects of plate tectonics that are important for technology.
Plate tectonics is an important part of continent building. Continents provide vast areas of dry land. Dry land is needed to make and control fire, which as Michael Denton argued in Fire-Maker, is the key starting point for advanced technology. Dry land also provides ready access to diverse minerals at or very near the surface, concentrated there by biological and geologic processes, including plate tectonics. Think of gold, copper, iron, uranium, salt, and coal, among many others.
The Continents Hold Other Treasures
There too we find time-stamped archives of Earth’s deep history, where we can dig up fossils and sample ice cores in the polar regions. Some fossils are of ancient sea creatures that died and ended up on the seafloor, covered by sediment, and were later transported to the continents or uplifted by plate motions. Yes, Earth’s dynamic geology destroys much information about its past, but at the same time it preserves often delicate features of ancient life. (See the photo at the top, a fossil leaf from the Eocene, 34 million years old, which I found at the Florissant Fossil Quarry in Colorado. The site is world famous for the quality and variety of its fossils.)
Plate motions also build mountain ranges. Mountains are important for a diverse biosphere. They are also important for mining minerals and for astronomical observations. Mountain ranges greatly increase the exposed surface area, making mineral deposits more accessible. The biggest, most expensive observatories are placed on high mountains to get above most of the mass of the atmosphere. A planet having only tectonics (without plates moving) might have a few high volcanic mountains, but they would remain active for long periods, preventing safe operation of observatories at their summit. This contrasts with, say, the Hawaiian Islands, which are over a hot spot in the crust with the oceanic plate slowly moving over it. The biggest volcano on Hawaii has already moved off the hot spot, causing it to be inactive and serving as a platform for observatories.
The Magnetic Field
Plate tectonics also contributes to the generation of Earth’s magnetic field. The magnetic field serves as a kind of global positioning system. Yes, people have used magnetic navigation for centuries, but I have in mind something more subtle. Geologists use the remnant magnetic field in ancient lava flows to reconstruct the motions of the continents over a large portion of Earth’s history. One aspect of the magnetic field that makes it especially useful to scientists is its semi-regular polarity reversals. This creates a kind of unique bar-code pattern over geologically long periods. It was this pattern, measured on the seafloor, that convinced geologists of the superiority of plate tectonics theory over competing theories in the early 1960s.
Earthquakes and Earthquake Zones
Plate motions generate earthquakes, which generate seismic waves that travel throughout Earth’s interior. Geologists have installed seismometers around the world to measure them and locate the earthquake epicenters and make a 3D map of Earth’s interior. This wouldn’t be possible on water worlds. Remarkably, geologists have discovered that earthquakes overwhelmingly occur in certain restricted regions, namely the crustal plate boundaries. We don’t know when earthquakes are going to happen, but we do know where they happen. Though people haven’t taken full advantage of this information, they could greatly reduce deaths from earthquakes by moving away from earthquake-prone areas.
Plate tectonics is yet another example of the correlation between the requirements for life and the requirements for doing science that we describe in The privileged planet.
Monday 2 September 2024
More on "Junk" DNA Proving to be junk science.
Hey, Please Ask Dawkins About His “Junk DNA” Goof
Our friend Brian Keating, a cosmologist at UC San Diego, does wonderful interviews for his Into the Impossible podcast. A particularly fun recent one was with Richard Dawkins. Near the end, Dr. Keating asked Dr. Dawkins for an example of a memorable scientific error he’s made. I leaned forward with curiosity. Dawkins volunteered that he had made a mistake about the so-called “handicap principle” relating to sexual selection. What I was hoping was that he would admit to the really major goof he made on “junk DNA,” a topic with so much consequence for the debate about intelligent design. But no.
Keating mentions that this is only Part 1 of a two-part conversation with Dawkins. Be sure to subscribe to Into the Impossible so that you’ll know right away when that one comes out. Perhaps Dr. Keating will consider asking Dawkins about “junk DNA” and what evolution would expect. On that, Dawkins seemed to changed his mind in a remarkable fashion. As of 2009 in his book The Greatest Show on Earth, he wrote, “the greater part (95 per cent in the case of humans) of the genome might as well not be there, for all the difference it makes.” Got that? 95 percent of the human genome is useless detritus, evolutionary garbage. And that would make sense if Darwinism is correct. It’s also the opposite of what ID proponents predicted.
With the Greatest of Ease
But the ID folks were dramatically vindicated. As of 2012, just three years later, after the results of the ENCODE project were published, Dawkins had completely flipped. Now, because ENCODE had indicated widespread function in the genome, putting the “junk” thesis out of business, Dawkins turned his earlier contention on its head. With the greatest of ease, he now argued that widespread function was just what Darwinian evolution would expect.
In a Conversation with Rabbi Jonathan Sacks, he said:
I have noticed that there are some creationists who are jumping on [the 2012 ENCODE results] because they think that’s awkward for Darwinism. Quite the contrary it’s exactly what a Darwinist would hope for, is to find usefulness in the living world […] we thought only a minority of the genome was doing something, mainly that minority which only codes for protein, and now we find that actually the majority of it is doing something. What it’s doing is calling into action the protein coding genes. […] The program that’s calling them into action is the rest that had previously been written off as junk.
Before, junk DNA fit beautifully with evolution. In the 2012 presentation, the opposite is the case: function rather than junk is “exactly what a Darwinist would hope for.” What a difference three years can make.
Watch the full podcast with Professor Keating below. And for more, see Casey Luskin’s post here, “‘Junk DNA’ from Three Perspectives: Some Key quotes.”
Sunday 1 September 2024
We continue our pursuit of straight answers from trintarians.
AservantofJEHOVAH:
"Is it compatible with trinitarian orthodoxy to claim that Jesus of Nazareth is the MOST High God?"
Designed intelligence?
There Is No Known Evolutionary Rule for Animal Intelligence
Cambridge neuropsychologist Nicholas Humphrey argues that warm-bloodedness (endothermy) enables mammals and birds to be more sentient than, say, cold-blooded reptiles and fish. In an excerpt from his book, Sentience: The Invention of Consciousness (MIT Press 2023), he argues that that development put these endotherms on the road to consciousness.
For one thing, as temperature goes up various bodily processes actually become more energetically efficient, so the costs can be partially offset. In particular, the cost of sending an impulse along a nerve decreases until it reaches a minimum at about 37 degrees Celsius. The result is that, although the overall running costs for the body go up with being warm-blooded, the costs for the brain are reduced. This means that mammals and birds can support larger and more complex brains with relatively little extra outlay of energy.
NICHOLAS HUMPHREY, “DID WARM-BLOODEDNESS PAVE THE PATH TO SENTIENCE?,” MIT PRESS, APRIL 15, 2024
He asks us to consider how warm-bloodedness might specifically affect the qualities we associate with intelligence:
It’s a well-established fact of physiology that the functional characteristics of neurons change with temperature. It’s been found for a range of animals — warm and cold-blooded — that the conduction speed for all classes of neurons increases by about 5 percent per degree Centigrade, while the refractory period decreases by roughly the same amount. This implies that when the ancestors of mammals and birds transitioned from a cold-blooded body temperature of, say, 15 degrees Celsius (59 degrees Fahrenheit) to a warm-blooded temperature of 37 degrees Celsius, the speed of their brain circuits would have more than doubled.
We’ve remarked already on the “lucky accidents” that have, at several points, played a part in the evolution of sensations. If warm-bloodedness played these key roles, first in changing the way animals thought about the autonomy of the self, second in preparing the brain for phenomenal consciousness, here was an accident as lucky as they come.
HUMPHREY, “PATH TO SENTIENCE?”
But the Situation Is Not Clear-Cut
When researchers have tested reptiles, using the same tests used on birds, the results have been surprising:
The lizards’ success on a worm-based test normally used on birds was “completely unexpected,” said Duke biologist Manuel Leal, who led the study.
He tested the lizards using a wooden block with two wells, one that was empty and one that held a worm but was covered by a cap. Four lizards, two male and two female, passed the test by either biting the cap or bumping it out of the way.
The lizards solved the problem in three fewer attempts than birds need to flip the correct cap and pass the test, Leal said. Birds usually get up to six chances a day, but lizards only get one chance per day because they eat less. In other words, if a lizard makes a mistake, it has to remember how to correct it until the next day, Leal said. He and Duke graduate student Brian Powell describe the experiment and results online in Biology Letters.
ASHLEY YEAGER, “BRAINY LIZARDS PASS TESTS FOR BIRDS,” DUKE TODAY, JULY 12, 2011
Significantly, the lizards had to learn a new task. They don’t feed themselves in the wild by flipping caps. And when the researchers raised the bar by switching which well held the worm, two of the lizards figured it out. As a result, the researchers named them Plato and Socrates.
That’s hardly the only instance of reptile intelligence observed by researchers. For example, the New York Times interviewed comparative psychologist Gordon M. Burghardt on monitor lizards:
Other studies have documented similar levels of flexibility and problem solving. Dr. Burghardt, for instance, presented monitor lizards with an utterly unfamiliar apparatus, a clear plastic tube with two hinged doors and several live mice inside. The lizards rapidly figured out how to rotate the tube and open the doors to capture the prey. “It really amazed us that they all solved the problem very quickly and then did much better the second time,” Dr. Burghardt said. “That’s a sign of real learning.”
EMILY ANTHES, “COLDBLOODED DOES NOT MEAN STUPID,” NEW YORK TIMES, NOVEMBER 19, 2013
Training a reptile.
Anoles and monitor lizards are considered to be among the most intelligent lizards. But it hasn’t been customary until recently to credit any lizards with much intelligence. That may be due to mishandling in some cases. Anthes notes at the Times that tests for reptile intelligence should take into account normal differences between, say, mammal behavior and reptile behavior: “By using experiments originally designed for mammals, researchers may have been setting reptiles up for failure. For instance, scientists commonly use “aversive stimuli,” such as loud sounds and bright lights, to shape rodent behavior. But reptiles respond to many of these stimuli by freezing, thereby not performing.”
Warm-bloodedness enables the mammal and the bird to be active for much longer than the reptile and to be active in colder temperatures. Thus, mammals and birds likely encounter more situations where they can (and must) demonstrate sentience and intelligence. But warm-bloodedness does not seem to be an essential component of those qualities.
Animal Intelligence Remains Something of a Mystery
One thinks of the invertebrate octopus and the brainless crab, which pass animal intelligence tests while breaking all the rules about which life forms are supposed to be smart. If there is a fixed evolutionary rule about which types of animals are intelligent, it has not been discovered yet.
Molecular biology is only the complex beginning of Darwinism's explanatory deficits?
The Extracellular Space: Where the Rest of Life Takes Place
When it comes to the discussion of how life came into being, whether by intelligent design or by the unguided processes proposed by evolutionary biology, I have a pet peeve.
It’s that almost all of the discussion from both camps revolves around just molecular and cellular biology — DNA, RNA, genes and their regulatory networks (GRNs), proteins and their various shapes, sizes, and functions, the cell membrane and cytoskeleton, and all the other fascinating intricacies of the cell.
Don’t Get Me Wrong
When it comes to the dialogue about the causal hurdles that life must overcome, every component mentioned above is important. And to my mind, they all favor ID.
After all, as chemist James Tour wrote in his chapter in The Mystery of Life’s Origin: The Continuing Controversy, when considering what is known about the laws of chemistry, “we’re still clueless about the origin of life.” Biologist Douglas Axe, in his book Undeniable: How Biology Confirms Our Intuition That Life Is Designed, tells us that “of the possible genes encoding protein chains 153 amino acids in length, only about one in a hundred trillion trillion trillion trillion trillion trillion is expected to encode a chain that folds well enough to perform a biological function.”
Zooming Out
But what about multicellular organisms, like us? Isn’t there more to think about and explain than just molecular and cellular biology? Here’s how Steve Laufmann and I posed the problem in our book Your Designed Body.
Zooming out from a single cell, the human body as a whole is made up of around thirty trillion cells. It needs to solve all the same kinds of problems that a cell does, plus quite a few more. And it needs new ways to solve old problems, ways completely different from how the same problems were solved at the cellular level.
For example, a single-celled organism is like a microscopic island of life. The cell gets what it needs and gets rid of what it doesn’t need from its surrounding environment. In contrast, a large multi-cellular organism (like you) is more like a continent with a deep and dark interior. Most of the cells reside deep in the interior with no direct access to the body’s surrounding environment. For a multi-cellular organism, then, harvesting the raw materials its cells need and getting rid of toxic byproducts becomes a major logistical problem.
Several hundred such problems must be solved for a complex body to be alive. And many of the solutions to these basic problems generate new problems that must also be solved, or that constrain other solutions in critical ways. The result is that for a complex body to be alive, thousands of deeply interconnected problems must be solved, and many of them solved at all times, or life will fail.
The bottom line is that, as hard as it is for a cell to maintain life, it’s much harder for an organism with a complex body plan like yours.
Besides knowing what’s going on inside our cells (within the intracellular space), don’t we also need to consider what’s going on outside our cells (but within our body) — in the extracellular space? Where one-third of our body’s total water resides? Where the various biomolecules that provide the framework for structure and support to all the different tissues in our body are located? Where the precise chemistry allowing for tissue survival and proper nerve and muscle function must be present? And much, much more.
My Experience as a Physician
As a hospice physician, I can tell you that all this is a matter of “life and death.” It’s something that evolutionary biologists rarely mention. This may be, at best, because they’ve never considered or understood it, or at worst, because they can’t explain it and it undermines their theory.
Let me give you a practical example from what I see and do every day. That way, you can understand why adding what goes on inside the extracellular space as a causal hurdle for multicelluar life is important. Meet my patient Joe.
Joe had had several heart attacks and now his heart wasn’t pumping as well as it should. In fact, it was doing so at one-quarter its normal strength — meaning he had heart failure. Since his heart wasn’t pumping efficiently, it caused a reduction in the force of arterial blood flow which turned on certain hormone systems in his body. These systems were designed (yes — designed) to try to correct such a situation. Unfortunately, this caused Joe’s body to start holding on to excessive amounts of water.
Joe’s body’s inability to control how much water was in his extracellular space put him at risk of death. Fluid was taking up more and more space in his lungs, making it harder and harder to breathe. Since he kept going in and out of the hospital and his physicians could not solve his recurrent fluid overload problem, he was put on hospice. By the time I first saw him, Joe could barely move or even talk without becoming short of breath. Fortunately for Joe, I knew exactly what medication adjustments were needed to safely remove his excessive fluid. Within a few months, we were able to discharge him alive from our service.
The above case (and I’ve had dozens of them) clearly shows that what’s going on in the extracellular space matters. It matters so much that to not even talk about it, in the context of biological origins, is frankly unscientific.
It also shows that my pet peeve about the absence of this discussion in the origins debate is my own fault. So, please watch this space for articles in the future on the extracellular space and ID.
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