ID is the science driver?

 It’s Intelligent Design, Not Darwinism, that Drives Scientific Progress

Casey Luskin

There’s a common objection to intelligent design that the positive case for ID helps us to answer. In his Kitzmiller v. Dover testimony, biologist Kenneth Miller referred to intelligent design as a “science stopper.”1 Similarly, in his book Only a Theory, Miller stated, “The hypothesis of design is compatible with any conceivable data, makes no testable predictions, and suggests no new avenues for research. As such, it’s a literal dead end…”2

Yet in fact, ID makes a variety of testable and successful predictions. This allows ID to serve as a paradigm guiding scientific research to make new discoveries. The list below shows various fields where ID is helping science to generate knowledge. For each field, multiple ID-friendly scientific publications are cited as examples.

How ID Inspires the Progress of Science

Protein science: ID encourages scientists to do research to test for high levels of complex and specified information in biology in the form of the fine-tuning of protein sequences.3 This has practical implications not just for explaining biological origins, but also for engineering enzymes and anticipating and fighting the future evolution of diseases.

Physics and cosmology: ID has inspired scientists to seek and find instances of fine-tuning of the laws and constants of physics to allow for life, leading to new fine-tuning arguments such as the Galactic Habitable Zone. This has implications for proper cosmological models of the universe, hinting at avenues for successful “theories of everything” that must accommodate fine-tuning, and other implications for theoretical physics.4

Information theory: ID leads scientists to understand intelligence as a cause of biological complexity, capable of being scientifically studied, and to understand the types of information it generates.5

Pharmacology: ID directs both experimental and theoretical research to investigate the limitations of Darwinian evolution to produce traits that require multiple mutations in order to function. This has practical implications for fighting problems like antibiotic resistance or engineering bacteria.6

Evolutionary computation: ID produces theoretical research into the information-generative powers of Darwinian searches, leading to the discovery that the search abilities of Darwinian processes are limited, which has practical implications for the viability of using genetic algorithms to solve problems.7

Anatomy and physiology: ID predicts function for allegedly “vestigial” organs, structures, or systems whereas evolution has made many faulty predictions of nonfunction.8

Bioinformatics: ID has helped scientists develop proper measures of biological information, leading to concepts like complex and specified information or functional sequence complexity. This allows us to better quantify complexity and understand what features are, or are not, within the reach of Darwinian evolution.9

Molecular machines: ID encourages scientists to reverse-engineer molecular machines — like the bacterial flagellum — to understand their function like machines, and to understand how the machine-like properties of life allow biological systems to function.10

Cell biology: ID causes scientists to view cellular components as “designed structures rather than accidental by-products of neo-Darwinian evolution,” allowing scientists to propose testable hypotheses about cellular function and causes of cancer.11

Systematics: ID helps scientists explain the cause of the widespread features of conflicting phylogenetic trees and “convergent evolution” by producing models where parts can be reused in non-treelike patterns.12 ID has spawned ideas about life being front-loaded with information such that it is designed to evolve, and has led scientists to expect (and now find!) previously unanticipated “out-of-place” genes in various taxa.13

Paleontology: ID allows scientists to understand and predict patterns in the fossil record, showing explosions of biodiversity (as well as mass extinction) in the history of life.14Genetics: ID has inspired scientists to investigate the computer-like properties of DNA and the genome in the hopes of better understanding genetics and the origin of biological systems.15 ID has also inspired scientists to seek function for noncoding junk-DNA, allowing us to understand development and cellular biology.16

Avenues of Discovery

Critics wrongly charge that ID is just a negative argument against evolution, that ID makes no predictions, that it is a “god of the gaps” argument from ignorance, or that appealing to an intelligent cause means “giving up” or “stopping science.” These charges are misguided. 

Ironically, when critics claim that research is not permitted to detect design because that would stop science, it is they who hold science back by preventing scientists from investigating the scientific theory of intelligent design. When researchers are allowed to infer intelligent agency as the best explanation for information-rich structures in nature, this opens up many avenues of discovery that are bearing good fruit in the scientific community.

Notes

Kenneth R. Miller, Kitzmiller v. Dover, Day 2 AM Testimony (September 27, 2005).

Kenneth R. Miller, Only a Theory: Evolution and the Battle for America’s Soul (New York: Viking Penguin, 2008), 87.

Axe, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors”; Axe, “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds”; Behe and Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues”; Axe, “The Case Against a Darwinian Origin of Protein Folds”; Gauger and Axe, “The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway”; Reeves et al., “Enzyme Families-Shared Evolutionary History or Shared Design? A Study of the GABA-Aminotransferase Family”; Thorvaldsen and Hössjer, “Using statistical methods to model the fine-tuning of molecular machines and systems.”

Guillermo Gonzalez and Donald Brownlee, “The Galactic Habitable Zone: Galactic Chemical Evolution,” Icarus 152 (2001), 185-200; Guillermo Gonzalez, Donald Brownlee, and Peter D. Ward, “Refuges for Life in a Hostile Universe,” Scientific American (2001), 62-67; Guillermo Gonzalez and Jay Wesley Richards, The Privileged Planet: How Our Place in the Cosmos Is Designed for Discovery (Washington, DC, Regnery, 2004); Guillermo Gonzalez, “Setting the Stage for Habitable Planets,” Life 4 (2014), 34-65; D. Halsmer, J. Asper, N. Roman, and T. Todd, “The Coherence of an Engineered World,” International Journal of Design & Nature and Ecodynamics 4 (2009), 47-65.

William A. Dembski, The Design Inference; William A. Dembski and Robert J. Marks II, “Bernoulli’s Principle of Insufficient Reason and Conservation of Information in Computer Search,” Proceedings of the 2009 IEEE International Conference on Systems, Man, and Cybernetics(October 2009), 2647-2652; William A. Dembski and Robert J. Marks II, “The Search for a Search: Measuring the Information Cost of Higher Level Search,” Journal of Advanced Computational Intelligence and Intelligent Informatics 14 (2010), 475-486; Øyvind Albert Voie, “Biological function and the genetic code are interdependent,” Chaos, Solitons and Fractals 28 (2006), 1000-1004; McIntosh, “Information and Entropy —Top-Down or Bottom-Up Development in Living Systems?”

Behe and Snoke, “Simulating evolution by gene duplication of protein features that require multiple amino acid residues”; Ann K. Gauger, Stephanie Ebnet, Pamela F. Fahey, and Ralph Seelke, “Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,” BIO-Complexity 2010 (2).

William A. Dembski and Robert J. Marks II, “Conservation of Information in Search: Measuring the Cost of Success,” IEEE Transactions on Systems, Man, and Cybernetics-Part A: Systems and Humans 39 (September 2009), 1051-1061; Winston Ewert, William A. Dembski, and Robert J. Marks II, “Evolutionary Synthesis of Nand Logic: Dissecting a Digital Organism,” Proceedings of the 2009 IEEE International Conference on Systems, Man, and Cybernetics (October 2009); Dembski and Marks, “Bernoulli’s Principle of Insufficient Reason and Conservation of Information in Computer Search”; Winston Ewert, George Montanez, William Dembski and Robert J. Marks II, “Efficient Per Query Information Extraction from a Hamming Oracle,” 42nd South Eastern Symposium on System Theory (March 2010), 290-297; Douglas D. Axe, Brendan W. Dixon, and Philip Lu, “Stylus: A System for Evolutionary Experimentation Based on a Protein/Proteome Model with Non-Arbitrary Functional Constraints,” Plos One 3 (June 2008), e2246.

       Jonathan Wells, “Using Intelligent Design Theory to Guide Scientific Research”; William Dembski and Jonathan Wells, The Design of Life: Discovering Signs of Intelligence in Living Systems (Dallas, TX: Foundation for Thought and Ethics, 2008).

Meyer, “The origin of biological information and the higher taxonomic categories”; Kirk K. Durston, David K.Y. Chiu, David L. Abel, Jack T. Trevors, “Measuring the functional sequence complexity of proteins,” Theoretical Biology and Medical Modelling 4 (2007), 47; David K.Y. Chiu and Thomas W.H. Lui, “Integrated Use of Multiple Interdependent Patterns for Biomolecular Sequence Analysis,” International Journal of Fuzzy Systems4 (September 2002), 766-775.

Minnich and Meyer. “Genetic Analysis of Coordinate Flagellar and Type III Regulatory Circuits in Pathogenic Bacteria”; McIntosh, “Information and Entropy—Top-Down or Bottom-Up Development in Living Systems?” 

Jonathan Wells, “Do Centrioles Generate a Polar Ejection Force?,” Rivista di Biologia / Biology Forum, 98 (2005), 71-96; Scott A. Minnich and Stephen C. Meyer, “Genetic analysis of coordinate flagellar and type III regulatory circuits in pathogenic bacteria,” Proceedings of the Second International Conference on Design & Nature Rhodes Greece (2004); Behe, Darwin’s Black Box; Lönnig, “Dynamic genomes, morphological stasis, and the origin of irreducible complexity.”

Lönnig, “Dynamic genomes, morphological stasis, and the origin of irreducible complexity”; Nelson and Jonathan Wells, “Homology in Biology”; Ewert, “The Dependency Graph of Life”; John A. Davison, “A Prescribed Evolutionary Hypothesis,” Rivista di Biologia/Biology Forum 98 (2005), 155-166; Ewert, “The Dependency Graph of Life.”

Sherman, “Universal Genome in the Origin of Metazoa: Thoughts About Evolution”; Albert D.G. de Roos, “Origins of introns based on the definition of exon modules and their conserved interfaces,” Bioinformatics 21 (2005), 2-9; Albert D.G. de Roos, “Conserved intron positions in ancient protein modules,” Biology Direct 2 (2007), 7; Albert D.G. de Roos, “The Origin of the Eukaryotic Cell Based on Conservation of Existing Interfaces,” Artificial Life 12 (2006), 513-523.

Meyer et al., “The Cambrian Explosion: Biology’s Big Bang”; Meyer, “The Cambrian Information Explosion”; Meyer, “The origin of biological information and the higher taxonomic categories”; Lönnig, “Dynamic genomes, morphological stasis, and the origin of irreducible complexity.”

Richard v. Sternberg, “DNA Codes and Information: Formal Structures and Relational Causes,” Acta Biotheoretica 56 (September 2008), 205-232; Voie, “Biological function and the genetic code are interdependent”; David L. Abel and Jack T. Trevors, “Self-organization vs. self-ordering events in life-origin models,” Physics of Life Reviews 3 (2006), 211-228.

Richard v. Sternberg, “On the Roles of Repetitive DNA Elements in the Context of a Unified Genomic– Epigenetic System”; Jonathan Wells, “Using Intelligent Design Theory to Guide Scientific Research”; Josiah D. Seaman and John C. Sanford, “Skittle: A 2-Dimensional Genome Visualization Tool,” BMC Informatics 10 (2009), 451.

This article is a modified excerpt from the recent book The Comprehensive Guide to Science and Faith: Exploring the Ultimate Questions About Life and the Cosmos. 

The world's most important corporation?

 

Another body blow to the "simple" lifeform trope?

 Quorum Sensing: A Clever Trick by Microbes

David Coppedge

You’re exploring in the dark on a secret mission. You need a dozen compatriots to initiate operations. How do you know when the minimum number is assembled, when you cannot see them or talk to them? The answer is quorum sensing: using techniques to silently count the friends near you. When you have a quorum, you start the mission.

These days, radio communication makes the imaginary secret mission a cinch. Without sight or sound, members of a team can know where their compatriots are on hand-held devices using encrypted messaging. In ordinary life, many people use apps like Apple’s “Find My Friends” to see where family members are before starting a birthday party. We take quorum sensing for granted, but we are purposeful, intelligent agents. Distributed robot systems designed by MIT use biomimetic algorithms pre-programmed into them by engineers.

Quorum sensing is used all the time by… (wait for it…) bacteria. Microbes can wait to commence an activity until a threshold density of neighboring conspecifics is detected. This skill has been observed in other microbes, like slime molds, and in higher organisms that exhibit collective behaviors, like insects, fish, and birds. Robot designers are learning tricks from the simplest of life forms: how to communicate with and respond to other unseen members of a population. Quorum sensing (QS) extends the concept of the interactome from intracellular to intercellular, converting a population of individuals into a super-organism. In this sense, a population of bacteria is a multicellular life form. This puts increased pressure on Darwinian notions of a “simple” cell. Could a lucky protocell, all alone, survive without a population of protocells able to communicate and coordinate their behaviors?

Requirements for Quorum Sensing

Consider the requirements for quorum sensing. The most rudimentary specifications include a sensor, a receptor, and a response plan. Bacteria employ QS by sending out specific molecules into the environment. On their surfaces, they post receptors for molecules from other members of their species. The incoming count is measured. When a threshold is reached, the signal triggers changes in gene expression, leading to pre-programmed actions coordinated with the other members of the swarm. These could include forming a biofilm, altering migration behavior, or switching on defensive maneuvers. Some bioluminescent microbes will only “turn on the lights” when a threshold density is detected.

Already we can see that a QS algorithm is irreducibly complex, but in real life examples, additional requirements become apparent. For instance, there is the need for “quorum quenching” — turning off the response when conditions change. The bacterium must also discern the degree of similarity of incoming signal molecules. In news about QS echoed on Phys.org, researchers from Aalto University in Finland likened the skill to understanding dialects and foreign languages:

“We did a ‘bacterial language check’ and found that bacteria using very similar languages can understand each other, just like a Dutch person might understand some German. We also tested communication between bacteria using very different languages and found that they couldn’t understand each other at all — just like a conversation between people speaking Finnish, Dutch and Arabic wouldn’t get far,” says Christopher Jonkergouw, the doctoral student who led the study. 

In the military, soldiers with different English dialects can generally understand one another to get by and continue their mission. They might even understand natives in other cultures who speak Pidgin, assisted by some gestures and facial expressions. There comes a point of “no comprendo” when the languages are too different, as anyone knows who has traveled abroad. The point is that beyond the threshold of comprehension, more is required for communication: language training, a smartphone translation app, or a human interpreter. Recall the consternation of Japanese soldiers in World War II listening in to the Navajo “code talkers” communicating American military strategies over the radio.

Bacteria Have a Similar Problem

The Aalto researchers identified over 160 bacterial “languages” spoken in molecular “words.” Molecules that are structurally similar can trigger a response up to a point, after which the bacteria do not respond. This knowledge is a first step for scientists wishing to intervene in bacterial responses like antibacterial resistance.

With these tools, the researchers have shown that we can accurately estimate the connections between bacterial languages and predict whether they can be understood. These findings will be valuable in further refining the team’s new treatment approach, and they also have implications for biotechnology — bacterial languages can be used to coordinate tasks between groups in bacterial communities, or even in bacterial microprocessors.

The team’s paper in Angewandte Chemie doesn’t use the language metaphor, but it elaborates on the methods for determining the limits of bacterial responses to similar molecules. Prior work on QS has focused on a few of these molecules, most prominently the homoserine lactones (HSLs). Like dialects, HSLs as a class include structurally similar forms, considered “cognate” — i.e., members of a family.

Here, we move beyond the commonly utilized HSL QS signalling systems and explore how chemical diversity in ligands can serve as a guiding principle to understand and circumvent non-cognate binding interactions. We explore the chemical diversity in a comprehensive set of known QS ligands and, based on the hypothesis that diversity in ligand chemical structures minimizes non-cognate interactions, experimentally assess a set of structurally similar as well as a diverging set of QS signalling systems (Figure 1). Using this approach, we significantly expand upon the known and available synthetic orthogonal QS signalling systems and provide a clear strategy towards future expansion efforts of additional synthetic orthogonal signalling systems.

Beyond the threshold of recognition, the signal molecule no longer triggers a response. The researchers “repaired” one such mutant molecule to see if the response could be regained:

Extensive screening from multiple ligation and transformation attempts generated a limited number of colonies that all contained non-synonymous mutations, resulting in amino acid substitutions. In the case of PauR, four sequenced colonies (from different ligations and transformations) all contained a point mutation in S129 a serine involved in AHL binding, within the autoinducer binding domain (Figure S2). Four clones of PluR contained non-synonymous mutations, all resulting also in amino acid substitutions. We hypothesized that constitutive expression severely affects viability in E. coli, so to overcome this, we controlled the expression of the receptor proteins with L-rhamnose (Figure 4b). This resulted in functional (and sequencing verified) constructs that we were able to experimentally assess.

It was a bit like intervening in a conversation to help a listener understand a word the speaker was mispronouncing. The mutations did not help the bacterium understand the signal. Less likely would a mutation help the listening bacterium come up with an improved response.

QS as a Life Trait

Rocks do not do quorum sensing. Could one boulder care how many others are around, using the information to initiate a programmed response? A critic might point to collective behaviors of particles in clouds, tornados, hurricanes, or other emergent phenomena. Such cases, however, do not send signals, receive signals, and respond by triggering embedded instructions. They simply respond to laws of physics. Life is different. From the smallest cell to the greatest whale or redwood tree, algorithmic processes like QS distinguish the biotic from the abiotic.

QS signalling systems are ubiquitous in prokaryotes, and novel [i.e., previously unknown] QS ligands are continually being identified. Furthermore, increasing evidence alludes to interspecies and even interkingdom signalling systems, expanding the range, scope, and complexity of intercellular signal recognition.

Within our own bodies there are examples of QS, for example in the immune system, hormone signaling, and blood clotting. Additionally, microbes in the gut use quorum sensing to respond to changes in food intake and wellness.

The authors know that QS is a characteristic of living things. They have nothing to say about Darwinian evolution, probably because we humans intuitively know intelligent design when we see it. Else why would scientists try to imitate it with engineering projects?

Cellular cooperation forms one of the defining features of higher organisms. The differentiation into various cell types allows cells to divide tasks and specialize. Prokaryotes have also developed methods to organizemore complex architectures. Bacteria utilize small molecules in quorum sensing (QS) as a form of intercellular signalling, which enables them to synchronize and organize behaviour on a population-wide or even community-wide level to facilitate bacterial biofilm architectures, promote plant colonization, or commence the production of a range of virulence factors. Consequently, these intercellular signalling systems have attracted widespread interest in biotechnology, where the potential to control community-wide responses has sparked innovations in microbiome therapeutics, microbial factories, and cellular computing.

Jonathan McLatchie wrote about quorum sensing here in 2010. His article embedded a TED talk by Bonnie Bassler that is worth watching again. Denyse O’Leary mentioned QS briefly in 2021 as an indicator of cognition, but there has been little mention of it otherwise in these pages. I hope this review of the latest news on QS will raise more awareness about this fascinating phenomenon. Perhaps it will prompt some ID scientists to take the lead in de-Darwinizing it for human health. In the meantime, all of us can use it as one more illustration of specified complexity and low probability that justifies the design inference

On the forgotten holocaust.

 

"Not so fast" re: saltation in Darwinism

 Hitting the Brakes on “Rapid Evolution”

Andrew McDiarmid

Evolutionary biologist Richard Lenski hopes to demonstrate Darwinian evolution in action. But one humble scientist from Northern Idaho says not so fast! On this episode of ID the Future, host Eric Anderson concludes his “Why It Matters” interview with microbiologist Dr. Scott Minnich. 

In Part 2, Dr. Minnich critiques Lenski’s famous Long Term Evolutionary Experiment. Through experiments of his own, Minnich has shown how the practical results of Lenski’s project on E. coli are easily repeatable under different conditions, and how some key changes to E. coli are even reversible, both of which speak more to an organism’s pre-existing capabilities than to a Darwinian explanation. “Overall, [Lenski’s] E. coli haven’t generated anything new,” observes Minnich. “They’re getting rid of stuff they don’t need…they have hyper mutational rates…but in the long run, that’s not an advantage, because you’re just going to acquire too many mutations, and that’s the road to extinction.”

Dr. Minnich also cautions that the authority of science can be abused, sharing his personal experience of being tasked by the Defense Intelligence Agency to look for biochemical weapons in Iraq. In the end, one of the things that most fascinates him about design in nature is DNA, with E. coli’s code-like logic that reminds us of the logical system operations programmed by human engineers.

Download the podcast or listen to it here. This is the second of a two-part conversation. Listen to part 1, 

On the irreducible complexity of sleep

 Sleep — Designed for Our Good

Eric Hedin

The other day, when I awoke from a restful sleep, the thought occurred to me that sleep, as an important part of our physical lives, holds some deep evidence of design. 

In reviewing research on sleep, I found that a common but somewhat surprising result is the acknowledgement of how incomplete our understanding is of why we sleep in the first place. 

Despite the fact that it’s been a universal of human experience for our entire existence as a species, it remains one of science’s greatest mysteries.1

Although it is apparent that humans need sleep, the current understanding of precisely why sleep is an essential part of life is still yet to be determined. We might suggest that the primary value of sleep is to restore natural balances among neuronal centers, which is necessary for overall health. However, the specific physiological functions of sleep remain a mystery and are the subject of much research.2

Darwinian evolution credits animal traits such as strength, speed, flight, and prowess to the selective mechanism of survival of the fittest (never mind how those complex functions arose in the first place), but survival of the unconscious? How reasonable is that?

Surely natural selection would weed out the unfit who fall prey in sleep and would favor those able to stay awake, wouldn’t it? Yet that is not the case in insects, reptiles, birds, mammals or humans.3

An Obstacle to Understanding

I would suggest that the evolutionary mindset operates as a major obstacle to the scientific understanding of sleep. In presupposing that all animals evolved from a common ancestor and that the universal biological need for the sleep-wake cycle evolved along with all organisms, two unsupported assumptions are exposed. One is that “survival of the fittest” has selected for the counterintuitive process of regularly going unconscious, and the other is that Darwinian mechanisms have the capacity to generate the high levels of information within the designed systems inherent in the process of sleep.

…if sleep doesn’t serve some vital function, it is the biggest mistake evolution ever made.4

Debate rages over why all but the simplest of animals have evolved to spend so much of their lives unconscious. One idea is that sleep conserves energy, but studies have shown we burn almost as many calories snoozing as we do when we are awake, so that seems unlikely.

Unfortunately, however, evolutionary theories are hard to prove, so for the moment we are left wondering how sleep emerged in the first place.5

Various studies have yielded some clues as to why we need sleep, based on physiological processes that occur during sleep. 

Researchers discovered that cells in the brains of sleeping mice shrink, allowing cerebrospinal fluid — the colourless liquid that circulates in the brain and spinal cord — to flow more easily, sweeping away debris that builds up around active cells during the day. This is carried to lymph glands and flushed out of the body. So perhaps sleep is vital because without it, these toxic by-products build up in the brain. The idea that sleep cleans up our brains is hard to test…6

Organisms without brains also exhibit evidence of a rhythm of sleep, revealing that even simple nerve responses to external stimuli may overtax the body without some regular period of respite.7

But although creatures with more primitive nervous systems don’t sleep quite the same way as more complex animals, they do in fact display regular sleeping behaviors.8

To Sleep, Perchance to Dream

Psychological studies reveal that our brains utilize the sleeping state to organize sensory information and thoughts received during waking hours.

During sleep, our brains sort through information taken in during the day, decide what to store, and make connections between new facts and memories. It is possible that dreams help with this…9

“Dropping off,” as we sometimes call going to sleep, involves a cascade of physiological modifications within our bodies that belies the seeming simplicity of the act of closing our eyes for a rest. 

Sleep is an extremely complicated process that consists of more than simply closing one’s eyelids and counting sheep. It is an active state of unconsciousness produced by the body where the brain is in a relative state of rest and is reactive primarily to internal stimulus. The exact purpos

An abbreviated description of just a few of the necessary processes for regulating sleeping and wakefulness are presented below. Sleep stages are distinguished by rapid-eye movement (REM) and non-REM stages.

Sleep-Promoting Processes

GABA [Gamma-aminobutyric acid] is the primary inhibitory neurotransmitter of the central nervous system, and it has been well established that activation of GABA-a receptors favors sleep. Sleep-promoting neurons in the anterior hypothalamus release GABA, which inhibits wake-promoting regions in the hypothalamus and brainstem. Adenosine also promotes sleep by inhibiting wakefulness-promoting neurons localized to the basal forebrain, lateral hypothalamus, and tuberomammillary nucleus.11

Wakefulness-Promoting Processes

Neurochemicals such as acetylcholine (Ach), dopamine, norepinephrine, serotonin (5-HT), histamine, and the peptide hypocretin maintain the waking state. Cortical ACh release is greatest during waking and REM sleep and lowest during NREM sleep…. The noradrenergic cells of the [locus coeruleus] inhibit REM sleep, promote wakefulness, and project to various other arousal-regulating brain regions, including the thalamus, hypothalamus, basal forebrain, and cortex.

Circadian rhythms, which begin to develop in humans at 2-3 months of age, follow a 24-hour cycle and affect several biological functions, including sleeping and waking.

The sleep cycle is regulated by the circadian rhythm, which is driven by the suprachiasmatic nucleus (SCN) of the hypothalamus. GABAergic sleep-promoting nuclei are found in the brainstem, lateral hypothalamus, and preoptic area.12

Transitions between sleep and wake states are orchestrated by multiple brain structures, which include:

Hypothalamus: controls onset of sleep

Hippocampus: memory region active during dreaming

Amygdala: emotion center active during dreaming

Thalamus: prevents sensory signals from reaching the cortex

Reticular formation: regulates the transition between sleep and wakefulness

Pons: helps initiate REM sleep. The extraocular movements that occur during REM are due to the activity of PPRF (paramedian pontine reticular formation/conjugate gaze center).13

As Steve Laufmann and Howard Glicksman lucidly describe in their recent book, Your Designed Body, a “push-pull principle” dominates in the proper regulation of many critically important bodily systems. Our body’s sleep-wake cycle exhibits this type of complex engineering design.

The mechanism through which sleep is generated and maintained is more of a balance between two systems located within the brain: the homeostatic processes, which are functionally the body’s “need for sleep” center, and the circadian rhythm which is an internal clock for the sleep-wake cycle.

Since the regulatory processes producing sleep and the return to wakefulness involve the coordinated activity of multiple brain structures and numerous neurotransmitters, calling it all irreducibly complex seems like quite the understatement. If getting to sleep is necessary for survival, returning to wakefulness is undeniably more so. All aspects of the process of sleeping and waking need to be in full operation before this “evolutionary mystery” could impart any survival advantage. For sleep to be able to accomplish its function of restoration and refreshment for body and mind, without leaving us to languish in the “land of nod,” is evidence of an intelligent designer whose purposes work for our blessing.14

Notes

“The Mystery of Sleep,” Penn Medicine News.

Aakash K. Pate, Vamsi Reddy, Karlie R. Shumway, John F. Araujo, “Physiology, Sleep Stages” (September 7, 2022).

“Sleep on It: Design in the Subconscious Brain,” Evolution News.

“Why do we sleep?” BBC Science Focus Magazine.

“The mysteries of sleep: everything we don’t know about why we snooze,” BBC Science Focus Magazine.

“Why do we sleep?” BBC Science Focus Magazine.

“The Simplest of Slumbers,” Elizabeth Pennisi, Science.

“The Mystery of Sleep,” Penn Medicine News.

“Why do we sleep?” BBC Science Focus Magazine.

Joshua E. Brinkman, Vamsi Reddy, Sandeep Sharma, “Physiology of Sleep” (April 3, 2023).

Aakash K. Pate, Vamsi Reddy, Karlie R. Shumway, John F. Araujo, “Physiology, Sleep Stages” (September 7, 2022).

Ibid.

Ibid.

“In peace I will both lie down and sleep; for you alone, O Lord, make me dwell in safety.” (Psalm 4:8 ESV)

Musing on the the thumb print of JEHOVAH.

 Stephen Meyer and Spencer Klavan on the Book of Nature: Is There an Author?

David Klinghoffer

At a Chanukah dinner over the weekend I met a man who had a passing awareness of intelligent design. When we got to talking about it, he criticized Stephen Meyer for being “disingenuous.” Why? Because, he informed me, “Meyer clearly believes that ID points to God but he won’t come out and say so directly.” Hah! Evidently, my new acquaintance hadn’t run across Dr. Meyer’s latest book, Return of the God Hypothesis: Three Scientific Discoveries That Reveal the Mind Behind the Universe. I told him about it and was glad the next day to be able to hand him a copy.

I thought of that as I was listening to a fascinating interview with Meyer on the Young Heretics podcast. The host, Spencer Klavan, is himself a very interesting person — a classicist with a love of science and an openness to considering challenging ideas. He calls Return of the God Hypothesis “one of the must-read books of the century thus far.” He and Meyer review several centuries of the history of science. They observe that intelligent design was the default understanding of nature and the cosmos — until the hostile takeover by Darwinian materialism in the middle of the 19th century. With new discoveries since then in biology and cosmology, science has been recovering the idea of purpose working through nature that it had lost.

And for our culture, that’s none too soon. As Meyer notes, citing new research from the Harvard Graduate School of Education, young adults are in a mental health crisis, beset by anxiety and depression tied to a failing sense of “meaning and purpose.” Perhaps knowing that the universe itself bears evidence of meaning and purpose can help address the roots of the crisis, summarized by psychologist Viktor Frankl in his classic 1946 book Man’s Search for Meaning.

The Book of Nature

Klavan, with his expertise in classical languages, is an insightful interviewer. He points out that the verse in Psalm 19 – “The heavens declare the glory of God, and the firmament showeth His handiwork” — uses a Hebrew verb, translated as “declare,” that shares a root with the word sefer, a “book.” The book of nature testifies to its author. And the Greek word cosmos, from which we get “cosmology,” comes from a verb that means to order or direct. So the study of cosmic origins fittingly reveals not just mindless material processes but, ultimately, the purposeful mind behind that ordering.

This is a terrific conversation between Meyer and Klavan, whose own recent book is How to Save the West: Ancient Wisdom for 5 Modern Crises. Listen to it here on Apple Podcasts or here on the episode website.

The enlightenment was not particularly enlightening? Pros and Cons.

OOL science keeps raiding I.D'S tool kit?

 Cronin-Tour at Harvard: How Researchers Smuggle Design into Their Theories

Brian Miller

I recently watched the debate hosted at Harvard between origins researcher Lee Cronin and synthetic chemist James Tour on the state of research into the origin of life. Günter Bechly already contrasted Tour’s presentation which focused on the most relevant chemistry with Cronin’s presentation that simply described his Assembly Theory while completely avoiding the details of the chemistry. Here, I will build upon Bechly’s insightful analysis by illustrating how all attempts by Cronin and others to justify belief in an undirected origin of life smuggle design into their theories in the guise of natural selection and self-organization. 

Cronin’s Assembly Theory

Cronin presented his Assembly Theory as a framework for understanding life’s origin. I believe he is correct but not in the way he intends. He describes Assembly Theory as a method for detecting life by identifying signatures of biological complexity. It quantifies the amount of biological information or “assembly” generated or residing in a biological system. He acknowledges that natural processes do not produce biological information or order, which is why the appearance of functional information and purposeful order points to life. His framework appears to function as a crude form of William Dembski’s design-detection apparatus presented in both editions of The Design Inference (here, here). The difference is that Cronin avoids the conclusion of design by assuming that the order is generated by natural selection. 

The problem is that so-called natural selection cannot commence until after a fully functional cell capable of high-accuracy self-replication already exists. Hypotheses of simple molecules self-replicating and evolving toward life are completely implausible for reasons Tour and I previously outlined (here, here). Even leading origins researcher Steven Benner acknowledged in his article “Paradoxes in the Origin of Life” that the spontaneous emergence of self-replicating molecules appears impossible. 

Self-Organization and Metastable States 

During the dinner conversation, physicist Randy Isaac and another physicist added self-organization to natural selection as life-creation mechanisms. They asserted that self-organizational process can generate a series of metastable states that could lead to life (here). 

Again, this claim is not based on evidence. Steven Benner and Michael Russel, another leading origin-of-life researcher, believe on faith that life-generating self-organizational processes must exist, but they acknowledge that the empirical evidence and everything known about physics and chemistry suggest that they cannot exist. Chemical systems never move toward life but always away from it. Experiments that generate patterns that are even remotely life-like only do so because of the systems being carefully engineered with that purpose in mind. 

Misleading the Public

Origins researchers intuitively recognize that life displays clear evidence for design, but their philosophical commitments prevent them from acknowledging where the evidence naturally leads. Instead, they invoke natural selection and self-organization not as real processes supported by empirical evidence but as secular demigods capable of any feat of creative genius. The public is easily misled since the bait-and-switch is concealed behind technical language that is impenetrable for the layperson. 

James Tour and others who have carefully studied the technical literature quickly came to realize that nearly all origin-of-life studies fall into one of three categories (here, here):

Prebiotic experiments: This class starts with molecules that could have existed on the early Earth. Energy is applied, and the product is analyzed. These studies consistently generate enormous numbers of molecules where only a tiny percentage is relevant to life. The large numbers of extraneous molecules prevent long chains of amino acids, nucleotides, or sugars from ever forming. All origins hypotheses collapse at this point. 

Synthesis experiments: This class typically starts with carefully chosen molecules in unrealistically high concentrations and purities. Experimental conditions are carefully designed to yield some life-relevant products such as amino acid chains. If such experiments started with realistic conditions, biological products would form in such trace quantities that they could never support future steps toward life. In addition, they would decompose on the early Earth into simpler molecules long before they would ever find a staging ground for a cell. 

Simulations and mathematical models: This class creates a simulation or mathematical model for some stage of an origin-of-life scenario. The models only produce interesting results if highly unrealistic parameters and starting conditions are employed. They have no relevance to what could ever have occurred on the early Earth. 

Claims that any of these classes of experiments demonstrates the plausibility of life forming through undirected processes represent gross exaggerations of their significance and media-driven hype. 

Tour also described how the public has been greatly misled by such unrealistic predictions as researchers creating life in a lab in a manner of years. Cronin attempted to downplay the hyperbole by citing other examples of researchers’ failed predictions, but the examples he cited pale in comparison to the highly misleading claims Tour mentioned. Such claims are comparable to a researcher discovering a new design for a battery and then claiming his research would allow NASA in a decade to colonize a planet in another galaxy. The problem is that presenting the truth about the evidence to the public would threaten the stranglehold that cherished materialist philosophies maintain over many institutions. 

On identifying the thumb print of JEHOVAH.

 

Loaded dice?

The thumb print of JEHOVAH and the foundation of science.

John Lennox: Against the Tide of Atheism

Evolution news 

On a classic episode of ID the Future, philosopher of science Dr. Stephen Meyer continues his conversation with Oxford mathematician and philosopher Dr. John Lennox about the recent documentary film Against the tide: Finding God in an Age of Science. 

In Part 2, Lennox talks about discovering the damage atheism does to people, by seeing it firsthand in Communist Eastern Europe and the former Soviet Union, and seeing what it does to rationality itself. He notes that if atheists like Richard Dawkins knew firsthand what hard atheism does to a society, they’d likely be a lot more careful to evaluate their position: “They are living on the basis of the Judeo-Christian legacy in culture,” says Lennox, “that founded the universities they worked in…and afforded them the luxury of the freedom to speak about these things.” Lennox learned that atheism in totalitarian regimes shuts down intellectual freedom of inquiry, a lesson that would prove useful to him in his later interactions with atheists in debate.

Lennox relates some of his experiences with famous religiously skeptical scientists, describing how he emphasized to these thinkers that the Judeo-Christian worldview did much to give us science. When skeptical scientists ask him how Christianity could have anything to say to science, Lennox is always ready with an answer. 

Download the podcast or listen to it here.

IL Duce vs. The Dons.

 

Pseudoscience is waging lawfare against science?

 

Pawn takes Knight?

 

No justice for the watchmen?

 

Against reductionism?

 Against the Tide: John Lennox and Stephen Meyer

Evolution news

Can one person push back against the strong currents of atheism, materialism, and naturalism so evident in academia and the public square today? On a classic episode of ID the Future, philosopher of science Dr. Stephen Meyer begins a three-part conversation with Oxford University mathematician and philosopher Dr. John Lennox about his recent documentary film Against the Tide: Finding God in an Age of Science. Lennox shows that one person can indeed push back when armed with knowledge, wisdom, and respect.

As Lennox explains, he grew up as the child of a uniquely non-sectarian Christian family in Northern Ireland, with parents who encouraged him to question broadly, read widely, and respect every person as a creature made in the image of God. Lennox tells of his encounters with C. S. Lewis at Cambridge University, relates a humorous story in which atheist Peter Atkins gave him the title of one of his books, and describes his front-row seat as he watched the scientific atheism of the 1960s transform into the aggressive and contemptuous New Atheism of more recent years — a story that includes Lennox’s own debate with Richard Dawkins.

Download the podcast or listen to it here.

The thumb print of JEHOVAH is pareidolia? Pros and Cons.

 

Islam is compatible with the republic? Pros and Cons.

 

Mapping the limits of evolution?

 William Whewell: Statesman of Science

Andrew McDiarmid

Are there natural limits to biological change? Is the evidence for design in nature well founded? On a new episode of ID the Future, concludes a conversation with historian of science Michael Keas about Christianity’s influence on the development of modern scientific inquiry.

Keas discusses the legacy of pioneering 19th century philosopher of science William Whewell. Considered the greatest methodologist of science during his lifetime, Whewell helped other scientists think through the implications of their work and was highly regarded by his contemporaries, including Charles Darwin. Keas contrasts Whewell’s perspective of the evidence for design with that of Darwin and discusses the importance of embracing a healthy form of methodological naturalism and methodological pluralism in scientific inquiry. 

Whewell “is a great example of an earlier leading figure in science doing something that today, the majority of scientists would not look too kindly on and maybe would even try to ostracize as being anti-science,” says Keas. Whewell demonstrated methodological pluralism, a view of scientific inquiry that allows for both intelligent and unintelligent causes and a plurality of causal agents, as long as the evidence supports it. Keas argues that we can adopt the same approach today.

Download the podcast or listen to it here 

America's forgotten war?

 

James Tour vs. The sphinx : post game commentary

 A Few Thoughts on the Cronin-Tour Debate

Gunter Bechly

Recently, the Cambridge Faculty Roundtable hosted a very interesting debate at Harvard about science and the origin of life. The main participants were chemistry professors Dr. James Tour and Dr. Lee Cronin. Tour is an organic chemist at Rice University and an outspoken critic of the current state of origin-of-life research, while Cronin is a British chemist and a prominent researcher in the field of chemical self-organization and abiogenesis. Cronin wants to reverse-engineer life from the bottom up and create artificial life, rather than explain the historically contingent event of the actual origin of the first living cell. 

Unlike James Tour’s earlier debate with YouTuber Dave Farina, this event was a very civil and respectful interaction between two distinguished scientists, who both have interesting and important things to say. Therefore, I want to use this opportunity to offer some personal thoughts. Since biochemistry, molecular biology, and information theory are outside my field of expertise, I will restrict my commentary to a more general issue that I found quite revealing. It is very much relevant to the status of intelligent design theory.

“False Claims by Cronin and His Group”

In the debate, Tour insisted on precise chemistry, while Cronin elaborated on vague ideas of Assembly Theory and selection doing its thing. Cronin proposed Assembly Theory in 2017. But it was only the recent publication on the subject in the prestigious journal Nature (Sharma et al. 2023) that made a real splash, generating headlines around the world. Tour quite correctly pointed out that Assembly Theory does not bring us a single step closer to understanding how a first cell, a first replicator, or even just the main building blocks of life could form under the conditions of the early Earth. Tour’s critique is echoed by other scientists including Dr. Hector Zenil at Oxford University. As Zenil wrote in an update to his article for Medium, “The 8 fallacies of Assembly Theory”:

While I may not share all of Prof. Tour’s set of beliefs regarding religion (he did not use any religious arguments to refute Cronin’s claims), I think he did a service to science and scientific practice by pointing out the many false claims by Cronin and his group.

A Precise Level of Complexity

Nevertheless, Assembly Theory has some interesting aspects. The most intriguing is that it provides an objective measure of the complexity of parts that arguably allows for a reliable empirical detection of life and its products, distinguishing it from any results of abiotic processes. This has important implications — for example, in the search for extraterrestrial life on exoplanets. However, this measure raises a question that was not addressed by Cronin: under the theory of an unguided process of chemical and biological evolution, should such a threshold of complexity, clearly identifying life and its activities, even be expected? 

I submit that it should not be expected at all. On the contrary, we should expect a smooth grade of complexity between abiotic and biotic processes, that does not allow for a clear distinction in the fuzzy transitional region. The fact that there seems to be a precise level of complexity, above which there is only life and its products and below which there is not, indicates to me a saltational phase transition. Such a transition does not fit with Cronin’s suggestion of an origin through unguided selection mechanisms.

Cronin’s Core Fallacy

A similar intuition seems to have pushed Cronin to commit the core fallacy that struck me in his presentation. I would call it the “If it were not” fallacy, or the fallacy of a ”naturalism of the gaps.” The fallacy admits that we have no clue how life originated. But it suggests that we will just have to wait, maybe for decades more of research, to see the problems solved. These twin fallacies are of course rooted in Cronin’s preferred worldview, which is explicitly one of materialist naturalism.

Cronin does not reason from the evidence with an unbiased inference to the best explanation. Instead, he excludes a priori the alternative of intelligent causation and restricts his search to material causes alone. Here is what Cronin said in his opening statement (timecode 1.04.30-1.04:50): “If we weren’t invented by some, … hmmm …well, if we are not in Elon Musk’s simulation and we are not some other fictitious creation, then there are other processes going on …”. This “If it were not” fallacy is a combination of the fallacy of the excluded middle and the fallacy of begging the question. But Cronin cannot justify his a priori exclusion of design with an appeal to methodological naturalism or to the scientific method. That is because Cronin himself mentioned in his talk fully naturalistic alternatives for intelligent causation such as the simulation hypothesis. 

His fallacy is therefore not rooted in a mere methodological naturalism but rather in a full-fledged ontological naturalism. He explicitly thinks that meaning, purpose, life, consciousness, memory, etc., are all emergent from material processes. In a previous conversation with James Tour he even made the absurd statement, “I don’t think consciousness exists” (see this episode of Unbelievable? with host Justin Brierley at timecode 1:11:28). In the recent debate, Cronin explicitly and unequivocally identified as a materialist, which fully explains his “If it were not“ fallacy and his “naturalism of the gaps.”

Excluding Intelligent Design

In my view this perfectly exemplifies the dynamic in modern science and its mainstream opposition against intelligent design theory: intelligent causation is a priori excluded from the set of allowed hypotheses under the false pretense of methodological naturalism. But this exclusion is actually rooted in ontological naturalism and crude materialism. The latter is an unfalsifiable metaphysical belief that has no justification for serving as an underlying paradigm for science. 

Even worse: the growing consensus in theoretical physics holds that spacetime is not fundamental but emergent from quantum entanglement. This implies an ultimate reality of quantum information beyond space and time. And that clearly contradicts materialism and reveals it to be an obsolete and anachronistic worldview, rooted in a 19th-century picture of a clockwork universe with billiard-ball-like elementary particles. Even if we were to grant for the sake of the argument that methodological naturalism is a core tenet of the scientific method, intelligent design is a valid form of causation that should and ultimately will return to the mainstream of science. When it does, we will be permitted to follow the evidence wherever it leads, without worldview blinders.

It's complicated IX

 

The great war:matrix of the mideast's turmoil?

 

Against "Christian" nationalism.

 

Global war on free speech?

 

The second horseman returns to the western hemisphere?

 

Specified complexity squared?

 The Interactome Multiplies Specified Complexity

David Coppedge

One aspect of the “Unknome” is starting to become clearer: the interactome. If the Unknome refers to the set of components in a cell we know nothing about, the Interactome refers to “the whole set of molecular interactions in a particular cell.” A recent paper has created a “wow moment” about the interactome. It found that there are far more interactions between proteins than previously thought.

A New Method

Publishing in Nature, seven researchers from Germany and Denmark explored the “social and structural architecture” of proteins in a eukaryotic organism. Michaelis et al. created a new method for investigating interactions between proteins. The interactome, they say, has been studied for two decades, but work has been tediously slow due to procedural challenges.

The large-scale study of cellular interactomes using mass spectrometry-based proteomics dates back over 20 years, culminating in 2 studies in which nearly half the expressed yeast proteome was successfully purified with identified interactors. These datasets have been mined extensively, leading to a network-based view of the cellular proteome. Given the importance of the interactome for functional understanding and the substantial improvements in mass spectrometry technology during the past decade, we set out to generate a substantially complete interactome of all proteins present in an organism in a given state. We made use of an endogenously GFP-tagged yeast library containing the 4,159 proteins that are detectable by fluorescence under standard growth conditions. 

They used a refined “pull-down” method to “bait” known proteins tagged with green fluorescent protein (GFP) and then observe what other “prey” proteins connected to them. 

Miniaturization and standardization of the workflow in combination with an ultra-robust liquid chromatography system with minimal overhead time coupled to a sensitive trapped ion mobility mass spectrometer utilizing the PASEF scan mode resulted in very high data completeness across pull-downs. This workflow required only 1.5 ml instead of litres of yeast culture, provided a constant throughput of 60 pull-downs per day and enabled the use of the same conditions for soluble or membrane proteins of vastly different abundances 

The new work doubles the number of proteins studied and triples the number of interactions found “compared with existing interactome maps.” They checked and cross-checked the data for accuracy. The results were startling. 

The replicate GFP pull-down measurement in the 4,147 yeast strains resulted in the enrichment of 82% of the baits (Extended Data Fig. 1). Our mass spectrometry data provided statistically significant evidence for more than 30,000 physical interactions, corresponding to an average of 15.8 interactions per protein. Most were supported by forward pull-down (35%), followed by forward pull-down and significant prey correlation (29%), whereas nearly all interactions with both forward and reverse evidence also had significant correlation z-scores (95%) 

More than two-thirds of the interactions discovered were novel, they said, not previously reported. While a small percentage of the baits did not retrieve “prey” proteins, that doesn’t mean they do not interact. 

Altogether, based on the total of 4,403 identified yeast proteins, with 74.1% having at least two interactors, 15.1% had one and only 10.8% had no discernable interaction partner. To investigate whether the latter set is truly ‘non-social’ or is an artefact of expression level or its tag position, we performed our workflow on a subset of the proteins using N-terminal tagged strains with identical promoters (Extended Data Fig. 5). This yielded additional interactors for about half of the proteins. Notably, the overall average of identified interactors in this set was around 2, compared with 16 in the main dataset, indicating that this set of proteins was indeed poorly connected (Supplementary Fig. 2). Although reciprocal tagging was beneficial, complexes with higher numbers of interactions would already be picked up by the redundancy effect of our screen. Given that some of our baits will have context-dependent interactions that are not captured here, our estimates are conservative and we conclude that almost all yeast proteins are ‘social’.

Remember, This Is Just Yeast

Keep in mind that all these 30,000+ interactions between 4,159 proteins are taking place in yeast — the smallest and simplest of eukaryotes! One can only imagine the enormous number of interactions taking place in the cells of higher organisms possessing tens of thousands of proteins. In complex multicellular organisms like us, furthermore, interactions extend upward into additional dimensions: between cells, between tissues, between organs, and between organisms.

This nearly saturated interactome reveals that the vast majority of yeast proteins are highly connected, with an average of 16 interactors. Similar to social networks between humans, the average shortest distance between proteins is 4.2 interactions.

The findings from Michaelis et al. blow the lid off any notion of “simple” cells. Stationary diagrams of cells tend to depict the parts as loners: a mitochondrion here, a ribosome there, a vacuole over yonder. This work shows that the parts are in a buzzing hive of activity, with everything communicating, touching, releasing, migrating, and reconnecting. By analogy, think of a still picture of a city compared to a time-lapse video of the scene, with cars and people moving about in a multitude of ways to talk, work and accomplish individual and collective goals. 

The Social Network

This paper also blows the lid off notions of cellular “junk.” If so-called “junk DNA” were generating “junk proteins,” much of the cell would be like hordes of the jobless on the streets taking up space and wasting resources. Instead, these proteins all have places to go and things to do. Everyone is contributing to the success of the social network. The unemployment rate in a cell is so low, it may not even be measurable. “The high connectivity of most proteins organizes almost all of them (3,839) into a single giant connected component,” the authors state, “accompanied by 41 small components (88 proteins)” acting, we might portray, like subcontractors. 

If so, there are no unemployed proteins. The situation recalls to mind the ENCODE project that found over 80 percent of the genome was transcribed. And the closer they looked, the more they found function in what was considered genetic junk.

The Design Inference

The interactome can be added to the huge list of biological phenomena exhibiting the two requirements for the design inference: specification and low probability. Explained in the newly expanded and revised edition of The Design Inference by William Dembski and Winston Ewert, those two qualities in every phenomenon — as evidenced by each case in which we have access to its history — rule out chance and natural law, leaving intelligent design as the inference to the best explanation. The “interactome” in a large company making jets or cars, for instance, would never come about by the law of electrodynamics or by random groups of people finding themselves in the same building. The purpose preceded the parts and actors.

Critics of ID try to carve out biology as a special case due to the presumed stepwise gains of natural selection. In the Introduction their book, Dembski and Ewert face the claim that natural selection is a designer substitute, a blind watchmaker that can climb Mount Improbable

Since the publication of the first edition of this book, the debate over the design inference and its applicability to evolution has centered on whether such gradual winding paths exist and how their existence or non-existence would affect the probabilities by which Darwinian processes could originate living forms. Design theorists have identified a variety of biological systems that resist Darwinian explanations and argued that the probability of such systems evolving by Darwinian means is vanishingly small. They thus conclude that these systems are effectively unevolvable by Darwinian means and that their existence warrants a design inference. In this book, we recap that debate and contend that intelligent design has the stronger argument.

The interactome adds more real-world evidence for the stronger argument.

Steelmanning design denial?

 

Yet more on the future of energy

 

21st Century alchemy.

Maybe if We Throw Enough Models at the Origin of Life..

Denyse O Leary

 

some of them will stick? This month's issue of The Scientist offers a look at "some of the most current origin-of-life science, from new research on how RNA may have been assembled from precursor molecules to what we now know about our last universal common ancestor." That ancestor, we are assured, is "not [Darwin's] 'primordial form,' but rather a sophisticated cellular organism that, if alive today, would probably be difficult to distinguish from other extant bacteria or archaea."

So one and a half centuries of research have not yet turned up a single entity that, like Thomas Huxley's hoped-for Bathybius haeckelii, is on its way to becoming life? Hardly for lack of trying! Here is a whirlwind tour of the waterfront:

Arsenic world: In December 2010, NASA researchers reported that they had taught microbes to metabolize arsenic instead of phosphorus, demonstrating that life could arise from unexpected chemicals, perhaps elsewhere in the galaxy. (Some researchers have suggested chlorine life instead.) Most researchers were unconvinced. In 2011, Science published eight articles questioning NASA's study in a single edition and arsenic-based life featured as one of The Scientist's top ten scandals of 2011.

Clay world: Some theorists argue that clay (or clay hydrogels) can select for molecules that can self-organize. The Scriptural associations of clay were a gift to science writers; the details did not impress researchers. Information theorist Hubert Yockey pointed out that clay crystal structures just repeat the same information indefinitely. By contrast, life's minimum information density is somewhere around the level of DNA. OOL theorist Leslie Orgel (1927-2007) said it wouldn't work for RNA either: If clay had the structural irregularities needed to enable RNA to emerge, it probably wouldn't reproduce it accurately.

Lagoons on the early Earth: Stanley Miller (1930-2007) of the textbooks' Miller-Urey experiment believed that the conditions on early Earth's beaches could foster pre-life reactions because chemicals would concentrate more there than out at sea. But Robert Shapiro, proponent of the "metabolism first" model, complained that "a large lagoon would have to be evaporated to the size of a puddle, without loss of its contents, to achieve that concentration. This process is not thought to occur today." He added, with an apparent touch of impatience,

The drying lagoon claim is not unique. In a similar spirit, other prebiotic chemists have invoked freezing glacial lakes, mountainside freshwater ponds, flowing streams, beaches, dry deserts, volcanic aquifers and the entire global ocean (frozen or warm as needed) to support their requirement that the "nucleotide soup" necessary for RNA synthesis would somehow have come into existence on the early Earth.

Metabolism first: Robert Shapiro (1935-2011) questioned Leslie Orgel's RNA world because of "the extreme improbability" that such a long, complex molecule as RNA would spontaneously arise and initiate life. His doubts earned him the title, Dr. No. Aspiring to somehow become Dr. Yes, he offered a model that life began via small molecules with a simple metabolism and progressed from there, hence "metabolism first." He hoped, among other things, to vindicatethe idea that "There's nothing freaky about life; it's a normal consequence of the laws of the universe."

Researcher Eric Smith, a physicist at the Santa Fe Institute, offers a more recent model of early metabolism: "It seems likely that the earliest cells were rickety assemblies whose parts were constantly malfunctioning and breaking down. ... How can any metabolism be sustained with such shaky support? The key is concurrent and constant redundancy." Or "millions of years of a poor replicator", as a summary article in Science put it, leaving unclear how hits could have mattered in those days but misses didn't.

"RNA first" proponent Leslie Orgel responded irritably to Shapiro's metabolism first model, "solutions ... dependent on 'if pigs could fly' hypothetical chemistry are unlikely to help." Near the end of his life, Orgel had perhaps forgotten that he himself once co-authored a paper with Francis Crick speculating that extraterrestrials might have started life.

Numerous less publicized models wallop through the science press, on the hope, perhaps, of a lucky strike: For example, not-obviously-promising substances such as hydrogen, ammonia, hydrogen cyanide, formaldehyde, or peptides, possibly kick started life. Maybe metals acted as catalysts. Or mica sheets. Otherwise, cold temperatures or ice helped life get started, despite the fact that cold reduces chemical reaction speed. Or a high salt environment. Or hot springs. No surprise that science writer Colin Barras observes that origin of life is "a highly polarised field of research." Most fields have only two poles, not twenty.

One model is noteworthy for the fact that it is the closest that origin of life theorists have come so far to an ancient pagan creation myth. Yet it was published in a popular science magazine (New Scientist):

Once upon a time, 3 billion years ago, there lived a single organism called LUCA. It was enormous: a mega-organism like none seen since, it filled the planet's oceans before splitting into three and giving birth to the ancestors of all living things on Earth today. ... LUCA was the result of early life's fight to survive, attempts at which turned the ocean into a global genetic swap shop for hundreds of millions of years. Cells struggling to survive on their own exchanged useful parts with each other without competition -- effectively creating a global mega-organism.

How did it all work? "It was more important to keep the living system in place than to compete with other systems."

Really? More important for whom? Who then existed for life to be more important to? The mega-organism itself? But that would imply selfhood and purpose. If selfhood and purpose were present at the origin of life, why is design a problem and not a solution?

 

The rise and fall of the Castle.

 

Scouting for truth vs. Fighting for truth.