Podcast appearances and mentions of Francis Crick

Most leading scientists agree that the old idea that life on Earth sprang into existence thanks to some happy accident 3.7 billion years ago is provably wrong. Top astronomers, such as Carl Sagan and the discoverer of DNA, Francis Crick, believe that life must have been deliberately planted here. And many biologists have suggested that there are large areas of our DNA that may contain a huge message for us to unlock. Christopher Knight and Alan Butler have spent 25 years studying the issue, and now, they have published irrefutable evidence that not only was DNA seeded on our planet but that the Earth, Moon, and the asteroid Ceres were carefully manipulated to ensure that living creatures on Earth would evolve and prosper in what amounts to a gigantic incubator. In this book, they provide details of the existence of conspicuous instructions on how to unlock the communication contained within our DNA coding. This short book will revolutionise how we think about the origin of life on Earth and our next steps of development. The evidence is overwhelming - checkable by anyone with a basic calculator. The data provided cannot be wrong, and the consequences are world-changing. Our species has arrived at a turning point, the originator of the message has carefully timed its discovery to this precise moment - when we have developed multiple ways of obliterating ourselves if left to our own devices. The call is made for a multi-disciplinary team of global experts to be assembled to carry out the mission of fully unlocking and implementing the contents of this message from the beginning of time.Christopher Knight is past chairman of companies from a UK national advertising agency of the year to a hi-tech augmented reality pioneer. He has a number of world-wide patents in the field of mobile communications. He is the author of many international best selling books from ‘The Hiram Key' in 1996, which went into The Sunday Times Top Ten list after just three days of sales, sold over two million copies in its first year and has been translated into over 40 languages.​For 25 years he has researched and written with Alan Butler in the field of ancient metrology and their book ‘Who Built the Moon?' was the acknowledged inspiration for the 2022 blockbuster movie ‘Moonfall' directed by Roland Emmerich.Become a supporter of this podcast: https://www.spreaker.com/podcast/earth-ancients--2790919/support.

En este episodio comparto una reflexión a partir de una frase que me marcó profundamente mientras leía "El almanaque de Naval Ravikant". No era un libro que me atrajera especialmente al principio, pero cinco años después de haberlo visto por primera vez, volví a él por casualidad tras escucharlo mencionado en un podcast. Esta vez lo leí con calma y me atrapó por completo.La frase que me hizo detenerme y pensar fue: “Redefinirte hasta ser el mejor en lo que haces.”A lo largo del episodio exploro qué puede significar esa idea. No se trata de fama, ni de competir con todo el mundo, sino de encontrar un encaje óptimo entre lo que eres, lo que sabes hacer y el valor que puedes aportar. Redefinirse no implica empezar desde cero, sino ajustar el enfoque, cambiar el marco mental, afinar lo que ya haces para convertirlo en algo realmente tuyo.Comparto también ejemplos reales que ilustran este proceso:- Una bioquímica que se convierte en divulgadora científica infantil. - Un músico que combina programación y composición para crear música en videojuegos. - Investigadores y figuras públicas como Francis Crick, Linus Pauling, Francis Mojica o Rosalía, que fueron capaces de cambiar de rumbo varias veces y redefinirse sin dejar de ser ellos mismos. Reflexiono además sobre cómo detectar si estamos en un momento de redefinición y qué señales pueden indicarlo: el estancamiento, la pérdida de interés, la repetición automática. Hablo de herramientas como el journaling, el feedback o simplemente detenernos a sentir si lo que estamos haciendo todavía tiene sentido para nosotros.También toco un tema que hemos tratado muchas veces en este podcast: cómo nuestras fortalezas únicas pueden marcar el camino, incluso cuando llevamos años en otra dirección. Porque a veces no se trata de aprender más, sino de reconocer lo que ya somos y afinarlo.Y como apunte final, aprovecho para comentar un cambio que quiero hacer en la intro del podcast, gracias a los comentarios que me habéis hecho llegar desde la comunidad de investigadores. Estoy trabajando en una nueva introducción musical, y si te apetece colaborar, eres bienvenido. Estoy reaprendiendo a usar Ableton Live, así que cualquier ayuda creativa será más que bienvenida.Por cierto, si te ha gustado el episodio, te agradecería muchísimo que lo valoraras con cinco estrellas en Spotify, iTunes o iVoox. Eso ayuda mucho a que el podcast llegue a más personas.Nos escuchamos en el próximo episodio. Sobre Naval Ravikant: https://nav.al/Más info y acceso a la comunidad: horacio.ps/comunidad

Tıptaki gelişmeler sayesinde artık milyonlarca hayat kurtuluyor. İnsanın yaşam kalitesini dramatik bir ölçüde arttıran birçok gelişme yaşanıyor bu alanda. Fakat bazı rahatsızlıklarda zaman en önemli şey. İşte zamana meydan okuyabilmek için birçok yeni şey deniyor bilim insanları. Ve bazıları bir insanın gelecekte hangi hastalıklara yakalanabileceğini öngören bazı çalışmalar yürütüyor. Hiçbir Şey Tesadüf Değil'in bu bölümünde o gelişmeleri inceliyoruz. DNA'mızın sarmallarında dolanıp, bizi öldürecek şeyin ne olduğunu bilsek, ne yapardık sorusunu sorguluyoruz.------- Podbee Sunar -------Bu podcast, On Dijital Bankacılık hakkında reklam içerir.Bankacılık On'la Rahat. Dünya Döndükçe EFT-Havale- Fast Ücreti Yok.ON Mobil'i İndir! Bu podcast, Pegasus hakkında reklam içerir.Yeni seyahat rotanı planlamak için hemen https://www.flypgs.com/'u veya Pegasus Mobil uygulamasını ziyaret et!Bu podcast, Garanti BBVA hakkında reklam içerir.See Privacy Policy at https://art19.com/privacy and California Privacy Notice at https://art19.com/privacy#do-not-sell-my-info.

They Built the EarthThen seeded life 3.7 billion years ago - Its time to unlock the message they leftby Alan Butler and Christopher KnightRelease date: MAY 01 2025Categories: Ancient mysteries & controversial knowledge, Ufos & extraterrestrialsCLICK HERE TO VIEW THE BOOK COVERA book that is set to open up a whole new direction for humanity by opening the message left for us from those who seeded life on Earth.Most leading scientists agree that the old idea that life on Earth sprang into existence thanks to some happy accident 3.7 billion years ago is provably wrong. Top astronomers, such as Carl Sagan and the discoverer of DNA, Francis Crick, believe that life must have been deliberately planted here. Many biologists have suggested that there are large areas of our DNA that may contain a huge message for us to unlock.Christopher Knight and Alan Butler have spent 25 years studying the issue, and now, they have published irrefutable evidence that not only was DNA seeded on our planet but that the Earth, Moon, and the asteroid Ceres were carefully manipulated to ensure that living creatures on Earth would evolve and prosper in what amounts to a gigantic incubator. In this book, they provide details of the existence of conspicuous instructions on how to unlock the communication contained within our DNA coding. This short book will revolutionise how we think about the origin of life on Earth and our next steps of development. The evidence is overwhelming - checkable by anyone with a basic calculator.The data provided cannot be wrong, and the consequences are world-changing. Our species has arrived at a turning point, the originator of the message has carefully timed its discovery to this precise moment - when we have developed multiple ways of obliterating ourselves if left to our own devices. The call is made for a multi-disciplinary team of global experts to be assembled to carry out the mission of fully unlocking and implementing the contents of this message from the beginning of time.BOOK LINK: https://www.collectiveinkbooks.com/6th-books/our-books/they-built-earth 

Mapa cerebral detallado: Investigadores cartografían un milímetro cúbico de cerebro de ratón con 3,2 kilómetros de conexiones neuronales  Por Félix Riaño @LocutorCo Un equipo científico superó los límites de la neurociencia al mapear millones de sinapsis en un fragmento cerebral microscópico. En 1979, el Nobel Francis Crick consideró que era imposible descifrar la maraña interna de un minúsculo trozo de cerebro. Décadas después, más de cien expertos reunieron 1,6 petabytes de información para demostrar lo contrario. Han analizado un milímetro cúbico de tejido cerebral de ratón que contiene millones de sinapsis y más de 3 kilómetros de filamentos neuronales. Las imágenes en alta resolución, capturadas mediante microscopía electrónica y combinadas con inteligencia artificial, han abierto nuevas ventanas para comprender enfermedades como Alzheimer o Parkinson. Este nivel de detalle asombra, porque revela patrones de conexiones que antes eran un misterio. ¿Qué hallazgos van a descubrir luego con esta nueva cartografía? La complejidad neuronal también despierta dudas sobre su verdadero alcance El proyecto MICrONS tomó un milímetro cúbico del cerebro visual de un ratón y lo partió en unas 25.000 secciones. Cada sección fue fotografiada con microscopio electrónico para obtener una visión detallada de cada célula. Esos datos se combinaron con grabaciones de la actividad cerebral en vida, mientras el animal miraba videos y contenidos en una pantalla. Luego, expertos de Princeton organizaron toda esa información en un modelo tridimensional. Así, se obtuvo el mapa de cientos de miles de neuronas con millones de sinapsis, en un volumen del tamaño aproximado de un grano de arena. Estas redes neuronales se representan con tonos de colores vivos que muestran cada célula y cada circuito, como si fuera un bosque iluminado. La gran dificultad surge al querer entender cómo se comunican las neuronas en semejante densidad de conexiones. Cada célula envía impulsos eléctricos y sustancias químicas a cientos o miles de células vecinas. Aun con la tecnología disponible, es complicado detectar si una neurona establece un vínculo directo o si su señal pasa por varias estaciones intermedias. Además, surge la necesidad de corregir errores en el trazado automático de rutas neuronales. El volumen masivo de datos —que puede equivaler a 22 años de video HD ininterrumpido— requiere enormes recursos computacionales y trabajo humano para revisar y ajustar. Esto explica por qué Francis Crick pensó que era un reto inalcanzable. Los avances fueron posibles gracias a algoritmos de inteligencia artificial y a un arduo trabajo en equipo. La reconstrucción final de este milímetro cúbico de cerebro de ratón aporta evidencias sobre cómo las células inhibitorias y excitatorias se organizan. Estas últimas son responsables de encender la actividad neuronal, mientras que las inhibitorias se encargan de regular y refinar ese impulso. Se creía que las células inhibitorias funcionaban como un simple freno. Ahora, se sabe que eligen de manera muy precisa a qué neuronas controlar. Este entramado complejo, repleto de detalles microscópicos, se vuelve un banco de pruebas para las teorías del aprendizaje profundo en máquinas y abre caminos para entender enfermedades neuronales. Las conclusiones podrían brindar nuevas pistas sobre la conciencia, la inteligencia y los trastornos que interrumpen la comunicación interna del cerebro. Investigadores de prestigiosas instituciones afirman que esta cartografía digital es comparable al Proyecto Genoma Humano por su valor transformador. Todo indica que vamos a seguir aprendiendo mucho de esta región cerebral diminuta. La iniciativa surgió como parte del MICrONS Project, financiado por la agencia IARPA en Estados Unidos. Baylor College of Medicine recabó datos de actividad cerebral en ratones despiertos. El Allen Institute se encargó de cortar el tejido en láminas ultrafinas de unas 0,25 micrómetros de grosor (casi 1/400 del espesor de un cabello humano) para fotografiarlas. Princeton aplicó algoritmos de visión por computador y aprendizaje profundo para reconstruir la forma completa de cada neurona. Estos procedimientos crearon un gran desafío de administración de datos y versiones, ya que cada error de interpretación podía cambiar todo el resultado. Herramientas personalizadas de control de versiones y de corrección automatizada permitieron avanzar. Además, la presencia de imágenes funcionales y estructurales en el mismo conjunto de datos ofreció un panorama integral, permitiendo correlacionar actividad eléctrica real con conexiones anatómicas. Este enfoque sienta bases sólidas para futuras investigaciones que van a explorar circuitos aún más complejos. En este Flash Diario revisamos el logro de mapear un trozo de cerebro de ratón y observar millones de sinapsis. El avance ayuda a comprender cómo se conectan las células y a diagnosticar padecimientos neurológicos. Te invitamos a seguir nuestro pódcast en Spotify llamado Flash Diario para descubrir más noticias así de fascinantes.BibliografíaThe New York TimesThe TimesThe GuardianNatureConviértete en un seguidor de este podcast: https://www.spreaker.com/podcast/flash-diario-de-el-siglo-21-es-hoy--5835407/support.

Le cancer du poumon à petites cellules représente environ 10 % des cas de cancer du poumon, mais se distingue par son agressivité et sa capacité de métastase extrêmement rapide. La survie moyenne des patients n’est que de 7 à 10 mois. Une équipe de chercheurs internationaux, dirigée par l'hôpital national de Taïwan, a pour la toute première fois démontré que ce cancer produit sa propre électricité, ce qui "favorise" directement sa propagation et son aggravation. Cette étude a été menée sous la direction de Leanne Li (李力恩), diplômée de médecine à l'Université nationale de Taïwan et actuellement chercheuse à l'institut Francis Crick du Royaume-Uni. Lors d’une conférence de presse sur ces résultats, le professeur Chen Jin-Shing (陳晉興), chef du département de chirurgie de l'hôpital de l'université nationale de Taïwan, a décortiqué cette "activité électrique" des cellules cancéreuses et le rôle clé de cette recherche dont les résultats ont été publiés dans la prestigieuse revue Nature. Retour en détails sur les enjeux et perspectives de cette découverte majeure pour l'oncologie et les futurs traitements des cancers, dans l'émission Taïwan en ébul'action.

Deciphering the structure of DNA was as complex as the double helix itself. On 28th February, 1953, Dr. James Watson and Dr. Francis Crick rushed to the pub and announced to their fellow drinkers in The Eagle, Cambridge that they had just found “the secret of life”.  But their work would not have been possible without the uncredited contribution of Dr. Rosalind Franklin - whose photographs of the X-ray diffraction pattern of DNA were the first to reveal its three-dimensional structure. And it was her colleague, Dr Maurice Wilkins, who first brought Franklin's work to the attention of Watson and Crick. In this episode, Arion, Rebecca and Olly consider how it came to be that Crick's wife, Odile; drew the iconic depiction of the structure published in Nature; explain why *technically* Dr Franklin didn't even have a degree; and recall how James Watson's legacy was tainted by his bitter and snide memoir, ‘The Double Helix'...  Further Reading: • ‘Double-Helix Structure of DNA' (ThoughtCo, 2020): https://www.thoughtco.com/double-helix-373302 • ‘The Geek Atlas - 128 Places Where Science and Technology Come Alive, By John Graham-Cumming' (O'Reilly Media, 2009): https://www.google.co.uk/books/edition/The_Geek_Atlas/rXH0AQAAQBAJ?hl=en&gbpv=1&dq=crick+watson+eagle+1953&pg=PA267&printsec=frontcover • ‘Rosalind Franklin: DNA's unsung hero - Cláudio L. Guerra' (Ted-Ed, 2016): https://www.youtube.com/watch?v=BIP0lYrdirI This episode first aired in 2023 Love the show? Support us!  Join 

On this day in 1953, the double-helix structure of DNA was discovered by James Watson and Francis Crick. 

En 1958, el físico Francis Crick, que poco antes había descubierto junto a Watson la estructura de la molécula de ADN, enunció el llamado Dogma Central de la Biología Molecular. Este concepto fundamental describe cómo fluye la información genética dentro de las células de los seres vivos. Un proceso, en definitiva, que define la vida tal y como la conocemos. Todo ello de la mano de José Blanca, Toni Monforte y Ximo Cañizares. Escucha el episodio completo en la app de iVoox, o descubre todo el catálogo de iVoox Originals

In this episode, Peter Bandettini interviews Matthew Cobb (https://en.wikipedia.org/wiki/Matthew_Cobb), the author of the book “The idea of the brain: The Past and Future of Neuroscience”. Episode producers: Omer Faruk Gulban Alfie Wearn

Since the discovery of the double helix by Francis Crick, James Watson and Rosalind Franklin in the 1950s, human knowledge of DNA and genetics has grown almost immeasurably. We now know that genes affect every aspect of our lives, from our appearance, our health and even our personality. But more than this, our genes are a living document of our evolutionary past, an ancient document that, if read properly, can reveal almost everything about how we came to be how we are. In this episode, we're joined by the evolutionary biologist and multi-million selling author Richard Dawkins to speak about his latest book The Genetic Book of the Dead: A Darwinian Reverie. He tells us how different species of animals hit on the same evolutionary strategies despite being separated by multiple continents, how natural selection doesn't necessarily always follow the perfect path and how a scientist of the future may one day be able to read the genetic code of any living animal like a book to uncover its entire evolutionary past. Learn more about your ad choices. Visit podcastchoices.com/adchoices

Jay McClelland is a pioneer in the field of artificial intelligence and is a cognitive psychologist and professor at Stanford University in the psychology, linguistics, and computer science departments. Together with David Rumelhart, Jay published the two volume work Parallel Distributed Processing, which has led to the flourishing of the connectionist approach to understanding cognition. In this conversation, Jay gives us a crash course in how neurons and biological brains work. This sets the stage for how psychologists such as Jay, David Rumelhart, and Geoffrey Hinton historically approached the development of models of cognition and ultimately artificial intelligence. We also discuss alternative approaches to neural computation such as symbolic and neuroscientific ones. Patreon (bonus materials + video chat): https://www.patreon.com/timothynguyen Part I. Introduction 00:00 : Preview 01:10 : Cognitive psychology 07:14 : Interdisciplinary work and Jay's academic journey 12:39 : Context affects perception 13:05 : Chomsky and psycholinguists 8:03 : Technical outline Part II. The Brain 00:20:20 : Structure of neurons 00:25:26 : Action potentials 00:27:00 : Synaptic processes and neuron firing 00:29:18 : Inhibitory neurons 00:33:10 : Feedforward neural networks 00:34:57 : Visual system 00:39:46 : Various parts of the visual cortex 00:45:31 : Columnar organization in the cortex 00:47:04 : Colocation in artificial vs biological networks 00:53:03 : Sensory systems and brain maps Part III. Approaches to AI, PDP, and Learning Rules 01:12:35 : Chomsky, symbolic rules, universal grammar 01:28:28 : Neuroscience, Francis Crick, vision vs language 01:32:36 : Neuroscience = bottom up 01:37:20 : Jay's path to AI 01:43:51 : James Anderson 01:44:51 : Geoff Hinton 01:54:25 : Parallel Distributed Processing (PDP) 02:03:40 : McClelland & Rumelhart's reading model 02:31:25 : Theories of learning 02:35:52 : Hebbian learning 02:43:23 : Rumelhart's Delta rule 02:44:45 : Gradient descent 02:47:04 : Backpropagation 02:54:52 : Outro: Retrospective and looking ahead Image credits: http://timothynguyen.org/image-credits/ Further reading: Rumelhart, McClelland. Parallel Distributed Processing. McClelland, J. L. (2013). Integrating probabilistic models of perception and interactive neural networks: A historical and tutorial review   Twitter: @iamtimnguyen   Webpage: http://www.timothynguyen.org

In this podcast, I am joined by Matthew Cobb, author of the fascinating book The idea of the Brain, to discuss the different concepts of the brain that have emerged over the centuries.Matthew Cobb is Professor of Zoology at the University of Manchester where he studies the neurobiology of the sense of smell.Matthew Cobb explores current and historical metaphors of the brain, from the machine and the mill to the battery and the computer.Matthew also flavours his history with gripping anecdotes, from Shakespeare's The Merchant of Venice to Mary Shelley's Frankenstein. And he draws lessons from such giants of science, from Galvani and Volta to Steno and Francis Crick.Matthew is also a non-professional historian, having written several other books, most recently Life's Greatest Secret: The Race to Crack the Genetic Code, and The Genetic Age: Our Perilous Quest to Edit Life.He is currently completing a biography of Francis Crick.

Charles Darwin's revolutionary observations of Galapagos tortoises and finches, explored how natural selection allows species to adapt over time. From the discovery of the hawk moth in Madagascar, predicted by Darwin, to the groundbreaking discovery of DNA by Rosalind Franklin, Francis Crick, and James Watson, we look at how genetic changes drive evolution. Please consider becoming a show Patron to help keep new episodes coming! Evolution Talk is also a book! You can find links to Amazon, Barnes & Noble and others on the front page of EvolutionTalk.com, or call your local bookstore and ask them to order a copy.   Music in this Episode Bright White by Podington Bear, License (CC BY 3.0): Artist website: soundofpicture.com Stars are Out by Podington Bear, License (CC BY 3.0): Artist website: soundofpicture.com

Prof. Mark Solms, a neuroscientist and psychoanalyst, discusses his groundbreaking work on consciousness, challenging conventional cortex-centric views and emphasizing the role of brainstem structures in generating consciousness and affect. MLST is sponsored by Brave: The Brave Search API covers over 20 billion webpages, built from scratch without Big Tech biases or the recent extortionate price hikes on search API access. Perfect for AI model training and retrieval augmentated generation. Try it now - get 2,000 free queries monthly at http://brave.com/api. Key points discussed: The limitations of vision-centric approaches to consciousness studies. Evidence from decorticated animals and hydranencephalic children supporting the brainstem's role in consciousness. The relationship between homeostasis, the free energy principle, and consciousness. Critiques of behaviorism and modern theories of consciousness. The importance of subjective experience in understanding brain function. The discussion also explored broader topics: The potential impact of affect-based theories on AI development. The role of the SEEKING system in exploration and learning. Connections between neuroscience, psychoanalysis, and philosophy of mind. Challenges in studying consciousness and the limitations of current theories. Mark Solms: https://neuroscience.uct.ac.za/contacts/mark-solms Show notes and transcript: https://www.dropbox.com/scl/fo/roipwmnlfmwk2e7kivzms/ACjZF-VIGC2-Suo30KcwVV0?rlkey=53y8v2cajfcgrf17p1h7v3suz&st=z8vu81hn&dl=0 TOC (*) are best bits 00:00:00 1. Intro: Challenging vision-centric approaches to consciousness * 00:02:20 2. Evidence from decorticated animals and hydranencephalic children * 00:07:40 3. Emotional responses in hydranencephalic children 00:10:40 4. Brainstem stimulation and affective states 00:15:00 5. Brainstem's role in generating affective consciousness * 00:21:50 6. Dual-aspect monism and the mind-brain relationship 00:29:37 7. Information, affect, and the hard problem of consciousness * 00:37:25 8. Wheeler's participatory universe and Chalmers' theories 00:48:51 9. Homeostasis, free energy principle, and consciousness * 00:59:25 10. Affect, voluntary behavior, and decision-making 01:05:45 11. Psychoactive substances, REM sleep, and consciousness research 01:12:14 12. Critiquing behaviorism and modern consciousness theories * 01:24:25 13. The SEEKING system and exploration in neuroscience Refs: 1. Mark Solms' book "The Hidden Spring" [00:20:34] (MUST READ!) https://amzn.to/3XyETb3 2. Karl Friston's free energy principle [00:03:50] https://www.nature.com/articles/nrn2787 3. Hydranencephaly condition [00:07:10] https://en.wikipedia.org/wiki/Hydranencephaly 4. Periaqueductal gray (PAG) [00:08:57] https://en.wikipedia.org/wiki/Periaqueductal_gray 5. Positron Emission Tomography (PET) [00:13:52] https://en.wikipedia.org/wiki/Positron_emission_tomography 6. Paul MacLean's triune brain theory [00:03:30] https://en.wikipedia.org/wiki/Triune_brain 7. Baruch Spinoza's philosophy of mind [00:23:48] https://plato.stanford.edu/entries/spinoza-epistemology-mind 8. Claude Shannon's "A Mathematical Theory of Communication" [00:32:15] https://people.math.harvard.edu/~ctm/home/text/others/shannon/entropy/entropy.pdf 9. Francis Crick's "The Astonishing Hypothesis" [00:39:57] https://en.wikipedia.org/wiki/The_Astonishing_Hypothesis 10. Frank Jackson's Knowledge Argument [00:40:54] https://plato.stanford.edu/entries/qualia-knowledge/ 11. Mesolimbic dopamine system [01:11:51] https://en.wikipedia.org/wiki/Mesolimbic_pathway 12. Jaak Panksepp's SEEKING system [01:25:23] https://en.wikipedia.org/wiki/Jaak_Panksepp#Affective_neuroscience

Esta semana, con motivo de los Juegos Olímpicos de París, hacemos un ejercicio un poco excéntrico: si tuviéramos que escoger una única figura para representar a la física, a la biología o a las matemáticas ¿a quién escogeríamos? ¿Quiénes deberían ser los *abanderados* de cada disciplina científica? Jugamos a este juego considerando dos candidatos para esas tres disciplinas: la física, la biología y las matemáticas (no nos cabían más *sad*). En Física escogemos entre Isaac Newton y Albert Einstein; en Biología, entre Charles Darwin y Francis Crick; y en Matemáticas entre Leonhard Euler y Carl Friedrich Gauss. Para cada uno trataremos de argumentar cuáles son sus méritos y por qué les estamos dando el honor de representar a toda su ciencia frente a la humanidad. Este programa se emitió originalmente el 18 de julio de 2024. Podéis escuchar el resto de audios de Más de Uno en la app de Onda Cero y en su web, ondacero.es

A political science major at a major university was having coffee with a campus pastor. The pastor knew that the student was wrestling with doubt about the existence of God and said to him, “John, you know all of us wonder at some point if it's all real or not. For example, there are quite a few stories in the Bible that are just hard to believe. Jonah and the whale and all that.” John smiled and said, “No, that's not my problem. What I wonder about is how God could care about me. I've done some really bad things and have had some really bad things done to me. I just can't understand the concept of forgiveness.”There you have it. Doubts about the faith come from all directions. While one person cannot bring herself to believe in miracles, another cannot forgive himself for the wrong things he's done, and can't fathom how God could. Thomas Jefferson actually cut out the miraculous sections of the Bible. He couldn't believe in what some would call the God of the Bible. Francis Crick, the co-discoverer of DNA, thought that Christianity was just a collection of mythical stories. And what about those who want to see the proof, they like evidence and feel a need to make an intellectual case for our faith. The New Testament writer Luke was like that. He wrote in Acts and the Gospel of Luke about the importance of eyewitness sightings of Jesus and His miracles. Lots of people debate whether evolution and religion are compatible or not. And this is a big stumbling block to believe for many. We all believe something, but our minds can struggle at times to grasp the big stuff, the infinite universe. While for others who doubt, the struggle is more internal. They're so grieved by their own sin, they can't accept that God could love them.Maybe the most famous verse in the Bible is John 3:16, which says, “For God so loved the world that he gave his one and only son, that whoever believes in him shall not perish, but have eternal life.” However, few quote the next verse which says, “For God did not send his son into the world to condemn the world, but to save the world through him.” It isn't God's wish to condemn you. Instead, He loves you and wants to give you assurance that life is more than struggle and molecules. Whether you're looking for evidence to believe the Bible or you just need to know that God loves you, try not to focus too much on your objections. Own them, but just tell God as a child would, that you're struggling to understand it all.Will you pray with me? Father, your grace saves us from a life of struggle with sin and we are accepted by you. Thank you for putting up with our up-and-down faith. In Jesus' name, amen.Change your shirt, and you can change the world! Save 15% Off your entire purchase of faith-based apparel + gifts at Kerusso.com with code KDD15.

¿Alguna vez te has preguntado de dónde venimos realmente?. Más allá de las explicaciones científicas y religiosas, ¿hay otras posibilidades?.Finalmente me animo a tocar un tema del que he querido hablar hace mucho tiempo, pero que hasta ahora no me había atrevido a traer.Hoy te voy a hablar de ¿quién nos creó?, vamos a cuestionar tus creencias más arraigadas sobre el origen de la vida en la Tierra.Vamos a contrastar lo que leí en la revista Icarus con lo que nos dicen los libros de historia sobre la civilización humana.Y por último te voy a hablar de tu código genético y su posible conexión con tus orígenes. ¿Qué guarda tu ADN sobre tu verdadera naturaleza?.Descubre que tu pasado puede ser mucho más complejo y misterioso de lo que te lo imaginas.Inscríbete en pre-lanzamiento al Programa de la Intuición y recibe el Bono para el Taller de Péndulo. Da click AQUÍ.EN ESTE EPISODIO¿De dónde vienen tus creencias acerca de tu origen en la tierra?Lo insólito que leí en la revista Icarus: "The 'Wow! signal' of the terrestrial genetic code" publicado en la revista Icarus (Volumen 224, Número 1, Mayo 2013,¿Qué dicen los libros de historia acerca de la civilización humana?¿Cuáles pudieron haber sido otras formas de llegar aquí?Nuestro ADN y qué puede hacer.Libros, autores y personas mencionadas:Francis Crick: el co-descubridor de la estructura del ADN.Zecharia Sitchin: Crónicas de la Tierra.Erich von Däniken: Chariots of the Gods.Peter Garayev descubrió el ADN cuántico.Pre-Inscripción al programa Cómo desarrollar tu intuición.  BONO:  Taller de péndulo en VIVO de 2 días. Da click AQUÍ.PROGAMA INTUICIÓN SEPT 2024Pre-Inscripción al programa Cómo desarrollar tu intuición. BONO: Taller de péndulo en VIVO de 2 días. AQUÍSESIONES CONMIGO ¿Buscas ayuda puntual? Separa una Sesión de Alkimia con balance de chacras para descubrir qué situación física, emocional, espiritual, de auto-sabotaje o de ancestros está impidiendo fluir tu energía. RESERVAR SESION DE ALKIMIA ¿Quieres adentrarte en tus vidas pasadas? Separa una Regresión con péndulo para que la energía te lleve a aquella vida que te ayuda a gestionar situaciones de tu vida presente. RESERVAR SESIÓN DE REGRESIÓN ME ENCUENTRAS ENInstagramWeb AlkimiaWeb Marcela HedeYouTube

Sam Harris speaks with Christof Koch about the nature of consciousness. They discuss Christof's development as a neuroscientist, his collaboration with Francis Crick, change blindness and binocular rivalry, sleep and anesthesia, the limits of physicalism, non-locality, brains as classical systems, conscious AI, idealism and panpsychism, Integrated Information Theory (IIT), what it means to say something “exists,” the illusion of the self, brain bridging, Christof's experience with psychedelics, and other topics. If the Making Sense podcast logo in your player is BLACK, you can SUBSCRIBE to gain access to all full-length episodes at samharris.org/subscribe. Learning how to train your mind is the single greatest investment you can make in life. That's why Sam Harris created the Waking Up app. From rational mindfulness practice to lessons on some of life's most important topics, join Sam as he demystifies the practice of meditation and explores the theory behind it.

Share this episode: https://www.samharris.org/podcasts/making-sense-episodes/374-consciousness-and-the-physical-world Sam Harris speaks with Christof Koch about the nature of consciousness. They discuss Christof’s development as a neuroscientist, his collaboration with Francis Crick, change blindness and binocular rivalry, sleep and anesthesia, the limits of physicalism, non-locality, brains as classical systems, conscious AI, idealism and panpsychism, Integrated Information Theory (IIT), what it means to say something “exists,” the illusion of the self, brain bridging, Christof’s experience with psychedelics, and other topics. Christof Koch is a neuroscientist at the Allen Institute and the Chief Scientist of the Tiny Blue Dot Foundation. He is the former president of the Allen Institute for Brain Science and a former professor at the California Institute of Technology. He writes regularly for Scientific American and is the author of five books, most recently Then I Am Myself the World: What Consciousness Is and How to Expand It. Website: https://christofkoch.com/ Learning how to train your mind is the single greatest investment you can make in life. That’s why Sam Harris created the Waking Up app. From rational mindfulness practice to lessons on some of life’s most important topics, join Sam as he demystifies the practice of meditation and explores the theory behind it.

The most enthralling conversation I've ever had with anyone on cancer. It's with Charlie Swanton who is a senior group leader at the Francis Crick Institute, the Royal Society Napier Professor in Cancer and medical oncologist at University College London, co-director of Cancer Research UK.Video snippet from our conversation. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with audio links and many external linksEric Topol (00:07):Well, hello, this is Eric Topol with Ground Truths, and I am really fortunate today to connect us with Charlie Swanton, who is if not the most prolific researcher in the space of oncology and medicine, and he's right up there. Charlie is a physician scientist who is an oncologist at Francis Crick and he heads up the lung cancer area there. So Charlie, welcome.Charles Swanton (00:40):Thank you, Eric. Nice to meet you.Learning from a FailureEric Topol (00:43):Well, it really is a treat because I've been reading your papers and they're diverse. They're not just on cancer. Could be connecting things like air pollution, it could be Covid, it could be AI, all sorts of things. And it's really quite extraordinary. So I thought I'd start out with a really interesting short paper you wrote towards the end of last year to give a sense about you. It was called Turning a failing PhD around. And that's good because it's kind of historical anchoring. Before we get into some of your latest contributions, maybe can you tell us about that story about what you went through with your PhD?Charles Swanton (01:26):Yeah, well thank you, Eric. I got into research quite early. I did what you in the US would call the MD PhD program. So in my twenties I started a PhD in a molecular biology lab at what was then called the Imperial Cancer Research Fund, which was the sort of the mecca for DNA tumor viruses, if you like. It was really the place to go if you wanted to study how DNA tumor viruses worked, and many of the components of the cell cycle were discovered there in the 80s and 90s. Of course, Paul Nurse was the director of the institute at the time who discovered cdc2, the archetypal regulator of the cell cycle that led to his Nobel Prize. So it was a very exciting place to work, but my PhD wasn't going terribly well. And sort of 18, 19 months into my PhD, I was summoned for my midterm reports and it was not materializing rapidly enough.(02:25):And I sat down with my graduate student supervisors who were very kind, very generous, but basically said, Charlie, this isn't going well, is it? You've got two choices. You can either go back to medical school or change PhD projects. What do you want to do? And I said, well, I can't go back to medical school because I'm now two years behind. So instead I think what I'll do is I'll change PhD projects. And they asked me what I'd like to do. And back then we didn't know how p21, the CDK inhibitor bound to cyclin D, and I said, that's what I want to understand how these proteins interact biochemically. And they said, how are you going to do that? And I said, I'm not too sure, but maybe we'll try yeast two-hybrid screen and a mutagenesis screen. And that didn't work either. And in the end, something remarkable happened.(03:14):My PhD boss, Nic Jones, who's a great guy, still is, retired though now, but a phenomenal scientist. He put me in touch with a colleague who actually works next door to me now at the Francis Crick Institute called Neil McDonald, a structural biologist. And they had just solved, well, the community had just solved the structure. Pavletich just solved the structure of cyclin A CDK2. And so, Neil could show me this beautiful image of the crystal structure in 3D of cyclin A, and we could mirror cyclin D onto it and find the surface residue. So I spent the whole of my summer holiday mutating every surface exposed acid on cyclin D to an alanine until I found one that failed to interact with p21, but could still bind the CDK. And that little breakthrough, very little breakthrough led to this discovery that I had where the viral cyclins encoded by Kaposi sarcoma herpes virus, very similar to cyclin D, except in this one region that I had found interactive with a CDK inhibitor protein p21.(04:17):And so, I asked my boss, what do you think about the possibility this cyclin could have evolved from cyclin D but now mutated its surface residues in a specific area so that it can't be inhibited by any of the control proteins in the mammalian cell cycle? He said, it's a great idea, Charlie, give it a shot. And it worked. And then six months later, we got a Nature paper. And that for me was like, I cannot tell you how exciting, not the Nature paper so much as the discovery that you were the first person in the world to ever see this beautiful aspect of evolutionary biology at play and how this cyclin had adapted to just drive the cell cycle without being inhibited. For me, just, I mean, it was like a dream come true, and I never experienced anything like it before, and I guess it's sizes the equivalent to me of a class A drug. You get such a buzz out of it and over the years you sort of long for that to happen again. And occasionally it does, and it's just a wonderful profession.Eric Topol (05:20):Well, I thought that it was such a great story because here you were about to fail. I mean literally fail, and you really were able to turn it around and it should give hope to everybody working in science out there that they could just be right around the corner from a significant discovery.Charles Swanton (05:36):I think what doesn't break you makes you stronger. You just got to plow on if you love it enough, you'll find a way forward eventually, I hope.Tracing the Evolution of Cancer (TRACERx)Eric Topol (05:44):Yeah, no question about that. Now, some of your recent contributions, I mean, it's just amazing to me. I just try to keep up with the literature just keeping up with you.Charles Swanton (05:58):Eric, it's sweet of you. The first thing to say is it's not just me. This is a big community of lung cancer researchers we have thanks to Cancer Research UK funded around TRACERx and the lung cancer center. Every one of my papers has three corresponding authors, multiple co-first authors that all contribute in this multidisciplinary team to the sort of series of small incremental discoveries. And it's absolutely not just me. I've got an amazing team of scientists who I work with and learn from, so it's sweet to give me the credit.Eric Topol (06:30):I think what you're saying is really important. It is a team, but I think what I see through it all is that you're an inspiration to the team. You pull people together from all over the world on these projects and it's pretty extraordinary, so that's what I would say.Charles Swanton (06:49):The lung community, Eric, the lung cancer community is just unbelievably conducive to collaboration and advancing understanding of the disease together. It's just such a privilege to be working in this field. I know that sounds terribly corny, but it is true. I don't think I recall a single email to anybody where I've asked if we can collaborate where they've said, no, everybody wants to help. Everybody wants to work together on this challenge. It's just such an amazing field to be working in.Eric Topol (07:19):Yeah. Well I was going to ask you about that. And of course you could have restricted your efforts or focused on different cancers. What made you land in lung cancer? Not that that's only part of what you're working on, but that being the main thing, what drew you to that area?Charles Swanton (07:39):So I think the answer to your question is back in 2008 when I was looking for a niche, back then it was lung cancer was just on the brink of becoming an exciting place to work, but back then nobody wanted to work in that field. So there was a chair position in thoracic oncology and precision medicine open at University College London Hospital that had been open, as I understand it for two years. And I don't think anybody had applied. So I applied and because I was the only one, I got it and the rest is history.(08:16):And of course that was right at the time when the IPASS draft from Tony Mok was published and was just a bit after when the poster child of EGFR TKIs and EGFR mutant lung cancer had finally proven that if you segregate that population of patients with EGFR activating mutation, they do incredibly well on an EGFR inhibitor. And that was sort of the solid tumor poster child along with Herceptin of precision medicine, I think. And you saw the data at ASCO this week of Lorlatinib in re-arranged lung cancer. Patients are living way beyond five years now, and people are actually talking about this disease being more like CML. I mean, it's extraordinary the progress that's been made in the last two decades in my short career.Eric Topol (09:02):Actually, I do want to have you put that in perspective because it's really important what you just mentioned. I was going to ask you about this ASCO study with the AKT subgroup. So the cancer landscape of the lung has changed so much from what used to be a disease of cigarette smoking to now one of, I guess adenocarcinoma, non-small cell carcinoma, not related to cigarettes. We're going to talk about air pollution in a minute. This group that had, as you say, 60 month, five year plus survival versus what the standard therapy was a year plus is so extraordinary. But is that just a small subgroup within small cell lung cancer?Charles Swanton (09:48):Yes, it is, unfortunately. It's just a small subgroup. In our practice, probably less than 1% of all presentations often in never smokers, often in female, never smokers. So it is still in the UK at least a minority subset of adenocarcinomas, but it's still, as you rightly say, a minority of patients that we can make a big difference to with a drug that's pretty well tolerated, crosses the blood-brain barrier and prevents central nervous system relapse and progression. It really is an extraordinary breakthrough, I think. But that said, we're also seeing advances in smoking associated lung cancer with a high mutational burden with checkpoint inhibitor therapy, particularly in the neoadjuvant setting now prior to surgery. That's really, really impressive indeed. And adjuvant checkpoint inhibitor therapies as well as in the metastatic setting are absolutely improving survival times and outcomes now in a way that we couldn't have dreamt of 15 years ago. We've got much more than just platinum-based chemo is basically the bottom line now.Revving Up ImmunotherapyEric Topol (10:56):Right, right. Well that actually gets a natural question about immunotherapy also is one of the moving parts actually just amazing to me how that's really, it's almost like we're just scratching the surface of immunotherapy now with checkpoint inhibitors because the more we get the immune system revved up, the more we're seeing results, whether it's with vaccines or CAR-T, I mean it seems like we're just at the early stages of getting the immune system where it needs to be to tackle the cancer. What's your thought about that?Charles Swanton (11:32):I think you're absolutely right. We are, we're at the beginning of a very long journey thanks to Jim Allison and Honjo. We've got CTLA4 and PD-1/PDL-1 axis to target that's made a dramatic difference across multiple solid tumor types including melanoma and lung cancer. But undoubtedly, there are other targets we've seen LAG-3 and melanoma and then we're seeing new ways, as you rightly put it to mobilize the immune system to target cancers. And that can be done through vaccine based approaches where you stimulate the immune system against the patient's specific mutations in their cancer or adoptive T-cell therapies where you take the T-cells out of the tumor, you prime them against the mutations found in the tumor, you expand them and then give them back to the patient. And colleagues in the US, Steve Rosenberg and John Haanen in the Netherlands have done a remarkable job there in the context of melanoma, we're not a million miles away from European approvals and academic initiated manufacturing of T-cells for patients in national health systems like in the Netherlands.(12:50):John Haanen's work is remarkable in that regard. And then there are really spectacular ways of altering T-cells to be able to either migrate to the tumor or to target specific tumor antigens. You mentioned CAR-T cell therapies in the context of acute leukemia, really extraordinary developments there. And myeloma and diffuse large B-cell lymphoma as well as even in solid tumors are showing efficacy. And I really am very excited about the future of what we call biological therapies, be it vaccines, an antibody drug conjugates and T-cell therapies. I think cancer is a constantly adapting evolutionary force to be reckoned with what better system to combat it than our evolving immune system. It strikes me as being a future solution to many of these refractory cancers we still find difficult to treat.Eric Topol (13:48):Yeah, your point is an interesting parallel how the SARS-CoV-2 virus is constantly mutating and becoming more evasive as is the tumor in a person and the fact that we can try to amp up the immune system with these various means that you just were reviewing. You mentioned the other category that's very hot right now, which is the antibody drug conjugates. Could you explain a bit about how they work and why you think this is an important part of the future for cancer?Antibody-Drug ConjugatesCharles Swanton (14:26):That's a great question. So one of the challenges with chemotherapy, as you know, is the normal tissue toxicity. So for instance, neutropenia, hair loss, bowel dysfunction, diarrhea, epithelial damage, essentially as you know, cytotoxics affect rapidly dividing tissues, so bone marrow, epithelial tissues. And because until relatively recently we had no way of targeting chemotherapy patients experienced side effects associated with them. So over the last decade or so, pioneers in this field have brought together this idea of biological therapies linked with chemotherapy through a biological linker. And so one poster chart of that would be the drug T-DXd, which is essentially Herceptin linked to a chemotherapy drug. And this is just the most extraordinary drug that obviously binds the HER2 receptor, but brings the chemotherapy and proximity of the tumor. The idea being the more drug you can get into the tumor and the less you're releasing into normal tissue, the more on tumor cytotoxicity you'll have and the less off tumor on target normal tissue side effects you'll have. And to a large extent, that's being shown to be the case. That doesn't mean they're completely toxicity free, they're not. And one of the side effects associated with these drugs is pneumonitis.(16:03):But that said, the efficacy is simply extraordinary. And for example, we're having to rewrite the rule books if you like, I think. I mean I'm not a breast cancer physician, I used to be a long time ago, but back in the past in the early 2000s, there was HER2 positive breast cancer and that's it. Now they're talking about HER2 low, HER2 ultra-low, all of which seem to in their own way be sensitive to T-DXd, albeit to a lower extent than HER2 positive disease. But the point is that there doesn't seem to be HER2 completely zero tumor group in breast cancer. And even the HER2-0 seem to benefit from T-DXd to an extent. And the question is why? And I think what people are thinking now is it's a combination of very low cell service expression of HER2 that's undetectable by conventional methods like immunohistochemistry, but also something exquisitely specific about the way in which HER2 is mobilized on the membrane and taken back into the cell. That seems to be specific to the breast cancer cell but not normal tissue. So in other words, the antibody drug conjugate binds the tumor cell, it's thought the whole receptor's internalized into the endosome, and that's where the toxicity then happens. And it's something to do with the endosomal trafficking with the low level expression and internalization of the receptor. That may well be the reason why these HER2 low tumors are so sensitive to this beautiful technology.Eric Topol (17:38):Now I mean it is an amazing technology in all these years where we just were basically indiscriminately trying to kill cells and hoping that the cancer would succumb. And now you're finding whether you want to call it a carry or vector or Trojan horse, whatever you want to call it, but do you see that analogy of the HER2 receptor that's going to be seen across the board in other cancers?Charles Swanton (18:02):That's the big question, Eric. I think, and have we just lucked out with T-DXd, will we find other T-DXd like ADCs targeting other proteins? I mean there are a lot of ADCs being developed against a lot of different cell surface proteins, and I think the jury's still out. I'm confident we will, but we have to bear in mind that biology is a fickle friend and there may be something here related to the internalization of the receptor in breast cancer that makes this disease so exquisitely sensitive. So I think we just don't know yet. I'm reasonably confident that we will find other targets that are as profoundly sensitive as HER2 positive breast cancer, but time will tell.Cancer, A Systemic DiseaseEric Topol (18:49):Right. Now along these lines, well the recent paper that you had in Cell, called embracing cancer complexity, which we've talking about a bit, in fact it's kind of those two words go together awfully well, but hallmarks of systemic disease, this was a masterful review, as you say with the team that you led. But can you tell us about what's your main perspective about this systemic disease? I mean obviously there's been the cancer is like cardiovascular and cancers like this or that, but here you really brought it together with systemic illness. What can you say about that?Charles Swanton (19:42):Well, thanks for the question first of all, Eric. So a lot of this comes from some of my medical experience of treating cancer and thinking to myself over the years, molecular biology has had a major footprint on advances in treating the disease undoubtedly. But there are still aspects of medicine where molecular biology has had very little impact, and often that is in areas of suffering in patients with advanced disease and cancer related to things like cancer cachexia, thrombophilia. What is the reason why patients die blood clots? What is the reason patients die of cancer at all? Even a simple question like that, we don't always know the answer to, on death certificates, we write metastatic disease as a cause of cancer death, but we have patients who die with often limited disease burden and no obvious proximal cause of death sometimes. And that's very perplexing, and we need to understand that process better.(20:41):And we need to understand aspects like cancer pain, for example, circadian rhythms affect biological sensitivity of cancer cells to drugs and what have you. Thinking about cancer rather than just sort of a single group of chaotically proliferating cells to a vision of cancer interacting both locally within a microenvironment but more distantly across organs and how organs communicate with the cancer through neuronal networks, for example, I think is going to be the next big challenge by setting the field over the next decade or two. And I think then thinking about more broadly what I mean by embracing complexity, I think some of that relates to the limitations of the model systems we use, trying to understand inter-organ crosstalk, some of the things you cover in your beautiful Twitter reviews. (←Ground Truths link) I remember recently you highlighted four publications that looked at central nervous system, immune cell crosstalk or central nervous system microbiome crosstalk. It's this sort of long range interaction between organs, between the central nervous system and the immune system and the cancer that I'm hugely interested in because I really think there are vital clues there that will unlock new targets that will enable us to control cancers more effectively if we just understood these complex networks better and had more sophisticated animal model systems to be able to interpret these interactions.Eric Topol (22:11):No, it's so important what you're bringing out, the mysteries that still we have to deal with cancer, why patients have all these issues or dying without really knowing what's happened no less, as you say, these new connects that are being discovered at a remarkable pace, as you mentioned, that ground truths. And also, for example, when I spoke with Michelle Monje, she's amazing on the cancer, where hijacking the brain cells and just pretty extraordinary things. Now that gets me to another line of work of yours. I mean there are many, but the issue of evolution of the tumor, and if you could put that in context, a hot area that's helping us elucidate these mechanisms is known as spatial omics or spatial biology. This whole idea of being able to get the spatial temporal progression through single cell sequencing and single cell nuclei, all the single cell omics. So if you could kind of take us through what have we learned with this technique and spatial omics that now has changed or illuminated our understanding of how cancer evolves?Charles Swanton (23:37):Yeah, great question. Well, I mean I think it helps us sort of rewind a bit and think about evolution in general. Genetic selection brought about by diverse environments and environmental pressures that force evolution, genetic evolution, and speciation down certain evolutionary roots. And I think one can think about cancers in a similar way. They start from a single cell and we can trace the evolutionary paths of cancers by single cell analysis as well as bulk sequencing of spatially separated tumor regions to be able to reconstruct their subclones. And that's taught us to some extent, what are the early events in tumor evolution? What are the biological mechanisms driving branched evolution? How does genome instability begin in tumors? And we found through TRACERx work, whole genome doubling is a major route through to driving chromosome instability along with mutagenic enzymes like APOBEC that drive both mutations and chromosomal instability.(24:44):And then that leads to a sort of adaptive radiation in a sense, not dissimilar to I guess the Cambrian explosion of evolutionary opportunity upon which natural selection can act. And that's when you start to see the hallmarks of immune evasion like loss of HLA, the immune recognition molecules that bind the neoantigens or even loss of the neoantigens altogether or mutation of beta 2 microglobulin that allow the tumor cells to now evolve below the radar, so to speak. But you allude to the sort of spatial technologies that allow us to start to interpret the microenvironments as well. And that then tells us what the evolutionary pressures are upon the tumor. And we're learning from those spatial technologies that these environments are incredibly diverse, actually interestingly seem to be converging on one important aspect I'd like to talk to you a little bit more about, which is the myeloid axis, which is these neutrophils, macrophages, et cetera, that seem to be associated with poor outcome and that will perhaps talk about pollution in a minute.(25:51):But I think they're creating a sort of chronic inflammatory response that allows these early nascent tumor cells to start to initiate into frankly tumor invasive cells and start to grow. And so, what we're seeing from these spatial technologies in lung cancer is that T-cells, predatory T-cells, force tumors to lose their HLA molecules and what have you to evade the immune system. But for reasons we don't understand, high neutrophil infiltration seems to be associated with poor outcome, poor metastasis free survival. And actually, those same neutrophils we've recently found actually even tracked to the metastasis sites of metastasis. So it's almost like this sort of symbiosis between the myeloid cells and the tumor cells in their biology and growth and progression of the tumor cells.Eric Topol (26:46):Yeah, I mean this white cell story, this seems to be getting legs and is relatively new, was this cracked because of the ability to do this type of work to in the past everything was, oh, it's cancer's heterogeneous and now we're getting pinpoint definition of what's going on.Charles Swanton (27:04):I think it's certainly contributed, but it's like everything in science, Eric, when you look back, there's evidence in the literature for pretty much everything we've ever discovered. You just need to put the pieces together. And I mean one example would be the neutrophil lymphocyte ratio in the blood as a hallmark of outcome in cancers and to checkpoint inhibitor blockade, maybe this begins to explain it, high neutrophils, immune suppressive environment, high neutrophils, high macrophages, high immune suppression, less benefit from checkpoint inhibitor therapy, whereas you want lymphocyte. So I think there are biomedical medical insights that help inform the biology we do in the lab that have been known for decades or more. And certainly the myeloid M2 axis in macrophages and what have you was known about way before these spatial technologies really came to fruition, I think.The Impact of Air PollutionEric Topol (28:01):Yeah. Well you touched on this about air pollution and that's another dimension of the work that you and your team have done. As you well know, there was a recent global burden of disease paper in the Lancet, which has now said that air pollution with particulate matter 2.5 less is the leading cause of the burden of disease in the world now.Charles Swanton (28:32):What did you think of that, Eric?Eric Topol (28:34):I mean, I was blown away. Totally blown away. And this is an era you've really worked on. So can you put it in perspective?Charles Swanton (28:42):Yeah. So we got into this because patients of mine, and many of my colleagues would ask the same question, I've never smoked doctor, I'm healthy. I'm in my mid 50s though they're often female and I've got lung cancer. Why is that doctor? I've had a good diet, I exercise, et cetera. And we didn't really have a very good answer for that, and I don't want to pretend for a minute we solved the whole problem. I think hopefully we've contributed to a little bit of understanding of why this may happen. But that aside, we knew that there were risk factors associated with lung cancer that included air pollution, radon exposure, of course, germline genetics, we mustn't forget very important germline variation. And I think there is evidence that all of them are associated with lung cancer risk in different ways. But we wanted to look at air pollution, particularly because there was an awful lot of evidence, several meta-analysis of over half a million individuals showing very convincingly with highly significant results that increasing PM 2.5 micron particulate levels were associated with increased risk of lung cancer.(29:59):To put that into perspective, where you are on the west coast of the US, it's relatively unpolluted. You would be talking about maybe five micrograms per meter cubed of PM2.5 in a place like San Diego or Western California, assuming there aren't any forest fires of course. And we estimate that that would translate to about, we think it's about one extra case of never smoking lung cancer per hundred thousand of the population per year per one microgram per meter cube rise in the pollution levels. So if you go to Beijing for example, on a bad day, the air pollution levels could be upwards of a hundred micrograms per meter cubed because there are so many coal fired power stations in China partly. And there I think the risk is considerably higher. And that's certainly what we've seen in the meta-analyses in our limited and relatively crude epidemiological analyses to be the case.(30:59):So I think the association was pretty certain, we were very confident from people's prior publications  this was important. But of course, association is not causation. So we took a number of animal models and showed that you could promote lung cancer formation in four different oncogene driven lung cancer models. And then the question is how, does air pollution stimulate mutations, which is what I initially thought it would do or something else. It turns out we don't see a significant increase in exogenous like C to A carcinogenic mutations. So that made us put our thinking caps on. And I said to you earlier, often all these discoveries have been made before. Well, Berenblum in 1947, first postulated that actually tumors are initiated through a two-step process, which we now know involves a sort of pre initiated cell with a mutation in that in itself is not sufficient to cause cancer.(31:58):But on top of that you need an inflammatory stimulus. So the question was then, well, okay, is inflammation working here? And we found that there was an interleukin-1 beta axis. And what happens is that the macrophages come into the lung on pollution exposure, engulf phagocytose the air pollutants, and we think what's happening is the air pollutants are puncturing membranes in the lung. That's what we think is happening. And interleukin-1 beta preformed IL-1 beta is being released into the extracellular matrix and then stimulating pre-initiated cells stem cells like the AT2 cells with an activating EGFR mutation to form a tumor. But the EGFR mutation alone is not sufficient to form tumors. It's only when you have the interleukin-1 beta and the activated mutation that a tumor can start.(32:49):And we found that if we sequence normal lung tissue in a healthy adult 60-year-old adult, we will find about half of biopsies will have an activating KRAS mutation in normal tissue, and about 15% will have an activating mutation in EGFR in histologically normal tissue with nerve and of cancer. In fact, my friend and colleague who's a co-author on the paper, James DeGregori, who you should speak to in Colorado, fascinating evolutionary cancer biologists estimates that in a healthy 60-year-old, there are a hundred billion cells in your body that harbor an oncogenic mutation. So that tells you that at the cellular level, cancer is an incredibly rare event and almost never happens. I mean, our lifetime risk of cancer is perhaps one in two. You covered that beautiful pancreas paper recently where they estimated that there may be 80 to 100 KRAS mutations in a normal adult pancreas, and yet our lifetime risk of pancreas cancer is one in 70. So this tells you that oncogenic mutations are rarely sufficient to drive cancer, so something else must be happening. And in the context of air pollution associated lung cancer, we think that's inflammation driven by these white cells, these myeloid cells, the macrophages.Cancer BiomarkersEric Topol (34:06):No, it makes a lot of sense. And this, you mentioned the pancreas paper and also what's going in the lung, and it seems like we have this burden of all you need is a tipping point and air pollution seems to qualify, and you seem to be really in the process of icing the mechanism. And like I would've thought it was just mutagenic and it's not so simple, right? But that gets me to this is such an important aspect of cancer, the fact that we harbor these kind of preconditions. And would you think that cancer takes decades to actually manifest most cancers, or do we really have an opportunity here to be able to track whether it's through blood or other biomarkers? Another area you've worked on a lot whereby let's say you could define people at risk for polygenic risk scores or various cancers or genome sequencing for predisposition genes, whatever, and you could monitor in the future over the course of those high-risk people, whether they were starting to manifest microscopic malignancy. Do you have any thoughts about how long it takes for the average person to actually manifest a typical cancer?Charles Swanton (35:28):That's a cracking question, and the answer is we've got some clues in various cancers. Peter Campbell would be a good person to speak to. He estimates that some of the earliest steps in renal cancer can occur in adolescence. We've had patients who gave up smoking 30 or so years ago where we can still see the clonal smoking mutations in the trunk of the tumor's evolutionary tree. So the initial footprints of the cancer are made 30 years before the cancer presents. That driver mutation itself may also be a KRAS mutation in a smoking cigarette context, G12C mutation. And those mutations can precede the diagnosis of the disease by decades. So the earliest steps in cancer evolution can occur, we think can precede diagnoses by a long time. So to your point, your question which is, is there an opportunity to intervene? I'm hugely optimistic about this actually, this idea of molecular cancer prevention.An Anti-Inflammatory Drug Reduces Fatal Cancer and Lung Cancer(36:41):How can we use data coming out of various studies in the pancreas, mesothelioma, lung, et cetera to understand the inflammatory responses? I don't think we can do very much about the mutations. The mutations unfortunately are a natural consequence of aging. You and I just sitting here talking for an hour will have accumulated multiple mutations in our bodies over that period, I'm afraid and there's no escaping it. And right now there's not much we can do to eradicate those mutant clones. So if we take that as almost an intractable problem, measuring them is hard enough, eradicating them is even harder. And then we go back to Berenblum in 1947 who said, you need an inflammatory stimulus. Well, could we do something about the inflammation and dampen down the inflammation? And of course, this is why we got so excited about IL-1 beta because of the CANTOS trial, which you may remember in 2017 from Ridker and colleagues showed that anti IL-1 beta used as a mechanism of preventing cardiovascular events was associated with a really impressive dose dependent reduction in new lung cancer primaries.(37:49):Really a beautiful example of cancer prevention in action. And that data weren't just a coincidence. The FDA mandated Novartis to collect the solid tumor data and the P-values are 0.001. I mean it's very highly significant dose dependent reduction in lung cancer incidents associated with anti IL-1 beta. So I think that's really the first clue in my mind that something can be done about this problem. And actually they had five years of follow-up, Eric. So that's something about that intervening period where you can treat and then over time see a reduction in new lung cancers forming. So I definitely think there's a window of opportunity here.Eric Topol (38:31):Well, what you're bringing up is fascinating here because this trial, which was a cardiology trial to try to reduce heart attacks, finds a reduction in cancer, and it's been lost. It's been buried. I mean, no one's using this therapy to prevent cancer between ratcheting up the immune system or decreasing inflammation. We have opportunities that we're not even attempting. Are there any trials that are trying to do this sort of thing?Charles Swanton (39:02):So this is the fundamental problem. Nobody wants to invest in prevention because essentially you are dealing with well individuals. It's like the vaccine challenge all over again. And the problem is you never know who you are benefiting. There's no economic model for it. So pharma just won't touch prevention with a barge pole right now. And that's the problem. There's no economic model for it. And yet the community, all my academic colleagues are crying out saying, this has got to be possible. This has got to be possible. So CRUK are putting together a group of like-minded individuals to see if we can do something here and we're gradually making progress, but it is tough.Eric Topol (39:43):And it's interesting that you bring that up because for GRAIL, one of the multicenter cancer early detection companies, they raised billions of dollars. And in fact, their largest trial is ongoing in the UK, but they haven't really focused on high-risk people. They just took anybody over age 50 or that sort of thing. But that's the only foray to try to reboot how we or make an early microscopic diagnosis of cancer and track people differently. And there's an opportunity there. You've written quite a bit on you and colleagues of the blood markers being able to find a cancer where well before, in fact, I was going to ask you about that is, do you think there's people that are not just having all these mutations every minute, every hour, but that are starting to have the early seeds of cancer, but because their immune system then subsequently kicks in that they basically kind of quash it for that period of time?Charles Swanton (40:47):Yeah, I do think that, I mean, the very fact that we see these sort of footprints in the tumor genome of immune evasion tells you that the immune system's having a very profound predatory effect on evolving tumors. So I do think it's very likely that there are tumors occurring that are suppressed by the immune system. There is a clear signature, a signal of negative selection in tumors where clones have been purified during their evolution by the immune system. So I think there's pretty strong evidence for that now. Obviously, it's very difficult to prove something existed when it doesn't now exist, but there absolutely is evidence for that. I think it raises the interesting question of immune system recognizes mutations and our bodies are replete with mutations as we were just discussing. Why is it that we're not just a sort of epithelial lining of autoimmunity with T-cells and immune cells everywhere? And I think what the clever thing about the immune system is it's evolved to target antigens only when they get above a certain burden. Otherwise, I think our epithelial lining, our skin, our guts, all of our tissues will be just full of T-cells eating away our normal clones.(42:09):These have to get to a certain size for antigen to be presented at a certain level for the immune system to recognize it. And it's only then that you get the immune predation occurring.Forever Chemicals and Microplastics Eric Topol (42:20):Yeah, well, I mean this is opportunities galore here. I also wanted to extend the air pollution story a bit. Obviously, we talked about particulate matter and there's ozone and nitric NO2, and there's all sorts of other air pollutants, but then there's also in the air and water these forever chemicals PFAS for abbreviation, and they seem to be incriminated like air pollution. Can you comment about that?Charles Swanton (42:55):Well, I can comment only insofar as to say I'm worried about the situation. Indeed, I'm worried about microplastics actually, and you actually cover that story as well in the New England Journal, the association of microplastics with plaque rupture and atheroma. And indeed, just as in parenthesis, I wanted to just quickly say we currently think the same mechanisms that are driving lung cancer are probably responsible for atheroma and possibly even neurodegenerative disease. And essentially it all comes down to the macrophages and the microglia becoming clogged up with these pollutants or environmental particulars and releasing chronic inflammatory mediators that ultimately lead to disease. And IL-1 beta being one of those in atheroma and probably IL-6 and TNF in neurodegenerative disease and what have you. But I think this issue that you rightly bring up of what is in our environment and how does it cause pathology is really something that epidemiologists have spent a lot of time focusing on.(43:56):But actually in terms of trying to move from association to causation, we've been, I would argue a little bit slow biologically in trying to understand these issues. And I think that is a concern. I mean, to give you an example, Allan Balmain, who works at UCSF quite close to you, published a paper in 2020 showing that 17 out of 20 environmental carcinogens IARC carcinogens class one carcinogens cause tumors in rodent models without driving mutations. So if you take that to a logical conclusion, in my mind, what worries me is that many of the sort of carcinogen assays are based on driving mutagenesis genome instability. But if many carcinogen aren't driving DNA mutagenesis but are still driving cancer, how are they doing it? And do we actually have the right assays to interpret safety of new chemical matter that's being introduced into our environment, these long-lived particles that we're breathing in plastics, pollutants, you name it, until we have the right biological assays, deeming something to be safe I think is tricky.Eric Topol (45:11):Absolutely. And I share your concerns on the nanoplastic microplastic story, as you well know, not only have they been seen in arteries that are inflamed and in blood clots and in various tissues, have they been seen so far or even looked for within tumor tissue?Charles Swanton (45:33):Good question. I'm not sure they have. I need to check. What I can tell you is we've been doing some experiments in the lab with fluorescent microplastics, 2.5 micron microplastics given inhaled microplastics. We find them in every mouse organ a week after. And these pollutants even get through into the brain through the olfactory bulb we think.Charles Swanton (45:57):Permeate every tissue, Eric.Eric Topol (45:59):Yeah, no, this is scary because here we are, we have these potentially ingenious ways to prevent cancer in the future, but we're chasing our tails by not doing anything to deal with our environment.Charles Swanton (46:11):I think that's right. I totally agree. Yeah.Eric Topol (46:15):So I mean, I can talk to you for the rest of the day, but I do want to end up with a topic that we have mutual interest in, which is AI. And also along with that, when you mentioned about aging, I'd like to get your views on these two, how do you see AI fitting into the future of cancer? And then the more general topic is, can we actually at some point modulate the biologic aging process with or without help with from AI? So those are two very dense questions, but maybe you can take us through them.Charles Swanton (46:57):How long have we got?Eric Topol (46:59):Just however long you have.A.I. and CancerCharles Swanton (47:02):AI and cancer. Well, AI and medicine actually in general, whether it's biomedical research or medical care, has just infinite potential. And I'm very, very excited about it. I think what excites me about AI is it's almost the infinite possibilities to work across scale. Some of the challenges we raised in the Cell review that you mentioned, tackling, embracing complexity are perfectly suited for an AI problem. Nonlinear data working, for instance in our fields with CT imaging, MRI imaging, clinical outcome data, blood parameters, genomics, transcriptomes and proteomes and trying to relate this all into something that's understandable that relates to risk of disease or potential identification of a new drug target, for example. There are numerous publications that you and others have covered that allude to the incredible possibilities there that are leading to, for instance, the new identification of drug targets. I mean, Eli Van Allen's published some beautiful work here and in the context of prostate cancer with MDM4 and FGF receptor molecules being intimately related to disease biology.(48:18):But then it's not just that, not just drug target identification, it's also going all the way through to the clinic through drug discovery. It's how you get these small molecules to interact with oncogenic proteins and to inhibit them. And there are some really spectacular developments going on in, for instance, time resolved cryo-electron microscopy, where in combination with modeling and quantum computing and what have you, you can start to find pockets emerging in mutant proteins, but not the wild type ones that are druggable. And then you can use sort of synthetic AI driven libraries to find small molecules that will be predicted to bind these transiently emerging pockets. So it's almost like AI is primed to help at every stage in scientific investigation from the bench all the way through to the bedside. And there are examples all the way through there in the literature that you and others have covered in the last few years. So I could not be more excited about that.Eric Topol (49:29):I couldn't agree with you more. And I think when we get to multimodal AI at the individual level across all their risks for conditions in their future, I hope someday will fulfill that fantasy of primary prevention. And that is getting me to this point that I touched on because I do think they interact to some degree AI and then will we ever be able to have an impact on aging? Most people conflate this because what we've been talking about throughout the hour has been age-related diseases, that is cancer, for example, and cardiovascular and neurodegenerative, which is different than changing aging per se, body wide aging. Do you think we'll ever changed body wide aging?Charles Swanton (50:18):Wow, what a question. Well, if you'd asked me 10 years ago, 15 years ago, do you think we'll ever cure melanoma in my lifetime, I'd have said definitely not. And now look where we are. Half of patients with melanoma, advanced melanoma, even with brain metastasis curd with combination checkpoint therapy. So I never say never in biology anymore. It always comes back to bite you and prove you wrong. So I think it's perfectly possible.Charles Swanton (50:49):We have ways to slow down the aging process. I guess the question is what will be the consequences of that?Eric Topol (50:55):That's what I was going to ask you, because all these things like epigenetic reprogramming and senolytic drugs, and they seem to at least pose some risk for cancer.Charles Swanton (51:09):That's the problem. This is an evolutionary phenomenon. It's a sort of biological response to the onslaught of these malignant cells that are potentially occurring every day in our normal tissue. And so, by tackling one problem, do we create another? And I think that's going to be the big challenge over the next 50 years.Eric Topol (51:31):Yeah, and I think your point about the multi-decade challenge, because if you can promote healthy aging without any risk of cancer, that would be great. But if the tradeoff is close, it's not going to be very favorable. That seems to be the main liability of modulation aging through many of the, there's many shots on goal here, of course, as you well know. But they do seem to pose that risk in general.Charles Swanton (51:58):I think that's right. I think the other thing is, I still find, I don't know if you agree with me, but it is an immense conundrum. What is the underlying molecular basis for somatic aging, for aging of normal tissues? And it may be multifactorial, it may not be just one answer to that question. And different tissues may age in different ways. I don't know. It's a fascinating area of biology, but I think it really needs to be studied more because as you say, it underpins all of these diseases we've been talking about today, cardiovascular, neurodegeneration, cancer, you name it. We absolutely have to understand this. And actually, the more I work in cancer, the more I feel like actually what I'm working on is aging.(52:48):And this is something that James DeGregori and I have discussed a lot. There's an observation that in medicine around patients with alpha-1 antitrypsin deficiency who are at higher risk of lung cancer, but they're also at high risk of COPD, and we know the associations of chronic obstructive pulmonary disease with lung cancer risk. And one of the theories that James had, and I think this is a beautiful idea, actually, is as our tissues age, and COPD is a reflection of aging, to some extent gone wrong. And as our tissues age, they become less good at controlling the expansion of these premalignant clones, harboring, harboring oncogenic mutations in normal tissue. And as those premalignant clones expand, the substrate for evolution also expands. So there's more likely to be a second and third hit genetically. So it may be by disrupting the extracellular matrices through inflammation that triggers COPD through alpha-1 antitrypsin deficiency or smoking, et cetera, you are less effectively controlling these emergent clones that just expand with age, which I think is a fascinating idea actually.Eric Topol (54:01):It really is. Well, I want to tell you, Charlie, this has been the most fascinating, exhilarating discussion I've ever had on cancer. I mean, really, I am indebted to you because not just all the work you've done, but your ability to really express it, articulate it in a way that hopefully everyone can understand who's listening or reading the transcript. So we'll keep following what you're doing because you're doing a lot of stuff. I can't thank you enough for joining me today, and you've given me lots of things to think about. I hope the people that are listening or reading feel the same way. I mean, this has been so mind bending in many respects. We're indebted to you.Charles Swanton (54:49):Well, we all love reading your Twitter feeds. Keep them coming. It helps us keep a broader view of medicine and biological research, not just cancer, which is why I love it so much.******************************************The Ground Truths newsletters and podcasts are all free, open-access, without ads.Please share this post/podcast with your friends and network if you found it informativeVoluntary paid subscriptions all go to support Scripps Research. Many thanks for that—they greatly helped fund our summer internship programs for 2023 and 2024.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff tor audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in. Get full access to Ground Truths at erictopol.substack.com/subscribe

Welcome back to The Trip Report Podcast, a production of Beckley Waves, a Psychedelic Venture StudioToday, we have the honor of speaking with distinguished neuroscientist and researcher of consciousness, Christof Koch, Ph.D.Christof is the Chief Scientist of the Tiny Blue Dot Foundation and Chief Scientist and President of the Allen Institute for Brain Science. He has been a prominent figure in the study of consciousness for over 40 years. His work includes collaborations with Nobel laureate Francis Crick and pioneering research in understanding the neural correlates of consciousness.Christof recently published a memoir of sorts titled Then I am Myself the World, where he discusses his profound experiences with psychedelics, including a near-death experience induced by 5-MeO-DMT. These experiences have significantly influenced his perspective on consciousness and the nature of reality.In our conversation, we explore:* Christof's journey from a devout Catholic upbringing to becoming a leading neuroscientist in the study of consciousness* His transformative experiences with psychedelics* The implications of these experiences on his understanding of consciousness and reality* The research and initiatives of the Tiny Blue Dot Foundation* The role of psychedelics, breathwork, and other techniques in expanding our perception and understanding of consciousness* The importance of integrating compassion, curiosity, and mindfulness in both personal and professional contextsChristof's insights offer a unique blend of scientific rigor and personal exploration, providing a fascinating perspective on the intersection of neuroscience and psychedelics.And now, I bring you my conversation with Christof Koch.Listen to the episode on Substack, Spotify, Google or Apple.Credits:* Hosted by Zach Haigney * Produced by Zach Haigney, Erin Greenhouse, and Katelin Jabbari* Find us at thetripreport.com* Follow us on Instagram, Twitter, LinkedIn and YouTubeTheme music by MANCHO Sounds, Mixed and Mastered by Rollin Weary This is a public episode. If you would like to discuss this with other subscribers or get access to bonus episodes, visit www.thetripreport.com

Christof Koch is a pioneering computational neuroscientist and neurophysiologist best known for his groundbreaking work on the neural basis of consciousness. He collaborated with Francis Crick, the co-discoverer of the structure of DNA, to establish a neurobiological framework for understanding consciousness. Christof served as the President and Chief Scientist of the Allen Institute for Brain Science in Seattle and continues his work there as a Meritorious Investigator. He is also the Chief Scientist of the Tiny Blue Dot Foundation in Santa Monica, CA, which funds research aimed at alleviating suffering, anxiety, and other forms of distress in people worldwide. Christof has authored over five books on consciousness, with his latest being "Then I Am Myself the World: What Consciousness Is and How to Expand It." This book delves into the subject of consciousness through the lenses of physics, psychology, neuroscience, philosophy, and computer science, as well as Christof's personal experiences exploring his consciousness. In this episode, Christof dives deep into what might explain the origin of consciousness and existing contradictions. We explore how our minds construct reality, the wonder of experience, and the profound implications of Integrated Information Theory. Christof also reflects on the importance of mindfulness, the power of belief, and the ongoing debate on free will. Our conversation includes: The origin of consciousness and the “Hard Problem Integrated Information Theory (IIT) How far down the phylogenetic tree consciousness might go The mind-body problem: physical structures and subjective experiences Panpsychism and how consciousness might be a fundamental aspect of matter. Qualities of experience and the perception box Mind-melding and the “uber” consciousness Why AI or any compute-based system may never be sentient The boundaries of consciousness and the dissolution of self The notion of "mind at large" Christoph's experiences with psychedelics Free will My hope is that this episode gives you a sense of awe about your mind so that you look at life and your experiences with a bit more wonder. Enjoy! For show notes and more, visit www.larryweeks.com 

From high school biology on up, we're taught the central dogma of biology - that biological information flows from DNA to RNA to proteins. This representation of the central dogma is, however, very much a simplification of its original formulation by Francis Crick and over-applying it can lead us down spurious paths and faulty conclusions. In this episode of Translating Proteomics, Parag and Andreas dive into the real meaning of the central dogma and discuss how modern biology research, including proteomics, shows we must drastically alter the ways we use and interpret the central dogma.Chapters:00:00 – What is the central dogma and how is it misinterpreted?08:06 – Regulation and control in biology11:58 – The need for new models in biology

Clark Smith has a Noam Chomsky story to tell. Clark Smith is in the studio for California Wine Country with Steve Jaxon and Dan Berger. Today he tells his MIT stories and more. The Clark Smith MIT story begins with his first two years of college, at Massachusetts Institute of Technology. This podcast episode is from the portion of the live show where Clark tells his personal story. Clark' last appearance on CWC was this episode of last March. The rest of Clark's conversation with Steve and Dan is about the wines he brought in today, so that has its own podcast episode, here. Clark Smith dropped out of MIT after two years and we finally hear the story today. At MIT, the senior faculty teach the Freshman courses. So he had Noam Chomsky for Linguistics, Francis Crick for microbiology, and several others. The trouble came when he had to declare a major at the beginning of his junior year, after earning straight As his first two years. He wanted to create his own major that combined science and art in some way. Today, that is a common practice in universities but at that time, he was not able to do it. So he dropped out thinking he would take a year to figure it out. The One-Way Cross Country Trip That is when Clark and a friend drove across the country and he ended up getting a job in a wine shop in Oakland. Someone asked him about a bottle of Paul Masson Emerald Dry wine. He didn't have the answer, so he started tasting the wines, eventually all of them. There were 250 wineries in the US and he visited a lot of them, maybe “all” of them. One day while visiting a winery he told his wife, that this was his calling. He is happy to have found the art plus science angle he was looking for. After that, he completed the BS and MS programs at UC Davis. Then he helped found RH Philips winery and he started his WineSmith consultancy. Click the logo to visit Davis Bynum Wines. When he was working for Benziger, their owner needed to find non-alcoholic wine. So he bought a reverse osmosis machine. One of the big problems of winemaking up to the 1970 was how to get rid of VA, Volatile Acidity, i.e. vinegar. In 1960 the average wine in California was 18.5% ABV, mostly Port and Sherry but that was before enough people learned how to really do it. There is great wine coming from places like South Africa and Australia, but most of the best product stays in the country of origin. Click the logo to visit our sponsor Rodney Strong for info on the 2024 Summer Concert series. Visit Clark's website to see the section about Forgeries and Oddities. Forgeries are wines that he makes exactly like wines from other places. His Cabernet Franc is Bordeaux style, made like a St. Emillion, and his Cabernet Sauvignon is made like a Pomerol. The Oddities are wines made from rare grapes you've never heard of, like Norton. Enter the promo code IKNOWCLARK all caps no spaces, for a 20% discount.

James Fadiman courtesy of Scott Kline Entheo*Anarcho*Animism / Endogenous Indigenuity Caroline is wildly enthused to welcome James Fadiman, PhD Who writes: “The work most worth doing for me has been helping myself and others remember how interwoven we are with the rest of the natural world. Only when we act out a dark fantasy of separation do we harm the very world in which we are enmeshed. Once awakened, exploitation of others, the destruction of any eco- system and that ultimate obscenity – war – all become as impossible to support as it would be to take a hammer and chisel (and) cut off one's own fingers. My different forms of self-expression: work, writing, photography are parts of who I have been and am. Psychedelic experiences have been the foundation stones of my worldview, as crucial now as when I had my first experience. If it is true, as one tradition suggests, that “God is as close to you as your jugular vein,” knowing that personally should be beneficial.” https://www.jamesfadiman.com/ connects to https://microdosingpsychedelics.com/ Support The Visionary Activist Show on Patreon for weekly Chart & Themes ($4/month) and more… *Woof*Woof*Wanna*Play?!?*   KPFA in Fund Drive The Psychedelic Exoporer's Guide = (for a pledge to KPFA of $100) Called “America's wisest and most respected authority on psychedelics and their use,” James Fadiman has been involved with psychedelic research since the 1960s. The Psychedelic Explorer's Guide addresses the immediate and long-term effects of psychedelic use for spiritual (high dose), therapeutic (moderate dose), and problem-solving (low dose) purposes. Fadiman outlines the best practices for safe, sacred entheogenic voyages learned through his more than 40 years of experience–from the benefits of having a sensitive guide during a session (and how to be one) to the importance of the setting and pre-session intention. James Fadiman reviews the newest as well as the neglected research into the psychotherapeutic value of visionary drug use for increased personal awareness and a host of serious medical conditions, including his recent study of the reasons for and results of psychedelic use among hundreds of students and professionals. He reveals new uses for LSD and other psychedelics, including extremely low doses for improved cognitive functioning and emotional balance. Cautioning that psychedelics are not for everyone, he dispels the myths and misperceptions about psychedelics circulating in textbooks and clinics as well as on the internet. Exploring the life-changing experiences of Ram Dass, Timothy Leary, Aldous Huxley, and Huston Smith as well as Francis Crick and Steve Jobs, James Fadiman shows how psychedelics, used wisely, can lead not only to healing but also to scientific breakthroughs and spiritual epiphanies. The post The Visionary Activist Show – Entheo*Anarcho*Animism appeared first on KPFA.

A cluster of brain cells in a dish, pulsing with electrical activity. A bee buzzing its way through a garden in bloom. A newborn baby staring up into his mother's eyes. What all these entities have in common is that we don't quite know what it's like to be them—or, really, whether it's like anything at all. We don't really know, in other words, whether they're conscious. But maybe we could know—if only we developed the right test.  My guest today is Dr. Tim Bayne. Tim is Professor of Philosophy at Monash University in Melbourne, Australia. He's a philosopher of mind and cognitive science, with a particular interest in the nature of consciousness. Along with a large team of co-authors, Tim recently published an article titled 'Tests for consciousness in humans and beyond.' In it, they review the current landscape of consciousness tests—or “C-tests”, as they call them—and outline strategies for building more and better tests down the road.  Here, Tim and I discuss what consciousness is and why theories of it seem to be proliferating. We consider several of the boundary cases that are most hotly debated right now in the field—cases like brain organoids, neonates, and split-brain patients. We sketch a few of the most prominent current consciousness tests: the command following test, the sniff test, the unlimited associative learning test, and the test for AI consciousness. We talk about how we might be able to inch our way, slowly, toward something like a thermometer for consciousness: a universal test that tells us whether an entity is conscious, or to what degree, or even what kind of conscious it is. Along the way, Tim and I talk about zombies, chatbots, brains in vats, and islands of awareness. And we muse about how, in certain respects, consciousness is like temperature, or perhaps more like happiness or wealth or intelligence, and maybe even a bit like fire.  I think you'll enjoy this one, friends—it's a thought-provoking conversation on a foundational topic, and one that takes us far and wide. So without further ado, here's my interview with Dr. Tim Bayne. Enjoy!   A transcript of this episode will be available soon.   Notes and links 4:45 – The philosopher Dan Dennett, who passed way in April, was known for his writings on consciousness—among them his 1991 book, Consciousness Explained. 7:00 – The classic paper on the neural correlates of consciousness, by Francis Crick and Christof Koch.   9:00 – A recent review of theories of consciousness by Anil Seth and Dr. Bayne. 10:00 – David Chalmers' classic paper on the “hard problem” of consciousness.  13:00 – Thomas Nagel's classic paper on what it's like to be a bat. 20:00 – A recent paper by James Croxford and Dr. Bayne arguing against consciousness in brain organoids. 23:00 – A recent paper by Dr. Bayne and colleagues about the emergence of consciousness in infants.  27:00 – A recent paper by Dr. Bayne and colleagues about consciousness in split-brain patients. An earlier paper by Dr. Bayne on the same topic. 30:00 – A paper by Dr. Bayne, Anil Seth, and Marcello Massimini on the notion of “islands of awareness.” 35:00 – The classic paper using the “(covert) command following test” in a patient in a so-called vegetative state.  38:00 – A 2020 paper introducing the “sniff test.”  40:00 – A recent primer on the “unlimited associative learning” test.  43:00 – An essay (preview only), by the philosopher Susan Schneider, proposing the AI consciousness test. 50:00 – The history of the scientific understanding of temperature is detailed in Hasok Chang's book, Inventing Temperature. 53:30 – Different markers of consciousness in infants are reviewed in Dr. Bayne and colleagues' recent paper. 1:03:00 – The ‘New York Declaration on Animal Consciousness' was announced in April. Read about it here.   Recommendations Being You, Anil Seth Into the Gray Zone, Adrian Owen Other Minds, Peter Godfrey-Smith   Many Minds is a project of the Diverse Intelligences Summer Institute, which is made possible by a generous grant from the Templeton World Charity Foundation to UCLA. It is hosted and produced by Kensy Cooperrider, with help from Assistant Producer Urte Laukaityte and with creative support from DISI Directors Erica Cartmill and Jacob Foster. Our artwork is by Ben Oldroyd. Our transcripts are created by Sarah Dopierala.  Subscribe to Many Minds on Apple, Stitcher, Spotify, Pocket Casts, Google Play, or wherever you listen to podcasts. You can also now subscribe to the Many Minds newsletter here! We welcome your comments, questions, and suggestions. Feel free to email us at: manymindspodcast@gmail.com.  For updates about the show, visit our website or follow us on Twitter: @ManyMindsPod.

Francis Crick, uno de los científicos que consiguió descifrar la estructura del ADN, compartió en primicia con su hijo en 1953 por carta uno de los mayores descubrimientos de la Humanidad. Nos cuenta la historia Laura Piñero en su #cartagrafía de un minuto especial para Todo por la Radio. 

A Note from James:I particularly want to reverse my aging. I'm not concerned about being able to run a mile or anything like that; I just want to reverse the aging of my brain. I feel there's a definite difference between my brain now and when I was younger. By the way, culturally, we acknowledge that the brain ages. Not only medically, but culturally, you have to adapt to being the wise older person rather than the sharp young person.We had a great conversation with Arthur Brooks about this. He wrote an excellent book, which I can't recommend enough, called "From Strength to Strength." That podcast with Arthur Brooks changed my life in how I view my brain aging. Additionally, several podcasts with David Sinclair about the aging process have also been life-changing.I have used the supplements he recommended and made the lifestyle changes he suggested back in 2019. David has conducted a lot of research in the five years since his book "Lifespan" was released, and I wanted to see what the current state of his research was. So, he came on the podcast.I'm very grateful; he doesn't do many podcasts. He shared some incredible discoveries and new information, giving me real insight. We discussed everything related to what he's doing in anti-aging and what he's discovered since the last time I had him on. At the special request of our listeners, I also asked him about testosterone.Towards the end of the podcast, I asked him about that, and his answer was very interesting. Here's David.Episode Description:Today, James discusses personal motivations for wanting to reverse aging, specifically targeting brain aging. The conversation moves into the broader cultural and scientific understandings of aging, touching on insights from Arthur Brooks and David Sinclair's research. Sinclair's work on anti-aging, including lifestyle changes and supplement use recommended by him, is highlighted, mentioning his book 'Lifespan' and the progress in his research over the past five years. Key discussions include the information theory of aging, the role of DNA and epigenetics in aging, and the concept of age reversal through maintaining or restoring the epigenome's integrity. The episode covers the potential of using Yamanaka factors for age reversal, the challenges in translating these findings from mice to humans, and regulatory considerations for human trials. Sinclair also touches on his ongoing work in developing chemical cocktails for age reversal, comparing lifestyle changes to these scientific advances.  Episode Summary:00:00 The Quest for Age Reversal: Personal Motivations and Influential Conversations01:11 Diving Deep into David Sinclair's Research on Anti-Aging02:24 Exploring the Information Theory of Aging and DNA's Role04:30 The Potential of Epigenetics in Reversing Aging07:14 The Challenges and Ethics of Age Reversal Technologies09:01 The Future of Anti-Aging: From Gene Therapy to Accessible Pills10:53 Debunking Myths and Addressing Controversies in Anti-Aging Supplements15:13 The Cutting-Edge of Aging Research: Yamanaka Factors and Epigenetic Reset25:05 The Philosophical and Practical Implications of Rejuvenation Research27:57 Unveiling New Breakthroughs in Cellular Biology28:19 Decoding the Mystery of Emanarcha Factors29:18 Exploring the Potential of Yamanaka Factors in Age Reversal29:43 The Future of Age Reversal: From Theory to Practice30:52 Innovative Approaches to Rejuvenation and Safety Measures31:52 Understanding the Complexity of Aging Across Different Organs34:57 The Fascinating World of Epigenetic Aging and Brain Plasticity37:20 Pushing the Boundaries: Chemical Cocktails for Rejuvenation39:46 Comparing Lifestyle Factors and Chemical Interventions in Aging40:56 Exploring the Possibilities of Reversing Menopause in Mice45:09 Navigating the Path to Human Trials and Regulatory Approval49:18 The Potential and Ethics of Off-Label Uses for Gene Therapy53:53 Personal Insights and Experiments in Anti-Aging ------------What do YOU think of the show? Head to JamesAltucherShow.com/listeners and fill out a short survey that will help us better tailor the podcast to our audience!Are you interested in getting direct answers from James about your question on a podcast? Go to JamesAltucherShow.com/AskAltucher and send in your questions to be answered on the air!------------Visit Notepd.com to read our idea lists & sign up to create your own!My new book, Skip the Line, is out! Make sure you get a copy wherever books are sold!Join the You Should Run for President 2.0 Facebook Group, where we discuss why you should run for President.I write about all my podcasts! Check out the full post and learn what I learned at jamesaltuchershow.com------------Thank you so much for listening! If you like this episode, please rate, review, and subscribe to “The James Altucher Show” wherever you get your podcasts: Apple PodcastsiHeart RadioSpotifyFollow me on social media:YouTubeTwitterFacebookLinkedIn

Rounding out the story begun in the previous installment, episode 13 of the DNA Papers centers on the publications in which the double helical structure for DNA was proposed, detailed, and its various implications speculated upon. It features four papers, all by Watson and Crick from Cambridge,. Together these papers not only proposed that DNA's three dimensional structure was a double-stranded helix, but also described the antiparallel and complementary nature of its two component strands and the specific pairing of the component nucleotide bases, namely, the purines, A and G, with the pyrimidines T and C respectively. The papers also discussed the implications of these features for the fundamental functions of DNA. For more resources on this topic, see https://www.chstm.org/video/144. Recorded on Dec. 11, 2023.

A true polymath, Moran started out in the Israeli military, in one of their elite intelligence units. Then ended up working as a hacker in computer security. And to this day is still in demand for that, but he had a weird experience when Francis Crick told him to junk hacking and get into working on neuroscience, and he did. And so Moran's had this amazing career some of the research that underpins things like Neuralink. These days, he's a professor in the business school at Columbia, where we recorded this conversation. I can't tell you how delightful Moran is. Super smart. Very insightful. Incredibly curious. He is difficult to pin down whenever I'm with him. He is somehow so good at asking questions and picking my brain that I hardly ever get to pick his brain. So the podcast was a perfect excuse to put him on the spot and I'm really thrilled that we get to share this with you guys. You'll notice that Moran still has a bit of an Israeli accent and he talks faster than anybody I've ever met. So most of you guys are used to putting podcasts on 2X. This one you might want to put on 0.5X. Important Links Moran's Website Moran on Wikipedia About Moran Cerf Moran Cerf is an American-French-Israeli neuroscientist, professor of business (at Colombia University), investor and former hacker.

Sir Paul Nurse, Director of the Francis Crick Institute in London, UK is a Nobel Prize winning geneticist and cell biologist whose research is recognised worldwide, particularly for his contributions to cell biology and cancer research. In this insightful interview with our sister publication, Research Features, Nurse discusses the institute's creative ‘bottom up' approach to research, his presidency of the Royal Society, science communication, and how he stays grounded despite a staggeringly successful career.Read more in Research Features: doi.org/10.26904/RF-150-5477109273Visit the Francis Crick Institute's website: crick.ac.uk

Jim Collins is one of the leading biomedical engineers in the world. He's been elected to all 3 National Academies (Engineering, Science, and Medicine) and is one of the founders of the field of synthetic biology. In this conversation, we reviewed the seminal discoveries that he and his colleagues are making at the Antibiotics-AI Project at MIT.Recorded 5 February 2024, transcript below with audio links and external links to recent publicationsEric Topol (00:05):Hello, it's Eric Topol with Ground Truths, and I have got an extraordinary guest with me today, Jim Collins, who's the Termeer Professor of Medical Engineering at MIT. He also holds appointments at the Wyss Institute and the Broad Institute. He is a biomedical engineer who's been making exceptional contributions and has been on a tear lately, especially in the work of discovery of very promising, exciting developments in antibiotics. So welcome, Jim.Jim Collins (00:42):Eric, thanks for having me on the podcast.Eric Topol (00:44):Well, this was a shock when I saw your paper in Nature in December about a new structure class of antibiotics, the one from 1962 to 2000. It took 38 years, and then there was another one that took 24 years yours, the structural antibiotics. Before I get to that though, I want to go back just a few years to the work you did published in Cell with halicin, and can you tell us about this? Because when I started to realize what you've been doing, what you've been chipping away here, this was a drug you found, halicin, as I can try to understand, it works against tuberculosis, c. difficile, enterobacter that are resistant, acinetobacter that are resistant. I mean, this is, and this is of course in mice models. Can you tell us how did you make that discovery before we get into I guess what's called the Audacious Project?Jim Collins (01:48):Yeah, sure. It's actually a fun story, so it is origins go broadly to institute wide event at MIT, so MIT in 2018 launched a major campus-wide effort focused on artificial intelligence. The institute, which had played a major role in the first wave of AI in the 1950s, 1960s, and a major wave in the second wave in the 1980s found itself kind of at the wheel in this third wave involving big data and deep learning and looked to correct that and to correct it the institute had a symposium and I had the opportunity to sit next to Regina Barzilay, one of our faculty here at MIT who specializes in AI and particularly AI applied to biomedicine and we really hit it off and realized we had interest in applying AI to drug discovery. My lab had focused on antibiotics to then close to 15 years, but primarily we're using machine learning and network biology to understand the mechanism of action of antibiotics and how resistance arise with the goal of boosting what we already had, with Regina we saw there was an opportunity to see if we could use deep learning to get after discovery.(02:55):And notably, as you kind of alluded in your introduction, there's really been a discovery void and the golden age of discovery antibiotics was in the forties, fifties and sixties before I was born and before you had the genomic revolution, the biotech revolution, AI revolution. Anyways, we got together with our two groups, and it was an unfunded project and we kind of cobbled together very small training set of 2,500 compounds that included 1,700 FDA approved drugs and 800 natural compounds. In 2018, 2019, when you started this, if you asked any AI expert should you initiate that study, they would say absolutely not, there's going to be two big data. The idea of these models are very data hungry. You need a million pictures of a dog, a million pictures of a cat to train a model to differentiate between the cat and the dog, but we ignored the naysayers and said, okay, let's see what we can do.(03:41):And we apply these to E. coli, so a model pathogen that's used in labs but is also underlies urinary tract infections. So it's a look to see which of the molecules inhibited growth of the bacteria as evidence for antibacterial activity and we could have measured and we quantified each of their effects, but because we had so few compounds, we just discretized instead, if you inhibited at least 80% of the growth you were antibacterial, and if you didn't achieve that, you weren't antibacterial zero in ones. We then took the structure of each molecule and trained a deep learning model, specifically a graphical neural net that could look at those structures, bond by bond, substructure by substructure associated with whatever features you look to train with. In our case, making for good antibiotic, not for good antibiotic. We then took the train model and applied it to a drug repurposing hub as part of the Broad Institute that consists of 6,100 molecules in various stages of development as a new drug.(04:40):And we asked the model to identify molecules that can make for a good antibiotic but didn't look like existing antibiotics. So part of the discovery void has been linked to this rediscovery issue we have where we just keep discovering quinolones like Cipro or beta-lactams like penicillin. Well, anyways, from those criteria as well as a small tox model, only one molecule came out of that, and that was this molecule we called halicin, which was named after HAL, the killing AI computer system from 2001 Space Odyssey. In this case, we don't want it to kill humans, we want it to kill bacteria and as you alluded, it turned out to be a remarkably potent novel antibiotic that killed off multi-drug resistant extensively drugs, a pan-resistant bacteria went after to infections. It was affected against TB, it was affected against C. diff and acinetobacter baumannii and acted to a completely new mechanism of action.(05:33):And so we were very excited to see how AI could open up possibilities and enable one to explore chemical spaces in new and different ways. We took them model, then applied it to a very large chemical library of 1.5 billion molecules, looked at a subset of about 110 million that would be impossible for any grad student, any lab really to look at that experimentally but we looked at it in a model computer system and in three days could screen those 110 million molecules and identified several new additional candidates, one which we call salicin, which is the cousin of halicin that similes broad spectrum and acts to a novel mechanism of action.Eric Topol (06:07):So before we go further with this initial burst of discovery, for those who are not used to deep neural networks, I think most now are used to the convolutional neural network for images, but what you use specifically here as you alluded to, were graph neural networks that you could actually study the binding properties. Can you just elaborate a little bit more about these GNN so that people know this is one of the tools that you used?Jim Collins (06:40):Yeah, so in this case, the underlying structure of the model can actually represent and capture a graphical structure of a molecule or it might be of a network so that the underlying structure itself of the model will also look at things like a carbon atom connects to an oxygen atom. The oxygen atom connects to a nitrogen atom and so when you think back to the chemical structures we learned in high school, maybe we learned in college, if we took chemistry class in college, it was actually a model that can capture the chemical structure representation and begin to look at sub aspects of it, associating different properties of it. In this case, again, ours was antibacterial, but it could be toxic, whether it's toxic against a human cell and the model, the train model, the graph neural model can now look at new structures that you input them and then make calculations on those bonds so a bond would be a connection between two atoms or substructures, be multiple bonds, interconnecting multiple atoms and assign it a score. Does it make, for example, in our case, for a good antibiotic.Eric Topol (07:48):Right. Now, what's also striking as you set up this collaboration that's interdisciplinary with Regina, who I know of her work through breast cancer AI and not through drug discovery and so this was, I think that new effort and this discovery led to this, I love the name of it, Audacious Project, right?Jim Collins (08:13):Right. Yeah, so a few points on the collaboration then I'll speak to Audacious Project. In addition to Regina, we also brought in Tommi Jaakkola, another AI faculty member and marvelous colleague here at MIT and really we've benefited from having outstanding young folks who were multilingual. We had very rich, deep trained grad students from ML on Regina and Tommi's side who appreciated the biology and we had very richly, deeply trained postdocs, Jon Stokes in particular from the microbiology side on my side, who could appreciate the machine learning and so they could speak across the divide. And so, as I look out in the next few decades in this exciting time of AI coming into biomedicine, I think the groups will make a difference of those that have these multilingual young trainees and two who are well set up to also inject human intelligence with machine intelligence.(09:04):Brings the Audacious Project. Now, prior to our publication of halicin, I was invited by the Audacious Project to submit a proposal, the Audacious Project is a new philanthropic effort run by TED, so the group that does the TED Talks that's run by Chris Anderson, so Chris had the idea that there was a need to bring together philanthropists around the world to go for a larger scale in a collective manner toward audacious projects. I pitched them on the idea that we could use AI to address the antibiotic resistance crisis. As you can appreciate, and many of your listeners can appreciate that we're doomed if we don't actually address this soon, in that the number of resistance strains that are in our communities, in our hospitals has been growing decade upon decade, and yet the number of new antibiotics being developed and approved has been dropping decade upon decade largely because the antibiotic market is broken, it costs just as much to develop an antibiotic as it does a cancer drug or a blood pressure drug.(09:58):But antibiotic you take once or maybe over the course of three to five days, blood pressure, drug cancer drug you might take for months if not for the rest of your life. Pricing points for antibiotics are small dollars, cancer drugs, blood pressure drugs, thousands if not hundreds of thousands. We pitched this idea that we can maybe turn to AI and use the power of AI to address this crisis and see if we could use our wits to outcompete the genes of superbugs and Chris and his team really were taken with this, and we worked with them over the course of nine months and learned how to make the presentations and pulled this together. Chris took our pitches to a number of really active and fantastic philanthropists, and they got behind us and gave us a good amount of money to launch what we have now called the Antibiotics-AI Project at MIT and in conjunction with it and also using funding from the Audacious Project, we've launched a nonprofit called Phare Bio which is French for lighthouse, so our notion is that antibiotics are public good that we need to get behind his community and Phare Bio, which is run by Akhila Kosaraju, she's the CEO and President, is the mission of which is to take the most promising molecules out of the antibiotics AI project and advance them towards the clinic through partnerships with biotech, with pharma, with other nonprofits, with nation states as needed.Eric Topol (11:18):Well, before I get to the next chain of discovery and as explain ability features, which we all like to see when you can explain stuff with AI, did halicin because of this remarkable finding, did it get into clinical trials yet?Jim Collins (11:36):It's being advanced quite nicely and aggressively by Phare Bio. So Phare Bio is in discussions with the Department of Defense and BARDA, and actually on an interesting feature of halicin is that it acts like a flash bomb in the gut, meaning that when delivered orally to the gut, it only acts briefly and very quickly in a fairly narrow spectrum manner as well, so that it can go after pathogens sparing the commensals. One of the challenges our US military face is one of the challenges many militaries face are gut issues when soldiers are first deployed to a new location, and it can disable the soldiers for three to four weeks. And so, there's a lot of excitement that halicin might be effective as a treatment to help prevent gut dysbiosis resulting from new deployments.Eric Topol (12:27):Oh wow. That's another application that I would never have thought of. Interesting, so you then moved on to this really big report in Nature, which I think this is now involving a transformer model as I recall. So you can explain the difference and you made a discovery from a massive, again, number of potential compounds to staph aureus resistant methicillin resistant agents that were very potent in vivo. So how did you make this big jump? This is a whole new structural class of antibiotics.Jim Collins (13:11):Yeah, so we made this jump, this was an effort led by Felix Wong, who's a really talented postdoc in my lab, and we got intrigued of to what extent could we expand the utility of AI and biology of medicine. As you can appreciate that, that many of our colleagues are underwhelmed by the black box nature of many AI models and by black box I mean that when you train your model, you then largely use it as a filter where you'll provide the model with some input. You look at the output and the outputs, what's of interest to you, but you don't really understand in most cases, what guided the model to make the prediction of the output that you look at and that can be very unsatisfactory for biology, interested in mechanism. It can be very unsatisfactory for physicians interested in understanding the underlying disease mechanism.(13:57):It can be unsatisfactory for biotech and drug discoveries that want to understand how drugs act and what maybe underlies meaningful structural features. So with Felix, we decided it'd be interesting if you could open up the box. So could you look inside the model to see what was being learned? We are able to open up, in this case actually, we primarily focused on graph neural nets. We now have a new piece we're just about to submit on transformers, but in this case, we could open up and look to see what were the rationales, what were the chemical substructures that the model was pointing to in each compound that was leading to the high prediction that it could make for a good antibiotic and these rationales we then used as hooks, I should notably say, that we were able to identify the rationales from these large collections using algorithms that would develop by DeepMind as part of their AlphaGo program.(14:51):So AlphaGo was developed by DeepMind as a deep learning platform to play and win go the ancient Asian board game and we used similar approaches called Monte Carlo Tree Search that allowed us to identify these rationales that we effectively then used as hooks and kind of organizing hooks on screens where you can envision or appreciate that most exposed screens give you one-offs. This molecule does what you want and silico screens are similarly designed with these rationales. We could use them as organizing hooks to say, ah, these compounds that are identified as making for very good antibiotics all have the same substructure and thus they likely in the same class and act in similar mechanism and this led us to identify five novel classes, one of which we highlighted in this piece that acts very effectively against MRSA, so methicillin-resistant staph aureus you alluded, which is probably the most famous of the antibiotic resistant pathogens that we even outside infectious are quite familiar with. It be devil's athletes, so NFL players are often hit with MRSA, whether from scraping their limbs on AstroTurf or from actually surgeries to say, for example, correct something at their knee. This new class had great efficacy in animal models, again, acting through a new mechanism.Eric Topol (16:12):Will you bring that forward like halicin through this same entity?Jim Collins (16:17):Yes. We've now provided the molecules to Phare Bio and they're digging in to see which of these might be the most exciting and interesting to advance clinically.Eric Topol (16:26):I mean, it's amazing because this area is so neglected. Maybe you can help explain, since we're talking about existential threats as we get more and more resistant antibiotics and the biopharma industry is basically not into this and it relies on the work that you've been doing perhaps or other groups, I don't know of any that are doing more than you. I mean, it's incredible to me. Is it just because of the financial aspects that there's no business in the life science industry?Jim Collins (17:03):It's an interesting challenge. So I've thought about it. I really haven't come up with a great solution yet, but I think you've got multiple factors at play. One is that I think all of us, every one of your listeners has lost someone to a bacterial infection, but in most cases you don't realize you lost them to a bacterial infection. It might be that your elderly relative went into the hospital with a condition but acquired hospital-based infection and died subsequently from that and happened quite quickly. Another cases, again, it's secondary. Notably, during the pandemic, one out of seven individuals hospitalized for Covid had a bacterial infection and 50% of those who died had a bacterial co-infection. And noted by going back to the Spanish flu of over a hundred years ago. It was as deadly as it was because we didn't have antibiotics and most of the folks that died had a bacterial co-infection.(17:56):So you have this in the backdrop, you then have that, nobody's kind of gotten behind it, so we don't have any major foundation addressing antibiotic resistance. There are no charity walks, there are no charity runs, there is no month, there is no color, there are no ribbons, there are no celebrity behind it, there's just not known so it hasn't captured the public's imagination. AThen you come with that, this backdrop of the broken market where I said shared, it's really expensive to develop a new antibiotic, but if you develop a new antibiotic, the tendency now will be to shelve it until it's desperate so now even the young companies that had developed and gotten an antibiotic through to approval often went bankrupt because the model, the market couldn't provide them with revenue to go after the next one or sustain their efforts. And so you have pharma biotech jumping out. I think we need two-pronged effort going forward. I do think we need nation states to come forward and get behind this, and I think we increasingly need philanthropists to come forward and go after it. As I share your term of existential threat, I think if you speak with most educated individuals, antibiotic resistance broadly, antimicrobial resistance will be on everyone's existential threat list but notably of that list, it's the cheapest one that can be solved.Eric Topol (19:09):Well, you're showing that you've got the most extraordinary candidates that have been found in decades. So that says a lot right there.Jim Collins (19:18):Important step, yeah. So I think we've got additional innovation needed in the models to address this, and until we have that address, then this interesting discoveries we and others are making will not get to patients. So we need to have that additional next step to close this gap.Eric Topol (19:32):Now, obviously this has relied on AI and the progress that's occurring in AI to enable some of your work. I am fascinated by the use of AlphaGo. Most times we hear about using AlphaFold2, but you actually use AlphaGo the original game DeepMind work but there also was the progress of from deep neural networks to transformer models and your ability now to basically exemplify what can be achieved in drug discovery using the progress in multimodal AI. Is this something that is making a difference for you and your group?Jim Collins (20:13):It is, it's huge. I think it's very early in terms of the introduction to these new tools extensively within drug discovery. Machine learning has been used for over two decades, both supervised learning and unsupervised learning. Now we're seeing groups coming in for the deep learning efforts. It's largely data-driven so in fact, with the exception of sequences, most of drug discoveries not yet big data in the big data phase, but it's beginning to change. It's truly been transformative for us, so we've used graph neural nets primarily for our discovery efforts. We're now beginning to incorporate language models as multimodal models along with the graph neural nets as well as to see to what extent pre-trained language models. For example, mobile form from IBM, which was trained on PubChem and the ZINC database could be fine-tuned with small amounts of training data, screening data from a resistant organism.(21:06):Third, and I made an indirect allusion already, we've been looking at using transformers and genetic algorithms in older form of AI tech for design of novel antibiotics so we've been now looking to see using fragments as a starting base, using trained models to build out novel antibiotics that can then be de novo designed. One of the big challenges in that space is how do you synthesize these molecules? So you have both the challenge of can you come up with a small number of steps that enable you to synthesize? And second is could you find somebody to synthesize them? And each of those remains very big challenges. My faculty colleague here at MIT, Connor Coley's probably one of the world leaders, easily, he's in using AI to calculate the synthesized ability of a molecule, but we still have gaps in that we don't have the community resources to make most of what we come up with.Eric Topol (21:58):Well, one of the features of large language models that David Baker at the Protein Design Institute exploited is its ability to hallucinate and come up with proteins that don't exist. Can you do the same thing in your design of antibiotic candidate molecules in a way that is not worrying about the synthesis, but just basically the hallucinatory behavior of large language models?Jim Collins (22:28):It's interesting, so yes and so David's work is marvelous and we're big fans and longtime friends of his work. Yes, so we've been driving these models truly to do de novo synthesis. So based on what has been learned, can you put together molecules that one's never seen before? We're doing it quite successfully. It becomes interesting from the hallucination in that it comes out really more of these models making stuff up and ours it's really more directing the hallucinations, right? Really looking to see can we harness the imagination of the models in order to move them forward in very creative design manners.Eric Topol (23:08):Yeah, I mean, I think most people have a negative connotation of hallucinations, but these are the smart variety potentially. This in many ways you could say there's so much crowded interest in the drug discovery AI world, but what you're doing now seems to be setting the pace in many respects for others to follow such remarkable advances in a short time. By the way, we'll link to that TED talk you gave in April 2020, where in seven minutes you went over what you're doing of course and who would've, and that was in 2020 that where you'd be three or four years later, and that was what you're going to do over the next seven years with seven new classes of new antibiotics. Now, before we wrap up, it isn't just that you're an AI antibiotic, you and your team antibiotic discover and doing compressing in time, what has taken decades that you're doing in months, but also you are a father of figure in the field of synthetic biology and I wonder if you, before we wrap up, can explain not only what synthetic biology is since a lot of people don't really know what that means, but how does that dovetail with your efforts in what we've been discussing?Jim Collins (24:33):Yeah, thanks. So synthetic biology is a relatively new field that's bringing together engineers with biologists to use engineering principles to model design and build synthetic gene networks and other molecular components that can be used to rewire and reprogram living cells and cell-free systems, endowing them with novel functions of a variety of applications. So the circuits, these programmable cells are impacting broad swats of the economy from food and water to health and sustainability of bioenergy to human health. Our focus is primarily human health and we've been advancing the idea that you can reprogram bacteria to detect and treat bacterial infections. So we've shown you can use this to go after cholera, we've shown you can use is to prevent antibiotic induced gut dysbiosis. We've also used synthetic biology to create whole new classes of diagnostics. For example, paper-based ones using RNA sensors for Ebola, for Zika and for Covid.(25:33):How it dovetails with what we talked about is that I think there's a great opportunity now to turn to AI to expand synthetic biology, both expanding the number of parts we have to re-engineer living systems as well as to better infer design principles that can be used to reprogram rewire living systems. We're beginning to advance, we're not yet at the SynBio AI project phase, but very early efforts and David's dominating the protein space and we and others are beginning to now movement to the RNA space. So to what extent can we create large libraries of RNA components, train language-based models, structure-based models that can both predict RNA structure more critically predict RNA function and as you know from your marvelous work and what's happening is that it's the exciting age of RNA of getting after RNA therapeutics, be it mRNA or CRISPR related and we still need to get better at our ability to design those therapeutics with certain functions in mind, and we think AI is going to help get us there faster.Eric Topol (26:34):Well, speaking of that, there was a paper this week in Cell by McCafferty and colleagues, and one of the sentences that struck me, we are standing on the cusp of a new era of biology, where the integration of multimodal structural datasets with multiscale physics-based simulation will enable the development of visible, virtual cells. This is yet another lineage or direction of where we're headed with AI, but this fusion of the advances that are occurring right now in biology with AI that extend in many different directions, it's so exciting and you are basically nailing it. I mean, you're putting points on the board, Jim, and I just have to say, I'm blown away by what you've been accomplishing in a time space that's so incredibly compressed.Jim Collins (27:40):Oh, well thanks. Well, you think back to the early days of molecular biology and physicists like Francis Crick and Max Delbrück played huge pioneering roles and then in the second wave in the eighties or so, you had other physicists like Walter Gilbert playing big roles. I do think physicists computer scientists are starting now to play big roles in this next phase where we need tools like AI in order to really grapple with and harness the complexity, both the biology and the chemistry that underlies living cells. They can kind of expand our intuitions both to understand and to really control these systems for good going forward.Eric Topol (28:15):Well, you're doing it and we're be cheering for the success of these drugs that you've come up with in the clinical trials as they go forward because they look so remarkably promising. You even highlighted ways that I wouldn't have envisioned where they could make a difference, so we'll follow your work, you and your colleagues with great interest. Thanks so much for joining,Jim Collins (28:37):Eric, thanks for having me. Enjoyed our conversation.******************************************************************************Thanks for listening to Ground Truths. Please share if you found this podcast informative.Full video interview will post here Get full access to Ground Truths at erictopol.substack.com/subscribe

The Discovery of DNA Join us today as we learn about how DNA was discovered. Sources: https://www.britannica.com/biography/James-Dewey-Watson  https://www.genome.gov/genetics-glossary/Double-Helix    Picture  https://kids.britannica.com/students/article/DNA/398123  https://www.britannica.com/science/DNA  https://profiles.nlm.nih.gov/spotlight/sc/feature/doublehelix  https://www.ducksters.com/biography/scientists/watson_and_crick.php  https://kids.britannica.com/kids/article/Francis-Crick/476244   Send us listener mail!  Send an audio message: anchor.fm/inquisikids-daily/message  Send an email: podcast@inquisikids.com   

Shownotes and Transcript Intelligent Design may not be an idea you are familiar with but it has interested me since I was a child.  I find it impossible to accept that the world we live in and the complexity of human beings is all based on luck and chance. There has to be an intelligent designer.  Stephen C Meyer is one of the most renowned experts on this very topic and his recent appearance on The Joe Rogan Experience has made many people question the theory of a universe without God.  At what point did intellectuals decide that scientific knowledge conflicts with traditional theistic beliefs? Is it even statistically possible for such complexity to just appear? What about the question of who is this intelligent designer?  Stephen Meyer will help you view the world around you with a brand new perspective. Dr. Stephen C. Meyer received his Ph.D. from the University of Cambridge in the philosophy of science. A former geophysicist and college professor, he now directs the Center for Science and Culture at the Discovery Institute in Seattle. In 2004, Meyer ignited a firestorm of media and scientific controversy when a biology journal at the Smithsonian Institution published his peer-reviewed scientific article advancing intelligent design. Meyer has been featured on national television and radio programs, including The Joe Rogan Experience, The NewsHour with Jim Lehrer, CBS's Sunday Morning, NBC's Nightly News, ABC's World News, Good Morning America, Nightline, FOX News Live, and the Tavis Smiley show on PBS. He has also been featured in two New York Times front-page stories and has garnered attention in other top-national media. Dr. Meyer is author of the New York Times bestseller Darwin's Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design and Signature in the Cell, a Times Literary Supplement Book of the Year. He is also a co-author of Explore Evolution: The Arguments For and Against Neo-Darwinism and Theistic Evolution: A Scientific, Philosophical, and Theological Critique. Connect with Stephen... WEBSITE           https://stephencmeyer.org/                            https://www.discovery.org/                            https://returnofthegodhypothesis.com/ X                         https://x.com/StephenCMeyer?s=20 BOOKS               https://www.amazon.co.uk/stores/author/B001K90CQC Interview recorded 13.12.23 Connect with Hearts of Oak... WEBSITE            https://heartsofoak.org/ PODCASTS        https://heartsofoak.podbean.com/ SOCIAL MEDIA  https://heartsofoak.org/connect/ TRANSCRIPTS   https://heartsofoak.substack.com/ Support Hearts of Oak by purchasing one of our fancy T-Shirts....  SHOP                  https://heartsofoak.org/shop/ *Special thanks to Bosch Fawstin for recording our intro/outro on this podcast. Check out his art https://theboschfawstinstore.blogspot.com/ and follow him on GETTR https://gettr.com/user/BoschFawstin and Twitter https://twitter.com/TheBoschFawstin?s=20  Transcript (Hearts of Oak) Dr. Stephen Meyer. It's wonderful to have you with us. Thank you so much for your time today. (Stephen C Meyer) Thanks for inviting me, Peter.  No, it's great to have you. And people can find you on Twitter @StephenCMayer. It's on the screen there. And also discovery.org, the Discovery Institute. And you obviously received your PhD in philosophy of sciences from England, from University of Cambridge, your a former geophysicist, college professor, and you now are the director of Discovery Institute, author of many books. The latest is Return of the God Hypothesis, Three Scientific Discoveries That Reveal the Mind Behind the Universe, and the links for those books will be in the description. But, Dr. Meyer, if I can maybe, I think I remember as a child, church loyalty, being at church and getting a stamp for attending. I remember asking for a book on creationism then, and we may touch on different creationism, intelligent design. I mean, it was 10 or 11. And I remember being fascinated by this whole topic of how God can be seen in the world around us. Maybe I can ask you about your journey. What has been your journey to being one of the, I guess, main proponents on intelligent design? Well, I've always been interested in questions at the intersection between science and philosophy or science and  larger worldview questions or science and religion the questions that are addressed about, you know, how do we get here and what is, is there a particular significance to human life, what is the meaning of life, in the early part of my scientific career I was working as a geophysicist as you mentioned the introduction and in the city where I was working, a conference came to town that was investigating that intersection of science and philosophy, science and belief, and it was addressing three big questions, and they were the origin of the universe, the origin of life, and the origin and nature of human consciousness. And the conference was unique in that it had invited leading scientists and philosophers representing both theism, broadly speaking, belief in God, and scientists and philosophers who rejected theism and who affirmed the more common view among leading scientists at that time, which was materialism or sometimes called naturalism. We have the New Atheist Movement with their scientific atheists and people of more of that persuasion. So it was, let's look at the origin of the universe from the standpoint. What do the data say, what do you theists say about it, what do you non-theist materialists say about it, and it was a fascinating conference and I was particularly taken by the panels on the origin of the universe and the origin of life because surprisingly to me it seemed that the theists had the intellectual initiative that the the evidence in those about the origin of the universe, and then about the complexity of the cell and therefore the challenges it posed to standard chemical evolutionary theories of the origin of life that in both these two areas, both these two subjects, it seemed that there were powerful, theistic friendly arguments being developed, in one case about the, what you might call, a reviving of the ancient cosmological argument because of the evidence that scientists had discovered about the universe having a beginning. And in the other case, what we now call the theory of intelligent design, that there was evidence of design in the cell, in particular, in the digital code that is stored in the DNA molecule, the information and information processing system of the cell. And was it that time? And still to this day is something that undirected theories of chemical evolution have not been able to explain. And instead, what we know from our experience is that information is a mind product, which is a point that some of these scientists made at this panel, that when we see digital code or alphabetic text or computer code, and many people have likened the information and DNA to a computer code, we always find a mind behind that. So this was the first time I was exposed to that way of thinking. I got fascinated with that. A year later, after the conference, I ended up meeting one of the scientists on the Origin of Life panel, a man named Charles Thackston, who had just written a book with two other co-authors called The Mystery of Life's Origin. He was detailing in that book, he and his colleagues were detailing sort of chapter and verse the problems with trying to explain the origin of the first cell from simpler chemicals in some alleged or presupposed prebiotic soup. And the three authors showed that this was implausible in the extreme, given what we know scientifically about how chemistry works versus how cells work. And over the ensuing year, he kind of mentored me and I got fascinated with the subject and ended up getting a fellowship. A Rotary Fellowship to study at Cambridge for a year and then ended up extending on. I did my master's thesis and then my PhD thesis both on origin of life biology within the History and Philosophy of Science Department at Cambridge. And while I was there, I started to meet other scientists and scholars who were having doubts about standard Darwinian and chemical evolutionary theories of life's origin. And by the early 90s, a number of us had met each other and connected and had some private conferences. And out of that was born a formal program investigating the evidence for intelligent design in biology, in physics, in cosmology, and in 96, we started a program at Discovery Institute. You were very kind to me to call me the director of the whole institute. I direct a program within the institute called the Center for Science and Culture, which is the institutional home. A network of scientists who are investigating whether or not there is, empirical scientific evidence for a designing mind behind life in the cosmos and and the program just continues to grow, the network especially continues to grow, we've got fantastic scientists from all around the world now who are sympathetic to that position and I would mention too that it's a position that's kind of reviving an ancient view going back to certainly the time of the scientific revolution. In particular, we've discovered back to the scientific revolution in Cambridge where I had been fortunate enough to study. There's a, in the college that I was part of, St. Catherine's, there was back in the 17th century, one of the founders of modern botany, who was also one of the first authors of what's called British National Theology. His name was John Ray. Ray was the tutor of Isaac Barrow, a mathematician who in turn tutored Newton and so this whole tradition of seeing the fingerprints of a creator in the natural world is something that was launched in Britain, particularly in Cambridge there were other figures like Robert Boyle who were in other places but the Cambridge tradition of natural theology was very strong from that time period in the 17th century, late 17th century, right up to figures like James Clerk Maxwell, the great physicist in the late 19th century who was critical, sceptical of Darwinism and articulated the idea of design. And I think that's now being revived within contemporary science. There's a growing minority of scientists who see evidence of design in nature.  Now, the understanding of intelligent designer, that's a new thinking, but through the millennia, that's been the norm. Individuals have viewed the world through the lens that there is a God, and that has helped them understand and see the world. But there must have been a point, I guess, when intellectuals decided that scientific knowledge conflicts with that that traditional belief, that traditional theistic belief. Yeah, that's a great way of framing the discussion, Peter. There's a historian of science in Britain named Steve Fuller, who's at Warwick. And he's argued that the idea of intelligent design has been the framework out of which science has been done since the period of the scientific revolution at least and that the the post Darwinian deviation from that, denying that there's actual design and only instead as the Darwinian biologists say the appearance or illusion of design, you may remember from Richard Dawkins's famous book the blind watchmaker, page one he says biology is the study of complicated things that give the appearance of having been designed for a purpose. And of course, for Dawkins and his followers, and for Darwinians from the late 19th century forward, the appearance of design is an illusion. And it was thought to be an illusion because Darwin had formulated an undirected, or had identified an undirected, unguided process, which he called natural selection that could mimic the powers of a designing intelligence, or so he argued, without itself being designed or guided in any way. And that's kind of where we've engaged the argument. Is that appearance of design that nearly all biologists recognize merely an appearance, or is it the product of an actual guiding intelligence? And that's why we call our theory intelligent design. We're not challenging the idea that there has been change over time, one of the other meanings of evolution we're not challenging even the idea of universal common descent though some of us myself included are quite sceptical of that, the main thing we're challenging with the theory of intelligent design is that is that the appearance of design is essentially an illusion because an unguided undirected mechanism has the capability of generating that appearance without itself being guided or directed in any way and that's, to us the key issue. Is the design real or merely apparent? You may remember that Francis Crick also once said that biologists must constantly keep in mind, that what they see was not designed, but instead evolved. So there's this, the recurrence of that strong intuition among people who have studied biological systems. And I would say, going back all the way to Aristotle, you know, this has been, the Western tradition in biology has been suffused with this recognition. That organisms look designed, they look like they're designed for purpose, they exhibit purpose of behaviour. And now in the age following Watson and Crick, following the molecular biological revolution of the late 50s and 1960s and 70s, we have extraordinarily strong appearances of design. We've got digital code. We have a replication system. We have a translation system as part of this whole information processing system. Scientists can't help but use teleological wording to describe what's going on. We see the purpose of nature, of all of the biological systems and subsystems. And so what we've argued is that, at least at the point of the origin of life, there is no unguided, undirected, or there is no theory that invokes, that has identified an unguided, undirected mechanism that can explain away that appearance of design. Many people don't realize that Darwin did not attempt to explain the origin of the first life. He presupposed the existence of one or a few very simple forms. And so he started it effectively with assuming a simple cell and then said, well, what would have come from that? We now know, however, that the simple cell was not simple at all and displays this many very striking appearances of design that have not been explained by undirected chemical evolutionary processes. Dawkins himself has said that the machine code of the genes is strikingly computer-like. And so you have this striking appearance of design at the very foundation of life that has not in any way been explained by undirected processes. Well, I want to pick up on a number of that, the new discoveries, how things have changed, the complexity. But I can go back, you're challenging, I guess, hundreds of years of new thinking that the complexity of the universe simply points to luck and chance. And I guess there's a statistical side of that, whether that's even possible. We look around and we see things just working perfectly. And I wonder whether it's even possible for a chance element to make all those things come together and make the world as it is. Well, in my book, Signature in the Cell, which was the first of the three books that I've written on these big topics, I look at the argument for the chance origin of life and even more fundamentally, the chance origin of, say, DNA and the protein products that the DNA codes for. And one of the first things to take note of in addressing the chance hypothesis is that no serious origin of life researcher, no origin of life biochemist or biologist today reposes much hope in the chance hypothesis, it's it's really been set aside and the reason for that, I explained the reason for that in in signature in the cell and then do some calculations to kind of back up the thinking that most origin of life biologists have adopted and that is that the cell is simply far too complicated to have arisen by chance. And you can, and the large biomacromolecules, DNA and proteins, are molecules that depend on a property known as sequence specificity, or sometimes called specified complexity. That is to say, they contain informational instructions in essentially a digital or typographic form. So you have in the DNA you have the four character chemical subunits that biologists actually represent with the letters A, T, G, and C. And if you want to build a protein, you have to arrange the A's, C's, G's, and T's or the evolutionary process or somehow the A's, C's, G's, and T's must have been sequenced in the proper way so that when that genetic message is sent to the ribosome, which is the the translation apparatus in the cell, then what comes out of that is a properly sequenced protein molecules. Proteins also are made of subunits called amino acids. There are 20 or so, maybe as many as 22 now, protein-forming amino acids. And to get the protein chain that is built from the DNA instructions to fold into a proper functional conformation or three-dimensional shape, those amino acids have to be arranged in very specific ways. If they're not arranged properly, the long peptide chain, as it's called, will not fold into a stable protein. And so in both cases, you have this property of sequence specificity that the function of the whole, the whole gene in the case of DNA or the whole protein in the case of the the amino acids, the function of the whole depends upon the precise sequencing of the constituent parts. And that's the difficulty, getting those things to line up properly. Turns out there's all kinds of difficulties in trying to form those subunits, those chemical parts, out of any kind of prebiotic chemical environment that we've been able to think of. But the most fundamental problem is the sequencing. And so you can actually run, because there's, if you think of the protein chain, you have 1 in 20 roughly chances of getting the right amino acid at each site. Sometimes it's more or less because in some cases you can have any one of, there is some variability allowed at each site, but you can run numbers on all this and get very precise numbers on the probability of generating even a single functional protein in the known history of the universe. And it turns out that what are called the combinatorials or the probabilities associated with combinatorials, the probabilities are so small that they are small even in relation to the total number of possible events that might have occurred from the Big Bang till now. In other words, here's an example I often use to use to illustrate, if you have a thief trying to crack a bike lock. If the thief has enough time, even though the combination is hidden among all the possibilities, and then the probability of getting the combination in one trial is very small, if the thief has enough time and can try and try and try again, he may crack it by sheer chance. But if the lock is, we have a standard four-dial bike lock, but if the thief encounters a 10-dial bike lock, and I've had one rendered by my graphic designer to get the point across, then in a human lifetime, there's not enough opportunities to sample that number of possible combinations. If you've got 10 dials, you've got 10 to the 10 possibilities, or 10, that's 10 billion. And if the thief spins the dial once every 10 seconds for 100 years and does nothing else in his entire life, he'll only sample 3% of those total combinations, which means it's much more likely that the thief will fail than it is that he will succeed by chance alone. And that's the kind of, that's the, so the point is that there are, there are degrees of complexity or improbability that dwarf what we call probabilistic resources, the opportunities. And that's the situation we have when we're talking about the origin of the first biomacromolecules by reference to chance alone. Only it's not just that you would with those events, you know, all the events that have occurred from the beginning of the universe until now could only sample about one, I think I've calculated about one ten trillion trillionth of the total possibilities that correspond to a modest length protein. So it's like the bike thief trying to sample that 10-dial lock, only much, much worse. You know, it turns out that 14 billion years isn't enough time to have a reasonable chance to find informational biomolecules by chance alone. I mean, is the whole scientific argument that removes God, is it just an attempt by science to play God, because whenever we are told that scientific principles break down and no longer exist at the very beginning, for instance, and it doesn't make sense, but we're told that that's just how it happened and you have to accept that. And it seems to be people jumping over themselves with a desperation to try and remove the idea that there is an intelligent designer. Well, I tend to think that the questions of motivation in these debates are kind of a wash. I think as theists, we have to, I'm a theist, okay, I believe in God. In my first two books, I argued for designing intelligence of some kind as being, of some unspecified kind as being the best explanation for the information, for example, in the cell or the information needed to build fundamentally new body plans in the history of life on earth. So, but in my last book, I extend that argument, I bring in evidence from cosmology and physics and suggest that the best explanation for that, the ensemble of evidence that we have about biological and physical and cosmological origins is actually a designing intelligence that has attributes that, for example, Jews and Christians have always described to God, transcendence, as well as intelligence. For example, no being within the cosmos, no space alien, and some scientists have proposed even Crick, Francis Crick in 1981 in a little book called Life Itself floated the idea that yes we do see evidence of design in life. The origin of life is a very hard problem, we can't see how it could possibly have happened on Earth so maybe there was an intelligent life form from space who seeded life here. He was subsequently ridiculed a bit and said, I think he was embarrassed that he'd floated this and said he would not, he foreswore any further speculation on the origin of life problem. It was too difficult, he said. But in any case, back to your question, I think the whole question is. Oh, I was finishing a thought, and that is that the evidence of design that we have from the very beginning of the universe and what's called the fine-tuning of the laws and constants of physics and the initial conditions of the universe, the basic parameters of physics, which were said at the beginning, are exquisitely finely tuned against all odds. And no space alien, no intelligence within the cosmos could be responsible for the evidence of design that we have from the very beginning of the universe because any alleged space alien would itself have had to evolve by some sort of naturalistic processes further down the timeline, once you have stable galaxies and planets and that sort of thing and so no being within the cosmos could be responsible for the conditions that made its future evolution possible nor could a space alien to be responsible for the origin of the universe itself. So when you bring in the cosmological and the physical evidence, I think the only type of designing intelligence that can explain the whole range of evidence we have is one that is transcendent, that is beyond the cosmos, but also active in the creation, because we see evidence of information arising later, and information, as I've mentioned, is a mind product based on our uniform and repeated experience.  But as to the motivation issue, I kind of think it's a wash. I think theists have to acknowledge that all people, including those of us who are theists, have a motivation, maybe a hope that there is a purposeful intelligence behind the cosmos. I think there's a kind of growing angst in young people. Harvard study recently showing that over 50% of young people have doubts about there being any purpose to their existence. And this is contributing to the mental health crisis. And so I think all of us would like, to be possible, for there to be life after death, for there to be an enduring purpose to our lives that does not extinguish when we die or when eventually there's a heat death of the universe. I think theism, belief in God, gives people a sense of purpose in relation, the possibility of a relationship to our creator. That's a positive thing. I think there's also a common human motivation to not want to be accountable to that creator and to have moral, complete moral freedom to decide what we want to do at any given time. And so oftentimes theists or God-believers, religious people will say, well, you just like these materialistic theories of origins because you don't want to be accountable to a higher power. That might be true, But it's equally true that the atheist will often say, well, but you guys just need a cosmic crutch. You need comfort from the idea of a divine being, a loving creator, father, whatever, you know, the divine father figure. And Freud famously critiqued or criticized religious belief in those terms. So I think that those two kind of motivation, arguments about motivation are something of a wash and that what I've tried to do in Return of the God Hypothesis is set all of that aside, look at the evidence that we have, and then evaluate it using some standard methods of scientific reasoning and standard methods of evaluating hypotheses, such as a Bayesian analysis, for example, that come out of logic and philosophy. And set the motivation questions aside. And my conclusion is that the evidence for an intelligent designer of some unspecified kind is extremely strong from biology, and that when you bring in the cosmological and physical evidence, the evidence of fine-tuning and the evidence we have that the material cosmos itself had a beginning, I think materialism fails as an explanation, and you need to invoke an intelligence that is both transcendent and active in the creation to explain the whole range of evidence. Well, let me pick you up on that change, because initially there is a change from someone who believes the evolutionary model, big bang, there is no external force. That step from there to there is an external force, there is intelligent design feeding into the universe we have. And then it's another step to take that to there is an intelligent designer, now there is a personal God. And that step certainly, I assume, is frowned upon in the scientific community. Tell us about you making that step, because it would have been much safer to stay, I guess, in the ID side and not to make the step into who that individual is. Tell us about kind of what prompted you to actually make the step into answering that who question.  Right. Well, I've been thinking about this question for 35, 36, I don't know, since the mid-80s when I was a very young scientist. And it was at the conference that inspired it, because at the conference, there were people already thinking about the God question, especially the cosmologists. At that conference, Alan Sandage announced his conversion from scientific agnosticism he was a scientific materialist to theism and indeed I think he became Christian, and he talked about how the evidence for the singularity at the beginning of the universe, the evidence that the material cosmos itself had a beginning was one of the things that moved him off of that materialistic perspective, that it was clear to him that as he described it, that the evidence we had for a beginning was evidence for what he called a super, with a space in between, natural events, nothing within the cosmos could explain the origin of the cosmos itself, if matter, space, time and energy have a beginning and as best we can tell they do and there are multiple lines of evidence and theoretical considerations that lead to that conclusion and I developed that in return of the god hypothesis, it is the evidence from observational astronomy and also developments in theoretical physics converge on that conclusion. And if that's the case, if matter and energy themselves have a beginning, and indeed if space and time themselves have a beginning, then we can't invoke any materialistic explanation to explain that. Because before there was matter, before the beginning of matter, there was no matter to do the causing. And that's the problem. There must be something. For there to be a causal explanation for the universe, it requires a transcendent something. And when you also consider that we have evidence for design from the very beginning in the fine-tuning of the initial physical parameters of the universe, the initial conditions of the universe, the initial establishment and fine-tuning of the physical laws, then you have evidence for that transcendent something being a transcendent intelligent something. And if something is intelligent, capable of making choices between one outcome or another, that's really what we mean by personhood. I mean, this is very close to a, the idea of a personal gun, now that entity may not want to have anything to do with us, but we're talking about a conscious agent when we talk about evidence for intelligent design, and then we have further evidence I think in biology with the presence of the information and information processing system inside cells. And so when you bring all that together, I think you can start to address the who question. So after I wrote Signature in the Cell and Darwin's Doubt, a lot of my readers were asking, OK, that's great. We have evidence of a designing intelligence, but who would that intelligence have been? Is it a space alien, something imminent within the cosmos, like Crick and others have proposed? Or is it a transcendent intelligence? And what can science tell us about that question? So I thought it's a natural question that flows from my first two books. I would stipulate that the theory of intelligent design, formally as a theory, is a theory of design detection. And it allows us to detect the action of an agent as opposed to undirected material processes. We have this example that we often use. If you look at the faces on the mountains at Mount Rushmore, you right away know that a designing intelligence of some kind was responsible for sculpting those faces. And those faces exhibit two properties which, when found together, invariably and reliably indicate a designing intelligence. And we've described those properties as high probability and what's called a specification, a pattern match. And we have evidence of small probability specifications in life. If something is an informational sequence, it's another way of revealing design, so that we can get into all of that. The point is, we've got evidence of design in life, but, the cosmology and fine-tuning allow us to adjudicate between two different design hypotheses, the imminent intelligence and the transcendent one. And I thought, well, let's take this on. It's a natural, it goes beyond the theory of intelligent design, formally speaking, and it addresses one of the possible implications of the evidence of design that we have in biology, that maybe we're looking at a theistic designer, not a space alien.  I just want to pick one or two things from different books. Signature in the Cells, you have it there behind you. And when you simply begin to look at the complexity of cells. You realize that they are like little mini cities, that actually everything, so much happens within. And I guess we are learning more and more about everything in life. And you talk to doctors and they tell you that they are learning more and more about how the body functions. And there's a lot of the unknown. But when you look at that just complexity of, we call it the simple cell, which isn't really very simple, that new research and that new understanding, surely that should move people to a position that, this is impossible, that this level of complexity simply just happens. So tell us about that, just the cell, which is not simple.  Yeah, that's the sort of ground zero for me in my research and interest in the question was this origin of life problem. That's what I did my PhD on. And I think it's really interesting. We could have debates about the adequacy of Darwinian evolutionary theory. I'm sceptical about what's called macroevolutionary theory. But set that all aside. Darwin presupposed one or a few simple forms. And in the immediate wake of the Darwinian Revolution, people like Huxley and Heckel started to develop theories of the origin of those first simple cells. And they regarded the cell in the late 19th century as a very simple, as Huxley put it, a simple homogenous globule or homogeneous globule of undifferentiated protoplasm. And they viewed the essence of the cell as a simple chemical, it's coming from a simple chemical substance they called protoplasm. And so it kind of, and they viewed it as a kind of jello or goo, which could be produced by a few simple chemical reactions. That viewpoint started to fall by the wayside very, very quickly. By the 1890s, early part of the 20th century, we were learning a lot more about the complexity of metabolism. When you get to the molecular biological revolution in the late 1950s and 1960s, nobody any longer thinks the cell is simple because the most important biomacromolecules are large information-bearing molecules that are part of a larger information processing system. And so this is where I think, and in confronting that. And so any origin of life theory has to explain where that came from. My supervisor used to say that the nature of life and the origin of life topics are connected. We need to know what life is in order to formulate a plausible theory of how it came to be. And now that we know that life is much more complex and that we have an integrated informational complexity that characterizes life, those 19th century theories and the first origin of life theories associated with figures like Alexander Oparin, for example, from the 1920s and 30s. These are not adequate to explain what we see. But what's happened, and this is what I documented in Signature in the Cell, is that none of the subsequent chemical evolutionary theories, whether they're based on chance or based on self-organizational laws or somehow based on somehow combining the two, none of those theories have proven adequate either. This problem of sequence specificity or functional information has defied explanation by reference to theories that start from lower level chemistry. It's proven very, very difficult, implausible in the extreme. Here's the problem. Getting from the chemistry to the code is the problem. And undirected chemical processes do not, when observed, move in a life-friendly, information-generative direction. And this has been the problem. So the impasse in origin of life research, which really began in the late 70s, was documented by this book I mentioned, the mystery of life's origin and books, another book, for example, by Robert Shapiro called, Origins, A Sceptic's Guide. That impasse from the 1980s has continued right to the present. Dawkins was interviewed in a film in 2009 by Ben Stein, the American economist and comic. And very quickly, Stein got Dawkins to acknowledge that nobody knows how we got from from the prebiotic chemistry to the first cell. Well, that's kind of a news headline. We get the impression from textbooks that the evolutionary biologists have this all sewed up. They don't by any means. This is a longstanding conundrum. And it is the integrated complexity and informational properties of the cell that have, I think, most fundamentally defied explanation by these chemical evolutionary theories. And I think that's very significant when you think of the whole kind of evolutionary story. Darwin thought that if you could start with something simple then the mutation selection, oh, he didn't have mutations, but the mutation, sorry, the natural selection variation mechanism, could generate all the complexity of life. You'd go from simple to complex very gradually. Well, if the simplest thing is immensely complex and manifest a kind of complexity that defies any undirected process that we can think of, well, then you don't have a seamless evolutionary story from goo to you. Because I guess when you're Darwin's doubt, the next book you wrote, I guess when Charles Darwin wrote Origin of the Species, he assumed it was settled. But science is never settled. There are always developments. And yet it seems, oh, that's sacrosanct, and that cannot be touched and must be accepted. Yeah, and what I did in the second book was show or argue that the information problem is not something that only resides at the lowest level in the biological hierarchy, at the point of the origin of the first cell, but it also emerges later when we have major innovations in the history of life as documented by the fossil record, events such as the Cambrian explosion or the origin of the mammalian radiation or the angiosperm revolution. There are many events in the history of life where you get this sudden or abrupt appearance in the fossil record of completely new form and structure. And we now know in our information age, as it's come to biology, that if you want to build a new cell, you've got to have new proteins. So you have to to have information to build the first cell. But the same thing turns out to be true at the higher level. If you want to build a completely new body plan, you need new organs and tissues. You need to arrange those organs and tissues in very specific ways. And you need new proteins to service the new cell types that make the organs and tissues possible. So anytime we see the abrupt appearance of new biological form, that implies the origin of a vast amount of new biological information.  And so in Darwin's doubt, I simply asked, well, is there, can the standard mutation natural selection mechanism explain the origin of the kind of information that arises and the amount of information arises? And I argue there that no, it doesn't. That we have, there are many, many kinds of biological phenomena that Darwin's mechanism explains beautifully, the small scale variation adaptation, that sort of thing. So 2016, a major conference at the Royal Society in London. First talk there was by the evolutionary biologist Gerd Müller. The conference was convened by a group of evolutionary biologists who think we need a new theory of evolution. Whereas Darwinism does a nice job of explaining small-scale variation, it does a poor job or a completely inadequate job of explaining large-scale morphological innovation, large-scale changes in form. And Mueller, in his first talk at this 2016 event, outlined what he called the explanatory deficits of Neo-Darwinism, and he made that point very clearly. And so it's, I think it's a new day in evolutionary biology, the word of this is not percolating so well perhaps but that was part of the reasons I wrote Darwin's doubt is that within the biological peer-reviewed biological literature it's well known that the problem of the origin of large-scale form, the origin of new body plans is not well explained by the mutation selection mechanism. At this 16 conference, the conveners included many scientists who were trying to come up with new mechanisms that might explain the problem of morphological innovation. Afterwards, one of the conveners said the conference was characterized by a lack of momentousness. Effectively, the evolutionary biologists proposing new theories of evolution and new evolutionary mechanisms had done a good job characterizing the problems, but had not really come up with anything that solves the fundamental problems that we encounter in biology when we see these large jumps in form and structure arising. And in Darwin's Doubt, I didn't just critique standard neo-Darwinian theories of evolution, but many of these newer theories as well, showing that invariably the problem of the origin of biological information and the form that arises from it is the key unsolved problem in contemporary evolutionary theory.  Mueller and Newman wrote a book with MIT Press called On the Origins of Organismal Form, which was a kind of play on the origin of species. Darwinism does a nice job of explaining speciation, small-scale changes within the limits of the pre-existing genomic endowments of an organism, but it doesn't do a good job of explaining new form that requires new genetic information. And these authors, Newman and Mueller, listed in a table of unsolved problems in evolutionary theory, the problem of the origin of biological form. That's what we thought Darwin explained back in 1859, and instead we realized that the mechanisms that he first envisioned have much more limited creative power and much more limited explanatory scope. So that's what my second book was about, and also I think it's still, this is still very much right at the cutting edge of the discussion in evolutionary biology. We can explain the small scale stuff, but not the big scale stuff. Let's just finish off with actually disseminating the information, because all of this is about taking issues which are complex and actually making it understandable to the wider public. And I guess part of that is, I mean, obviously being on the most popular podcast in the world, Joe Rogan, I was like, oh, there's Steve Meyer and Joe Rogan. And taking that information and that turbocharges that. So maybe just to finish off on the ability to disseminate this, because I think in the US, the ID movement is more understood, where I think maybe in Europe, it's certainly it's more misunderstood and not as accepted where there is an acceptance in the States. But tell us about that and how being on something like podcasts like that turbocharge the message. Yeah, well, I can tell you, you know, now that I'm getting introduced at conferences and things after The Joe Rogan Experience, it's as if I never did anything else in my life. No, that's the only thing people care to mention. I mean, he's got a monster reach. He's extremely, his questions on the interview were very probative. Of course, slightly to moderately sceptical, maybe more, but I thought they were fair. I thought it was a great discussion and it was a lot of fun. And, you know, we've had not only, I think he gets something like 11 million downloads on average for his podcast. We couldn't even believe these numbers when we were told them. But there have been over 25 million derivative videos that social media influencers and podcasters have made about the Rogan interview, analysing different sections of our conversation. So, yeah, that was a huge boost to the dissemination of our message. But one thing I realized in our conversation that there's a simple way to understand the information argument. And that's one of our tools in getting some of these ideas out is distilling some of these things that we've been talking about at a fairly deep level to a more understandable level. So let me just run that argument, that argument sketch or the distillation of the argument by your audience. And then they would talk about some of the things we're doing to get the word out. Our local hero in the Seattle area here is Bill Gates, the founder of Microsoft. And he has said, like Dawkins, that the digital code in the DNA, that the DNA is like a software program, but much more complex than any we've ever created. Dawkins, as I mentioned before, says it's like a machine code. It contains machine code. Well, if you think about that, those are very suggestive quotations because what we know from our uniform and repeated experience, which is the basis of all scientific reasoning, is that information always arises from an intelligence source. If you have a section of software, there was a programmer involved. If you have a hieroglyphic inscription, there was an ancient scribe involved. If you have a paragraph in a book, there was a writer involved. As we're effectively broadcasting, we're transmitting information, that information ultimately issues from our mind. So whenever we look at information, an informational text or sequence, and we trace it back to its ultimate source, we always come to a mind rather than a material process. All attempts to explain the origin of life based on undirected material processes have failed because they couldn't explain the information present in DNA, RNA proteins. So the presence of that information at the foundation of life, based on our uniform and repeated experience about what it takes to generate information is therefore best explained by the activity of a designing intelligence. It takes a programmer to make a program, to make a software program. And what we have in life is, from many different standpoints, identical to computer code. It is a section of functional digital information. So that's a kind of more user-friendly sketch of the argument but the point is some of these some of these key ideas that are that make intelligent design so, I think so persuasive at a high scientific level if you actually look at the evidence, can be also explained fairly simply and so we're generating a lot of not just Joe Rogan podcast interviews but coming on many many podcasts and that sort of thing but also we're generating a lot of YouTube video short documentaries that get some of these ideas across and for your viewers, one that I might recommend which is on of any it was out on the internet it's called science uprising and it's a series of 10 short documentary videos, another one that we've done called the information enigma which I think would would help people get into these ideas fairly quickly, the information enigmas I think it's a 20 minute short documentary it's up online and we've had hundreds of thousands of views so we're doing a lot to sort of translate the most rigorous science into accessible ideas and disseminate that in user-friendly ways. The best website for finding a lot of this compiled is actually the website for my most recent book, Return of the God Hypothesis. So the website there is returntothegodhypothesis.com. Okay, well, we will have the link for that in the description.  Dr. Stephen Meyer, I really appreciate you coming along. Thank you so much for coming and sharing your experience and understandings of writing and making that understandable, I think, to the viewers, many of them who may not have come across this before.  So thank you for your time today. I really appreciate you having me on, Peter.

In this episode:00:54 Franklin's real roleWhen it comes to the structure of DNA, everyone thinks they know Rosalind Franklin's role in its discovery. The story goes that her crucial data was taken by James Watson without her knowledge, helping him and Francis Crick solve the structure. However, new evidence has revealed that this wasn't really the case. Rosalind Franklin was not a ‘wronged heroine', she was an equal contributor to the discovery.Nature Podcast: 25 April 2023Comment: What Rosalind Franklin truly contributed to the discovery of DNA's structure14:37 An automated way to monitor wildlife recoveryTo prevent the loss of wildlife, forest restoration is key, but monitoring how well biodiversity actually recovers is incredibly difficult. Now though, a team has collected recordings of animal sounds to determine the extent of the recovery. However, while using these sounds to identify species is an effective way to monitor, it's also labour intensive. To overcome this, they trained an AI to listen to the sounds, and found that although it was less able to identify species, its findings still correlated well with wildlife recovery, suggesting that it could be a cost-effective and automated way to monitor biodiversity.Nature Podcast: 25 October 2023Research article: Müller et al.27:11 Research HighlightsThe first brain recording from a freely swimming octopus, and how a Seinfeld episode helped scientists to distinguish the brain regions involved in understanding and appreciating humour.Research Highlight: How to measure the brain of an octopusResearch Highlight: One brain area helps you to enjoy a joke — but another helps you to get it30:24 Why multisensory experiences can make stronger memoriesIt's recognized that multisensory experiences can create strong memories and that later-on, a single sensory experience can trigger memories of the whole event, like a specific smell conjuring a visual memory. But the neural mechanisms behind this are not well understood. Now, a team has shown that rich sensory experiences can create direct neural circuit between the memory regions involved with different senses. This circuit increases memory strength in the flies, and helps explain how sense and memories are interlinked.Nature Podcast: 25 April 2023Research article: Okray et al.38:58 Briefing ChatHow elephant seals catch some shut-eye while diving.New York Times: Elephant Seals Take Power Naps During Deep Ocean Dives Hosted on Acast. See acast.com/privacy for more information.

On this ID the Future from the archive, host Stephen Meyer concludes his three-part conversation with Oxford mathematician and philosopher John Lennox on Lennox's new film Against the Tide: Finding God in an Age of Science. Science depends on word, on logos, says Dr. Lennox, meaning the rational intelligibility of the universe. Francis Crick, co-discoverer of DNA, wished to disprove the need for God, but the language of DNA has turned out to be a signpost to an intelligence, Lennox contends: a logos behind nature. Scientists still claim authority to pronounce against theism, but according to Lennox, such pronouncements come not from science but from a dogma known as scientism. Far from being “science vs. God,” it's really a collision of competing worldviews. Enjoy the conclusion to this conversation and then watch the movie Against the Tide, also starring actor Kevin Sorbo. Dig Deeper Rent or buy Dr. Lennox's film Against the Tide. Watch the trailer: Source

Christof is a neurophysiologist and computational neuroscientist best known for his work on the neural basis of consciousness on which he worked with Nobel Prize winner Francis Crick for 24 years. He is the president and chief scientist of the Allen Institute for Brain Science in Seattle. Christof describes his passion in life as "to understand how I came to be in this wonderful, mysterious universe. Not so much me, personally, but me as a conscious, experiencing thing surrounding by other conscious organisms and trees, stars, and the sea." Over the last decade, he has worked closely with the psychiatrist and neuroscientist Giulio Tononi. Together they advocate for an Integrated Information Theory (IIT) of consciousness - often seen as a modern version of panpsychism that only ascribes consciousness to entities with some degree of irreducible cause-effect power. Christof is the author of the books Consciousness: Confessions of a Romantic Reductionist. , The Quest for Consciousness: A Neurobiological Approach, and Biophysics of Computation: Information Processing in Single Neurons. His forthcoming book, Then I am Myself the World, is due out in 2024. In Sentientist Conversations we talk about the two most important questions: “what's real?” & “who matters?” Sentientism is "evidence, reason & compassion for all sentient beings." The video of our conversation is ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠here on YouTube⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. We discuss: 00:00 Clips! 01:09 Welcome - "My dog... Mr. Felix... a sentient being" - The dedication from Christof's forthcoming book "Then I Am Myself The World": "... to all fellow travellers on the river of time who howl, bark, cry, screech, whine, bellow, shriek, buzz, sing, speak or those without a voice - for it is only in compassion with all life that we can redeem ourselves." 03:52 Christof's Intro - Physicist turned neurobiologist - "I've always been fascinated by the question of #consciousness" 04:45 What's Real - Growing up in a devout Roman #catholic family, raised kids Catholic - "One thing that always irked me... the belief that my dogs... somehow didn't have a soul and wouldn't be resurrected... that always bothered me... whatever it is we all share" - "I lived in two worlds - like many scientists do. On Sunday you go to church and you pray... during the week, the rest of the time, you're a scientist - you try to explain everything using natural explanation... this split... I couldn't support any more" - "Progressively I lost my faith... I'm a naturalist... I try to explain everything... using natural laws" - A priest acknowledging that non-human animals are "parts of god's creation" and can suffer, but "they do not partake in the same way we do" - Human exceptionalism "many religions believe that humans are exceptional... we're in charge of the universe... everything gets subsumed under human demands - that struck me as wrong" - "Who has what faith - it's totally random - it depends where you were born and in which family you were born... how can this be true?" - JW: Topics that draw even some naturalists back towards the mystical: Origins & nature of the universe, life, humanity, consciousness... 13:47 What and Who Matters? 39:45 What are Consciousness and Sentience? 1:14:09 A Better World? 1:17:35 Follow Christof - christofkoch.com - Christof at the Allen Institute - Christof on Wikipedia ...and much more. Full show notes at ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Sentientism.info⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Sentientism is “Evidence, reason & compassion for all sentient beings.” More at ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠Sentientism.info⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Join our ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠"I'm a Sentientist" wall⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠ via ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠this simple form⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Everyone, Sentientist or not, is welcome in our groups. The biggest so far is ⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠here on FaceBook⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠⁠. Come join us there! --- Send in a voice message: https://podcasters.spotify.com/pod/show/sentientism/message

Is History driven by heroic individuals or by variation and selection? What determines the speed of innovation? Matt Ridley is a science writer, journalist, and businessman. His books include The Red Queen, The Origins of Virtue, Genome, Nature via Nurture, Francis Crick, The Rational Optimist, The Evolution of Everything, and How Innovation Works.Matt and Greg discuss the integral role freedom, idea exchange, and trade play in driving innovation. They delve deep into the concept of creative destruction and how it's essential for large corporations to reinvent themselves to stay competitive or be allowed to cease to exist suddenly. Matt talks about the debate surrounding the origin of COVID-19, its implications for virology, and the spread of false information in our interconnected world. The discussion examines the controversial lab leak hypothesis and the impact of China's rise on global innovation.*unSILOed Podcast is produced by University FM.*Episode Quotes:Why is it that evolutionary thinking is like the gift that keeps on giving?02:25: The message of my book, "The Evolution of Everything," is that we don't want to let this insight remain confined to biology. It's just as useful as a way of understanding human society in lots of different aspects. Not just economics, but social change as well. Because really, the simple idea that if there's variation, if there's trial and error, if there's experimentation going on, then some ideas are going to survive at the expense of others. And that's going to lead to progressive adaptation. That's going to lead to progressive improvement in some technology, in some social habits, whatever it might be.Innovation is more about rearranging the world14:20: Recombination of existing genes is the main way that innovation happens in evolutionary biology, much more common than de novo mutation, and that's true of us too. Most of the new products we produce in the world by innovation are actually just the same old materials combined in new and interesting ways. Innovation is more about rearranging the world than it is about coming up with completely new things.Crony capitalism extends corporate lifespans, stifling innovation27:41: Crony capitalism, corporate favoritism, is a tried-and-true and tested way to stay in the game. But it tends to come at the expense of innovation, and it tends to leave you more and more vulnerable to collapse when you do. Get to face real competition. It tends to leave the company vulnerable to disappearing. Everybody thinks they know innovation, but only few people can pin it down30:46: The main reason we're living lives of far greater comfort than we did 500 years ago is still somewhat mysterious. We can tell you things like it needs freedom, it needs trial and error, and things like that, but we can't switch it on and off, let alone tell you when and where it's going to happen. In that sense, it's a surprisingly slippery thing, innovation. Everybody talks about it. Everybody thinks they know about it, but surprisingly, few people can really pin it down. And as I say, you can't put it in a mathematical model, at least not in a very convincing way.Show Links:Recommended Resources:Intentional stanceGreat man theoryFrancis CrickInfinite Improbability DriveMemeGeoffrey WestLinear modelFrancisco MojicaCOVID-19 lab leak theoryZoonosisMichael ShellenbergerGuest Profile:Speaker's Profile on Chartwell SpeakersMatt Ridley's WebsiteMatt Ridley on LinedInMatt Ridley on XMatt Ridley on YouTubeMatt Ridley on TEDTalk Matt Ridley on Talks at GoogleHis Work:Viral: The Search for the Origin of COVID-19The Rational Optimist: How Prosperity EvolvesHow Innovation Works: And Why It Flourishes in FreedomThe Evolution of Everything: How New Ideas EmergeThe Red Queen: Sex and the Evolution of Human NatureGenome: The Autobiography of a Species in 23 ChaptersThe Origins of VirtueNature Via Nurture: Genes, Experience, and What Makes Us HumanFrancis Crick: Discoverer of the Genetic CodeClimate Change: The Facts 2017

(NOTAS Y ENLACES DEL CAPÍTULO AQUÍ: https://www.jaimerodriguezdesantiago.com/kaizen/179-el-misterio-de-la-vida-iv-identidad-consciencia-y-cerebro/)Menudo lío en el que me he metido. Uno de los temas que quería tratar esta temporada es el de la consciencia. Algo así sencillito, para pasar el rato. Un día, comiendo con Samuel Gil se lo mencioné y hablamos de un autor, Sam Harris, que escribe sobre mindfulness entre otros muchos temas. Y unas semanas después me vi metido en un grupo de whatsapp con el propio Samuel y con Ion Cuervas-Mons, que tiene un podcast muy recomendable del que te he hablado alguna vez: intercambio iónico. Habían hablado entre ellos y les había parecido muy buena idea que hiciéramos algún tipo de especial los tres sobre estos temas. Y se pusieron a intercambiar en el grupo cosas hiper-frikis sobre el asunto de la consciencia, la meditación, el libre albedrío, la realidad y muchas otras que ni me he enterado porque no sido capaz de seguir su ritmo. No sé bien qué saldrá de todo eso, pero he pensado que, o me pongo las pilas, o vete tú a saber qué cuento cuando nos juntemos a charlar. Por eso hoy vamos a dar los primeros pasos, seguramente torpes, para acercarnos a otro de esos grandes misterios insondables que nos depara esto de ser humanos y estar vivos. Porque si la vida, su origen y su evolución, ya son de por sí enigmas, nuestra consciencia, el hecho de que seamos conscientes de que estamos vivos, que existimos, y de que experimentamos cosas constantemente, que seamos conscientes también de que algún día parece que dejaremos de hacerlo y todo lo que eso significa sobre quiénes somos, es un misterio por lo menos igual de grande.Uno al que nos vamos a asomar hoy, así que tiene pinta de que vamos a acabar con agujetas neuronales. ¡Ánimo!

Kat Arney chats with Professor Matthew Cobb about what really happened between James Watson, Francis Crick and Rosalind Franklin during the discovery of the double helix structure of DNA.Full show notes, transcript and references online at GeneticsUnzipped.com Follow us on Twitter @GeneticsUnzipThis episode of Genetics Unzipped was written and presented by Kat Arney with audio production by Emma Werner and Sally Le Page.This podcast is produced by First Create the Media for the Genetics Society - one of the oldest learned societies dedicated to promoting research, training, teaching and public engagement in all areas of genetics.

Scientific Evidence for Intelligent Design, How Mutations Fail To Invent and The  Remarkable Coincidences in Photosynthesis. ACU Sunday Series.  Stephen Meyer Investigates Scientific Evidence for Intelligent Design (Lecture 1) Michael Behe Exposes How Mutations Fail To Invent Michael Denton Remarkable Coincidences in Photosynthesis   Stephen Meyer Investigates Scientific Evidence for Intelligent Design (Lecture 1) https://youtu.be/C5Z6h_RVhIw Discovery Science Visit https://www.discoveryu.org/courses/meyer for the full course. For the first time, you can have living room access to over seven hours of teaching by intelligent design pioneer Stephen Meyer in a brand-new online course. A favorite of students young and old(er), Meyer will delight both as he explores the scientific evidence for intelligent design (ID) found in physics, cosmology, biology and the chemical origin of life. Join Stephen as he investigates the scientific evidence for intelligent design in the origin of life, the development of biological complexity, and physics and cosmology. In 42 short video lectures, Meyer explores the scientific basis for the theory of intelligent design—the idea that key features of life and the universe are best explained as the product of an intelligent cause rather than an unguided process. In this course, Meyer will guide you through the major concepts and information presented in his path breaking books Signature in the Cell and Darwin's Doubt, as well as previewing some of the material about physics and cosmology in his book The Return of the God Hypothesis. Each video lecture is accompanied by a short quiz, and a special digital certificate of completion is offered for those who finish the course. For more about the course visit https://www.discoveryu.org/courses/meyer. Check out these videos as well: Information Enigma: Where does information come from? https://youtu.be/aA-FcnLsF1g Michael Behe Investigates Evolution & Intelligent Design (Lecture 1) https://youtu.be/XCTTy0ylf7A Stephen Meyer Shatters The Myth Of The Multiverse (Science Uprising EP4) https://youtu.be/WR51OrawqIg ============================ The Discovery Science News Channel is the official Youtube channel of Discovery Institute's Center for Science & Culture. The CSC is the institutional hub for scientists, educators, and inquiring minds who think that nature supplies compelling evidence of intelligent design. The CSC supports research, sponsors educational programs, defends free speech, and produce articles, books, and multimedia content. For more information visit https://www.discovery.org/id/ http://www.evolutionnews.org/ http://www.intelligentdesign.org/ Follow us on Facebook and Twitter: Twitter: @discoverycsc Facebook: https://www.facebook.com/discoverycsc/ Visit other Youtube channels connected to the Center for Science & Culture Discovery Institute: https://www.youtube.com/user/Discover... Dr. Stephen C. Meyer: https://www.youtube.com/user/DrStephe... The Magician's Twin - CS Lewis & Evolution: https://www.youtube.com/user/cslewisweb Darwin's Heretic - Alfred Russel Wallce: https://www.youtube.com/user/AlfredRW...   Course Overview Join philosopher of science Stephen Meyer as he investigates the scientific evidence for intelligent design in the origin of life, the development of biological complexity, and physics and cosmology. In 42 short video lectures, Meyer explores the scientific basis for the theory of intelligent design—the idea that key features of life and the universe are best explained as the product of an intelligent cause rather than an unguided process. In this course, Meyer will guide you through the major concepts and information presented in his pathbreaking books Signature in the Cell and Darwin's Doubt, as well as previewing some of the material about physics and cosmology in his book The Return of the God Hypothesis. Each video lecture is accompanied by a short quiz, and a special digital certificate of completion is offered for those who finish the course. About the Professor Stephen C. Meyer received his PhD from the University of Cambridge in the history and philosophy of science. A former geophysicist with ARCO and professor of philosophy at Whitworth University, he currently directs the Center for Science and Culture at the Discovery Institute in Seattle. He is author of the New York Times-bestseller Darwin's Doubt (2013) as well as Signature in the Cell (2009) and The Return of the God Hypothesis (forthcoming in 2021). Recommended Texts and Resources You are encouraged to dig deeper into the topics explored in this course by consulting the following books and resources: Signature in the Cell: DNA and the Evidence for Intelligent Design (book) Darwin's Doubt: The Explosive Origin of Animal Life and the Case for Intelligent Design (book) Debating Darwin's Doubt (book) Signature of Controversy: Responses to Critics of Signature in the Cell (book) Explore Evolution: The Arguments for and against Neo-Darwinism (book) The Return of the God Hypothesis (book) DarwinsDoubt.com (website) The Information Enigma (video) The Intelligent Design Collection—Darwin's Dilemma, The Privileged Planet, Unlocking the Mystery of Life (videos) Course Outline Unit 1: Evidence of Intelligent Design in the Origin of Life Introduction to Course. What is intelligent design, and why is it controversial? In this first lecture, Meyer introduces the topic of intelligent design. Darwin's Challenge to Intelligent Design. What does evolution mean? Meyer explains adaptation and explains how Darwin's theory challenges the idea of intelligent design. Theories of the Origin of Life in the Nineteenth Century. Darwin conceived of the origin of life happening possibly in a “warm little pond.” Meyer explains the state of origin of life research at Darwin's time and later. Oparin's Theory of the Origin of Life. Meyer delves into Alexsandr Oparin's theory on the origin of life, put forward in 1936. Learn about evolutionary abiogenesis and the experiment that sought to prove it. The Amazing Complexity of Proteins. What do proteins look like? How has science progressed in its understanding of these basic building blocks of life? Meyer traces the work of protein scientists in the 1930s up through the 50s. What is the importance of a protein's shape? And how is this shape determined? The Role of DNA. How did our understanding of the cell change in the 1950s and 60s? Meyer discusses the discovery of the stable double helix structure of DNA and the key scientists involved. The DNA Enigma. Meyer examines Francis Crick's sequence hypothesis and then goes on to delve into the question of code and biological information, explaining what he calls “the DNA enigma.” What Kind of Information Does DNA Contain? Meyer explores types of information, explains mathematical Shannon information, and discusses what kind of information Francis Crick, Richard Dawkins, and Bill Gates see in life's code. Explanations for the Origin of Life: Chance. Could the information in the cell come about by chance? Today, learn the history of origin of life research from the 1950s to the present. What is prebiotic soup, anyway? Explanations for the Origin of Life: Self-Organization. Can self-organization explain the origin of biological information? In this lesson, learn about Dean Kenyon and his idea of ‘biochemical predestination' of amino acids. How does DNA fit into this whole picture? 2 Explanations for the Origin of Life: Pre-Biotic Natural Selection. What is prebiotic natural selection? Listen in as Dr. Meyer examines Oparin's hypothesis and modern attempts to reconcile evolution with the origin of life. Introduction to Intelligent Design. Meyer recounts his introduction to the design hypothesis and his quest to shape it into a rigorous scientific argument as he explores historical science methods. Objections to Intelligent Design: Is Intelligent Design Science? Meyer responds to a key philosophical objection to intelligent design. Objections to Intelligent Design: Argument from Ignorance? Some critics claim design proponents make an argument from ignorance. Is this true? Meyer discusses the intelligent designer of the gaps objection and illustrates why it is not applicable. Objections to Intelligent Design: RNA World, pt 1. Is it possible to avoid the cell's chicken and egg problem? Listen in as Meyer discusses the RNA world scenario. Can genetic information and biochemically relevant functions be present without either DNA or protein? Objections to Intelligent Design: RNA World, pt. 2. Can the RNA world scenario overcome the information problem? Listen in as Dr. Meyer analyzes this popular proposal. Objections to Intelligent Design: RNA World, pt. 3. Have scientific developments “overtaken Meyer's book” as Stephen Fletcher claims? Listen in as Meyer examines Fletcher's supposed evidence. Objections to Intelligent Design: Junk DNA. Critics claim that junk DNA disproves intelligent design. Meyer takes on this objection. Unit 2: Evidence of Intelligent Design in the Development of Life Another Information Problem in the History of Life. Is the origin of life the main problem with the materialistic evolutionary account of origins? Meyer delves into the modern evolutionary synthesis. Is information a problem here too? The Cambrian Explosion. What does the fossil record reveal about life's history? Meyer discusses how Darwin found the Cambrian explosion particularly striking and puzzling. The Mystery of the Missing Fossils: The Burgess Shale. Darwin tried to propose an explanation for the mystery of the missing fossils. But have later discoveries confirmed his predictions? Meyer introduces a 1909 discovery – the Burgess Shale. The Mystery of the Missing Fossils: The Chenjiang Fauna. Meyer details a fossil find with great diversity: the Cambrian era Chenjiang fauna. 3 What Does It Take to Build an Animal? Meyer discusses the process of how to get a Cambrian animal. Challenges to the Neo-Darwinian Mechanism: Combinatorial Searches, pt. 1. What does combinatorial search mean? And how would the neo-Darwinian mechanism produce the new genetic information needed to build new animals? Challenges to the Neo-Darwinian Mechanism: Combinatorial Searches, pt. 2. How hard is it to get a new protein? Meyer does the math, further examining the efficacy of the neo-Darwinian synthesis. Challenges to the Neo-Darwinian Mechanism: Developmental Mutations and Gene Regulatory Networks. It's a catch-22: random mutation and organism development. Meyer gets beyond the numbers and uncovers the challenges posed for NeoDarwinism by developmental mutations and developmental gene regulatory networks. Challenges to the Neo-Darwinian Mechanism: Information beyond DNA. Do protein folds and developmental gene regulatory networks pose the biggest problems to Neo-Darwinism? Meyer discusses a third devastating challenge to evolution. He also discusses new evolutionary theories proposed to overcome it. The Positive Case for Intelligent Design, pt. 1. Can one make a positive case for intelligent design using accepted methods of reasoning? Meyer examines inductive, deductive and abductive reasoning, and lays out what intelligent design proponents need to demonstrate to make a strong case for design. The Positive Case for Intelligent Design, pt. 2. Meyer applies historical scientific methods to evaluate potential causes of the Cambrian explosion. The Positive Case for Intelligent Design, pt. 3. Meyer discusses genetic algorithm computer programs, the reason why the random mutation/natural selection mechanism is doomed, and why intelligence uniquely can account for functional information. Responding to Critics: Charles Marshall. Paleontologist Charles Marshall challenged Meyer's arguments in Darwin's Doubt, and here Meyer responds. Response to Critics: Dennis Venema and Deborah Haarsma. Meyer evaluates an objection to his book from theistic evolutionists Dennis Venema and Deborah Haarsma. Can evolution's mechanism of natural selection acting on random mutations account for new protein folds? And what does the evolution of nylonase demonstrate? Responding to Critics: Lawrence Krauss and Richard Dawkins. Meyer responds to atheists Lawrence Krauss and Richard Dawkins. 4 Who Is the Designer? Who is the designing intelligence? Was it an alien? Or a transcendent being? Meyer addresses this question, distinguishing between evidence from biology that merely points to mind, and separate evidence that may shed light on the identity of the designer. Unit 3: Evidence of Intelligent Design in Physics and Cosmology One Man's Journey. Meyer recounts the story of an astronomer's journey from atheism to intelligent design. What do the stars reveal? What Is Fine-Tuning? Meyer discusses the laws and constants of physics, highlighting striking examples of fine-tuning. How Do We Recognize Design? Meyer discusses William Dembski's theory of design inferences, and applies that to fine-tuning. Weak Anthropic Principle and Natural Law. Meyer gives an overview of the weak anthropic principle and natural law as explanations for fine-tuning. The Multiverse, pt. 1. Meyer describes a popular explanation for fine-tuning and the two cosmological models physicists employ. The Multiverse, pt. 2. Meyer analyzes the multiverse theory. How does it stack up against intelligent design? The Multiverse, pt. 3. Meyer delves deeper into universe generating mechanisms and what they require. Who Is the Designer? In this final video lecture, Stephen Meyer shares his thoughts on this important question.     Michael Behe Exposes How Mutations Fail To Invent (Science Uprising EP6) https://youtu.be/_ivgQFIST1g Discovery Science Are chance mutations really “the key to our evolution” like they claim in the X-Men films? Or are there strict limits to what mutations can accomplish, limits that point to the need for an overarching designer and the failure of Darwinian evolution to create fundamentally new things? Be sure to visit https://scienceuprising.com/ to find more videos and explore related articles and books. In this episode of Science Uprising, we'll take a look at the real evidence for the supposed powerhouse of evolution. The featured expert is biochemist Michael Behe of Lehigh University, author of the books Darwin's Black Box, The Edge of Evolution, and Darwin Devolves. Well-known scientists have been preaching a materialistic worldview rather than presenting the public with all the evidence. We are here to change that. The objective scientific evidence does not prove our universe is blind and purposeless. It does not show we are simply meat machines. It does not prove that evolutionary mechanisms can completely account for the diversity of life on earth. This is what THEY want you to think. Think for yourself and make an informed decision. Are you ready? The uprising has begun. In a lecture, Phillip Johnson cited physicist Richard Feynman on a scientist's obligation to be honest — not only with himself or in other scientific contexts but, not one bit less, when speaking to the lay public. “You should not fool the laymen when you're talking as a scientist.” That such a thing would need to be said is itself revealing. What's more, Feynman insisted, you should “bend over backwards to show how you may be wrong.” The comments are taken from a Commencement address by Feynman in 1974 at Caltech. Johnson, a founding father of modern intelligent design, was so moved by this that he said “I wish it could be set to music.” As far as I know it hasn't been set to music. But the idea is a major theme in the new Science Uprising series. Scientists fool themselves and they fool non-scientists, not about dry technical details with no special significance, but about matters that bear on huge, life-altering world picture issues. One example is the role of mutations in evolution. That is the topic of Episode 6 of Science Uprising, “Mutations: Failure to Invent.” It's out now; see it here: The Alternative Perspective The idea that random genetic mutations lead to wondrous, creative innovations is so influential that it forms the premise of a movie franchise, X-Men, that has grossed $6 billion worldwide over the past couple of decades. That's a lot of “fooling the laymen”! The alternative perspective would be open to the possibility of creative evolution requiring intelligence guidance. The producers of the X-Men movies aren't scientists. However, the science media have done their best to mislead about the work of real scientists, including National Academy of Sciences member Richard Lenski. We're all victims of that hype, including Hollywood moviemakers. Dismantling the hype about Lenski occupies biochemist Michael Behe for a significant part of his recent book, Darwin Devolves. Super-Challenges Not Super-Powers As Professor Behe explains in Science Uprising, the Long-Term Evolution Experiment conducted by Lenski has demonstrated not the creative power of unguided evolution but the occasional benefits of devolution, of breaking or disabling genes. That's the opposite lesson from the one drawn by media such as the New York Times in reporting on Lenski's efforts. “Think about it,” says the masked narrator of Science Uprising, against the backdrop of poignant images of people suffering from genetic illnesses, “significant mutations don't create superpowers. They create super-challenges. Sometimes those mutations are even life-threatening.” Check out some of our other videos: Information Enigma: Where does information come from? Information drives the development of life. But what is the source of that information? https://youtu.be/aA-FcnLsF1g Science Uprising Episode 1 - Reality: Real vs. Material Has science proven we are all just matter? Or does reality extend beyond what we can see and touch? https://youtu.be/Fv3c7DWuqpM Bijan Nemati: Rare Earth https://youtu.be/vn3YpOWCrc4 Check out other videos from this playlist: https://www.youtube.com/playlist?list... Subscribe to our channel: https://www.youtube.com/user/Discover...     Michael Denton Remarkable Coincidences in Photosynthesis -- ID The Future Podcast https://youtu.be/12i2RKct5RM Discovery Science On this episode of ID the Future, we listen in on a few minutes from a lecture given by CSC Senior Fellow Michael Denton. We've all heard of the importance of photosynthesis as an oxygen creating process. In this segment, Denton explains the “remarkable set of coincidences” which makes the creation of oxygen through photosynthesis possible. From the specific energy of visible light to the unique properties of water, this degree of improbability screams DESIGN. For more and to download this episode go to: https://www.discovery.org/multimedia/... For more on how the cosmos is designed for life, watch Discovery Institute's documentary Priviledged Species, featuring Michael Denton, at http://privilegedspecies.com/. The ID The Future (IDTF) podcast carries on Discovery Institute's mission of exploring the issues central to evolution and intelligent design. IDTF is a short podcast providing you with the most current news and views on evolution and ID. IDTF delivers brief interviews with key scientists and scholars developing the theory of ID, as well as insightful commentary from Discovery Institute senior fellows and staff on the scientific, educational and legal aspects of the debate. You've heard the hype, now learn the truth. Subscribe to the podcast Intelligent Design: The Future. Exploring issues central to the case for intelligent design from the Big Bang to the bacterial flagellum and beyond. https://itunes.apple.com/us/podcast/i... ============================ The Discovery Science News Channel is the official Youtube channel of Discovery Institute's Center for Science & Culture. The CSC is the institutional hub for scientists, educators, and inquiring minds who think that nature supplies compelling evidence of intelligent design. The CSC supports research, sponsors educational programs, defends free speech, and produce articles, books, and multimedia content. For more information visit https://www.discovery.org/id/ http://www.evolutionnews.org/ http://www.intelligentdesign.org/ Follow us on Facebook and Twitter: Twitter: @discoverycsc Facebook: https://www.facebook.com/discoverycsc/ Visit other Youtube channels connected to the Center for Science & Culture Discovery Institute: https://www.youtube.com/user/Discover... Dr. Stephen C. Meyer: https://www.youtube.com/user/DrStephe... The Magician's Twin - CS Lewis & Evolution: https://www.youtube.com/user/cslewisweb Darwin's Heretic - Alfred Russel Wallce: https://www.youtube.com/user/AlfredRW...  

Today we're continuing our series on doubt. We're in part four of five.    A political science major at a major university was having coffee with a campus pastor. The pastor knew that the student was wrestling with doubt about the existence of God and said to him, “John, you know all of us wonder at some point if it's all real or not. For example, there are quite a few stories in the Bible that are just hard to believe. Jonah and the whale and all that.” John smiled and said, “No, that's not my problem. What I wonder about is how God could care about me. I've done some really bad things and have had some really bad things done to me. I just can't understand the concept of forgiveness.”   There you have it. Doubts about the faith come from all directions. While one person cannot bring herself to believe in miracles, another cannot forgive himself for the wrong things he's done, and can't fathom how God could.    Thomas Jefferson actually cut out the miraculous sections of the Bible. He couldn't believe in what some would call the God of the Bible. Francis Crick, the co-discoverer of DNA, thought that Christianity was just a collection of mythical stories. And what about those who want to see the proof, they like evidence and feel a need to make an intellectual case for our faith.    The New Testament writer, Luke, was like that. He wrote in Acts and the Gospel of Luke about the importance of eyewitness sightings of Jesus and His miracles. Lots of people debate whether evolution and religion are compatible or not. And this is a big stumbling block to believe for many. We all believe something, but our minds can struggle at times to grasp the big stuff, the infinite universe. While for others who doubt, the struggle is more internal, they're so grieved by their own sin, they can't accept that God could love them.   Maybe the most famous verse in the Bible is John 3:16, which says, “For God so loved the world that he gave his one and only son, that whoever believes in him shall not perish, but have eternal life.” However, few quote the next verse which says, “For God did not send his son into the world to condemn the world, but to save the world through him.” It isn't God's wish to condemn you. Instead, he loves you and wants to give you assurance that life is more than struggle and molecules.    Whether you're looking for evidence to believe the Bible or you just need to know that God loves you, try not to focus too much on your objections. Own them, but just tell God as a child would, that you're struggling to understand it all.   Will you pray with me?    Father, your grace saves us from a life of struggle with sin and we are accepted by you. Thank you for putting up with our up-and-down faith. In Jesus' name, amen.

“Who you are depends on where you've been. Your brain is a relentless shape-shifter, constantly rewriting its own circuitry—and because your experiences are unique, so are the vast, detailed patterns in your neural networks. Because they continue to change your whole life, your identity is a moving target: it never reaches an endpoint. That's From Neuroscientist and Stanford Professor, David Eagleman's, The Brain: The Story of You. Now that REALLY made me STOP and THINK as I am about to write this next episode. I wonder: What's my identity-or what makes me-me, especially if it's a moving target. I'm not just Andrea, the host of the Neuroscience Meets SEL Podcast (imagining my brain, and all its neural networks that consist of ALL the years of experience that make me, who I am today) and each day, my experiences change who I am right down to the books I'm reading, what I'm studying and learning, the people around the world I interact with, making me the person I am today. Then I wonder, who are YOU listening to this podcast? What's YOUR identity, wherever you are tuning in from around the world (and I imagine YOUR brain, and the neural networks you've created with YOUR own specific and unique life experiences. And if our identity (who we are at this point in time) is a moving target that never reaches an endpoint, can we then, create our own reality and future by continuing to re-wire our own circuitry with NEW information, and NEW ideas, that create NEW experiences that change who we could be in the future? Thus, changing our conditions, our circumstances, and our environment? That is the goal of this podcast, (to help all of us to re-wire our brains (with new information) that we'll put into action (using the most current, evidence based research) taking our results to new heights.  This is what keeps ME coming back time and time again to write new episodes.  I've put an image in the show notes that came from my study with Mark Waldman on the Default Mode Network, showing exactly what our brain looks like when we are using our imagination network to take this information we are learning, and use it in a creative way. Our whole brain lights up, connecting all of our brain regions in this process. With that thought, I want to welcome you back to our final episode of Season 9 of The Neuroscience Meets Social and Emotional Learning Podcast, where we cover the science-based evidence behind social and emotional learning (for schools) and emotional intelligence training (in the workplace) with tools, ideas and strategies that we can all use for immediate results, with our brain in mind.  I'm Andrea Samadi, (and while we know I'm not just) an author, or an educator with a passion for learning (I think after today's episode, we will see that we are much more than our work and life experiences) and it's this understanding that will encourage us all to continue re-wiring our brains, taking us to new, and often unimaginable heights.     I'm recording this episode the end of May 2023, and plan to take some time away from the recording studio (my office) this summer. We'll be back with the start of Season 10 the end of June, as we move into the 5th year of this podcast, and our second half of “Going Back the Basics” where we'll continue through our past episodes, to see what we can add to them, with new research and ideas to take our personal and professional results to these new heights. As I started writing this episode that tied back into some of our Brain Fact Fridays on Learning, I couldn't think of what to cover specifically, because learning is behind EVERY episode we produce. I wonder, as we move towards our 5th year, and a new season when we return, what else can we uncover when it comes to “learning” with our brain in mind. Or in other words, how can we take our “learning” to new heights, or look at learning through a new lens? I glanced through some of the episodes we covered on how we learn (procedural vs declarative learning) on EP 131[i], neuroplasticity on EP 133[ii], spaced repetition, distance learning, the neuroscience of learning EP #167[iii], learning and how our emotions impact our memory EP #127[iv] , even the importance of learning skills with our non-dominant hand. While all of these topics are fascinating, I wondered what could we cover today that would take us deeper into the circuitry of our brain, and guarantee a shift of thinking for all of us, causing a lasting change with our results. Then I remembered a documentary I watched YEARS ago, from a Neuroscientist at Stanford University, and Internationally best-selling author, David Eagleman, called The Brain: The Story of You[v]. I know it was in the early days of when I was trying to make sense of why this understanding of the brain would be important for us (specifically as it related to education) so I took clear and detailed notes, and found his documentary to be interesting because it was applicable to our daily life, and I remember it changed my way of thinking. You can see the options for how to watch this documentary today, and also buy his book, The Brain: The Story of You[vi] on Amazon, which I did, even though I had detailed notes on each chapter. What caught my attention with this documentary is that David Eagleman wanted to get away from a textbook inquiry of the brain, (which we all know can be confusing at times with the terminology, and also sometimes boring). Eagleman wanted to “illuminate a deeper level of inquiry” that dives into the question of “who am I” which he says “depends on where you've been” or the experiences we've had and that “because our experiences are unique, so are the vast, detailed patterns in our neural networks.” He goes on to say that “they continue to change your whole life (and that) your identity is a moving target: it never reaches an endpoint.” So to close out Season 9 of our podcast, on “Diving Deeper into The Neuroscience of Learning: Unlocking the Mystery of Individuality and Uniqueness” we will look at our content, through David Eagleman's lens, and see how we can rewire our brain, with new experiences, taking our identity to new heights, in this episode and beyond.  I'm looking for sustainable, long-lasting change to occur for all of us. On today's episode #290 on “Diving Deeper into The Neuroscience of Learning” we will sharpen our focus of what our understanding of the brain REALLY means to us as we cover: ✔ Who Are We (Self-Awareness) as we move through life as an infant, teenager and into adulthood. ✔ Understanding our Identity (What Makes YOU-YOU) By Looking at Our Unique Experiences ✔ What Neuroplasticity Really Means for Us: How Can We Shape Our Brain for a Better Future? ✔ 3 Tips for Re-Wiring Our Brain to Change Our Identity   Who Am I? Chapter 1 of The Brain: The Story of You We started this podcast covering self-awareness: know thyself, on EP #2[vii] where we covered six tips for being self-aware, and then I remember when we dove deeper with a graphic on the levels of consciousness, from EP 251[viii] where we looked at our levels of consciousness from low awareness, like when we are in a coma, under general anesthesia, moving up towards drowsiness or that state called hypnagogia (between wakefulness and sleep), right into our actual sleep, REM state, and dreams and finally into full consciousness.  We explored full-consciousness and the question of “who am I” with Chantel Prat and her book, The Neuroscience of You, on EP #255.[ix]   But what does David Eagleman have to say about our consciousness and who we are? He says,  “It turns out your conscious mind-the part you think of as you—is really the smallest part of what's happening in your brain, and usually the last one to find out any information.” Which made me stop and think for a minute. I thought “wait, should I REALLY be using my conscious mind—the part I think is me-- to write this episode, “the smallest part of what's happening in my brain?” according to Neuroscientist David Eagleman. I thought back to that image of our conscious mind as an iceberg, showing me that logical and critical thinking (that I'm using to write) consist of only 10% of my mental capacity, and that the other 90% that holds my beliefs, emotions, habits, values, long term memory, imagination and intuition are all in my subconscious mind. What else can we do to tap into this other part of our brain to take our results to new heights? I have just started reading David Eagleman's book, and he's already started to challenge my thinking.  He takes us back to when we were babies and born with a brain that “allows itself to be shaped by the details of life experience.” (Eagleman, The Brain, Ch. 1). What's the secret behind “the flexibility of young brains” he asks us? He says, “it's not about growing new cells, the secret lies in how those cells are connected.” (Eagleman, The Brain, Ch 1). So now I'm thinking that who we are really IS based on our life experiences, that create these neural connections in our brain, and if we don't like where we've ended up in life, or the circumstances we've created, then we can change our environment by doing something new. But REMEMBER: To truly discover WHO we ARE, we've got to dive into the depths of our subconscious mind. Eagleman reminds us that “your actions, your beliefs and your biases are all driven by networks in your brain to which you have no conscious access.” That's why it takes some time to peel back the layers of who we are, in our efforts to become the best version of ourselves. PUT THIS INTO ACTION: LEARN NEW THINGS AND YOU WILL RE-WIRE YOUR BRAIN If the adult brain can change (neuroplasticity) then we can change our brain, and create improved versions of ourselves with our life experiences that does take time.  Eagleman noted that when Albert Einstein's brain was examined, it didn't reveal why he was a genius, but it did show that “the brain area devoted to his left fingers had expanded—forming a giant fold in his cortex called the Omega sign, shaped like the Greek symbol” (Eagleman, The Brain, Ch 1). This Omega sign was also found in violin players, showing clearly how detailed movement can in fact change the brain.   LONDON CAB DRIVER'S PROVED THIS TO BE TRUE: We've also mentioned on this podcast about how London Cab drivers changed their brains but David Eagleman went into detail of how these cabbies had to memorize London's extensive roadways that “covers 25,000 individual streets, and 20,000 landmarks of interest (hotels, theaters, restaurants, embassies, police stations, sports facilities, and anywhere a passenger wants to go.” (Eagleman, The Brain, Ch 1). When the brains of these cab drivers were studied, they found “visible differences:  the posterior (back) part of the hippocampus had grown physically larger than those in the control group—presumably causing their increased spatial memory.” (Eagleman, The Brain, Ch 1). Eagleman mentioned that “the longer the cabbie had been doing their job, the bigger the change in the brain region” suggesting the result came from the practice. Now I'm thinking back to some early episodes where we covered the importance of “spaced repetition” or “daily practice” to yield new results over time. So, if we want to re-wire our brain, or create a stronger 2.0 version of ourselves, here are 3 TIPS for implementing this concept. IDEAS FOR IMPLEMENTING SOMETHING NEW INTO OUR LIFE TO RE-WIRE OUR BRAIN: LISTEN: To new podcasts, take notes, and implement what you learn. I'm always discovering new podcasts, and just need to find the time for all of this new learning. I'm sure if you are listening to us here, that you have also found the benefit to learning through this medium. TRAVEL: Go somewhere you've never been before. This summer we are traveling to somewhere we've never been before. Instead of planning the same old summer vacation, this year, we will be going somewhere where the internet doesn't work well, to create new life experiences for all of us. Pick a place you've never been before to open yourself and your brain to NEW life experiences. BE OPEN TO LEARNING SOMETHING NEW, EVEN SOMETHING WEIRD: Like with a new meditation or something. I can't say enough about how much I learned from my review of Jose Silva's The Silva Mind Control Method[x] that we covered earlier in the year. It looks like this episode was also a hit for those listening, with over 4K downloads the last time I looked. The book was eye-opening, but the online course completely blew my mind open with new ideas that I could spend the rest of my life practicing and implementing. As I read through some of the topics, I definitely can say they stretched my mind beyond where I have ever gone before. REVIEW AND CONCLUDE To review and conclude this final episode of Season 9 on taking a “Diving Deeper into The Neuroscience of Learning” we covered: ✔ Who Are We (Self-Awareness) as we move through life as an infant, teenager and into adulthood. ✔ Understanding our Identity (What Makes YOU-YOU) By Looking at Our Unique Experiences ✔ What Neuroplasticity Really Means for Us: How Can We Shape Our Brain for a Better Future. ✔ 3 Tips for Re-Wiring Our Brain to Change Our Identity As we looked into changing our identity, diving into our subconscious mind, we know that consciousness is something that neuroscientists continue to debate over, and this is a topic that you can see from the graphic I created, that I'm interested in studying, learning more here, and sharing what I learn with you on the podcast. As we continue to study, we will become more consciously aware of WHO WE ARE. Here is something profound that David Eagleman shared. He said: Have you ever looked at someone's work written on a wall like David Eagleman is recalling with Francis Crick's work? I absolutely love seeing ideas written on walls, and my office is always full of thoughts, ideas and plans. We can gain inspiration from each other's ideas and plans. I think back to the movie “Good Will Hunting” where Matt Damon was solving math problems on the wall, while he was working as a caretaker at MIT, inspiring more than just the students who saw his work, but the teachers who wondered who this student was. Our experiences can change our brain, and then when we share them with others, we can then go on to inspire others with our thoughts, ideas and knowledge.   But what has meaning for YOU, might mean something completely different to ME, and so the search for what we find “meaningful” continues. To close out this episode I'll end with the SAME quote we opened up with. “Who you are depends on where you've been. Your brain is a relentless shape-shifter, constantly rewriting its own circuitry—and because your experiences are unique, so are the vast, detailed patterns in your neural networks. Because they continue to change your whole life, your identity is a moving target: it never reaches an endpoint. Neuroscientist and Stanford Professor, David Eagleman's, The Brain: The Story of You. With that final thought, I encourage all of us to keep learning, and improving WHO we are as individuals, because this is only the beginning. When we next look at the impact we can have on others, bringing our unique neural networks together, we open up an entire new universe to explore. I'll see you the END of June for SEASON 10 of the podcast, and our 5th YEAR of The Neuroscience Meets SEL Podcast. . We will continue with our Theme of Going Back to The Basics with: ✔ What Can We Really Learn from Looking at Someone Else's Brain? (Einstein, Walt Whitman, Parkinson's, Alzheimer's). ✔ Continue This NEW Learning to Build the Best 2.0 Version of Ourselves REFERENCES: [i]Neuroscience Meets Social and Emotional Learning Podcast EPISODE #131 on “understanding How We Learn: Declarative vs Procedural Systems”  https://andreasamadi.podbean.com/e/brain-fact-friday-understanding-how-we-learn-declarative-vs-procedural-systems/ [ii]Neuroscience Meets Social and Emotional Learning Podcast EPISODE #133 on “Applying Neuroplasticity in Your School or Workplace”  https://andreasamadi.podbean.com/e/brain-fact-friday-applying-neuroplasticity-to-your-school-or-workplace/ [iii]Neuroscience Meets Social and Emotional Learning Podcast EPISODE #167 on “The Neuroscience of Learning”  https://andreasamadi.podbean.com/e/brain-fact-friday-on-the-neuroscience-of-learning/ [iv]Neuroscience Meets Social and Emotional Learning Podcast EPISODE #127 on “How Emotions Impact Learning, Memory and the Brain” https://andreasamadi.podbean.com/e/brain-fact-friday-how-emotions-impact-learning-memory-and-the-brain/ [v] David Eagleman The Brain https://www.pbs.org/show/brain-david-eagleman/ [vi] The Brain: The Story of You by David Eagleman Published October 6, 2015 https://www.amazon.com/Brain-Story-You-David-Eagleman-ebook/dp/B0104EOGQ0/ref=tmm_kin_swatch_0?_encoding=UTF8&qid=1684456595&sr=8-1 [vii]Neuroscience Meets Social and Emotional Learning Podcast EPISODE #2 “Self-Awareness: Know Thyself”  https://andreasamadi.podbean.com/e/self-awareness-know-thyself/ [viii] Neuroscience Meets Social and Emotional Learning Podcast EPISODE #251 on “Exploring Consciousness Using Neuroscience” https://andreasamadi.podbean.com/e/brain-fact-friday-on-exploring-consciousness-using-neuroscience-to-expand-our-awareness/ [ix] Neuroscience Meets Social and Emotional Learning Podcast EPISODE #255 with Chantel Prat on “The Neuroscience of You.” https://andreasamadi.podbean.com/e/chantel-prat-phd-on-the-neuroscience-of-you-how-every-brain-is-wired-differently-and-how-to-understand-yours/ [x] Neuroscience Meets Social and Emotional Learning Podcast EPISODE #261 on PART 1 of The Silva Mind Control Method https://andreasamadi.podbean.com/e/a-deep-dive-with-andrea-samadi-into-applying-the-silva-method-for-improved-intuition-creativity-and-focus-part-1/  

James Watson and Francis Crick, who detailed the double-helix structure of DNA in 1953, are perhaps two of the most iconic scientists of the 20th Century. Yet the story of how they made their incredible discovery is perhaps equally famous, with a notorious narrative suggesting that they only identified the structure after taking the work of Rosalind Franklin and using it without her permission. Now, 70 years after the discovery of DNA's structure, it is perhaps time to rewrite the tale. New evidence has now been unearthed, in the form of an overlooked news article and an unpublished letter, that shows that Franklin was truly an equal contributor to the discovery, and Watson and Crick were not as malicious as previously assumed. Together with Matthew Cobb of the University of Manchester, Nathaniel Comfort from Johns Hopkins University, and Angela Creager of Princeton University, Gaia Vince discusses this tantalising tale and finds out more about how this discovery could bring a whole new twist to the story of DNA. Presenter: Gaia Vince Producer: Harrison Lewis Assistant Producer: Jonathan Blackwell

In this episode:00:57 Franklin's real roleWhen it comes to the structure of DNA, everyone thinks they know Rosalind Franklin's role in its discovery. The story goes that her crucial data was taken by James Watson without her knowledge, helping him and Francis Crick solve the structure. However, new evidence has revealed that this wasn't really the case. Rosalind Franklin was not a ‘wronged heroine', she was an equal contributor to the discovery.Comment: What Rosalind Franklin truly contributed to the discovery of DNA's structure13:41 Research HighlightsHow the growth of tiny iodine-engined satellites could damage the ozone layer, and how a pill-like detector that could measure radiotherapy dosages.Research Highlight: How CubeSats could harm the ozone layerResearch Highlight: An easy-to-swallow pill monitors X-ray dosage16:06 Why multisensory experiences can make stronger memoriesIt's recognized that multisensory experiences can create strong memories and that later-on, a single sensory experience can trigger memories of the whole event, like a specific smell conjuring a visual memory. But the neural mechanisms behind this are not well understood. Now, a team has shown that rich sensory experiences can create a direct neural circuit between the memory regions of fruit fly brains. This circuit increases memory strength in the flies, and helps explain how sense and memories are interlinked.Research article: Okray et al.23:44 Briefing ChatWe discuss some highlights from the Nature Briefing. This time, how video calls could help parrots feel less isolated, and a new method for recycling wind turbine blades.The Guardian: Parrots taught to video call each other become less lonely, finds researchNature Video: How to recycle a wind turbine in a test tubeSubscribe to Nature Briefing, an unmissable daily round-up of science news, opinion and analysis free in your inbox every weekday. Hosted on Acast. See acast.com/privacy for more information.

James Watson and Francis Crick first published their discoveries about the structure of DNA on 25 April 1953. Their findings were to revolutionise our understanding of life. We hear archive recordings of their memories, 70 years on. This programme, presented by Louise Hidalgo, was first broadcast in 2010. (Photo: James Watson and Francis Crick. Credit: Getty Images)

Data collated from swab samples taken in Wuhan's market in the early days of the Covid pandemic suggest animals sold in the market were carrying the virus at the time. It's the strongest evidence yet for an intermediate species – one which passed the virus on to humans after becoming infected by bats carrying the virus. Dr Florence Debarre from the Institute of ecology and environmental sciences, in Paris and Professor Eddie Holmes from Sydney University discuss the findings. Beethoven's genome has been reconstructed from samples of his hair. It reveals some of his medical history, but also unexpected findings on his paternity. We discuss the ethics of such genetic analysis with Tom Booth who studies ancient DNA at the Francis Crick institute. And microbes may help us survive and thrive in space according to Astrobiologist Rosa Santomartino, not only that but their recycling capabilities could also help us on earth

Seventy years since James Watson and Francis Crick first revealed DNA's double-helix structure, Dr Kersten Hall shares the story of the scientist who almost beat them to their major discovery: molecular biologist William Astbury. Speaking with Emily Briffett, Kersten details how, despite missing this major opportunity, Astbury forged a new discipline, made pioneering steps in the field of X-ray crystallography – and also wore a coat made of peanuts. (Ad) Kersten Hall is the author of The Man in the Monkeynut Coat: William Astbury and How Wool Wove a Forgotten Road to the Double-Helix (Oxford University Press, 2014). Buy it now from Waterstones: https://go.skimresources.com?id=71026X1535947&xcust=historyextra-social-histboty&xs=1&url=https%3A%2F%2Fwww.waterstones.com%2Fbook%2Fthe-man-in-the-monkeynut-coat%2Fkersten-t-hall%2F9780198704591 Learn more about your ad choices. Visit podcastchoices.com/adchoices

Dr. Peterson's extensive catalog is available now on DailyWire+: https://utm.io/ueSXh Dr. Jordan B. Peterson and Matt Ridley go in depth to explore the Covid 19 outbreak, scrutinizing the lack of criticism, the inherent red flags widely accepted as benign, the possible motive for a multi-government cover up, and ultimately the demise of the scientific enlightenment as it bends to a more fearsome pandemic: totalitarianism. Matt Ridley is a British writer, journalist, and public speaker. His books collectively have sold over a million copies, and have been translated into 31 languages. His books include The Red Queen, The Origins of Virtue, Genome, Nature via Nurture, Francis Crick, The Rational Optimist, The Evolution of Everything, and How Innovation Works. He is also frequently published in the Wall Street Journal, and in the Times (London), as a columnist. As a speaker, Ridley has seen over two million views for his TED talk, “When Ideas Have Sex.” Ridley focuses on the area of science for his writings, and held the role  of science editor at the Economist for nine years. -Sponsors- Birch Gold: Text "JORDAN" to 989898 for your no-cost, no-obligation, FREE information kit  Audible: Try Audible FREE for 30 days. Visit https://audible.com/peterson or text “PETERSON” to 500-500.  Exodus90: Is it time for your Exodus? Find resources to prepare at https://exodus90.com/jordan.  Black Rifle Coffee: Get 10% off your first order or Coffee Club subscription with code JORDAN: https://www.blackriflecoffee.com/ - Links - For Matt Ridley: Matt Ridley's newest book, Viral, is now available in a revised and expanded edition, find it here https://www.amazon.com/Viral-Search-COVID-19-Matt-Ridley/dp/006313912X or the audio/digital version here https://a.co/d/aVdU6zV Matt Ridley's Website https://www.mattridley.co.uk/ Twitter https://twitter.com/mattwridley?ref_src=twsrc%5Egoogle%7Ctwcamp%5Eserp%7Ctwgr%5Eauthor Facebook https://www.facebook.com/authormattridley/  - Chapters - (0:00) Coming up(1:31) Intro(4:25) The origin of the Covid 19 outbreak(7:39) Adapted for humans(11:42) Immediate effectiveness(13:50) Inserted genetic information(16:29) Early concerns of engineering, the pangolin problem(20:00) Reputation management, potential cover up(25:00) The smoking gun, Project Defuse(28:24) The impossibility of ethical science in a totalitarian country(33:50) When presumptions don't add up(37:00) Framing the pandemic as political, a distraction(45:16) 80,000 animals tested in Wuhan, 0 infected(50:30) The lack of criticism for the Chinese government(53:53) Potential darkness, spreading totalitarianism(57:03) China envy, recalling the USSR(1:01:23) Other possible motives(1:05:24) The sad evolution of scientific inquiry(1:09:30) The demise of the enlightenment(1:17:15) The antagonism between religion and science(1:22:07) Truth over consequence(1:28:01) The conflation of religion as a faith and as an institution(1:36:00) The spirit of inquiry(1:38:37) Dawkins; not seeking the answer, following the questions(1:43:20) The truth will set you free // SUPPORT THIS CHANNEL //Newsletter: https://mailchi.mp/jordanbpeterson.com/youtubesignupDonations: https://jordanbpeterson.com/donate // COURSES //Discovering Personality: https://jordanbpeterson.com/personalitySelf Authoring Suite: https://selfauthoring.comUnderstand Myself (personality test): https://understandmyself.com // BOOKS //Beyond Order: 12 More Rules for Life: https://jordanbpeterson.com/Beyond-Order12 Rules for Life: An Antidote to Chaos: https://jordanbpeterson.com/12-rules-for-lifeMaps of Meaning: The Architecture of Belief: https://jordanbpeterson.com/maps-of-meaning // LINKS //Website: https://jordanbpeterson.comEvents: https://jordanbpeterson.com/eventsBlog: https://jordanbpeterson.com/blogPodcast: https://jordanbpeterson.com/podcast // SOCIAL //Twitter: https://twitter.com/jordanbpetersonInstagram: https://instagram.com/jordan.b.petersonFacebook: https://facebook.com/drjordanpetersonTelegram: https://t.me/DrJordanPetersonAll socials: https://linktr.ee/drjordanbpeterson #JordanPeterson #JordanBPeterson #DrJordanPeterson #DrJordanBPeterson #DailyWirePlus