Portal:19: Bret Weinstein - The Prediction and the DISC/lang-it

Descrizione
Tutti i nostri Topi sono Rotti. In questo episodio de "Il Portale", Bret e Eric Weinstein si siedono per la loro prima comparsa in pubblico insieme. Senza alcun piano.

C'era tuttavia una significativa storia scientifica al contempo nelle migliori e peggiori perspettive che, per anni, non è stata raccontata. Dopo un'iniziale battibecco, abbiamo spolverato le ragnatele e deciso di ricostruirla nel suo stato brado e di condividerla con voi, il nostro audience de "Il Portale", per la prima volta. Non penso che sarà l'ultima, poiché stiamo riscoprendo vecchi appunti per prepararla al meglio per il prossimo racconto. Speriamo la troverete interessante, e che ispirerà voi più giovani e meno affermati scienziati a raccontare la vostra storia utilizzando questo nuovo format di podcast a lunga durata. Speriamo che il prossimo luogo dove sentirete raccontare questa storia sia nelle sala per seminari dei dipartimenti di biologia di, forse, Cambridge, Chicago, Princeton, della Bay Area o altrove. Fino ad allora, state bene e ascoltate questa cruda versione iniziale.

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Relevant Links
Bret Weinstein's Wikipedia, Personal Webpage, Youtube Channel, and an archived version of Bret's website, Telomere.org

Papers and articles

 * Bret Weinstein and Deborah Ciszek's 2002 paper in Experimental Gerontology, "The Reserve-Capacity Hypothesis"


 * Bret Weinstein and Deborah Ciszek's 2002 unpublished manuscript, "Life's Slow Fuse"


 * Bret's PhD Thesis, Evolutionary Trade-offs: Emergent Constraints And Their Adaptive Consequences


 * Carol Greider and Mike Hemann's 2000 paper in Nucleic Acids Research


 * Bret Weinstein's 2005 paper in Evolution and Human Behavior


 * 2012 HuffPost article about Bret's telomere length discovery


 * "An Unsolved Problem of Biology", Medawar (1952), a classic paper on senescence


 * "Laboratory Life", a 2010 NY Times Opinionator article that mentions Bret and cites Greider's 2000 paper

Evolutionary Biologists

 * Dr. Carol Greider Wikipedia, NobelPrize.org Bio, Johns Hopkins Faculty page, Research page Twitter NY Times article


 * Dr. Michael Hemann MIT Faculty page


 * Dr. Richard D. Alexander Wikipedia


 * Dr. Richard Dawkins Wikipedia, personal website, Twitter


 * Dr. Robert Trivers Wikipedia


 * Dr. Heather Heying personal website


 * Dr. Elizabeth Blackburn Wikipedia, NobelPrize.org Bio


 * Dr. Jack Szostak Wikipedia, Harvard Faculty research page, NobelPrize.org Bio


 * Dr. George C. Williams Wikipedia


 * Bill Hamilton Wikipedia


 * Dr. John Maynard Smith Wikipedia


 * Dr. Judith Campisi Wikipedia


 * Peter Medawar Wikipedia

Laboratory mice info

 * Laboratory mice general info on Wikipedia


 * Genetics and Strains of laboratory mice


 * Mus (genus)


 * Mus musculus (aka house mouse)


 * JAX Lab Wikipedia, company website


 * JAX Lab's popular mouse strains

Other Concepts and Terms

 * Xanthopan (moth)


 * Darwin's Orchid (Angraecum sesquipedale)


 * Ophrys orchid


 * Eusocial


 * Hymenoptera


 * Haplodiploidy


 * Naked Mole-rat


 * Telomeres


 * Hayflick Limit


 * Senescence


 * Somatic cell


 * Germline


 * Genome


 * Pleiotropy


 * Antagonistic Pleiotropy Hypothesis


 * Telomerase


 * (Environmental) Insult


 * Histology


 * Rofecoxib (Vioxx)

Margot O'Toole, Imanishi-Kari & David Baltimore story

 * Thereza Imanishi-Kari Wikipedia


 * David Baltimore Wikipedia


 * NY Times article


 * MIT article


 * Nature News and Views: Margot O'Toole's Record of Events


 * People.com article

Institutions

 * Evergreen State College Wikipedia

Events

 * Takeover at Straight Hall at Cornell in 1969


 * Chronicle article about Bret's stand against racism at UPenn in 1987


 * NY Times opinion article about Evergreen Student Takeover in 2017


 * Bret's conversation with Richard Dawkins in 2018

Books

 * The Tapir's Morning Bath - Elizabeth Royte


 * Fertilisation of Orchids - Charles Darwin

Remaining Questions
1) Telomere length delta from wild type in both absolute length and variance.

2) Changes and variation in lab-bred rodent telomere length over time.

3) Notification history of all of the above to all affected parties.

4) Estimated impacts of all of the above deltas from wild type.

5) Communication protocol with the JAX lab and other suppliers and pharma companies for journalists and researchers wishing to understand all of the above.

Transcript
Eric: Ciao. Sono Eric Weinstein. Sto registrando una piccola introduzione a questo episodio perché penso sia ad oggi il più importante episodio de “Il Portale”. Detto questo, sotto normali circostanze, avrei probabilmente apportato pesanti modifiche o non lo avrei pubblicato affatto. Inizia molto lentamente e prima di prendere il ritmo diventa leggermente sconfortante. Ora, quello che è successo è che il protagonista di questa intervista non è ben che meno mio fratello Bret Weinstein. Nel caso di Bret, se lo conosceste, lo ricordereste come l’eroico professore che sfidò quello che può essere solamente descritto come – sono sincero, non me lo sto inventando – l’insurrezione Maoista in un college americano del Nord-Ovest Pacifico, il college statale Evergreen. È stata una situazione molto strana perché in qualche modo i media nazionali che penseremmo avrebbero riportato una storia di questo tipo – quei media, per esempio, che riportarono l’assedio della Straight Hall della Cornell negli anni sessanta – sono quasi del tutto scomparsi. O perlomeno si sono mantenuti assenti molto a lungo prima di prendere parte a questo gioco. E qual è la ragione di ciò? Perché la storia seguiva una traiettoria totalmente opposta allo standard: gli studenti del college statale Evergreen che si stavano comportando in maniera razzista erano in realtà studenti di colore, per l’appunto una narrativa totalmente opposta. E Bret, che si oppose a questa insurrezione razzista, aveva già allora un record per aver preso posizione contro il razzismo. Lui, infatti, era stato uno studente della Università della Pennsylvania, la mia alma mater, una Ivy League, che ha dovuto lasciare a causa di minacce di morte quando si mise dalla parte delle donne di colore che venivano molestate per il divertimento e vizio sessuale degli studenti bianchi delle fraternite. Per questo dovreste essere familiari del nome di Bret, da una vecchia storia nazionale, lui che fu inoltre l’eroe di un libro chiamato “Il bagno mattutino del Tapiro”.

Ma per qualche ragione, i mezzi di informazione, che decisero di non riportare la storia Evergreen, non erano neanche interessati a scoprire chi fosse Bret poiché le notizie dimostravano l’esistenza di una contraddizione con la narrativa principale. In qualche senso, questo verrà ripreso in questo episodio. C’è anche una narrativa ufficiale per quanto riguarda l’episodio scientifico, e c’è una narrativa che è molto più vicina alla verità, della quale io sono uno dei pochi testimoni. Ora la domanda chiave è se raccontare la storia o meno, e voi noterete che entrambi [Bret ed Io] abbiamo una certa trepidazione e energia attorno a questa questione: se rompere o meno questo lungo silenzio pubblico. Quando Bret ha capito di essere un professore in esilio a fianco di sua moglie, Heather Heying, avrei pensato che l’establishment americano per la biologia avrebbe realizzato che uno dei loro era stato gettato in mare come una zavorra, e che lo avrebbero quindi invitato a dare seminari di biologia.

Mi ci volle qualche tempo per realizzare che, essendo lui del college statale Evergreen, le persone che insegnavano a quelle università di alto rango lo ritenevano più un insegnante che un ricercatore. Infatti, lui era stato uno dei migliori studenti di uno dei più grandi teoretici evoluzionari negli Stati Uniti, Richard Alexander all’università del Michigan, e anche di Bob Trivers, formalmente di Harvard, che fu uno dei grandi teoretici evoluzionari viventi, ora a Rutgers. Bret era stato uno di quelli che ha condotto un lavoro davvero interessante nella sua tesi, e per qualche ragione, il sistema trovò inquietante considerare tutte le implicazioni del suo lavoro.

Penso che faremo qualcosa di interessante in questo episodio. Io vedo Bret in due luci separate: da un lato, lo vedo come una figura eroica e un persona assolutamente brillante. È stato un piacere stuzzicarsi nel corso della mia vita. Tuttavia, sono anche il suo fratello maggiore e mi coglierete difficile da sopportare, provocandolo un po’. Il punto non è di sopprimerlo, ma proprio il contrario. Sono molto competitivo in quanto fratello maggiore di Bret e non voglio competere con la sua versione più debole, il professore e l’esiliato. Invece, voglio farlo sedere ancora una volta all’interno delle istituzioni di cui ha sempre fatto parte. E per farlo, voglio che racconti la storia, non abbellendola, ma come è successa per davvero, perché penso che sia uno degli episodi più affascinanti della biologia moderna che io abbia mai sentito.

Così, spero che vi piaccia. Lo mettiamo di fronte al vostro scrutinio come un esperimento e cercheremo di capire se ho ragione o meno, se saremo capaci di influenzare i normali canali [di informazione].

Credo che molti di noi siano seduti su oro intellettuale. Non penso che la storia che il lavoro di qualcuno non abbia raggiunto la luce del giorno, o che sia stato attribuito a qualcun altro, sia così esotica quanto le istituzioni vogliano farvi credere. Infatti, penso che sia molto comune. Penso che molti di noi non abbiano carriere nelle scienze perché qualcosa andò storto in un periodo quando eravamo molto vulnerabili. E la mia speranza è che alcuni di voi ascoltatori, che so stanno avendo difficoltà come laureati o come postdoc o come laureandi, ascolterete questa storia e troveranno il coraggio di prendere una posizione, perché, molto sinceramente, se scegliete di non farlo per fare i carini nel vostro campo, le possibilità di avere una carriera nel lungo termine hanno una bassa probabilità. Potete quindi correre per le recinzioni [tagliare la corda], schiarirvi la gola e raccontare la vostra storia come è realmente accaduta, senza paura.

Non so se questo avrà successo, ma faremo questo esperimento e penso che sia io che Bret siamo all’altezza di scoprire qualunque siano le conseguenze. L’unica cosa che voglio aggiungere è che chiunque sia coinvolto nella storia e voglia raccontare la sua versione degli eventi, sarà un’onore ospitarti ne “Il Portale”. Non ci sono molte persone nella storia, in mia opinione; ci sono molti pessimi incentivi. E se vogliamo davvero aggiustare il sistema, dobbiamo guardare oltre le relazioni interpersonali. Ma il punto di questo, secondo me, è che è abbastanza riaprire il caso e sedersi con Bret Weinstein dentro il sistema universitario – cioè, il sistema universitario di ricerca a cui lui è sempre appartenuto. Ascoltate e spero rimarrete soddisfatti.

(00:06:01)

Eric: Ciao, hai trovato “Il Portale”. Sono il tuo conduttore, Eric Weinstein, e oggi ho l’onore di ospitare nientemeno che mio fratello, il Dr. Bret Weinstein. Bret, benvenuto.

Bret: Grazie per l’invito.

Eric: Okay, bene, cosa facciamo? Cosa ne pensi?

Bret: Wow. Beh, non saprei. Mi immagino che una certa frazione del tuo pubblico sta attraversando la solita sorta di una –

Eric: Ci chiamano casualmente o Bret o Eric.

Bret: Sì.

Eric: Fin qui è l’unica cosa che posso dire.

Bret: Che è anche una cosa che i nostri genitori facevano mentre crescevamo.

Eric: Penso sia vero.

Bret: Anche i nomi degli animali domestici si inoltravano di tanto in tanto, se ricordo bene.

Eric: È vero. Okay. Allora, se non ti dispiace, cercavo di pensare al fatto che abbiamo un’opportunità di fare qualcosa che potrebbe essere leggermente diverso perché io e te abbiamo molto in comune e pensavo che dovremmo iniziare a fare buona attenzione ad un’area della tua specializzazione in biologia piuttosto che alla tangente per cui molte persone ti hanno conosciuto di recente. Così posso chiederti di spiegare, in 30 secondi, come il mondo ha iniziato a riconoscerti se vieni riconosciuto affatto?

Bret: Certo. Quanto io venga riconosciuto è dovuto tipicamente al meltdown all’ Evergreen e alla mia posizione –

Eric: Stai parlando del college stata Evergreen.

Bret: College statale Evergreen in Olimpia, Washington, dove ho insegnato per 14 anni, al fianco di mia moglie, Heather Heying, che ha insegnato lì per 15 anni. Abbiamo affrontato una folla di persone che mi accusavano di razzismo. E questi erano studenti, studenti che non avevo mai conosciuto. E l’evento fu così pittoresco, che una volta che il mondo scoprì il fatto che questa protesta, che divenne una rivolta, era stato caricato tramite video su internet, e così le persone poterono vedere l’intero evento anche dalla loro perspettiva, venne colto l’interesse di certi quadranti. Così, per esempio, finì per andare nel programma di Joe Rogan, che è il posto da cui spesso molti mi riconoscono. E tu lo sai, durante la mia prima apparizione lì, parlammo della situazione ad Evergreen. E comunque, è da lì che la maggior parte delle persone mi riconosce.

Eric: Molto bene. Così tu eri un biologo che insegnava in un college relativamente sconosciuto che prima veniva riconosciuto per attivismo sociale. E non mi è piaciuta la tua introduzione perché quando dici, “Beh, gli studenti mi accusarono di razzismo” questo lascia aperta una strana domanda. Per esempio, “Perché è stato accusato di razzismo?” Permettimi di risolvere questo puzzle immediatamente – forse tu non riusciresti – perché quella fu finora la cosa più vicina a una insurrezione Maoista all’interno degli Stati Uniti d’America. Sembrava come se fosse un caso d’insania e i video dimostrarono che lo fu infatti e se fino a quel momento non fossi stato indottrinato a credere in qualche forma di Maoismo, rieducazione Maoista, come normale, il resto del mondo disse “O mio Dio! Quello che sta succedendo è pura follia –”. Non fu solo come uno di quei pezzi di follia collegiale. Quello che si avvenne lì fu un episodio di completa follia istituzionale. Il video esiste. E se avessi preso le persone che cercavano di farti passare per un razzista nei loro termini, sarebbe stato sufficiente – sarebbe come un narratore inaffidabile. Stavano disintegrando loro stessi negli occhi di tutti quelli che non erano stati incantati da questa particolare forma di follia.

Bret: Beh, c’è anche un qualcosa in più nel senso che furono totalmente impreparati a un uomo bianco che diceva “No, semplicemente, non sono un razzista”. E non gli passò mai nella testa che quello sarebbe successo. E non si aspettarono che i miei studenti non sarebbero scappati alla loro parte nel momento in cui presentarono le loro accuse, perché questo sarebbe stato normale in questo ambiente. Ma, nel mio caso, crebbi in una casa – c’erano molte falle in quella casa, come sai – ma uno di quei posto che non penso avesse una falla e quello era quello sui problemi di inegualità e giustizia di razza. E così io, io avevo il senso che questi problemi non mi suonassero come nuovi e avevo molti casi al liceo, molti studenti di colore–

(00:10:43)

Eric: Lo stai spiegando troppo. E non voglio passare per rude, ma, erano semplicemente pazzi.

Bret: Erano impazziti. Ma il mio punto è: l’accusa è in e da sé così potente nelle moderne circostanze che le persone, l’idea di affermare la propria posizione non passa nella maggior parte delle persone. E il fatto fu che neanche io avevo preso una posizione abbastanza chiara. La cosa decadde in follia. Decadde letteralmente in anarchia con studenti armati, nomadi nel campus, quella stessa gentaglia mi stava cercando, passando da macchina a macchina, per esempio. Fu una situazione davvero pericolosa.

Eric: Con mazze da baseball…

Bret: Con mazze da baseball... Ma quello a cui sto arrivando è che mi confrontai con me stesso e non mi sentii vulnerabile da queste accuse. Capii che molte persone non avrebbero potuto resistere a questa pressione, ma io ero in quella posizione e in uno modo strano-

Eric: Ti hanno dovuto allontanare dalla tua stessa università come laureando per esserti alzato contro il razzismo.

Bret: Infatti.

Eric: Questo persone hanno invertito il manoscritto e poi ti hanno detto “se non ti iscrivi al nostro razzismo, sei razzista” Certo!

Bret: Lo fecero.

Eric: Io non. Lo sai. Il fatto è questo. Ho due documenti che ho studiato e che hanno una certa longevità. Uno inizia con, “Riteniamo che queste verità siano evidenti” e l’altro inizia con “In principio”. E penso che abbiamo fatto un errore gigantesco ad aver preso questo come un argomento. È una posizione non-seria mantenuta da deficienti e idioti, o da persone che sono state indottrinate e infette con un’idea che c’è qualcosa di sinistra nell’essere razzista. Non sono interessato a quello e penso anche che sia smettere di rispettare queste persone. È come, è molto importante escluderle dalla conversazione, perché se c’è bisogno di un simposio di tre giorni sul come o no il razzismo posso essere ridefinito in un modo che rende impossibile per certe persone di essere razziste e rende impossibile per altre persone non esserlo, allora non c’è un punto. C’è bisogno di buttarlo nella spazzatura perché è solamente un’idea suicida che spreca il tempo di tutti e affonda il mondo nella stupidità, pazzia e nell’odio.

Bret: Beh, sia io che te siamo in totale accordo sulla necessità di escludere attori maligni dalla conversazione.

Eric: Ottimo.

Bret: Sono molto preoccupato di un largo gruppo di persone che rappresenta uno dei due campi. O sono confusi, o soffrono di tale codardia che si iscriverebbero ad idee che dovrebbero sapere sono sbagliate.

Eric: Sì. Ma non penso che tu stia ricevendo il messaggio. Abbiamo fatto un enorme errore e mi rifiuto di perdere tempo perché queste persone hanno deciso che questa sia una tassa da pagare, che questo sia un punto serio. È una posizione non-seria. È una terrificante non-seria posizione poter ridefinire il razzismo come anti-razzismo e l’anti-razzismo come razzismo.

Bret: Nessuno lo sa meglio di me.

Eric: Ottimo. Okay. Siamo a posto?

Bret: Sì.

Eric: Bene. Con questo a parte, il mio dubbio – lo sai che mi piace giocare a questo gioco, che si chiama “Cos’è la cosa meno interessante che c’è di interessante in X?” dove prendo una persona e prendo la loro caratteristica più importante. Così per esempio, la cosa meno interessante che c’è di interessante di Dolly Parto è che è una tettona. La cosa più interessante è che è una geniale cantautrice e una ottima businesswoman. Non è importante. Il punto principale è che ci siamo aggrappati ad una caratteristica stupida e superficiale, e non vediamo la cosa davvero interessante o maestosa di una persona e penso che questo sia accaduto a te. Penso, su un certo livello, avendoti conosciuto per un certo tempo, che tu sia una persona davvero interessante per una ragione totalmente diversa da quella ragione che ti ha reso famoso. E vorrei usare questo episodio e, comunque, sei sempre benvenuto. Amerei fare una serie con te. Amerei, lo sai, rendere questa una parte regolare delle nostre vite se alle persone piace.

(00:14:43)

Bret: Interessante. Penso to lo sappia, entrambi abbiamo molta curiosità su come sia la nostra relazione, e come le nostre discussioni suonino. E penso che ci sia molto spazio per questo.

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(00:16:57)

Eric: Cosa vorrei fare è provare ad essere per te il vegliante che nessun altro può essere, perché ho iniziato a seguire la storia molto presto. E tra l’altro, quando originariamente iniziai a cercare arrivare aiuto e alleati, penso che l’unica persona che poté capire quello che stava accadendo allo statale Evergreen era il nostro mutuale amico, Sam Harris, che aveva intenzione di amplificare e ritwittare questo, perché era così disorientante che la maggior parte del resto del mondo non aveva mai visto questo tipo di argomenti. E ora è molto più comune per le persone essere a conoscenza di questi problemi. Ma quando iniziò, non avevamo neanche un contesto su come riflettere su queste cose.

Bret: Sì, ed infatti, Sam, mi ricordo persino il contenuto del suo tweet quando ha preso parte nella discussione, dove ha suggerito che quello che era necessario sarebbe stato deporgrammare queste persone. E vivendo all’interno di questo sconvolgente scenario, sentire un messaggio di ragione dall’esterno, che era evidente quanto pazzo fosse questo, significò molto per me. Davvero, ha cambiato le cose. Fu come confermare le osservazioni finora fatte.

(00:18:00)

Eric: Sì. Sam fu un eroe per quanto riguarda quello. È fantastico che arrivò presto e fu così corretto. E, sai, meglio per lui.

Bret: Sì.

Eric: Okay. Come sai, io non ero felice che tu fossi al college statale Evergreen, molto prima che nascesse questo problema. Mi sembrava che ti stessi come ritirando in questo veramente oscuro college e usassi questi maturandi come se fossero studenti laureati, insegnando loro concetti avanzati, e offrendo uno strano tipo di programma simile ad Harvard con materiale davvero avventuroso, con nessuna riconoscenza che questo tipo di strano ambiente educazionale stesse cambiando. Giusto? Sbagliato?

Bret: Beh, è per gran parte giusto. Non era proprio un posto appropriato. Ma non ho rimorsi. Penso che per l’ultimo o li ultimi due anni, Heather e Io stessimo vivendo col coltello alla gola, che questo avrebbe potuto colpirci in maniera peggiore e sarebbe potuto arrivare in ogni momento. Ma la cosa del lavoro che avevo era quella positiva in un pazzo esperimento educazionale. I fondatori del college ruppero ogni regola di una università normale, e la metà delle cose che fecero fu brillante. Nessuno si prese la briga di separare il prototipo e, sai, riparare il pezzo rotto. Non accadde. Ma, l’amministrazione non aveva alcun potere, e molta poca conoscenza di quello che stava accadendo nelle classi, ciò significava che potevo creare un ambiente di studio e lavorare dal mio punto di vista sugli obiettivi per avanzare il programma di ricerca che, in franchezza, non avrei mai potuto mantenere in un college normale. Sarei stato così soppresso dagli impegni educativi che non avrei potuto combinare le due cose. Così comunque, penso che uno abbiamo bisogno di capire come sopravvivere finanziariamente. Uno deve capire come crescere i figli. E da molti punti i vista, per quanto ci fosse poca corrispondenza tra me e Evergreen in molti modi, in altri, non era un brutto posto dove parcheggiare. Mi diede – ero anonimo dal punto di vista del mondo e potevo fare progressi in biologia. Così ho molti meno rimorsi di quanto potrei averne.

(00:20:36)

Eric: Okay. Questo è così scomodo, ma è anche la vera sostanza della nostra relazione. Ho sempre risentito il fatto che tu fossi eccellente e trovassi gioia nell’ insegnare per quanto hai potuto, e l’hai sempre visto come un posto dove giocare con idee, insegnare agli studenti e condurre una vita felice, in salute all’aperto, etc, ect, blah, blah blah. E vedo ancora queste caratteristiche dentro di te, e mi fa impazzire perché sei il più grande nemico di te stesso in qualche modo, dal mio punto di vista. Quello che per me sei, in realtà, per me, è un incredibile pensatore e ricercatore, e all’ombra di questo amichevole e carino pedagogista si trova un pensatore che il mondo non conosce. E ho seguito di recente le tue interazioni con Richard Dawkins, ed era assolutamente infuriante. Voglio dire, lo sai, lui è molto chiaro. È come, “Beh, Bret è un vero eroe, per quanto riguarda la libertà di parola e per rispondere ad altre inchieste contro la libertà. Ma è molto confuso.” Beh, no, non penso che sia giusto. Penso che abbiate avuto una davvero sostanziale interazione di biologia, che penso lui voglia spendere molto più tempo su quella perché lui è fenomenale quando è concentrato, e tu sei fenomenale. E quella doveva essere una conversazione completamente diversa. Ma perché ti abbiamo conosciuto nel modo sbagliato, in mia opinione, rimani sempre quello che è stato abbastanza forte per confrontare gli studenti in un posto oscuro, e questo maschera completamente quello che sei sempre stato, e non ti dimostri volenteroso a prendere responsabilità per quel ruolo più importante per te.

(00:22:21)

Bret: Beh, non so se non sono volenteroso. Penso che tu ed io abbiamo un approccio diverso a questo e potrebbe essere che, lo sai, l’ordine in cui si nasce o chissà, ma, lo sai, e anche io, ho il beneficio di averti al mondo, facendo quel che fai, e ogni tanto mi chiedo cosa mi sarebbe successo ad Evergreen avendo solo i miei strumenti a disposizione. È molto possibile che sarei stato effettivamente escluso in privato e non so cosa starei facendo in questo momento. Come succede, la storia Evergreen divenne combustibile che mi spinse in uno strato dove ci sono molte cose interessanti da fare, che non sono esattamente quello di cui tu stai parlando, ma che fanno senso.

(00:23:07)

Eric: Sì, è infuriante. Sto provando – Non penso tu capisca quello che sto cercando di fare. Credo che tu sia stato messo nella categoria sbagliata e non ci arrivi che questa è la mia opportunità -

Bret: No, capisco. Ci sono arrivato. Quello che ci distingue è che abbiamo due stili diversi nell’approcciare le cose. Io, per esempio, prendo un certo piacere perverso a vedere Dawkins muoversi lentamente nella mia direzione, che è quello che credo stia accadendo.

Ora. Vorrei che fosse più veloce. Non è un uomo giovane ed io penso sia veramente importante che riconosca dove sono gli errori nel suo pensiero. E ad essere onesto, credo di sapere dove molti di questi risiedono e so che li troverebbe anche lui se fosse condotto a capire la natura di questi errori e confrontare, francamente, il portale che si apre se passi attraverso un’altra porta di quella che lui ha attraversato. Ma lo sai, non ha funzionato in una sera – Mi sono sempre chiesto se sarebbe potuto succedere, ma c’è comunque la possibilità che lui avrà un’epifania che spero lui avrà.

(00:24:27)

Eric: Davvero non capisco dove siamo in questa conversazione.

Bret: Okay.

Eric: Okay. Non ci arrivi. Ti hanno trovato al college statale Evergreen. Questa è una comunicazione al mondo che non eri molto bravo.

Bret: Sì.

Eric: E ogni volta che provo a dirlo viene sempre male, manchi – non prendi la palla che ti è stata tirata addosso, cosa che, non capisci cosa stai confrontando. Lui non ti prende seriamente perché non hai la lista di pubblicazioni all’altezza di quello che sei, o che hai fatto, o dove sei stato, e come risultato, continui ad essere il ragazzo buono, che parla molto bene, pieno di idee, dice cose interessanti, e costantemente lascia andare potere ad altre persone.

(00:25:14)

Bret: Mmm, non penso. C’è un modo per affrontare le opportunità che ricevi, le carte che ti sono date, e penso che tu ed io condividiamo una certa delizia – dove facciamo i nostri esercizi e scopriamo qualcosa di interessante e assolutamente nessun altro ci arriva?

Eric: Mm-hmm.

Bret: Quello farebbe star male la maggior parte della gente, perché si sentirebbero come “Cosa sto facendo di sbagliato? Perché nessun altro capisce questo punto?” Io e te ci sentiamo bene. È il sapere di aver raggiunto qualcosa, aver scoperto qualcosa e che nessuno sia in grado di riconoscerlo, ti dà una sorta di senso di quanto di fronte agli altri potresti essere. La questione è cosa fare con quelle cose, e lì, penso che la questione sia se. Mi è successa una cosa – ho detto qualcosa di smoderato a i “Nuovi atei” e di colpo Steven Pinker, Jerry Coyne, Michael Shermer, Richard Dawkins, and Neil Shubin mi diedero contro allo stesso tempo, non nel punto dove sono stato offensivo – su uno completamente diverso. Hanno preso qualcosa dal mio canale Youtube. Jerry Coyne dichiarò di avermi smentito. Sbagliato, ma ha comunque aggiunto energia così che potessero attaccarmi. Il loro punto fu che non avevo capito la selezione naturale e che, per quello potevo credere di sapere qualcosa che altre persone non potevano sapere, la cosa giusta sarebbe stata spedirla ad un giornale scientifico e andare attraverso peer review. Ho sottolineato che la peer review non era nello stile di Richard Dawkins e che infatti ha avanzato di molto il campo, sostanzialmente, ma ha pubblicato solo pochi articoli. Questo li ha messi in ritirata e il tono camibò a “Beh, allora un libro? Questo è quello che ha fatto Dawkins.” E per me è una vittoria. L’idea – Non sono contro peer review. Voglio che altri colleghi controllino il mio lavoro, ma non voglio che venga denigrato in privato. E così, per quanto quella piccola battaglia fosse il risultato della loro sottostima nei miei confronti e non sapendo che sarebbe arrivata qualche risposta convincete e reattiva per il mondo come fu e veder loro arretrare e dire “Sì, un libro sarebbe una cosa accettabile.” Quello fu una buona mossa dalla mia perspettiva. Mi hanno sottostimato e sono dovuti arretrare. Quindi non posso avere molti rimossi. Per me, su una scala temporale diversa, penso di star facendo progresso verso un obiettivo che tu ed io concordiamo sia quello giusto, ma non sono sicuro che raggiungerlo sparando a destra e a manca sia la strada da prendere.

(00:28:16)

Eric: Beh, sono felice di interrompere l’intervista esattamente qui ed ora, perché è adorabile, è dolce, ed è incredibilmente paziente, ed è un sentimento bellissimo, ma mi sento anche di aver attraversato tutte le guerre e le battaglie per portare le tue idee al mondo, e non voglio finanziare quel programma.

Bret: Ti sembra che mi stia arrendendo?

Eric: No, mi sembra che tu mi stia annoiando. Come, questo è davvero poco interessante.

Bret: *sigh*

Eric: Se penso a quello che è davvero successo -

Bret: Sì.

Eric: Questa è una burla. Non è neanche onesto.

Bret: Okay. Il palco è tuo.

Eric: Okay. Voglio parlare di qualcosa che chiamo il DISC, il Distributed Idea Suppression Complex [Complesso Distribuito di Soppressione d’Idee] e non ha niente a che fare con Richard Dawkins e peer review e Jerry Coyne e una massa di altre cose che non interessa a nessuno. Ha a che fare con circa un periodo di 50 anni in cui grandi idee sono state sotterrate indipendentemente da dove originarono. Perché grandi idee avevano grande probabilità di essere dirompenti ad un ordine istituzionale. E tra te e tua moglie, me e mia moglie, tre delle nostre quattro tesi incorsero in grandi problemi, perché provavano a guadagnare nuovo terreno. E la quantità di ritardo che hai sofferto, voglio dire, sei cinquantenne ora. Questo è un inizio di carriera molto tardo. Viene da un luogo veramente non auspicabile. Sei stato arredato con una storia, che è “lui è un ragazzo molto dolce che si alzò contro gentaglia e questo è il suo diritto alla fama” e non stai veramente capendo che non vieni preso totalmente seriamente come un biologo. In parte quello che Jerry Coyne ti sta dicendo è “Hey, sei veramente uno sconosciuto. Io sono a Chicago. Richard Dawkins è a Oxford.” Lo sai, lui è stato il Professore “Simonyi” per -

Bret: La pubblica comprensione della Scienza.

Eric: Esatto. Il punto è che non sei parte di questo Super Club. Non confonderti. Tu sei semplicemente qualcuno che ha fatto valere la sua posizione.

Bret: Oh, capisco. Questo è quello che stanno dicendo.

Eric: Okay, allora il mio punto è che non ho tempo per il diario della tua fiaba su una salutare, gentile e dolce -

Bret: Chi ha detto qualcosa sull’essere salutare? Io sono, guarda, sono interessata a vincere per un paio di ragioni: uno, il pagamento. Certo, l’intuito che apre il portale della biologia che non sappiamo perché abbiamo avuto cattivi strumenti Darwiniani, e per quelli che hanno preso questo per un attacco al Darwinismo, non lo è. Il Darwinismo ha bisogno di essere aggiustato, e non c’è niente sbagliato con quello che ha contribuito Darwin – è quello che è successo dopo.

Eric: Puoi farmi un favore?

Bret: Certo.

Eric: Io veramente, tu hai il tuo podcast. Si chiama Dark Horse (Cavallo Oscuro), giusto? Il Dark Horse podcast. Penso che questo sia il grande posto per te al fine di esplorare un cambiamento graduale, progressione incrementale, stravolgere le menti, aprire cuori, tutte queste cose. Questo non è il tuo podcast.

Bret: Sì.

Eric: Questo è il mio podcast.

Bret: Giusto. Ma stiamo parlando della mia vita. Giusto?

Eric: Stiamo parlando della tua vita, ma se questo è quello che vuoi fare, non so se sono così interessato nel fare quello che avevo intenzione, che era provare a portare le tue idee nel mondo, curate da qualcuno che non è te.

(00:31:43)

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(00:32:52)

Eric: Sai una delle cose, e comunque, ho avuto questo problema con te -

Bret: Siamo veramente in un podcast in questo momento?

Eric: Siamo in un podcast. Oh, credimi, te lo farò pesare perché ti stai ritirando dal tuo ruolo nella storia e ne sono stanco. Guarda, ti amo come, come se fossi mio fratello.

Bret: Fantastico.

Eric: Okay. Il caso è che tu hai sempre fatto questo, e vuol dire che non prendi propriamente il tuo posto. E io sono dovuto andare a convincere il tuo supervisore, Richard Alexander, uno dei più grandi teorici evoluzionari dei nostri tempi -

Bret: Assolutamente.

Eric: Giusto? Uno dei più grandi in assoluto. Membro della Accademia Nazionale delle Scienze, con una cattedra all’università del Michigan. Ho dovuto convincerlo a scriverti una lettera di raccomandazioni per te così da avere qualche documento, poiché stava invecchiando, su chi tu fossi, perché sapevo che Evergreen non sarebbe stato – Non è parte del gioco.

(00:33:59)

Bret: È vero.

Eric: Okay. Qui è quello che lui ha avuto da dire. “Bret Weinstein potrebbe essere uno dei più grandi studenti che io abbia mai conosciuto. La sua difesa della tesi riguardava solo uno dei quattro temi capitoli della tesi, e sono quella era molto più che sufficiente per una tesi. Non conosco nessuno che sa più di Bret su una grande varietà di temi non solo in biologia evolutiva, ma anche sui problemi e le possibilità di cambio culturale e i modi di unire le persone e solvere problemi difficili. Per 40 anni, ho condotto frequenti, a volte giornalieri, seminari con i miei dottorandi in biologia evolutiva. Mentre era uno studente, Bret era tra i principali elementi in tutti questi seminari. Quando parlava, c’era quasi sempre un rispettoso silenzio, persino quando era il novello tra le persone coinvolte. I temi della tesi di Bret sono così significativi e attuali, e trattati così bene rispetto ai modelli di vita degli umani e di altre specie, la funzione e l’importanza dei telomeri e spiegare la lunghezza della vita controbilanciata dal cancro e molti altri temi importanti come la diversità delle specie e la selezione naturale, che ha convertito drammaticamente, sul momento, due riluttanti – ” E comunque, riluttanti è una sottostima britannica qui – “vorrei dire moderatamente e scetticamente evoluzionisti membri della commissione. Io penso, nonostante la sua giovane età, in termine delle caratteristiche che ho citato sopra, Bret è il candidato migliore.”

Sei stato lo studente numero uno di Richard Alexander, che è finito al college statale Evergreen, un errore enorme. Ed è sempre stato un errore. Non avresti mai dovuto essere lì. Avevo completamente ragione. Mi dispiace di essere ripetitivo su questo, ma, come, per quanti anni ti ho detto, “Devi andare via da questo posto.”

Bret: Beh, vedi, prima di tutto, Dick era stato molto chiaro con me sul fatto che, avesse lui provato a competere nell’accademia moderna, non crede che avrebbe potuto avere successo. E lui era chiaro sul fatto che non ci fosse una buona soluzione al problema. Così, lo sai. Non posso dire di aver mai sentito quella lettera. Penso che tu mi abbia quotato parti di essa.

(00:36:06)

Eric: Sì, perché poi farai quella cosa dove minimizzi la tua dote ed è vomitevole. Ne sono stanco. Ne ho avuto abbastanza. E una parte di questo, quello che è successo è che ora stai storcendo la storia della scienza. Tu hai un posto nella storia della scienza che non stai prendendo, non lo stai difendendo, c’è qualcosa che non ti piace a riguardo.

Bret: No, no, non penso che sia vero. Penso che lo sto seguendo – forse lo sto perseguendo in un modo che non funzionerà alla fine, o forse lo sto perseguendo in una maniera che avrà frutto, forse c’è più di un percorso.

Eric: Ho fatto così tanto per aiutarti, provando a farlo accadere, fino al punto che le persone si rendessero conto della complessità di idee che hai provato a portare avanti, e il mio sentimento su questo è che tu mantieni questa bellissima, calmissima posizione, e ora è abbastanza. Come, tu hai una storia e questa storia è una storia esplosiva. Voglio dire, sono felice di sotterrare questo podcast affinché nessuno lo ascolti, ma voglio davvero esplorare la verità, piuttosto che questo estremamente buono per te, alto contenuto di fibre, lo sai, poco zucchero, ciotola di ceriali.

Bret: Io solo non penso di sapere dove siamo. Sono stato molto chiaro in pubblico riguardo al fatto che io penso che il mio intero campo sia infangato, che si sono intrappolati in poche cattive assunzioni e che stanno sprecando decadi nelle erbacce per nessuna buona ragione, che c’è una via d’uscita, che non sapevo cosa fosse per molto tempo. Ho scoperto cosa fosse, e ottenere l’attenzione sulla questione di quello che stanno facendo è un compito Erculeo. L’ho chiarito. La questione è quale sia il miglior uso dell’opportunità che ho ottenuto, le carte che ho in mano, e abbiamo una differenza di opinione su quello che potrebbe essere. E tu potresti aver ragione. Non sto dicendo che non hai ragione, ma sto dicendo che c’è almeno una discussione da avere sulla via migliore di giocare le –

(00:38:01)

Eric: Perché non parliamo di questo sul tuo podcast? Accetto l’invito a venire. Questo è il mio podcast. Lo faremo a modo mio.

Bret: Facciamolo a modo tuo allora.

Eric: Tutto a posto. Sono il fratello maggiore.

Bret: Ho notato di avere il problema del mercato Marcia Marcia definitivo.

Eric: Tutto a posto. Bret, questa non è la storia della carriera e della tua vita. Quello che è successo è che ti sei bloccato all’università del Michigan per un periodo di tempo molto lungo, perché hai scomodato delle persone. Quello che sta dicendo nella lettera di raccomandazione è che hai scritto quattro diverse tesi, finché la memoria mi aiuta, e che erano su temi vastamente diversi. In aggiunta, qui c’è una cosa interessante: nessuno che conosco, nonostante la quantità di discussione che è stata spillata in inchiostro su Evergreen è riuscito a collegarti con l’eroe di un libro chiamata The Tapir’s Morning Bath [Il bagno mattutino del Tapiro], che apparve anni prima.

Bret: È strano che non sia mai apparso.

Eric: Vero? Non è mai apparso. E poi sei anche il recipiente del premio Golden Gazelle [Gazzella d’Oro], penso della Organizzazione Nazionale delle Donne, per aver preso posizione contro ZBT all’università della Pennsylvania. E sei stato espulso, effettivamente, da una università di prestigio a causa di minacce di violenza fisica per aver difeso donne nere che veniva sfruttaate da uomini bianchi. Voglio dire, è come, poi è come se tu fossi, l’assistente sul campo e studente principale come laureando di un altro leggendario evoluzionista teorico, Bob Trivers. E in qualche modo, lo sai, Richard Dawkins ti sta trattando come un ragazzo che non è davvero un suo pari. “Tu non sei davvero uno dei grandi teorici. Sei molto confuso e hai bisogno di imparare di più sul fenotipo esteso” e tutto questo è senza senso. E sei così gentile che non sei neanche, non so, penso che tu sia fuori a pranza. Senza offesa.

Bret: Capisco. Capisco. E lo sai, come ho detto, potresti avere ragione.

Eric: Okay. Voglio parlare delle materie a cui tu sei più associato partendo dalla tua tesi. E voglio entrare nella loro scienza usando il podcast. Se le persone rimangono indietro, rimangono indietro.

Bret: Okay.

Eric: Okay. Ora Dick Alexander è una leggenda in teoria evoluzionaria perché è molto difficile usare teoria evoluzionaria per fare predizioni che possono essere verificate nel mondo. È una sorta di collezione di tecniche e punti di vista sciolti e amorfi. E persone pensano a volte che non sia neanche una teoria perché non sembra essere così predittiva.

(00:40:37)

Eric: E poi ci sono poche predizioni. Così, ho ragione? Darwin iniziò questo gioco predicendo che ci sarebbe stata una falena con una lingua molto lunga perché c’era un fiore che richiedeva una lunga distanza prima di raggiungere il nettare e tirarlo fuori.

Bret: Sì, ricevette una orchidea da Bateson, forse, con il tubo della corolla lungo un piede. E ragionò molto direttamente che non avrebbe avuto alcun senso per questa pianta aver investito su questa struttura molto lunga se non ci fosse una lingua che potesse raggiungere il nettare. E penso che non abbia vissuto per vedere la scoperta di questo animale.

Eric: Questo non lo sapevo.

Bret: Ma aveva totalmente ragione. C’è una falena che possiede questa bellissima lunga lingua. È una falena sfingide, una sorta di questi colibrì-esque falena, e comunque, sì, è una delle predizioni maggiori, dimostrazioni, che la teoria evoluzionaria può realmente essere usata per predire fenomeni che non sei in grado di osservare.

(00:41:34)

Eric: Okay. And you know, Darwin famously couldn't, for example, like, I don't know how much I've talked about this in the open, but my favorite Darwin book is the one he wrote after Origin of Species, which is On the Various Contrivances by Which British and Foreign Orchids are Fertilized by Insects. It makes absolutely no sense as a title, I think that's what's so funny about it. But because orchids are so highly speciated, it turned out to be the perfect place to explore the consequences of evolution. And he couldn't figure out my favorite, I don't know whether it's clade or a group—

Bret: Clade is pretty safe.

Eric: Yeah, clade of orchids, the Ophrys system, which is just unbelievable because it mimics the pollinators, the female of the pollinator species using pheromones and some sort of replica good enough to fool males into copulating with the lower pedal of an orchid—

Bret: A 3D replica of the female that smells like her. And it just so happens that when the male lands on it to copulate, he gets these pollen packets glued to him, and then he screws up and makes the same mistake at another flower and delivers—

Eric: Well, he may, he may or may not

Bret: Put it this way—

Eric: Only the ones that screw up twice get to fertilize.

Bret: The reason that it gets glued to him is that it has worked enough times for this strategy to have been so beautifully refined.

Eric: Right. So Darwin saw that there was this mimicry going on, but he couldn't put it together. He spent pages and pages not getting it. So I think it's very funny. So he predicts some things, but he can't predict something else in a very closely related system. Okay. Fast forward, Dick Alexander comes out with a crazy prediction, which I still don't fully— I mean, it's just amazing that he made it— where he says, I bet that you will find the kind of behavior we associate with wasps and bees, which is in this clade called Hymenopteran ants of eusocial breeding patterns and organization, but in mammals that will live underground.

Bret: So, I think, the way this story actually worked, he didn't say you will find it—

Eric: Or, you could find it.

Bret: What he said is, in principle, there's no reason that a eusocial animal has to be an insect. That in fact, you could get such a thing in a mammal. And then he predicted—I forget how many characteristics there were—but he named some large—

Eric: So we should say that there's something funny about the system of ants, bees, wasps, which is that they've got this very strange haplodiploid chromosomal characteristic. Do you want to say a word about that? Cause that makes the prediction more—

Bret: Sure. So it has long been understood that the Hymenoptera behave in this incredibly cooperative fashion, which effectively all of the workers of the colony forgo reproduction in order to advance the reproductive interests of the queen. And it was late discovered that actually their genetic system is unlike our genetic system, and that males have basically half a full complement of genes. They have enough greens to function, but they have half the female complement of genes. And, for reasons that are mathematically slightly complicated and require a chalkboard, the females are more closely related to the daughters produced by their mother than they would be to their own offspring, their three quarters relatives to her offspring. And there they would be 50% relatives to their own offspring.

Eric: Spot on.

Bret: So, they are actually evolutionarily favored by very standard mechanisms. Once you understand the crazy genetics underlying the thing, they are favored to engage in behavior where they forgot reproducing and fostered.

Eric: So, once you understand the chromosomal difference of the system, it is far less surprising that it would behave as a loosely coupled, in some way—don't overreact—unified organism, which is distributed. That there are ways in which the hive behaves as a superorganism, and there are ways in which it does not.

(00:45:40)

Bret: Yeah. Well, all I want to say is, I'm not sure how clear we have the story with respect to what precedes what— it's completely plausible that the behavior precedes the evolution of the genetic system.

Eric: Right.

Bret: And I actually, frankly just don't know where that research stands at the moment. We have found many other insect systems that have various versions of this. Interestingly, though, the termites are not hymenopteras.

Eric: Right.

Bret: And the termites engage in this behavior—

Eric: Termites are eusocial, but they're not haplodiploid.

Bret: They’re eusocial, they behave very much like ants.

Eric: Okay.

Bret: But they don't have the strange genetic system, proving that the behavior can evolve even in the absence of this genetic system—

Eric: Well, the reason I bring this up is that if you look at, for example, Prince Peter Kropotkin, the great anarchists theorist, he was obsessed by finding analogs in nature of preferred human structures. And so it's very simple to say, why can't we work together the way an ant colony all works together? And then there's a counter to that, which is, well, they have different chromosomal structures, and then you say, well, but yes, but that's a kind of a cheap way of achieving eusociality. There are other ways of—so through this crazy kind of investigation, we get to Dick Alexander, who, and I think you're quite correct, says there is nothing prohibiting us from finding a mammalian species that exhibits ant- and wasp-like behavior. And it would be likely to have these characteristics, it would live underground, in a—

Bret: Yeah, underground, I believe eating tubers, was on the thing. It was a crazy list. And you know, my understanding from, from Dick—Dick is now unfortunately dead. He died a couple of years ago. But my understanding from him was that he didn't actually expect to find such an animal. He was speaking very abstractly, just completely theoretically. And at the point that he unleashed this idea, it may even have been in a talk, rather than a paper. The information made it back to him, actually—what about naked mole-rats? They match your characteristics, and study reveals then that actually they are eusocial, they behave very much like ants, bees, wasps, termites, et cetera.

Eric: And this is like one of the great moments in modern science.

Bret: I really think it is. It's certainly the moment that people who know who Dick Alexander was, reference as sort of the high watermark because it's comprehensible. You know, Dick did a lot of things. He was very interested in people and other things, but this particular demonstration was so, it would be impossible to have predicted such a thing and have gotten lucky. He had to have understood some things that were extremely deep in order for that to have worked out. And so, yeah, it's really, I don't know of another example in evolutionary theory of a prediction that clean, of something that obscure.

Eric: I know one.

Bret: Oh yeah?

Eric: Yeah. I once heard a story about a graduate student who predicted that the breeding protocols of laboratory rodents would compromise the laboratory system in terms of its relationship to so called “wild type” versions of the same species. So you have the bred rodents and you have the wild rodents, and that they would be distinguished by virtue of the fact that the non-coding nucleotide sequence at the end of the chromosome, known as “telomeres”, would be wildly different in length if the prediction were true from pure evolutionary theory.

Bret: Wow.

Eric: Yeah.

Bret: Yeah. Yeah, that story that didn't happen exactly the way you said it, but you know, it's been a lot of years, and it takes a second to get back there.

Eric: Yeah. I mean it's, you, you did that.

Bret: Yeah, I did that.

Eric: And that story, unfortunately, has not really been told, and it is, in some sense, your central origin story as a biologist.

Bret: It's a pretty good one, and it definitely changed the way I saw myself in a way that has been very productive.

Eric: Okay. I want you to talk to me about that story, and because I lived with you, I know that it happened, and I know that it got buried, and I know that it's part of what I'm calling the Distributed Idea Suppression Complex because, quite frankly, you were not the only person who was a part of the story, and the story had to die because it said something, which is that the power of your theory was sufficient to predict, from first principles, a manifestly observed and surprising result, within molecular biology, from pure evolutionary principles.

(00:50:47)

Bret: Yup. All right. I'll try to do a short version of it.

Eric: You know, this is long form podcasting, and you tell—however long the story is, I guarantee you when people finally figure out that it may be that the rodents that we've used to test drugs on, let's say, might be compromised, and compromised in a way that would be potentially extra permitting of potential toxins in the form of pharmaceuticals. I think that it's going to be fascinating. And it's going to repay the study that it will take to understand the story. The floor is yours.

Bret: All right, so let me just set the stage a little bit. Evolutionary biology has—

Eric: But, do me a favor.

Bret: Yeah.

Eric: You can get into a very patient careful pedagogical mode. This is an exciting story. Tell it the way it actually occurred.

Bret: I'm going to tell it the way it actually occurred. And I'm going to be careful. I'm going to try not to be—there are parts of it that were for a very long time kind of emotionally fraught. But anyway, I think I remember it well enough to do a sparse but complete version.

Eric: Okay.

Bret: Evolutionary biology has long been biased in the direction of abstraction. Rather than thinking about mechanism, that is to say we deal in the phenomenology of things. We talk about gross patterns that we see in nature rather than talking about the fine detail of what drives them. That has been changing in recent decades, but it has a long history, and it comes from a very mundane place. That mundane place is that we just haven't had the tools to look, for example, inside of cells and we haven't been able to read genomes. You know, we could have been able to read a gene here and there at great expense, but the ability to peer into genomes is pretty new. The ability to peer into these molecular pathways is pretty new. So anyway, there's a historical bias in evolutionary biology against mechanism and in the direction of phenomenology. I have never been particularly fond of that bias. I have always been interested in mechanism. I'm interested in the phenomenology too, but I've always kept my foot in the door with respect to mechanism. And as an undergraduate, I took lots of mechanism classes. I took a development class at the time, developmental biology was in my opinion, a bit stuck. It is now unstuck in a very dramatic way. But anyway, I took a developmental biology class. I took some or immunobiology. And anyway, I was armed with these things in an environment in evolutionary biology where most people were not, most people were in the phenomenology. And one day I happened to be in a seminar. Dick Alexander was running a seminar for graduate students, and a student was there who was very out of place. He was studying cancer, and he, on a lark, decided to take an evolution seminar that looked good to him in the catalog, and it wasn't right for him. And he gave a talk at some point, and his talk was on his work with cancer and frankly, because all the other people in the room were evolutionarily oriented, nobody was really tracking what he was saying. But what he said struck me like a bolt of lightning. He said that in the realm of cancer research, people were looking at telomeres, which are these repetitive sequences at the ends of chromosomes. And they were toying with the possibility that the fact that these telomeres shorten every time a cell divides, that that is providing a resistance to tumor formation. Very straightforward—counter counts down, and that would prevent—

Eric: So just for the audience that maybe needs a tiny refresher, we're taught in general that DNA is a string of letters called nucleotides, A, C, T and G, and that, in general, three of those that are adjacent to each other form words called codons. And for every word there is an amino acid or an instruction to stop coding for amino acids. So this is the instruction tape that tells us how to string together amino acids into proteins to make machines, molecular machines. This is some weird different thing, where the region of DNA could be interpreted as coding for a protein, but in fact might be instead just counting how many nucleotides are at the end. So it comes across as a counter.

(00:55:33)

Bret: It's a little better. It was known not to be a coding sequence. It wasn't a useful sequence. So what you had is a bunch of DNA at the ends of chromosomes that were just repetitive, and the length of the number of repeats varies. And the number of repeats correlates with basically how many times the cell can divide before it refuses. This being interpreted as a cancer prevention thing made perfect sense. But the reason it struck me like a bolt of lightning was that I was well aware of the existence of tumors and their implication in something entirely different. What they had been implicated in, as far as I was aware, was something called Hayflick limits, which were the tendency of perfectly healthy, happy cells to grow and grow and grow and grow in a Petri dish, until they hit some number of divisions and then to stop without apparent dysfunction. So—

Eric: So this was the theory of Leonard Hayflick?

Bret: Yup. It was the discovery of Leonard Hayflick, who basically overturned the prior wisdom about cells, which was that they would grow indefinitely as long as you kept feeding them and making an environment that was conducive to division. So I don't exactly know why that result had been misunderstood at first. Maybe somebody had a cancerous cell line and so they got the wrong idea and it just spread, but Hayflick checked it and it turned out to be false. It turned out there was a number of cell divisions that healthy cells would go through, and then they'd stop. The mechanism was not obvious to Hayflick, but later it became clearer and clearer that the mechanism was these sequences at the ends of chromosomes which shorten each time the cell divides. And the implication was that, potentially, this was a cause of what we call “senescence”. What in common parlance would often be called “aging”, the tendency to grow feeble and inefficient with age. If your cells are each in a cell line and that line has a fixed number of times that it can replace itself before it has to stop, then some point your repair program starts to fail. And that repair program, failing across the body, looks like what you would expect aging—aging follows the pattern you would expect if cell lines one-by-one stopped being able to replace themselves. So—

Eric: We know that there's a special sort of a, I don't want to call it cell line cause you keep correcting me for every tiny mistake I make in speech. But, if we divide our body into two kinds of cells, soma and germ, where germ lines are that which has a hope of immortality through reproduction, then it's the somatic cells that have finite limits on their ability to undergo mitosis and cellular repair and whatnot.

(00:58:25)

Bret: And the germline can't because if it did, your lineage would go extinct as a result of small—

Eric: Small addendums.

Bret: So it's the soma, the parts of your body that don't go on to produce babies, that have this effect. The reason it struck me like a bolt of lightning was that I was aware of another very elegant piece of research done by a guy named George Williams. George Williams had finally—

Eric: One of the greatest of modern—

Bret: One of the greatest modern evolutionary biologists. I actually knew him a bit too. He is also now gone, unfortunately. But George Williams had laid out in a beautifully elegant paper, the evolutionary theory of senescence. It is an absolutely elegant argument that says that, in a lifetime there are, well, let's start somewhere else. A creature is built of parts and traits. It has a relatively small genome and a relatively high complexity. At the time it was thought there might be 100,000 genes or something and you have maybe 30 trillion cells with a ton of complexity. In order to get that small number of genes to dictate how to produce a creature that complex, the genes are doing multiple things.

William's point was when a gene has multiple effects, what we call a pleiotropy, those effects may be good or bad. If effects are good early in life—

Eric: By good we mean contributing to fitness—

Bret: Fitness enhancing traits at some costs late in life, then they will tend to be accumulated by selection. And the reason for that is because, well, there are two ways to think of it, really. If a negative trait occurs very late in life, then a large number of individuals who have the gene for that trait will not live long enough to experience the harm. So if it came bound to a positive thing early in life and you're dead before the late life harm accrues, you got away with it. Right? So William's point was, he was building on earlier work of Medawar, but let's skip that for the moment.

His point was, because of tradeoffs, you will have lots of traits that are good early and bad late. Selection sees the early traits much more clearly than it sees the late traits, and it prioritizes them because of the discounting that arises because so many individuals aren't around to experience the late-life harm, and if they are around experienced the late-life harm, a lot of their reproduction is behind them anyway. So they count less. Selection counts more early in life. And this timer starts at the moment of first reproduction, the usual moment of first reproduction for your species. So this was a beautiful hypothesis, and it was beautifully articulated with many predictions, which is the way really good work is done. And we knew, at the point that I was entering graduate school, we knew that the hypothesis was right. It was a theory.

(01:01:36)

Bret: And the reason that we knew it was real,

Eric: The hypothesis is the Antagonistic Pleiotropy Hypothesis.

Bret: The Antagonistic Pleiotropy Hypothesis for senescence. We knew that it was right because it predicted so many phenomenon in nature that we could readily go out and measure. And this is again where the phenomenology versus mechanism comes out.

Eric: Okay.

Bret: We know that creatures that are poisonous or have a shell that protects them or can fly away from danger, are disproportionately long-lived for their size. Small creatures tend to live shorter lives than large creatures. But if you can fly, then you're off the line of the other creatures of your size. So for example, their small bats who have been recovered after 30 years in the wild. So creatures that have special protections have disproportionate longevity. This matches William's hypothesis, because it is their ability to fly away from danger that makes the likelihood of their experiencing late-life costs go up.

Eric: Yep.

Bret: So selection sees their late life more easily than it sees a small Creek.

Eric: I just want to say something. This is a podcast. It's an unusual podcast and we can talk science and I'm thrilled, but we always have our colleagues in our minds when we're talking to a general audience and the colleagues are always in a “gotcha” mode. Well, you forgot about this. You didn't mention that. I'm even interjecting little bits because I want to make sure that you're immunized from all the bullshit that the academics, so I just want to make a general statement, which is we can come back and get into any level of specificity that somebody wants to, if they want to take you down, I don't care. What I'd love to do is to tell the story with enough punch that people understand what happens.

Bret: So we're about to jump into the meat of the matter. The theory of antagonistic pleiotropy was well established, but in four decades of research on the genome, nobody had found a gene that matched it, so that we knew that this explanation was right, but we couldn't find the genes that caused it. The mechanism was missing. So, anyway—

Eric: Does that mean, to be a gene, it has to be protein encoding?

Bret: Yeah. Anyway, I knew this assertively, I was well familiar with William's paper. At the point that I saw this talk on cancer and I knew already about the question of senescence, everything came together. This was obviously the answer, where the missing pleiotropy was. Well, the missing pleiotropy had to do with a telomere, which wasn't exactly a gene. It was genetic, it was DNA, but it wasn't a gene, but it was perfectly capable of producing exactly the effects that we see in senescence across the body, tissue—

Eric: So a counter, and not a protein, could be the answer.

Bret: Right. Now, I saw this instantly at the point I heard this talk, I raised my hand, and I tried to articulate what was so obvious in that moment, and I couldn't compel a single person in the room. They couldn't even understand what I was trying to say—

Eric: Which is bizarre.

Bret: It was bizarre. I mean Dick was in the room and you know, Dick was very broad-minded and I just couldn't make it clear.

Eric: Look, let me just interject something, and you can correct me if I'm wrong, but my impression of it is that it was a very simple idea attended to by an outrageous amount of irrelevant complexity that had to be very carefully pried off of the central idea.

(01:05:04)

Bret: Yeah, I think, I think that's well said. So anyway, I left the room feeling like I had just glimpsed something so important, kind of, you know, I wondered could it be right and I started to just do the first bit of library research to figure out whether somebody else knew what I knew or—

Eric: So I'm not even sure that you fully said it. I want to make sure that I'm even clear on it and I'm going to, I think I'm right, but correct me if I'm wrong. What you're saying is, “What if the Hayflick limit is a protection against dying from immortality at a cytological level”, that some cell gets a dream of immortality that it shouldn't have because, let's say, it's a somatic cell, and it says, “Okay, I just want to keep dividing and dividing and dividing”. Nature knows how to do this, and that immortality, which sounds good at first, is actually called cancer. And so in computer science we would say, okay, you've introduced a recursion limit into a while loop or a for loop to make sure that you don't have a resource leak, which is what a tumor is.

Bret: Yeah, so let me say it this way. If you have a damage to a tissue cut on your arm or something, the cells on both sides of that cut suddenly become aware that there is a problem, a gap, because the can't hear a neighbor on one side of them and their natural reaction is to start growing into the gap until they can hear a neighbor which is the sign to stop. If you imagine that something like that is occurring in every tissue, or almost every tissue, the problem is that that means that every tissue in your body for which that story is about right, is in danger of having damage from radiation or whatever, turn it deaf to its neighbors. A single cell that has turned deaf to its neighbors will suddenly start replicating, and if it is deaf to its neighbors, then there's no message that it's going to hear that's going to tell it to stop. So that thing, imagine any cell in your body just taking off and growing and growing and growing—

Eric: Okay, this is terrifying. What you're saying to me is, is that if I'm comprise of let's say 30 trillion cells and I view them as each let's say subroutines, any subroutine that is not denucleated, right? Like this wouldn't happen in the in the lens of your eye because the nucleus has been removed, but any other reasonable cell is potentially your assassin, because it's mitosis process might completely go rogue.

Bret: It can run away.

Eric: Okay.

Bret: And so the rather elegant and very simple idea is that there would be a hard limit so that any cell that had become damaged, so it started down this path would just simply run into the number of cell divisions it was allowed in a lifetime and it would stop.

Eric: So like, the moles on my face that some of my less couth commenters loved to talk about—

Bret: Yep.

(01:08:01)

Eric: Are effectively attempts to kill me that may have stopped. And that the perimeter where they stop is where the Hayflick limit took over and said, “This cell line must die so that the patient will live”?

Bret: Yeah. The name I gave him was “prototumor” and the idea is a prototumor is a patch of cells arrested at their Hayflick limit. Because they had become unregulated. If you go to the dermatologist and you say, what do I look for? You know, they tell you certain things to look for. So a round patch of cells that suddenly becomes irregular in shape. Well that's what would happen if you took one of those cells and gave it a second mutation and it started growing again.

Eric: Got it.

Bret: Right. So anyway, the idea that a limit on cellular reproduction—

Eric: Yep.

Bret: Is adaptive to protect you from cancer—

Eric: K, so there's a little bit of a mind bender because what you're telling me is that I've got to avoid immortality, which can kill me, and that the solution to not dying is death.

Bret: Yes, and that what selection does is it balances these two competing forces to give you as much vigor and longevity as it can.

(01:09:00)

Eric: So all of the other diseases and insults and things that I can die from sort of start to fade away. And at the complete core of biology, in this theory, there are two things that I can't get away from, one of which is death by immortality, and the other one is death by recursion limit.

Bret: That's it.

Eric: It's a very elegant thing. And now the problem is, is that there's all this weird attended complexity that you had to deal with.

Bret: Right

Eric: So it was like stem cells versus germ versus ...

Bret: So when I went into the literature, what I found was that people had played around in the neighborhood, but that there was a particular fact which blocked every attempt to make sense of what was going on. And the fact was that rodents were understood to have ultra long, hypervariable telomeres. And I didn't know what that meant at first, but the more I looked into this possibility, the more I realized that dozens of longstanding problems would be solved if my hypothesis was true, but that my hypothesis couldn't be true because basically mice have long telomeres in short lives. Why is that? And I banged my head on the table for a couple of weeks trying to figure out what was going on.

Eric: Figuratively

Bret: Yes, maybe even literally on occasion. But the question was, I began to wonder if there was something wrong with the idea that mice had long telomeres. Sometimes, like in Hayflick's case it turned out that a bunch of people were copying some wrong result, so it seemed like a lot of people had seen it, but only one had. And I checked, was it true, that there was some, that everybody was parroting one study that said mice had long telomeres?

Eric: Right.

Bret: It turns out lots of people had tested it. Mice have long telomeres like 10 times the length of human telomeres. It just didn't fit. So finally, it occurred to me that it was possible that what was going on—I discovered something in trying to figure out what they meant by “mice”. Right? There's a lot of species of mice, but all the mice that we use in the lab, with rare exception, are from one genus, and often from a particular target species.

Eric: So you were focused, if I recall correctly, on mus spretus

Bret: Mus musculus, which is the common one. What shocked me was that it turned out all the mus musculus that were being used in labs across the country, and in many cases, farther afield than that were coming from one place, which I had no idea. There was one—

Eric: I remember getting a phone call when you said, what do you know about the JAX Lab?

Bret: The JAX Lab in Bar Harbor Maine, right? They seemed to be the source of everybody's mice. And so it began to be—it was a possibility I could not shut down in my mind, that there was something about what was going on at the JAX Lab that had resulted in the mice that were being sent out to all these other labs—

Eric: Is it that they were representative animals—

(01:12:04)

Bret: Right, these are a model organism. People were just using mice because mice were a convenient mammal, but they're all coming from one place, and it began to occur to me that that one place was not just a source of mice in the sense that we might think it, it was actually a selective environment that was impacting those mice. And when I dug deeper, it turned out that the mice had all, they were descendants of a long lineage that had lived in captivity under conditions at the JAX Lab. And at some point I realized that the most likely thing going on was that there was something about this environment that had wildly elongated the telomeres of these mice. And that was simultaneously an unbelievable idea, but the only one I could think of that made sense of everything I had seen. And so—

Eric: Well, it's unbelievable because the consequences, I mean, look, I have not even heard whether anyone has said, “Yeah, we did that, we screwed that up.” But it is, like, your favorite model organism for mammalian trials being screwed up by a central facility. Because also there's this weird thing where medical people very often stop taking into account evolutionary theory because they treat that as “Well, that's that class I took in college or the beginning of graduate school.”

Bret: Right. So I began to focus on this question and I did something that was the right thing to do, but I did it in a way I will forever regret. I found somebody who was represented in the literature, who I regarded as very well versed. They made sense to me, their papers. Her name was Carol Greider. Carol Greider is now a Nobel Laureate. She was not at the time. She was the co-discoverer of the enzyme telomerase, which is the enzyme that elongates telomeres, when that occurs—

(01:14:01)

Eric: With the famous and co-Nobel recipient—she was the student of Elizabeth Blackburn.

Bret: Elizabeth Blackburn. Exactly. She was her student and they shared the Nobel prize with Szostak. In any case, her work seemed good to me. I called her up, cold, you know, I went into the insect division office and I sat down at the phone. I called her, I said, Carol, you don't know me. I'm a graduate student at Michigan. I'm an evolutionary biologist. I'm racking my brains trying to understand something. Can you tell me, is it possible that mice don't have ultra long telomeres? That it's only laboratory mice that do? And she said, huh, that's really interesting. I'm pretty sure that mice have long telomeres universally. But it is odd that if you order mus spretus instead of mus musculus and you order from European suppliers, the lengths are very different than what you get if you order mus musculus from the JAX Lab. I said, Whoa.

And she said, yeah, that's really interesting. And then she said, I can't remember if it was the same phone call or if we had a second phone call, but she said she was gonna put her student, her graduate student, Mike Hemann, who I think is now at MIT, on the project. And he was going to do a little work to figure out whether there was anything to this. And Mike did some work. They sourced some different strains of mice that were, they were actually not wild mice. Wild mice would have been the right test, but she couldn't get wild mice for obvious reasons.

Eric: You’d have to go out into the woods.

Bret: Right, exactly. And so she got several different strains of mice that had just been in captivity much less time. She actually got one strain of mice that was treated very differently in captivity. But nevermind. She put her graduate student on it, and he measured their telomere lengths. And I get this excited email. Mike Hemann sends me any email that says effectively, “Whoa! The hypothesis is true, mice have short telomeres!” Right? Now—

Eric: I'm sorry, this is like as close to a who'd done it Discovery J'accuse— the mice, you know, I remember, you were over the moon.

Bret: I still am! I still can look at this email and it is the moment at which I realized, A, there's no way I'm kidding myself about how well I understand this.

Eric: Right.

Bret: Right? That prediction was—

Eric: How old are you?

Bret: Now? Or then?

Eric: No, when you get this email.

Bret: When I got that email it was 1999? 98? Something like that.

Eric: Okay. So over 20 years ago.

Bret: Yeah. So I get this email, and—

Eric: By the way, that puts you at about 30. You're at the beginning of your career, and you—in this story, you've just predicted that—

Bret: It's a stunning coup for a graduate student. And, it wasn't in my advisor’s wheelhouse, so it was clearly my own work. And, I mean, Dick was great about not blurring those things, but—

Eric: Okay, either you are a dirty dog liar—

Bret: Right

(01:17:10)

Eric: And I was there at the time—

Bret: Yeah.

Eric: Or, so we're both dirty dog liars about this particular story—

Bret: Or—

Eric: Or, one of the great moments in evolutionary theory, which is—and let me just curate this, because I'm not a biologist, but I think I can more or less get this—because it's a breeding protocol that is the alteration in the evolutionary landscape for these laboratory mice, and because it's acting on a non-protein coding region, the adaptation to a change in the breeding protocol can be extremely rapid. It doesn't have to undergo some sort of completely crazy typical Darwinian story about random mutation and some of them being retained and others being rejected.

Bret: It's even better than that. The creatures are presumably—so we haven't gotten to what the breeding protocol has to do with this—but the creatures are built in some sense to detect how dangerous their environment is, and to the extent that the level of extrinsic danger changes, their telomeres respond quickly so that they are better adapted to the environment. So, they're built to detect the environment and then what is actually a strict matter of market forces.

Eric: Okay, so there are no predators in this environment.

Bret: No predators in this environment.

Eric: And we're not killing them particularly early based on their skills. So environmental insult is sort of absent.

Bret: Environmental insult is more or less absent. What we are doing is imposing an economic rule on breeding so that we can maximize the rate at which we turn mouse chow into mice, which is obviously economically the right thing to do, if you're selling mice to all these labs, you want to produce as many mice as cheaply as possible. So producing as many mice as people—

Eric: The genius of the market!

Bret: It's the genius of the market.

(01:19:08)

Eric: There you go.

Bret: So in order to produce as many mice as cheaply as possible, what you do is you don't breed animals past eight months. They breed faster when they're younger because of senescence. And so you don't breed older mice. You throw them out and you replace them with younger mice who breed faster. What that effectively did was it eliminated the selection against cancer, and it turbocharged the selection in favor of youthful vigor

Eric: Well let me see if I get this—in general, almost all cancers, like, cancer of the germline happens early in life, but all the other cancer, in general, is much more common later in life.

Bret: I gotta pause. I realize I forgot to tell you one thing Carol told me in my first phone call with her that’s vital.

Eric: Sure.

Bret: In addition to telling me that there was something funny about mus spretus, she told me that, consistent with the hypothesis that I was conveying to her, that all mice die of cancer. She said, “If you let them live long enough, and then you do the necropsy, you find cancer of one kind or another”, and that was perfectly consistent because they had these wildly long telomeres and no cancer protection. That would be the prediction of the hypothesis—

Eric: That’s an extrapolation—it's not really all mice. It's all mice that we see in the lab, which happens to be the mice that are ordered.

Bret: Right. She was still speaking from the mindset of somebody who thought that the mice she was getting in the mail representative representative of mice in the wild.

Eric: Got it.

Bret: Okay, so let me clear up why the breeding protocol—and I should say, that it is the breeding protocol that is causing this? That part, I would say, is still a hypothesis. It has not been directly tested by anybody, but, what I would say is that many hypotheses were tested in the aftermath of the discovery, that lab mice have bizarrely long telomeres, and wild mice don’t, and no other hypothesis has stood up to scrutiny. So it is the last hypothesis standing and I'm all but certain that it will turn out to be true.

Eric: Yeah.

Bret: The reason that the breeding protocol has this weird effect, is that when you throw out the mice at eight months of age, you eliminate selection against cancer, you turbocharge selection in favor of—

Eric: Sorry, when you throw out the mice, for breeding purposes, at eight months of age.

Bret: Right,

Eric: Okay.

Bret: When you throw them out for breeding purposes at eight months of age, you are increasing the importance of their early life breeding, and you are discounting anything related to their ability to fend off cancer because they don't live long enough in that period of time to get cancers that kill them. And so what has happened, according to this hypothesis, is that the mice that have longer telomeres have driven out the other animals from the colony. The trait of having long telomeres has swept through the colony and the telomeres have been elongated to an absurd degree, creating animals that do all die of cancer. And interestingly enough, another thing that's evident from the literature is that if you look at their tissues, their tissues do not age in the way that a normal mammal’s tissues age, they remain young.

Eric: So there's one aspect of aging, but that there's a far darker interpretation of what you've just said. If I'm understanding you—correct me, I’ve never taken a class in biology, but I lived this adventure with you—those tissues have, at a histological level, the level of how cells are organized, the possibility of radical histological repair.

Bret: Yes, radical effectively indefinite capacity to repair, which is going to come back in this story in the worst possible way. So—

Eric: This is like a—I mean, I just forget how great of a—

Bret: Me too, I go years sometimes without thinking deeply about it.

Eric: Without telling the story. Alright.

(01:23:06)

Bret: Yeah. Okay. So the story now gets kind of ugly. I recognize I've got all the pieces of the puzzle necessary to tell the story correctly. I have taken on a coauthor, we've found the literature necessary to do it in proper scientific form.

Eric: This came from you, but I want to mention your coauthor’s name.

Bret: Yeah. Debbie Ciszek.

Eric: Okay.

Bret: And Debbie was an excellent coauthor, strong contributor to the paper. Anyway, we put together over the course of a year, I took a break from, effectively, my real dissertation work, and wrote a paper. Dick thought it was a fantastic paper. He was blown away by it—

Eric: Well I remember the revisions, and I remember this was like, I mean, if I think about what's on the line, like this combines one of these freak situations where you're using evolutionary theory to predict something, and in this case it's at the level of molecular biology, so with Darwin's orchid it's a tongue, and with Dick's thing, its behavior in naked mole rats. This thing is actually at a molecular level, and, it couldn't be more important if mice are going to be the major system in which we are going to test drugs, which are highly sensitive to what? Histological repair.

Bret: Yup. It's so profound on several different levels that I'm super energized about getting this into the world. It's transformative. Dick looks at the paper, he says, “This is fantastic”. He puts me through the ringer to get it really tight. We get it tight. We send it to George Williams, the—

Eric: The number one guy in the world.

Bret: The number one senescence guy at the evolutionary level in the world, and he writes a beautiful recommendation letter for this piece. We're going to send it to Nature. George Williams tells Nature, you need to take this piece very seriously. We send it to Nature and they send it back with one of their absurd form letters that says that “The nature of the article is such that it's probably not—

Eric: Of limited interest—

Bret: To their readers. And we're, you know, I mean, we had a good laugh about that. You know, it's cancer, it's senescence—

(01:25:10)

Eric: Dude, it's so bad. Like, this is a response that indicates either malfeasance, or an Eliza program, or the janitor ended up responding who didn't know any bio—

Bret: It’s the craziest thing, and you know, the cherry on top is that they're turning down George Williams recommendation? Like, how cra— do they know who he is? Like, what? Where?

Eric: On what planet?

Bret: On what planet do you turn down his recommendation to look at something about senescence? So, anyway, I get back this rejection, and I have purposefully not shown Carol Greider the paper in preparation, which I am afraid she might've read some way. The reason I didn't show it to her was because I wanted to preserve her independence as a reviewer for the paper. I was hoping, because I still thought she was an ally of mine, I was hoping that Nature would send it to her to review, and that she would look favorably on it, especially since it was, you know, very clear that she had done—

Eric: It was her lab that made the confirmation.

Bret: Yeah. And I, oh, another thing I forgot, I asked her at some point, something that now rings in my ears—I asked her, Carol, you've now got this result about, no, actually lab mice have long telomeres, but wild mice have short telomeres. That's a big result.

Eric: That’s a hell of a delta.

Bret: Where are you going to publish it so that I can cite it—

Eric: Right.

Bret:In my paper, which is the natural thing to do. And she says, “we're not going to publish it. We're going to keep the information “in house.” That was her phrase. I was too young to understand what the hell she was talking about.

Eric: I'll be honest, I'm 54 and I don't quite understand it myself.

Bret: Well, it's so heartbreaking. What she has effectively done is decided, “I could publish this result”

Eric: And then everyone would have it.

Bret: It would be huge, but then I'm on a level playing field with everybody else. If I don't publish this result—

(01:27:16)

Eric: I have a stream of papers I can get at.

Bret: Then I can start predicting other results. Nobody will know how I am doing that thing. I will look like a super genius. And so, holding it “in house” is a mechanism for a whole slew of papers.

Eric: to be, to be 100. You can afford to bend over backwards and not make inferences. Let's say the following, holding it in house is any seemingly inexplicable decision in science, but for the fact that it fits at least one story of this kind, which is that it is consistent with wishing to publish a stream, rather than the source of the information that would allow you—so you can either do one discovery or you can do a stream of predictions and that makes a certain amount of sense, given the ruthlessly competitive grant-winning environment. And we don't know exactly what happened, but there is no world that I know of in which you're allowed to hold back that kind of information, because, in part, of what's on the line.

Bret: Right. So—

Eric: I mean, this is not just a question of academic interest—

Bret: No.

Eric: Because these mice are used for medical testing.

Bret: Not even that. It's medical testing, but it's also all of the science relative, at least, to cancer, senescence, wound healing—all of the science that is stacked on these mice that is contingent on their function relative to their tiers is all compromised. You're letting year after year of this stuff accumulate. It's malpractice at an incredible level. So, I don't know that she has turned on me, but I call her up, and I say, “Carol, we are stunned to find that our paper was turned away without review from Nature—”

Eric: Without review.

Bret: Without review. We need your help. Can I send you the paper and have you look at it? And she says yes. And I sent her the paper and she sends back the paper with an unbelievable number of intense criticisms that are not sensible. She pans the paper, does not believe it—

Eric: Do you still have that copy?

Bret: I have that paper, I have that paper with her handwriting. I believe I also have the FedEx envelope in which she sent it to me. But she hates the paper, and I have now forgotten a bit of the sequence. But as I am attempting to fix this up for another journal—oh, here's a, sorry, I hate to tangle this story, but it's important to get it right.

Eric: No but you haven’t told this in enough—

Bret: I haven't told it in a very long time. After the rejection from nature, after Carol has seen the paper, and said it's cruddy, I get a letter I don't expect from a journal I don't—I know it exists, but I'm not super familiar with it, Experimental Gerontology. Experimental Gerontology says, “We are the editors of experimental gerontology. We have heard a rumor of your work. We're very interested. Would you be willing to submit a version to our journal?” and, oh, this is happening prior to Carol looking at my paper and panning it.

Eric: So the only way they would have known about this would have been from Nature or from Dick, or—

Bret: I'm pretty sure I know, based on what they, again, I was too young to sort out really what they were saying, but they indicate that they're fans of antagonistic pleiotropy, so what happened was George Williams, having heard that it got rejected, contacted some friends of his and was like, you should really take a look at this. So I begin the process of revising it. I've shown it to Carol, she's panned it. I send the revised version to experimental gerontology. They send it out for review. As you know, review is blind. You don't know who your reviewers are, but you can often tell who they are. It's not as obscure—

Eric: If it’s a small field.

(01:32:00)

Bret: Yeah. So they read the acknowledgements of my paper, which are now on alert about Carol. I have to thank her in the paper for the work she did, but I'm now on alert that she's gone strange on the subject matter of this paper, and so I've broken her out separately in the acknowledgements. I don't want to be as gracious to her, because she's being hostile to me.

Eric: Right.

Bret: But I don't want to not acknowledge her, so I acknowledge her separately. Experimental Gerontology then—I am 99% sure—sends the paper to her as the reviewer. She pans it. Absolutely brutal critiques, just pages and pages and pages of them. They are not high quality critiques. I could go through every single one.

Eric: Don’t bother, this is a podcast, just—

Bret: No, I can't do it here, but I could have then—

Eric: No, okay?

Bret: But I didn't know what to do because she was in line for a Nobel Prize, that was well understood. I didn't want to accuse a leading light of the field of,

Eric: Okay, this is exactly why I got angry with the beginning of the podcast, you moron. No, no offense. You were in line for a Nobel Prize. You didn't. I mean, I'm sorry. There is an aspect of this about giving away your power, before you’ve even accumulated—you don't even have a PhD at this time.

Bret: I'm just saying, at the time, if you mentioned her name, people would say, “Oh yeah, her Nobel Prize is one of these years.” Right? So my point was, I was in the awkward position—I didn't understand what I was supposed to do. I didn't want to send back a review that said, “I don't know who the person is who reviewed this, but they don't understand the material, and all of their critiques suck”, because I didn't want to accuse somebody who was that powerful of not getting it.

Eric: I mean, here's the problem. What do you do? You don't actually have evidence in the hard form where like you have got videotape, but on the other hand, these are small worlds. This, all of this is preposterous.

Bret: Right. So I sit on the review for too long, not knowing what to—

Eric: Well you don't know how to play the game!

Bret: I don't know how to handle it.

Eric: I'm sorry, but, like, I had no advisor. Your advisor was not equipped for the modern era.

Bret: He wasn't equipped for the modern era. He wasn't equipped for molecular biology.

Eric: That's true.

Bret: I finally settle on a strategy that I can live with and I send back a note. I send back the review and my note says, “I don't know why, but this entire list of critiques is not high quality. If you would like to point me to any of the critiques in this list that you would like me to address, I am more than happy to do it, but I don't think it makes sense to address the entire list”, and as I recall it, I hit send on the email, and within minutes, maybe it was an hour, I got back a response: “Your paper has been accepted for publication”, which blew me away because I—

Eric: It makes no sense according to regular protocols.

Bret: Right. It makes no sense, because, clearly, they're supposed to send it out for review. The reviewer is supposed to say whether it's supposed to get published. The reviewer said it shouldn't be published. I said, “I refuse to address these critiques unless you ask me to.” The editors have overridden the reviewer. They understood the reviews were cruddy. They needed me to say that in order to justify the move that they wanted to make. They knew the paper was good and the review was crap. So they effectively overrode normal peer review. Was my paper peer reviewed? Well, it was by the editors who were experts.

(01:35:28)

Eric: Let me jump in. Peer review is a cancer from outer space. It came from the biomedical community, it invaded science. The old system, because—I have to say this because many people who are now professional scientists have an idea that peer review has always been in our literature and it absolutely motherfucking has not.

Bret: Right.

Eric: Okay? It used to be that the editor of a journal took responsibility for the quality of the journal, which is why we had things like Nature crop up in the first place, because they had courageous, knowledgeable, forward thinking editors. And so I just want to be very clear, because there's a mind virus out there that says “peer review is the sine qua non of scientific excellence, yada, yada, yada, bullshit, bullshit, bullshit”. And if you don't believe me, go back and learn that this is a recent invasive problem in the sciences.

Bret: Recent invasive problem that has no justification for existing in light of the fact that—

Eric: Well, no, not only does it have no justification for existing. When Watson and Crick did the double helix, and this is the cleanest example we have, the paper was agreed should not be sent out for review because anyone who is competent would understand immediately what its implications were. There are reasons that great work cannot be peer reviewed. Furthermore, you have entire fields that are existing now with electronic archives that are not peer reviewed. Peer review is not peer review. It sounds like peer review. It is peer injunction. It is the ability for your peers to keep the world from learning about your work.

Bret: Keep the world from learning about your work—

Eric: Because peer review is what happens— real peer review is what happens after you've passed the bullshit thing called peer review.

(01:37:18)

Bret: Yes. Okay, so the paper was accepted by Experimental Gerontology. They went on to publish it.

Eric: This is called “Life’s Slow Fuse”?

Bret: No, “Life’s Slow Fuse” was the title as sent to Nature, and I changed the title because I did not want to compromise the story—I didn't want to confuse the story.

Eric: The original submission was called “Life’s Slow Fuse”.

Bret: Right.

Eric: We probably have a copy of that somewhere?

Bret: Oh, of course.

Eric: All right. Then the Experimental Gerontology paper, what is it called?

Bret: The Reserve Capacity Hypothesis, which is a much less catchy title, but, nonetheless, the paper, I'm very proud of how it's written. People read it who were not expert, could understand it. The abstract is extremely clear, and it ends with the clear point that, because we have unearthed, we have predicted, and Carol Greider has shown, that wild mice telomeres are short, and the telomeres had been elongated by captivity, that there is a clear danger that the mice we are using for drug safety testing are biased in an egregious way. And the bias would look like this: a mouse that has very long telomeres has an indefinitely large capacity to replace damaged tissue, and, it has a vulnerability to cancer that is preternaturally high. So, we may be overrating—if we use these mice, we may be overrating the danger of causing cancer, and vastly underrating the danger of toxicity. And, in fact, one of the things—so, the point was you give a mouse who's got an effectively infinite capacity to replace its tissues, a toxin, and either the toxin is so deadly that it dies right away, but if it doesn't die right away, it just eats up the insult. So those animals would lead us to release drugs—

Eric: By insult, what you mean is cellular necrosis?

Bret: Damage. Yeah. What this would cause us to do is release drugs onto the market for human use that are highly toxic across the body.

Eric: Wait a second—if the mouse standard was the last standard—

Bret: Well, no, even if it's not the last standard, because—

Eric: Well, it’s important to say this—

Bret: The problem is, I mean, you can imagine how hard it is to test on large, slowly reproducing animals.

Eric: Well, and the ethics of testing on humans is very—

Bret: Absolutely.

Eric: —restricted, so mice is the last cheap place—

Bret: It's the last cheap place—

Eric: —to get large N data.

Bret: Not only large N, but it's the one place that you can make the following move. You can imagine that in many circumstances the accelerated lifespan, the accelerated life cycle of mice allows you to see long term damage as it would accrue in humans on a very short timescale. That doesn't work with monkeys. It doesn't work with human patients. It works with mice, maybe, but in the case of mice with ultra long telomeres, those insults will be invisible.

(01:40:36)

Eric: Let's just, I want to back up because I think this is a really important part of the story. What you're saying is if you take an organism that has an expected, let's say, 40 year lifetime, it's very expensive timewise to say, “We ran this experiment and found that there was no immediate damage that was visible, but towards the very end of their lives we saw a marked increase in morbidity” or—

Bret: Yeah, I mean if you took a drug and it knocked 15 years off your life on average, that might not show up in any notable way in a short term study.

Eric: If there was pressure to—

Bret: Right. And nobody is going to want to let drugs, you know, you don't want to wait 40, 50 years to find out what happens to these patients. So what we do is we make the assumption that if we give large amounts of a drug to an animal that lives a very short life, we will see those effects early. And if the animal happens to have ultra long telomeres, you won't see those effects early. So, it's a perfect storm for causing us to release drugs that should never have been released into public.

Eric: Can you think of one?

Bret: Oh, I sure can. Vioxx, for example. So Vioxx was discovered to do heart damage, right? Heart damage. How do you, why do we know that it's heart damage? Well, the thing about hearts, for reasons we can get into maybe another time, hearts have a very low capacity for self-repair, right? That's why they're vulnerable to heart attack.

Eric: Not much turnover.

Bret: Not much capacity for repair, and not much turnover. Now, there's an adaptive reason for that, but hearts don't repair themselves very well in a healthy person. And when they fail, it's hard to ignore, right? If somebody who's 30 has their heart fail, there's questions asked, right? So anyway, Vioxx was released into the public having passed drug safety testing.

Eric: This isn’t the only system that doesn't have a lot of mitosis, like for example, neurons.

Bret: Neurons don't have a lot, cartilage doesn't have a lot.

Eric: Got it.

Bret: Your eye cells don't. Now note, all of the tissues I've just mentioned, when's the last time you heard about anybody having, you know, cancer of the cartilage, of their knee, cancer of the heart,

Eric: If they get brain cancer, it tends to be glial—

Bret: It’s glial cells, exactly. So the tissues that have very low capacity for self repair do tend to wear out and they don't tend to get cancer, which is exactly one of the predictions of my paper.

Eric: Right.

Bret: Okay. So Vioxx is known to do heart damage. That created a big scandal because how the hell did it get through drug safety testing? It turns out a lot of drugs have done this. We've seen it with Gleevec, Fen Phen, Arithromycin. Your doctors probably still doesn't know that Arithromycin does heart damage—

Eric: Yikes

Bret: Right. There's all of these cases of drugs that were released and then later understood to do heart damage. Now my claim is they don't actually do heart damage. They do cellular damage and the heart is the most conspicuous.

Eric: Yeah, yeah, yeah, yeah. Geez. This is like another layer of this thing.

Bret: It's like a huge fucking nightmare, right? Because—

Eric: Well, but it's this thing about, like, perseverance and disagreeability. You've got all sorts of things that sound like something that invalidates the theory, and then it’s sort of theories upon theories that allow you to see the original simplicity of the idea. I see the original idea is very simple—

Bret: Yep.

Eric: —but if you know a lot of weird facts about what you think are just mice, or something about hearts, you can't put together what is going on. The idea that ambient damages only manifest in the heart because that's the one system—you know, or the neural system—that, like, really doesn't have a lot of mitosis.

(01:44:17)

Bret: So, well, piece of advice to anybody who finds themselves in remotely similar waters. The signal that you are on the right track is that stuff starts canceling. Complexity in the story, which has accumulated because something was missing, starts disappearing in the story. You begin to take on a model. Anyway, so yes, we've got a situation where we've got a bunch of drugs mysteriously producing heart damage.

Eric: K, so now you've got a paper that's out. You've got a real world application. You've got a theory coming out of evolutionary theory. It's making a molecular prediction.

Bret: Yup. Successfully predicts mouse telomeres.

Eric: One of the world's leading labs has confirmed the prediction.

Bret: Yup.

Eric: Where are we now? What year is this?

Bret: God, well, let's see. The paper came out

Eric: And my recollection—and, just to be horrible about this—is that your fucking department at the university of Michigan, which has some great people, is also holding you back and enervating you year after year by not allowing—because this is groundbreaking stuff. This is Nobel quality work, at least one or two times over, in my opinion. I could be wrong. I'm biased because I'm your brother, but what concerns me here is that you are not comfortable with what this story really might be.

Bret: No I— Look, it's not mine to judge. I'm very proud of this work and the work—

Eric: But the problem, Bret, is that Jerry Coyne and Richard Dawkins did not know that Dick Alexander, Leonard Hayflick, and George Williams were all on this thing, because that community had broken down.

(01:45:59)

Bret: You know, the irony is, I sent a letter to Dawkins when this was going on, asking for his help, and he sent back a letter saying, “This is very interesting. It's not my area of specialty. You should talk to Bill Hamilton.” And I was in the process of writing a letter to Bill Hamilton on Dawkin’s suggestion, at the point that Bill Hamilton came back from Africa having—he was pursuing a remote hypothesis about humans having accidentally unleashed AIDS into the world with a polio vaccine. But anyway, so—

Eric: Bill Hamilton, I'm sorry, not everybody's going to know—this is the guy who came up with inclusive fitness?

Bret: Yes. He was one of the great geniuses of evolutionary biology in the late 20th century.

Eric: He was held back by John Maynard, right?

Bret: I don't know that story. I, you know—

Eric: I think Maynard is interviewed on Web of Stories where you—

Bret: Maynard Smith.

Eric: Yeah, sorry. Yeah. Maynard Smith. Right.

Bret: Yeah.

Eric: And Maynard Smith talks about like, you know, “It was very unfortunate. I didn't really understand who he was.” You should check it out. It's pretty amazing.

Bret: Well, as long as we're doing this, years after this story had cooled—

Eric: Yeah.

Bret: —I ran across a paper from John Maynard Smith that, I now don't remember exactly what its nature was, but it appeared to predict my whole story.

Eric: Uh-huh

Bret: Right? And John Maynard Smith was dead. I couldn't contact him. I really wanted to say, “Oh my God, you nailed it.” Right. But anyway, so I was in the process of writing to Bill Hamilton to get his help. You know, he was sort of on a par with George Williams, and he went into a coma on his trip back from Africa having contracted malaria. And then there was, I think complication with the aspirin that he took or something. And he never woke from his coma and he died, tragically. So he never got the letter, and who knows what he would've done.

Eric: Okay, but look, that's a tragic and interesting story, but Hayflick was positive towards you. Williams was positive towards you and Dick Alexander. Those were the three that blew me away. That's a huge amount of firepower.

Bret: That’s a lot of firepower, and it wasn't enough. But, here's the punchline to the story, effectively. At the point that my paper is out—

Eric: Right.

Bret: —and it very directly alleges the danger with these drugs being released when they're not safe, and the drugs have started emerging and turning out not to be safe, and the government is now really interested in what's going on, the government puts together a FDA commission to study the question of—the book that they put out, literally a book that they put out, at the end of their study is called The Future of Drug Safety

Eric: I hope it’s a Blue Ribbon panel.

(01:48:53)

Bret:It's not exactly clear what it was. What is clear is that you can search the manuscript of this book. Nowhere does it mention “mouse”—

Eric: Antagonistic pleiotropy?

Bret: It doesn't mention antagonistic pleiotropy. It doesn't mention the genus “mus”. It doesn't mention “telomeres”. It's not in there. It's alleged in the literature in broad daylight that this is what is causing the problem, and—

Eric: Now you're—see, this is the Vampire Effect, where you don't exist if nobody reacts.

Bret: Right. And, so I start going to members of the press, I think, “This is a huge goddamn story. Somebody is going to make—

Eric: “Oh my god, you’re self promoting!”

Bret: —career on it”, and I call up members of the press, and it's always the same, right?

Eric: Always the same.

Bret: It’s always the same. They're very excited about this story.

Eric: No, they’re initially, the reporter—

Bret: The reporter is excited.

Eric: Yep

Bret: And then the reporter—

Eric: Talks to someone.

Bret: They talk to someone, and then either they stop returning your calls, or they say, “I'm sorry, the story doesn't hang together”. It's again and again and again.

(01:49:48)

Eric: Yeah.

Bret: And there's just nothing you can do.

Eric: Remember what I said about the Distributed Idea Suppression Complex

Bret: Yeah. And the people who man it don't even know what they are. For most of them, they don't know what role they're playing.

Eric: Look, you see the same thing with like string theory because none of the reporters are actually string theorists, so they're dependent upon this. You saw this with this woman alleging that she had the Epstein story three years earlier, but that the editors said, well, we might lose access to the baby pictures of the Royal grandchildren like, you know, you're seeing this with catch and kill. There's this, I mean, I want you to take this seriously. You're just showing a part of what I'm calling the DISC, the Distributed Idea Suppression Complex. We have 50 years of such stories, and it happens that in our family, three out of four of us created such a story trying to get a PhD. And the idea for me is that every time you have to go into some closed system, like, there's a committee meeting or there's a blue ribbon commission or there's a peer review process, or there's a, what do they call them, the panels—study groups, for grants. That's where the DISC lives. We know that it's localized to the things that protect the integrity of science. It's an autoimmune disease, where what we have is an ability to stop highly disruptive ideas from getting a hearing in the general population of experts, by virtue of the fact that a carefully chosen group of experts can stop publication. Because look, if you're wrong about this stuff, there's a cost. It's not, it's not cheap.

Bret: No, I mean, in fact, it would have been career ending. I'm pretty sure, had I been—

Eric: I don't know that it would be career ending if it was done in good faith, but you know, this is my, my problem with this is that you're sitting on one of the great scientific stories—I would say that I've ever heard. But you know, I'm sort of, kind of saying, “Well, Bret, what happens next?” You know, obviously I know a lot of this stuff. I've forgotten it, but I lived this with you and this is, I can vouch that this is more or less the order of events as it was taking place, as we didn't understand what was happening.

Bret: So I have to go through the final Carol Greider chapter. In order for this story to fully make sense,

Eric: Where the Nobel Prize is given?

Bret: That's the very tail end.

Eric: Make sure you include that.

(01:52:46)

Bret: Okay. So at the point that my relationship with Carol is changing its tenor and she is becoming hostile and I'm not clear on what's going on, I contact her and I discover through talking to her that she and Mike are about to publish their paper on the long telomeres of laboratory mice.

Eric: So this is the Delta between a wild type and laboratory mice.

Bret: Yeah. And I'm shocked because she's told me they're keeping it in house and instead they've got a paper that there, she says in final revisions there that day submitting their final revisions to nucleic acid research with their paper. And I say, Carol, can I see the paper? And she says yes. And she sends me a manuscript, not the pre-print of the paper. She sends me a manuscript of the paper, no acknowledgements, no figures. And I contact her and I say, can I see the acknowledgements and the figures? She sends them to me, and I contact her and I say, “Carol, I'm disturbed. This was my hypothesis that you were testing. I should probably be an author on this paper, but at the very least I need to be an acknowledgement in this paper so that I can go back and point to it and say that was”—

Eric: It changes everything. That it was a prediction. It wasn't just something that was stumbled upon.

Bret: Absolutely.

Eric: Yeah.

Bret: And her response is, “I have been through my email and I see no evidence of the communications you are talking about.” Now, when I said at the beginning that—

Eric: You had called her.

Bret: I had called her.

Eric: Holy Shit.

Bret: That was my error.

Eric: This is such fucked up. I mean, I don't swear a lot in this program.

Bret: Yeah.

Eric: But this is such fucking academic, petty, stupid ass bullshit. This is like one of the great stories of all times.

Bret: One of the great stories of all time, maybe, and human life hangs in the balance on this one.

Eric: No kidding.

Bret: Right. Okay. So Carol does get awarded the Nobel prize, Carol Greider, Elizabeth Blackburn and Szostak. Szostak, who mentions at the point that the Nobel Prize is awarded that he was shocked as all hell to get a Nobel Prize because his work was so deep in the history of telomeres that he just didn't expect it. And suddenly—

(01:55:14)

Eric: No, I should say, I want to be very clear, right. All of these people have made fantastic Nobel-worthy discoveries.

Bret: Totally.

Eric: There's zero allegation that these people—

Bret: Weren't deserving. No,

Eric: Absolutely.

Bret: No. And they, you know, Carol and Elizabeth got their Nobel prize for the discovery of telomerase, which is a huge, huge progress. So anyway, I don't deny that they were worthy of this prize. What Carol Greider does with her Nobel lecture, right. Nobel lecture being the biggest lecture a scientist will ever give, the lecture that—

Eric: And filmed.

Bret: And filmed—is she delivers a paper in which she very oddly has now embraced my entire set of hypotheses about the effect. She has come over from the comparison between the paper of mine that she panned and said didn't make any sense. She is now a total convert to the idea that senescence across the body is being caused by Hayflick limits that are telomere based.

Eric: Okay, and this is the first public incident that we know of in which the delta between the negative comments on your paper, which is not an anonymous peer review.

Bret: We have it in an envelope from her.

Eric: Got it. And it's immediately after the Nobel prize that the wisdom of that line of thinking is embraced.

(01:56:43)

Bret: Right. But there's more to the Nobel lecture. So she spends her Nobel lecture on what is admittedly a very beautiful presentation of the connection between telomeres and senescence. She goes through tissue after tissue, says cirrhosis of the liver is what happens when you have short telomeres and your liver, etc. She goes through tissue after tissue. She projects the data, the blot actually from the paper with Mike Hemann, the paper that I should have been a coauthor on, she projects it on the screen, but she does some weird freaking dance, where she, instead of describing the long telomeres of laboratory mice as a major bug in the system, she describes it as a happy accident, effectively, because it allows us to test certain things like, “Oh, isn't it delightful that they have long telomeres?” And it's like, what the hell are you doing? There is so much riding on correcting this and you're presenting it like it’s just a bonus. And she, in her presentation, she's got several experiments that I did not know she had run that I had suggested to her and I said, you know, things like, “Carol, do you have any idea if a cell has many different telomere lengths, is it the shortest telomere that controls how many reproductions a cell can do?” She's run that experiment. Interesting. Low and behold, it's the shortest telomere. It's a good guess. But anyway, so, she goes through this. There's no mention of me, there's no mention of the actual implications of the the long telomeres for things like science and safety testing and all of that. And I can't seem to raise the issue of the safety question with anybody. Right? At best, I get journalists who are interested until they call somebody, and the somebodies on the other end, I know what they say. They say “everybody that mice aren't great models”. In fact, there's a paper out there that says something like the mice lie. It's not about this issue. It's just about the fact that mice aren't a perfect match. The issue in question could be solved. It could be addressed thoroughly. And, for all I know, once the JAX Lab figured out what they were doing—

Eric: They could change the protocols.

Bret: For all I know they quietly have fixed this and there was a private, you know, I've heard that there was a private meeting in which they decided—

Eric: Look, this is the thing.

Bret: Yep.

Eric: You see something like this in statistics, everybody knows that most distributions that are bell-shaped are not normal. Right?

Bret: Yup.

Eric: And on the other hand, we all use normal distributions, and as a result, there are lots of things that at one level everybody knows—

Bret: Yep.

Eric: But don't percolate down to the important layers in which we test things. And I don't know where, like you and I have never been able to fully put together, cause we're not molecular researchers and I'm not even a biologist. How important are these results? How robust are they? Has there been a change? This is a quiet world at some level.

Bret: It's a quiet world. But I think what I have concluded, yeah, working backwards from the phenomenology of the field and how it reacts to this problem, is that there's a tremendous amount resting on failing to acknowledge the error. Even though the error was obviously an honest error to begin with, they would rather sweep it under the rug. I mean, imagine you've got all these knockout mice, right? These knockout mice, there's a major investment in them. It takes a lot of work to knock out a particular gene.

Eric: No, dude, you've got a central, you've got a single point of failure—

Bret: Right.

Eric: Whose projections are tendrils into everything.

Bret: Right? And you've got how many careers built on papers that are now suspect.

Eric: This is like an era. This is like a centralized irreproducibility crisis.

(02:00:37)

Bret: Yes, it's that bad or worse.

Eric: Okay.

Bret: And, and you know what happens if, let's say somebody hears this podcast and they check into it and they find out, lo and behold, this story is true.

Eric: Yeah.

Bret: Well now the FDA has a problem.

Eric: What would, wait, wait a second. I don't want to get too far out over our skis. We have enough listeners that people will get a chance to hear an unbelievable story. And if there are things in the story that are not true or misremembered or unkind or there've been changes or maybe we don't really fully understand how the drug testing works. I'm open and I, and I want to be very clear, and I want this in the podcast, I'm open to the idea that the most straightforward implications of the story are subject to adjustment. However, having lived the story, I can say that this was an egregious story at multiple points, with conflicts between the evolutionary community, the biomedical community, the professional publishing community. This is a terrible story, and it's also an amazing and beautiful and wonderful story. And you know, I felt really lousy at the beginning of this podcast goading you and prodding you. But I am so bored of you, no offense, as the guy who stood up to the funny kids at Evergreen, and you know, we know what's in the heads of these people. If you're at Evergreen, you're not that good.

Bret: Yep.

Eric: Right. And that was like, this is the, I just want to be open about it.

(02:02:17)

Bret: No, I look, I appreciate it, and I'm glad to have this story out. The story has many different layers of meanings. I know, I remember where I was when I finally sat down to watch Carol Greider's Nobel lecture and I had one of the oddest experiences of my life. I was actually in a hammock watching her lecture, watching her present my hypothesis without my name anywhere on it, and then she projects this image from her paper with Mike Hemann, and I was flooded with two simultaneous emotions that are just completely incompatible. Right? I've never felt anything like it. I was absolutely elated to see my work projected on a Nobel stage, right? That changed me.

Eric: You know I called the horse and rider problem?

Bret: No.

Eric: The point of the official complex of science is to knock the rider and take the horse, where the horse is the theory and the rider is the attribution.

Bret: Well, this was it. I was elated and livid simultaneously, and I can still almost feel what it was almost like my body was trying to figure out one half supposed to feel one thing and the other feels the other? But, this story has many levels of importance. Personally, it gave me the ability—I was already, as you are, very good at not being persuaded by the fact that everybody else disagrees with you, that that has an implication. Every great idea starts with a minority of one and you have to be able to endure being alone with a great idea in order to advance the ball significantly. This story was so extreme and so clear in the end that it just left no doubt. And I must say, I don't know how young students can arrange to confront materials so that if they're really good, they get a clear demonstration like this, that they're really good. So they know to keep going.

(02:04:40)

Eric: Bret, look, I think you're selfish, and I don't mean to be horrible about it. I think that the story is an inspiration. I've lived the story with you. I have my own version of the story where instead of it being the slide from the paper of Grider and Hemann, it's equations that are known as the Sieberg-Witten equations. And you see what you did, with somebody else putting, you know, putting it up on a board, it starts to change the field, and you suddenly say, you mean I'm not an idiot? Right? And what I'm claiming is that the next layer of this is, “Well, why don't you just submit a paper? If you have ideas, submit a paper, submit a paper, submit a paper.” Who is this fucking suppose to fool?

Bret: Well, right, and this, this—

Eric: I mean, I just, I think the idea is that if you have a seat on the exchange, you know that by submitting a paper, your paper will get reviewed because you have, you present a credible threat. It doesn't occur to you that what you're saying is effectively like “let them eat cake”, to somebody whose paper is going to be reviewed by the person who's, like, holding them back.

Bret: No, this is exactly—when Jerry Coyne came at me with, you know, “Bret doesn't understand his, his explorer mode stuff is, is nonsense”. And then Richard Dawkins echoed it “Bret doesn't understand natural selection. And, you know, if he did, he'd submit a paper.” My feeling is, I lived this story, and you're going to pretend that there is even a mechanism to get a proper hearing?

Eric: Look, here's my proposal proposal. All right?

Bret: Yeah.

Eric: I think that you, Pia. and myself are indicative of an entire layer of GenX academicians, and now probably millennial academicians, whose work was suppressed, and we don't feel comfortable saying these words, which is that the purpose of the university system, in the time that we were there, was in large measure to make sure that big disruptive new ideas did not upset the apple cart because there was the ability to deny, I mean, this is what you guys call interference competition, which is that you keep people from sitting down in the chairs in a game of musical chairs. And then the idea is we have lovely parting gifts for our contestants. Doug Prasher, who did green fluorescent protein, ends up driving a shuttle bus in Huntsville, Alabama, features in the, you know, I don't know, was it the front page of the Science Times? A year later he's still driving a fucking shuttle bus in Huntsville, Alabama. Meanwhile, we're being told that Americans don't care about STEM. We're not really good at science, but thank God, thank God our friends in Asia are amazing at science, because, as bad as our children are thinking for themselves, we've got huge numbers of people who want to come from China, South Korea, India, and Taiwan in order to do the study in the labs, which is actually work, and I'm the guy who found the secret study in 1986 which says, “Hey, we're going to have to pay these American academicians over six figures very soon because of the supply demand relationships.” And then they took away the demand curves and they only showed the supply curves. They said this was a demographic rather than an economic analysis, so price and wage certainly didn't enter into it. Like, our problem is that the American scientific enterprise, headquartered in the National Science Foundation, National Academy of Sciences, and our university systems is fraudulent, and it serves to suppress radical new ideas. And I'm not saying that everything is guaranteed to be right about your story, but this is a story that you and Carol should have warred out, in public, without your submitting into a system where you don't know who reviewed this, you don't know how to respond to the comments. You can't measure the delta where somebody in one year says, “this is crap” and the next year they say, “this is my theory”. Right? And what I want. I would love to invite Carol Greider onto this program, because I think she deserves the right to rebut what you're saying.

(02:08:58)

Bret: Yup. That'd be cool.

Eric: And Elizabeth Blackburn is fantastic. I'd love to have—and these are great scientists.

Bret: Frankly, you're going to say, this is me being too nice.

Eric: Yeah.

Bret: I'd even like Carol to come clean and just put this behind us. I'm not, you know, at this point—

Eric: No, it's not a question of that Bret, there is—you have the right to offer somebody a hand up.

Bret: Yup.

Eric: But you're skipping the step of—let me be blunt—how many universities offered you a position after you were run out of this crappy Evergreen State College by a weak president who refused to stand up for academic freedom, freedom of speech, and anti-racism, which you exemplified.

Bret: Professorship? Zero.

Eric: How many biology lectures were you invited to give at top tier AAU universities? American Association of Universities? Or, Association of American Universities.

Bret: None

Eric: Okay. What the fuck is that? I mean, let's, let's just say the word “fuck” a lot, cause I had Andrew Yang in that chair. I don't say fuck a lot.

Bret: Yeah.

Eric: Okay. So the idea is you have a Maoist insurgency against a student of Dick Alexander, who is supported by George Williams, with support from Leonard Hayflick. He's predicting something from evolutionary theory, registers in molecular biology. It may have drug testing implications, and, like, nothing, silence. And you're terrified to talk about this.

Bret: I don't think I'm terrified to talk about it.

Eric: Well, I'm sorry. Can you tell me something? Where have you told— you have a podcast?

Bret: Yeah.

Eric: Where is the story written up? Where is the story lodged? You and I have the ability to lodge it. I'm forcing you to do this on my podcast. I haven't heard you do a podcast about this. I hear you talking about free speech. I hear you doing things with the Heterodox Academy. I hear you doing things in the Intellectual Dark Web, something with Andy Ngo, something with Antifa. Okay. The whole purpose of the Intellectual Dark Web is to keep the channel open based on merit, because if we do something like the diversity of ideas, you know, for all I know, the people who are suppressing you are more diverse than you are, you know? Okay. These are ideas that needed to come out. There are health implications potentially of these ideas. This is not ethical to suppress. In effect, it's not ethical for you not to talk about, not to be rude.

Bret: No, no. Look, I get this. I tried for a decade to get this story to come out. Now, I'm sure I would have been less aggressive on the social front. I would have let Carol go in order to get the story out and get the drug safety issue addressed. I don't know what you regard that as. Maybe that's—

Eric: It's not a question of this. Look, there is a Carol Greider and Elizabeth Blackburn and everybody else in like senescence land, Judith Campisi, who knows. Everybody's got a problem, which is there's way too much transparency, and there's too little funding, and there's not enough autonomy, and there's too much peer review, and for whatever reason, a new game has cropped up where everybody says we need more transparency, more diversity. We need to make sure that we're not wasting taxpayer dollars. We have, you know, ever more oversight. All of this is denaturing our society. We have to compete with China now. We are going to have issues with Iran and Russia, and we are losing our minds because we are serving a baby boom group. Almost, like, you pick a leading university. It is headed currently by a Baby Boomer. That's almost true without even telling—if I ask you, “Hey Bret, pick a university. Don't tell me which one it is.” I will tell you that the number of administrators that that university has soared above the levels of admissions, the tuition has soared above medical inflation, which is above regular inflation. If I ask you about the grant structure, older professors that are winning more grants and younger people are winning fewer grants. This is a giant complex. I am going to have somebody from Sugar Baby University, which is a subset of Seeking Arrangement, because the Baby Boomers made student debt non-dischargeable in bankruptcy. And now this group is offering older men the ability to date younger women with an allowance, right? So we're starting to get into gray area sex work, where the Baby Boomers to keep this lifestyle to which they've become accustomed are effectively enslaving—

(02:13:44)

Bret: Well, they're hoarding wellbeing on every front, including the sexual, which is no surprise at all.

Eric: But here’s my claim: we are in a holding pattern. I'm in my 50s. You're in your 50s. I've done work that has never seen the light of day. You've done work that's never seen the light of day. Pia has done work that's never seen the light of day. I don't know about Heather. My claim is: it's time to crash land the planes into the control tower. It's enough.

Bret: Wholeheartedly agree.

Eric: Okay. Bret, it's been an absolute pleasure having you on. Come back anytime. I want to say that anybody who is misportrayed by this podcast is welcome. We are not claiming to have absolute and universal knowledge. You are more than welcome to correct the story if you have knowledge about this that checks out. But the problem is that this is a story that needs to be told. It's like the story of Margot O'Toole and David Baltimore that played out at MIT, when, I believe that she found that she couldn't reproduce the work of Dr. Imanishi-Kari. And of course the system turned on the person who was trying to say, “Hey, I'm seeing irregularities. I'm seeing problems.”

We have a biomedical complex that needs whistleblowers. It needs iconoclasts. It needs challengers. The food pyramid has been off for years. Our health recommendations are completely off. I think that this is an essential story. You need to move out of Intellectual Dark Web stuff, which was about keeping the pipe open. Let somebody else do that. And it is time to hire you as a professor at a top tier university. And I'll be happy to talk to you about what happened when you and Richard Dawkins encountered each other on stage in Chicago, because I think in terms of pure evolutionary theory, it is time to boost a young Richard Dawkins who contributed two of the most important ideas in the form of extended phenotype in the mean, which largely dislodges the old Richard Dawkins and his hatred of religion, which has appeared to take over his thinking as regards his own contributions to biology. We got a lot of work to do.

Bret: No question.

Eric: All right, my friend.

Bret: Well, thanks for having me.

Eric: Thanks for coming. You've been through The Portal with Dr. Bret Weinstein, professor in exile from the Evergreen State College. Please subscribe on Apple or on Stitcher or on Spotify, wherever you listen to podcasts, navigate over to our YouTube channel and not only subscribe, but remember to click the bell icon to be notified with our next episode drops. And hope to see you back on the next episode of The Portal.

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