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== Description ==
{{EpisodeInfoBox
 
|title=The Prediction and the DISC
All of our Mice are Broken. On this episode of The Portal, Bret and Eric sit down alone with each other for the first time in public. There was no plan.
|image=[[File:The-portal-podcast-cover-art.jpg]]
|guest=[[Bret Weinstein]]
|length=02:17:18
|releasedate=18 January 2020
|youtubedate=19 February 2020
|customlabel1=OmnyFM
|customdata1=[https://omny.fm/shows/the-portal/19-bret-weinstein-the-prediction-and-the-disc Listen]
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|youtube=[https://www.youtube.com/watch?v=JLb5hZLw44s Watch]
|link4title=Portal Blog
|link4=[https://theportal.group/19-bret-weinstein-the-prediction-and-the-disc/ Read]
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All of our Mice are Broken. On this episode of [[The Portal Podcast|The Portal]], [[Bret Weinstein|Bret]] and [[Eric Weinstein|Eric]] Weinstein sit down alone with each other for the first time in public. There was no plan.


There was however, a remarkable story of science at its both best and worst that had not been told in years. After an initial tussle, we dusted off the cobwebs and decided to reconstruct it raw and share it with you, our Portal audience, for the first time. I don't think it will be the last as we are now again looking for our old notes to tighten it up for the next telling. We hope you find it interesting, and that it inspires you younger and less established scientists to tell your stories using this new medium of long form podcasting. We hope the next place you hear this story will be in a biology department seminar room in perhaps Cambridge, Chicago, Princeton, the Bay Area or elsewhere. Until then, be well and have a listen to this initial and raw version.
There was however, a remarkable story of science at its both best and worst that had not been told in years. After an initial tussle, we dusted off the cobwebs and decided to reconstruct it raw and share it with you, our Portal audience, for the first time. I don't think it will be the last as we are now again looking for our old notes to tighten it up for the next telling. We hope you find it interesting, and that it inspires you younger and less established scientists to tell your stories using this new medium of long form podcasting. We hope the next place you hear this story will be in a biology department seminar room in perhaps Cambridge, Chicago, Princeton, the Bay Area or elsewhere. Until then, be well and have a listen to this initial and raw version.


<span class="button">[[ep18 | Previous Episode]]</span> <span class="button">[https://art19.com/shows/the-portal/episodes/7591b76e-f107-4cba-beff-f5ec3f5da2f2 Listen to Episode 19]</span> <span class="button">[https://www.youtube.com/watch?v=JLb5hZLw44s Watch Episode 19]</span> <span class="button">[[ep20 | Next Episode]]</span>
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[[File:ThePortal-Ep19 BretWeinstein-EricWeinstein.png|600px|thumb|right|Eric Weinstein (right) talking with his brother, Bret Weinstein (left), on episode 19 of The Portal Podcast]]


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== Relevant Links ==
== Relevant Links ==
'''Bret Weinstein's''' [https://en.wikipedia.org/wiki/Bret_Weinstein Wikipedia], [https://bretweinstein.net/ Personal Webpage], [https://www.youtube.com/channel/UCi5N_uAqApEUIlg32QzkPlg Youtube Channel], and an archived version of Bret's website, [https://web.archive.org/web/20020722173540/http://www.telomere.org/ Telomere.org]
'''Bret Weinstein's''' [https://en.wikipedia.org/wiki/Bret_Weinstein Wikipedia], [https://bretweinstein.net/ Personal Webpage], [https://www.youtube.com/channel/UCi5N_uAqApEUIlg32QzkPlg Youtube Channel], and an archived version of Bret's website, [https://web.archive.org/web/20020722173540/http://www.telomere.org/ Telomere.org]


===Papers and articles===
===Papers and articles===
* Bret Weinstein and Deborah Ciszek's 2002 paper in Experimental Gerontology, [https://www.sciencedirect.com/science/article/abs/pii/S0531556502000128 "The Reserve-Capacity Hypothesis"]
* Bret Weinstein and Deborah Ciszek's 2002 paper in Experimental Gerontology, [https://www.sciencedirect.com/science/article/abs/pii/S0531556502000128 "The Reserve-Capacity Hypothesis"]


* Bret Weinstein and Deborah Ciszek's 2002 unpublished manuscript, [https://web.archive.org/web/20030316223515/http://www.telomere.org/Downloads/LifesSlowFuse.pdf "Life's Slow Fuse"]
* Bret Weinstein and Deborah Ciszek's 2002 unpublished manuscript, [https://web.archive.org/web/20030316223515/http://www.telomere.org/Downloads/LifesSlowFuse.pdf "Life's Slow Fuse"]


* Bret's Thesis, [https://deepblue.lib.umich.edu/bitstream/handle/2027.42/63672/fruitbat_1.pdf?sequence=1 Evolutionary Trade-offs: Emergent Constraints And Their Adaptive Consequences]
* Bret's PhD Thesis, [https://deepblue.lib.umich.edu/bitstream/handle/2027.42/63672/fruitbat_1.pdf?sequence=1 Evolutionary Trade-offs: Emergent Constraints And Their Adaptive Consequences]


* Carol Greider and Mike Hemann's [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC113886/ 2000 paper in Nucleic Acids Research]
* Carol Greider and Mike Hemann's [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC113886/ 2000 paper in Nucleic Acids Research]
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* Dr. Richard D. Alexander [https://en.wikipedia.org/wiki/Richard_D._Alexander Wikipedia]
* Dr. Richard D. Alexander [https://en.wikipedia.org/wiki/Richard_D._Alexander Wikipedia]
* Dr. Richard Dawkins [https://en.wikipedia.org/wiki/Richard_Dawkins Wikipedia], [https://www.richarddawkins.net/ personal website], [https://twitter.com/RichardDawkins Twitter]


* Dr. Robert Trivers [https://en.wikipedia.org/wiki/Robert_Trivers Wikipedia]
* Dr. Robert Trivers [https://en.wikipedia.org/wiki/Robert_Trivers Wikipedia]
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===Other Concepts and Terms===
===Other Concepts and Terms===
* [https://en.wikipedia.org/wiki/Xanthopan Xanthopan (moth)]
* [https://en.wikipedia.org/wiki/Angraecum_sesquipedale Darwin's Orchid (Angraecum sesquipedale)]
* [https://en.wikipedia.org/wiki/Ophrys Ophrys orchid]
* [https://en.wikipedia.org/wiki/Eusociality Eusocial]
* [https://en.wikipedia.org/wiki/Hymenoptera Hymenoptera]
* [https://en.wikipedia.org/wiki/Haplodiploidy Haplodiploidy]
* [https://en.wikipedia.org/wiki/Naked_mole-rat Naked Mole-rat]
* [https://en.wikipedia.org/wiki/Telomere Telomeres]


* [https://en.wikipedia.org/wiki/Hayflick_limit Hayflick Limit]
* [https://en.wikipedia.org/wiki/Hayflick_limit Hayflick Limit]
* [https://en.wikipedia.org/wiki/Senescence Senescence]
* [https://en.wikipedia.org/wiki/Somatic_cell Somatic cell]
* [https://en.wikipedia.org/wiki/Germline Germline]
* [https://en.wikipedia.org/wiki/Genome Genome]
* [https://en.wikipedia.org/wiki/Pleiotropy Pleiotropy]


* [https://en.wikipedia.org/wiki/Antagonistic_pleiotropy_hypothesis Antagonistic Pleiotropy Hypothesis]
* [https://en.wikipedia.org/wiki/Antagonistic_pleiotropy_hypothesis Antagonistic Pleiotropy Hypothesis]


* [https://en.wikipedia.org/wiki/Telomere Telomeres]
* [https://en.wikipedia.org/wiki/Telomerase Telomerase]
 
* [https://en.wikipedia.org/wiki/Insult_(medical) (Environmental) Insult]


* [https://en.wikipedia.org/wiki/Senescence Senescence]
* [https://en.wikipedia.org/wiki/Histology Histology]


* [https://en.wikipedia.org/wiki/Rofecoxib Rofecoxib (Vioxx)]


===Margot O'Toole, Imanishi-Kari & David Baltimore story===
===Margot O'Toole, Imanishi-Kari & David Baltimore story===
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== Transcript ==
== Transcript ==
[https://theportal.wiki/images/c/c8/19_Bret_Weinstein.vtt Raw transcript file]


'''Eric:''' Hello. This is Eric Weinstein. I'm going to be recording a short introduction to this episode because I think it's probably the most important episode of The Portal to date. That said, under normal circumstances, I probably would have either edited this heavily or not released it at all. It starts off quite slow and it gets quite awkward before finding its pace. Now what's going on is that the interview subject is none other than my brother Bret Weinstein. In Bret's case, you probably know him if you know him at all as the heroic professor who stood up against what can only be described—I swear I'm not making this up—as an Maoist insurrection at an American college in the Pacific Northwest, the [https://en.wikipedia.org/wiki/Evergreen_State_College Evergreen State College]. It was a very strange situation because somehow the national media that we would normally have thought would have covered such a story—for example, the media that covered the [https://en.wikipedia.org/wiki/Willard_Straight_Hall#1969_building_takeover takeover of Straight Hall at Cornell] in the 60s—that media was almost absent completely.  At least, they were absent for a very long time before they entered late in the game. And why is that? Because the story ran counter-narrative—that is, the students at the Evergreen State College who were behaving in a racist fashion were actually students of color, and this was an exactly counter-narrative story. And Bret, who stood up to this racist insurrection, was in fact somebody with a history of standing up against racism. He had, in fact, been a student at the University of Pennsylvania, my Alma mater, an Ivy league school, and had to leave because of death threats when he stood up for women of color who were being abused for the amusement and the sexual amusement of white fraternity students. So Bret was supposed to be familiar to many of you from that, from an old national news story, and he was also the hero of a book called [https://www.goodreads.com/book/show/476218.The_Tapir_s_Morning_Bath The Tapir’s Morning Bath].
'''Eric:''' Hello. This is Eric Weinstein. I'm going to be recording a short introduction to this episode because I think it's probably the most important episode of The Portal to date. That said, under normal circumstances, I probably would have either edited this heavily or not released it at all. It starts off quite slow and it gets quite awkward before finding its pace. Now what's going on is that the interview subject is none other than my brother Bret Weinstein. In Bret's case, you probably know him if you know him at all as the heroic professor who stood up against what can only be described—I swear I'm not making this up—as an Maoist insurrection at an American college in the Pacific Northwest, the [https://en.wikipedia.org/wiki/Evergreen_State_College Evergreen State College]. It was a very strange situation because somehow the national media that we would normally have thought would have covered such a story—for example, the media that covered the [https://en.wikipedia.org/wiki/Willard_Straight_Hall#1969_building_takeover takeover of Straight Hall at Cornell] in the 60s—that media was almost absent completely.  At least, they were absent for a very long time before they entered late in the game. And why is that? Because the story ran counter-narrative—that is, the students at the Evergreen State College who were behaving in a racist fashion were actually students of color, and this was an exactly counter-narrative story. And Bret, who stood up to this racist insurrection, was in fact somebody with a history of standing up against racism. He had, in fact, been a student at the University of Pennsylvania, my Alma mater, an Ivy league school, and had to leave because of death threats when he stood up for women of color who were being abused for the amusement and the sexual amusement of white fraternity students. So Bret was supposed to be familiar to many of you from that, from an old national news story, and he was also the hero of a book called [https://www.goodreads.com/book/show/476218.The_Tapir_s_Morning_Bath The Tapir’s Morning Bath].
Line 142: Line 201:
I think in this episode we're going to do something interesting. I see Bret in two separate ways: On the one hand, I view him as a very heroic figure and he's an absolutely brilliant person. It's been a pleasure sparring with him throughout my life. However, I'm also his older brother and you're going to hear me at sort of my overbearing best, brow beating him a bit. Now the point isn't to push him down, but quite the contrary. I'm rather competitive as Bret's older brother and I don't want to compete with the weakest version of Bret, the professor and exile. Instead, I want him seated again inside of the institution where he always belonged. And in order to do that, I want him to tell the tale, not with embellishment, but as it actually happened, because I think it's one of the most fascinating episodes in modern biology that I've ever heard.  
I think in this episode we're going to do something interesting. I see Bret in two separate ways: On the one hand, I view him as a very heroic figure and he's an absolutely brilliant person. It's been a pleasure sparring with him throughout my life. However, I'm also his older brother and you're going to hear me at sort of my overbearing best, brow beating him a bit. Now the point isn't to push him down, but quite the contrary. I'm rather competitive as Bret's older brother and I don't want to compete with the weakest version of Bret, the professor and exile. Instead, I want him seated again inside of the institution where he always belonged. And in order to do that, I want him to tell the tale, not with embellishment, but as it actually happened, because I think it's one of the most fascinating episodes in modern biology that I've ever heard.  


So I hope that you like it. We're going to put it in front of you as an experiment and we're going to test to see whether or not I'm correct that can be used to augment the usual channels.  
So I hope that you like it. We're going to put it in front of you as an experiment and we're going to test to see whether or not I'm correct that The Portal can be used to augment the usual channels.  


I believe that a lot of us are sitting on intellectual gold. I don't think that the story that somebody’s work didn't see the light of day, or got attributed to somebody else, is as exotic as the institutions would have you believe. In fact, I think it's quite common. I think many of us find that we don't have careers inside of science because something goes wrong quite early when we're quite vulnerable. And my hope is that some of you listening, who I know are struggling as graduate students or as postdocs or as undergraduates, will listen to this and find some courage to stand up for yourself, because, quite frankly, if you choose not to do it in order to make nice with your fields, the chances are you will probably won't have a career in the long term. You might as well swing for the fences and you might as well clear your throat and tell your story as it actually happened, without fear.  
I believe that a lot of us are sitting on intellectual gold. I don't think that the story that somebody’s work didn't see the light of day, or got attributed to somebody else, is as exotic as the institutions would have you believe. In fact, I think it's quite common. I think many of us find that we don't have careers inside of science because something goes wrong quite early when we're quite vulnerable. And my hope is that some of you listening, who I know are struggling as graduate students or as postdocs or as undergraduates, will listen to this and find some courage to stand up for yourself, because, quite frankly, if you choose not to do it in order to make nice with your fields, the chances are you will probably won't have a career in the long term. You might as well swing for the fences and you might as well clear your throat and tell your story as it actually happened, without fear.  
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(00:40:37)
(00:40:37)


'''Eric:''' And then there are a few predictions. So, am I right? Darwin started this game off by predicting that there would be a moth with a really long tongue because there was a flower that had a really long distance to go before you could get the nectar out of it.  
'''Eric:''' And then there are a few predictions. So, am I right? Darwin started this game off by predicting that there would be [https://en.wikipedia.org/wiki/Xanthopan a moth with a really long tongue] because there was [https://en.wikipedia.org/wiki/Angraecum_sesquipedale a flower that had a really long distance to go] before you could get the nectar out of it.  


'''Bret:''' Yeah, he had been sent an orchid by Bateson, maybe, with a foot long corolla tube. And he reasoned very straightforwardly that it would make no sense for this plant to have invested in this very long structure if there were not a tongue that could reach down to gather the nectar. And I believe he did not live to see the discovery of that animal.  
'''Bret:''' Yeah, he had been sent an orchid by Bateson, maybe, with a foot long corolla tube. And he reasoned very straightforwardly that it would make no sense for this plant to have invested in this very long structure if there were not a tongue that could reach down to gather the nectar. And I believe he did not live to see the discovery of that animal.  
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'''Bret:''' Clade is pretty safe.  
'''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—
'''Eric:''' Yeah, clade of orchids, the [https://en.wikipedia.org/wiki/Ophrys 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—
'''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—
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'''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.  
'''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 clay called hymenopteran ants of eusocial breeding patterns and organization, but in mammals that will live underground.  
'''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 [https://en.wikipedia.org/wiki/Eusociality 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—  
'''Bret:''' So, I think, the way this story actually worked, he didn't say you will find it—  
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'''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—  
'''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—
'''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 [https://en.wikipedia.org/wiki/Haplodiploidy 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.  
'''Bret:''' Sure. So it has long been understood that the [https://en.wikipedia.org/wiki/Hymenoptera 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.
'''Eric:''' Spot on.
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'''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—
'''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.  
'''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 [https://en.wikipedia.org/wiki/Naked_mole-rat 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.  
'''Eric:''' And this is like one of the great moments in modern science.  
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'''Bret:''' Oh yeah?
'''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.
'''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 “[https://en.wikipedia.org/wiki/Telomere <span title="A telomere is a region of repetitive nucleotide sequences at each end of a chromosome, which protects the end of the chromosome from deterioration or from fusion with neighboring chromosomes. Over time, due to each cell division, the telomere ends become shorter. They are replenished by an enzyme, telomerase reverse transcriptase.">telomeres</span>]”, would be wildly different in length if the prediction were true from pure evolutionary theory.


'''Bret:''' Wow.  
'''Bret:''' Wow.  
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'''Eric:''' Okay.  
'''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—
'''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 [https://en.wikipedia.org/wiki/Mechanism_(biology) 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.  
'''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.  
Line 514: Line 573:
'''Eric:''' So this was the theory of [https://en.wikipedia.org/wiki/Leonard_Hayflick Leonard Hayflick]?  
'''Eric:''' So this was the theory of [https://en.wikipedia.org/wiki/Leonard_Hayflick 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—  
'''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 [https://en.wikipedia.org/wiki/Senescence “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.
'''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 [https://en.wikipedia.org/wiki/Somatic_cell somatic cells] that have finite limits on their ability to undergo mitosis and cellular repair and whatnot.


(00:58:25)
(00:58:25)


'''Bret:''' And the germline can't because if it did, your lineage would go extinct as a result of small—  
'''Bret:''' And the [https://en.wikipedia.org/wiki/Germline germline] can't because if it did, your lineage would go extinct as a result of small—  


'''Eric:''' Small addendums.  
'''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—
'''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 [https://en.wikipedia.org/wiki/George_C._Williams_(biologist) George Williams]. George Williams had finally—


'''Eric:''' One of the greatest of modern—  
'''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.  
'''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 [https://en.wikipedia.org/wiki/Genome 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—  
William's point was when a gene has multiple effects, what we call a [https://en.wikipedia.org/wiki/Pleiotropy pleiotropy], those effects may be good or bad. If effects are good early in life—  


'''Eric:''' By good we mean contributing to fitness—  
'''Eric:''' By good we mean contributing to fitness—  
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'''Bret:''' And the reason that we knew it was real,  
'''Bret:''' And the reason that we knew it was real,  


'''Eric:''' The hypothesis is the Antagonistic Pleiotropy Hypothesis.
'''Eric:''' The hypothesis is the [https://en.wikipedia.org/wiki/Antagonistic_pleiotropy_hypothesis 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.  
'''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.  
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'''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.”
'''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 [https://en.wikipedia.org/wiki/Carol_W._Greider 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—
'''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 [https://en.wikipedia.org/wiki/Carol_W._Greider Carol Greider]. Carol Greider is now a Nobel Laureate. She was not at the time. She was the co-discoverer of the enzyme [https://en.wikipedia.org/wiki/Telomerase telomerase], which is the enzyme that elongates telomeres, when that occurs—


(01:14:01)
(01:14:01)
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'''Eric:''' Can you think of one?
'''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.
'''Bret:''' Oh, I sure can. [https://en.wikipedia.org/wiki/Rofecoxib 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.
'''Eric:''' Not much turnover.
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'''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.
'''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 mytosis, like for example, neurons.
'''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.  
'''Bret:''' Neurons don't have a lot, cartilage doesn't have a lot.  
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'''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.
'''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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