Speaker 1: Hello everyone, and welcome to Talk Nerdy. Today is Monday,
Speaker 1: June twenty ninth, twenty twenty six, and I'm the host
Speaker 1: of the show Doctor Kara Santa Maria, and I do
Speaker 1: want to apologize for not putting out a new episode
Speaker 1: last week. It has been just a hell of a
Speaker 1: time over here. In addition to if you listen to
Speaker 1: The Skeptics Guide to the Universe, the other show that
Speaker 1: I work on, you may have heard that, in addition
Speaker 1: to something as innocuous as having an endoscopy kolenoscopy in
Speaker 1: the middle of the week that threw things off, two
Speaker 1: such large concerns as Evan Bernstein's resignation from the SGU,
Speaker 1: and I would turn you to the most recent episode
Speaker 1: of SGU to learn more about that, all the way
Speaker 1: to the tragic news that we recently received at my
Speaker 1: work in the hospital of the death of my direct supervisor.
Speaker 1: It's just been it's been a trying week, and unfortunately
Speaker 1: I just wasn't able to make it to air last week.
Speaker 1: So I appreciate your patients, and I'm glad that you're
Speaker 1: sticking with me, because this week we've got a really
Speaker 1: good one for you. But before we do dive into
Speaker 1: this week's episode. As always, I want to thank those
Speaker 1: of you who make Talk Nerdy possible. Remember, this show
Speaker 1: is and will always be one hundred percent free to download,
Speaker 1: and the way we can offset that fee basically provide
Speaker 1: this free service, especially for all those who either can't
Speaker 1: afford or just you know, can't prioritize paying for podcasts
Speaker 1: in their life. It's that individuals like you are offsetting
Speaker 1: that cost. The way we do it is using the
Speaker 1: Patreon model, which means you pledge your support on an
Speaker 1: episodic basis. And so right now, I just want to
Speaker 1: thank my top patrons this week. They include Chuck Blell,
Speaker 1: David J. E. Smith, Daniel Lang, Mary Neva, Will Defrain,
Speaker 1: David Compton, Brian Holden, Gabo, Jay l Rica Hagman, Pasqually Gelati,
Speaker 1: Rica Maharaj and Joe Wilkinson. Thank you all, and if
Speaker 1: you're interested in pledging your support, all you've got to
Speaker 1: do is visit patreon dot com slash Talk Nerdy to
Speaker 1: learn more. All right, this week I had the opportunity
Speaker 1: to chat with Roxanne Camsie. She is an author and
Speaker 1: a science communicator. She's written for a ton of outlets,
Speaker 1: that you read New York Times, The Economist, Popular Science, Scientific,
Speaker 1: American Slate, Nott, GEO, on and on and on. She
Speaker 1: is a contributing writer for The Atlantic. Currently and historically,
Speaker 1: she served as chief news editor at Nature Medicine, which is,
Speaker 1: you know, a huge research journal. She did that for
Speaker 1: over a decade, and before that she was a reporter
Speaker 1: for New Scientist magazine, which is also a widely circulating
Speaker 1: UK based science magazine. She also has taught at stony
Speaker 1: Brook University in Long Island through the Allen Alda Center
Speaker 1: for Communicating Science, and at the Craig Newmark Graduate School
Speaker 1: of Journalism at the City University New York. And she
Speaker 1: served on the editorial advisory board of ted MEHD. She
Speaker 1: has a new book. She has her first book, so
Speaker 1: this is very very exciting. It's called Beyond Inheritance, Our
Speaker 1: Ever Mutating Cells and a New Understanding of Health.
Speaker 2: So, without any.
Speaker 1: Further ado, here she is Roxanne Camsie.
Speaker 2: Well, Roxanne, thank you so much for joining me today.
Speaker 3: Thank you. Garrett's great to be here.
Speaker 1: I always love to talk to a veteran science journalist,
Speaker 1: especially one who writes a full length book, because I
Speaker 1: don't know I struggle. Man. I don't know how you
Speaker 1: do it. It's so much work. Does it come easy
Speaker 1: for you? Or was it like a real slog?
Speaker 3: And I always wanted to write a book that that
Speaker 3: was one of my goals when I was growing up.
Speaker 3: I think part of it, you know, I think, you know,
Speaker 3: like as you get older, you realize how And I've
Speaker 3: been doing science journalism for two decades, so I feel
Speaker 3: like I can kind of say say something with that
Speaker 3: kind of statement. But I do feel that you understand
Speaker 3: how much just wanting to do something and feeling like
Speaker 3: the idea comes to you and you have to really
Speaker 3: run with it is a large part of what keeps
Speaker 3: you going through it. And I was really curious what
Speaker 3: it would be like because this was a topic that
Speaker 3: I felt I couldn't do in just a magazine feature.
Speaker 3: This idea in this book is about how our DNA
Speaker 3: changes every single day of our lives. And there were
Speaker 3: a bunch of different scientists from a different fields that
Speaker 3: were coming to the same conclusion, but just like really
Speaker 3: not talking to one another, not understanding how this idea
Speaker 3: has been percolating throughout decades of history. So I felt
Speaker 3: like there's no way to do that in five thousand
Speaker 3: words or ten thousand words. It's really an idea you
Speaker 3: want to sit with and like peel apart like an onion.
Speaker 1: Yeah, And for some journalists who are writing long form,
Speaker 1: when they finally write the book, they're like, oh, I
Speaker 1: had this one piece, or I wrote multiple pieces and
Speaker 1: I was able to kind of synthesize, but add to it.
Speaker 1: Have you nibbled around the edges of this in any
Speaker 1: of your publications in magazines or is this the first time?
Speaker 3: So I went to Florida in twenty seventeen and I've
Speaker 3: gotten this tip from a scientist that there was like
Speaker 3: this interesting stuff going on in the field of cancer,
Speaker 3: where you know, they're basically getting the idea that like
Speaker 3: it's not just one or two mutations that causes cancer
Speaker 3: to form in your body, it's a whole bunch. And
Speaker 3: then there's like sometimes even like what's called a big
Speaker 3: bang of mutations in the cancer. So there's like thousands
Speaker 3: of mutations in one person's tumor. And then there were
Speaker 3: these scientists that the Moffit in Tampa, Florida, and they
Speaker 3: they were trying to understand how they could like play
Speaker 3: cancer cells against one another by removing and restarting therapy
Speaker 3: at like specific intervals. So like they'd take away the
Speaker 3: drugs that were giving these patients with prostate cancer and
Speaker 3: like let the drug sensitive cells like grow faster than
Speaker 3: the drug resistance cells, and then they'd hit the cancer
Speaker 3: with the treatment and like be able to knock out
Speaker 3: more of it using that approach. So just kind of
Speaker 3: just the way in the wilderness, like certain animals compete
Speaker 3: against one another for like resources. They were taking that
Speaker 3: idea and applying it to the cancers to help this
Speaker 3: essentially the cancer cells with the less worse mutations take over.
Speaker 1: And so how did you even start thinking about that?
Speaker 1: Like how did you even get to the place where
Speaker 1: this was on your mind?
Speaker 3: Oh? Well, yeah, so I didn't finish that thought really,
Speaker 3: So like that was that was from a tip from
Speaker 3: a scientist who was like, hey, like cancer biologists are
Speaker 3: really taking this idea of like evolution in the body
Speaker 3: like is happening, and we can leverage it. But then
Speaker 3: when I came back, I was like looking at research
Speaker 3: papers for another part of my job at the time.
Speaker 3: I was in addition to like writing for you know, Wired,
Speaker 3: where I published that story and the new York Times
Speaker 3: magazine is like a freelance journalist. I had a day
Speaker 3: job as an editor at a research journal called Nature Medicine,
Speaker 3: and I was like doing a news roundup and I
Speaker 3: found this paper that was talking about how mutant blood cells,
Speaker 3: so cells that are acquired mutations in the blood were
Speaker 3: linked to an increased risk of heart disease and stroke.
Speaker 3: And I was like, well, that's that's different from cancer.
Speaker 3: Like I knew that we could acquire mutations as we
Speaker 3: grow older, but I didn't know that that caused more
Speaker 3: than cancer. And then I was just like dug around
Speaker 3: and I found out, Okay, well it's not just like cancer.
Speaker 3: It's not just heart disease. It's also like epilepsy, it's
Speaker 3: like Alzheimer's, it's liver conditions. Like all sorts of mutations
Speaker 3: can pile up in the body, and ultimately it's probably
Speaker 3: the main driver of aging, or potentially a large driver
Speaker 3: of agent. Just the idea that we rack up errors
Speaker 3: in our DNA over time and they stay in ourselves
Speaker 3: because it's easy to get a mutation, but it's hard
Speaker 3: to like erase it. So I just I saw these
Speaker 3: threads coming together and I was like Okay, Like I
Speaker 3: got to pitch this as a book, and I wrote
Speaker 3: it and I recorded the audiobook, and I feel kind
Speaker 3: of like, I feel like I needed to spend time
Speaker 3: with it and to really dig into the historical archives
Speaker 3: and find how this idea has just like been like
Speaker 3: over a century in the making, and why we're we're
Speaker 3: going to be talking about it so much more in
Speaker 3: the future.
Speaker 1: Well, and also just why not many people are talking
Speaker 1: about it. I mean, even as you're introducing this concept,
Speaker 1: and you know, my bias is that I now work
Speaker 1: as a psychologist in a cancer center in addition to
Speaker 1: doing you know, the public science communication that I continue
Speaker 1: to do, I can't help but think, Okay, what you
Speaker 1: were describing, Like, gosh, I don't even phrase this question
Speaker 1: with regards to other disease states.
Speaker 2: How now, how do we define cancer?
Speaker 1: Right?
Speaker 3: Yeah? Like, yeah, Well, I mean that's the thing. It's
Speaker 3: like a lot of the scientists when they talk about
Speaker 3: mutant cells, they have to kind of preface it by saying, Okay,
Speaker 3: these are like these.
Speaker 2: Are non.
Speaker 3: Non malignant, but like non cancer cells, but there are
Speaker 3: mutant cells in the body. And it's interesting because you know,
Speaker 3: you talk about cancer patients and you know psychology and
Speaker 3: there you're talking about. You know, obviously with cancer there's
Speaker 3: mutant cells that drive like that, like growth, and also
Speaker 3: oftentimes the resistance to the chemotherapy and all the treatments
Speaker 3: and blood vessels and yeah, yeah, there are a lot
Speaker 3: of things they do are like rewiring themselves essentially. But
Speaker 3: then on top of that, it's interesting because then you're
Speaker 3: also hving psychology in the brain and you know, there
Speaker 3: is that sense of DNA change. We know that happens
Speaker 3: in our bodies that causes cancer, but like you're saying,
Speaker 3: like a lot of people haven't yet really fully understood
Speaker 3: that even the healthy quote unquote healthy cells in our bodies,
Speaker 3: in our brains, for example, we're picking up trillions of
Speaker 3: mutations every day. Like by the time a person is
Speaker 3: one hundred years old, they've looked at centenarians and they've
Speaker 3: taken cells from their blood and they've found that, you know,
Speaker 3: there's around three thousand mutations in a given cell that
Speaker 3: aren't all in the other parts of the body. So
Speaker 3: you know, we're just kind of every day our cells
Speaker 3: through wear and tear break, their DNA breaks, and like
Speaker 3: we have DNA repair enzymes, but they don't always do
Speaker 3: a perfect job. I like to say they're human too, right,
Speaker 3: So if a mistake's made in the patching up, it
Speaker 3: just carries to all the daughter cells. So see, I
Speaker 3: do think that this is something important for people to understand,
Speaker 3: not just on a metaphysical like you know, meaning of
Speaker 3: the universe thing where you and I are having this
Speaker 3: conversation and our brain cells are mutating even as we're talking,
Speaker 3: but also to understand like what it does mean for
Speaker 3: cancer treatment, what it does mean for the diagnosis of
Speaker 3: diseases like heart disease, and our risk factors for these things.
Speaker 3: So I'm kind of on a mission for people to
Speaker 3: get the idea that our biology is just like much
Speaker 3: more dynamic than they might have traditionally thought.
Speaker 1: Yeah, and so I feel like there's so many different
Speaker 1: ways to approach this, you know. I think, just as
Speaker 1: questions pop into my head, I'm going to approach it
Speaker 1: in the most nonlinear way possible and see if anyone
Speaker 1: can follow. But one of the questions that comes up
Speaker 1: right at the top is maybe we can talk.
Speaker 2: A little bit about like what is a mutation?
Speaker 1: What happens in our body when our genetic material does mutate,
Speaker 1: and like, what are some of the checks and balances,
Speaker 1: Because obviously you mentioned before like when there are times
Speaker 1: where the error correction does doesn't work, or where the
Speaker 1: like the load is too high, it may be passed on.
Speaker 1: But there are plenty of times where you know, mutations
Speaker 1: are happening all the time, and our cells are really
Speaker 1: good at correcting that, right.
Speaker 3: Yeah, absolutely, yeah, Well they're good at correcting certain like
Speaker 3: so mutations kind of I mean, if a scientist might
Speaker 3: consider a distinction between DNA damage and mutation, I don't
Speaker 3: because I think that ultimately the lay people kind of
Speaker 3: understanding them is the same thing. So it's a scientists mind.
Speaker 3: A mutation is usually when like there are let's just
Speaker 3: back up for a second. Our DNA in each of
Speaker 3: our cells is comprised of these essentially letters, like scientists
Speaker 3: will call them nucleotides, but they're actg for all intents
Speaker 3: and purposes here and there's three billion If you line
Speaker 3: up all the DNA in a given cell of yours,
Speaker 3: there be like three billion of the string of like
Speaker 3: three billion letters if you lined it all up together.
Speaker 3: And so imagine having to copy that every time you
Speaker 3: make a new right, they copy the DNA into the
Speaker 3: new cell. If I gave you a book with three
Speaker 3: billion letters and I was like, Kara, like write this
Speaker 3: all down with a pen, I mean, I trust in
Speaker 3: you very deeply, but I also think you like me,
Speaker 3: would probably accidentally, like if it was like attcg like
Speaker 3: maybe you'd say att, I don't know GCCC, I don't know,
Speaker 3: like you know, like there's.
Speaker 1: Yeah, like i'd switch some or some would get left out,
Speaker 1: or I might add a line somewhere on accident, and.
Speaker 3: I shouldn't put it on you. Let's talk about it.
Speaker 3: If I were to do this, I would make right
Speaker 3: so so even in just the copy and like, oh,
Speaker 3: we have so much cell turnover. So a mutation in
Speaker 3: this sense would be like if we did make if you,
Speaker 3: you are or me one of us made, or you
Speaker 3: or I made like an error in the copying, that
Speaker 3: would be considered a mutation. Because when the when the
Speaker 3: the next cell would like go on to like read
Speaker 3: that instruction booklet right of DNA to make the proteins
Speaker 3: that needs to process I don't know sugar or like
Speaker 3: I don't like run some kind of oration in the cell.
Speaker 3: It would it would kind of go to that gene
Speaker 3: and all of a sudden be like wait a second,
Speaker 3: like this gene this isn't working because there's an error.
Speaker 3: So that's when you get in trouble with mutations that
Speaker 3: they can happen in parts of the DNA that like
Speaker 3: don't have an effect, right or that cell might die,
Speaker 3: in which case, no biggie, it might happen somewhere where
Speaker 3: it does matter.
Speaker 1: And so oftentimes when it does happen, because like it's
Speaker 1: gonna happen, because that's just the nature of being alive,
Speaker 1: there are like mechanisms in place to like find it
Speaker 1: and either like you mentioned, kill that cell so that
Speaker 1: it doesn't wreak havoc or do some type of correction
Speaker 1: so that there's not a big downstream effect.
Speaker 3: But there are like error correction mechanisms in the cell.
Speaker 3: But it kind of works better where there's like a
Speaker 3: big mistake. The cell can spots when it's something where
Speaker 3: like there's a single letter change, and again that's kind
Speaker 3: of where we're talking about DNA breaks, which the cell
Speaker 3: is like easier, it's easier for them to recognize. But
Speaker 3: if it's just like one letter's wrong, I mean again,
Speaker 3: going back to the book. It's like, imagine if I
Speaker 3: like forgot, Like if there's like a paragraph and I
Speaker 3: pressed return in the middle of the paragraph, your eyes
Speaker 3: could like spot that. Yeah, But if I changed like
Speaker 3: H to C in a word like hat to cat, like,
Speaker 3: you might be like less able to catch that mistake.
Speaker 3: And yet a single letter changed like that can have
Speaker 3: huge effects. Like there are many, many, many inherited disorders,
Speaker 3: for example, where somebody's life is just truncated because of
Speaker 3: a single letter that's wrong, and it's uh. One of
Speaker 3: the injustices I think of our biology is that, like
Speaker 3: it's so fragile in some ways.
Speaker 1: Yeah, And so there's these examples like you mentioned, where
Speaker 1: there are mistakes, mutations, damage to DNA that get passed
Speaker 1: down generation to generation, especially in situations where maybe the
Speaker 1: symptoms don't come into later in life after somebody's already
Speaker 1: had kids, or situations where you only have like a
Speaker 1: one in four chance of getting that they tend to
Speaker 1: continue throughout the population.
Speaker 2: But there are other.
Speaker 1: Examples, as you mentioned before, where your own DNA is
Speaker 1: damaged throughout the life span due to mutagens, carcinogens, things
Speaker 1: like that, and then disease states can occur within a
Speaker 1: single life span as well.
Speaker 3: Right, Yeah, So part of my mission is to kind
Speaker 3: of reframe even how we hear the words genetic disease.
Speaker 3: Like I meant, you and me, if we had this
Speaker 3: conversation ten years ago and we said genetic disease, we
Speaker 3: would automatically think inherited disease inherent Oh I still do.
Speaker 1: I definitely think heretically when you say, yeah, genetic disease.
Speaker 3: Okay, So you know, we think about things like cystic bibrosis,
Speaker 3: where severely tragic disease where there's like you know, like
Speaker 3: a mutation that will disturb how cells kind of their
Speaker 3: channels work to move stuff around and what happens. Ultimately
Speaker 3: it affects different organs, but the lungs are primarily affected,
Speaker 3: where you are just more prone to these infections that
Speaker 3: you and I would not need to worry about assuming
Speaker 3: you don't have CF. Like a little asterix there, which
Speaker 3: is like there's these new drugs that have come that
Speaker 3: have completely changed the disease so that ninety percent of
Speaker 3: people with CF now have this great solution where essentially
Speaker 3: they can correct the gene function. But let's think about
Speaker 3: you know, that's an exception, A lot of these diseases
Speaker 3: don't yet have these easy to take medications. I'm getting
Speaker 3: a little sidetracked, but just to say that, like CF
Speaker 3: sickle cell does these muscular dystrophee. People probably heard some
Speaker 3: of these name Tay Sachs, PKU, like all these different
Speaker 3: inherited disorders where maybe like there's a metabolic error, they're
Speaker 3: they're generally things that have been passed generations, right. They
Speaker 3: c F has traced back thousands of years to Assistic
Speaker 3: fibrosis is traced back thousands of years to Europe. Some
Speaker 3: of the some of the mutations right for.
Speaker 1: Then you mentioned Tay Sachs. Like anybody who has done
Speaker 1: a DNA test and knows that they are predominantly Ashkenazi
Speaker 1: inherited in their heritage and is partnering with somebody who's
Speaker 1: ashkan Nazi, they'll often do a lot of genetic counseling
Speaker 1: before even deciding to have children, right, because there are
Speaker 1: genetic diseases that are so prevalent within that population.
Speaker 3: And these are just you know, like you say, like that,
Speaker 3: you can look in the family tree and you can
Speaker 3: just find a bunch of people affected by these because
Speaker 3: they are passed down. Now, now, genetic disease is not
Speaker 3: always inherited, like like you alluded to. In my book,
Speaker 3: I talk about how it could happen at any point,
Speaker 3: like anytime after for example, like the sperm and the
Speaker 3: egg that may do came together, and there's a lot
Speaker 3: of cell division that happens at the embryo development stage.
Speaker 3: I'm kind of laughing as I'm saying this because I
Speaker 3: have a son, and when I was pregnant with him,
Speaker 3: I kept, you know, all women who are pregnant are
Speaker 3: just get so thirsty. We're like drinking water all the time.
Speaker 3: And it's partly because like there's a lot of cell
Speaker 3: division that's happening, and you it's like very energetically intensive,
Speaker 3: it's very rapid. And I say this because, like imagine
Speaker 3: I asked you to I gave as I care here,
Speaker 3: like take this book and copy it like letter for letter,
Speaker 3: and you have let's say it's a two hundred page book,
Speaker 3: and I can give you six months. Okay, that's like
Speaker 3: basically the cell turnover of an adult. It's approximate. But
Speaker 3: then if I said I'm going to give you two
Speaker 3: days to do it, that's kind of what's going on.
Speaker 3: When it's early embryonic development, things just happen faster. The
Speaker 3: copying happens faster, and so I think, you know, there's
Speaker 3: a lot of errors that can happen, and they do,
Speaker 3: and so genetic disease can happen when embryonic cells acquire
Speaker 3: a mistake because the DNA was like there was a
Speaker 3: mistake in the in the replication, or it can happen.
Speaker 3: You know here what you and I are sitting, we
Speaker 3: might have a mutation that crops up in us that
Speaker 3: is pathogenic, could cause cancer, or it could cause could
Speaker 3: cause good things. I mean, my book also talks about
Speaker 3: how we rely on mutation to survive, and like as
Speaker 3: we get older, you know, one or to two out
Speaker 3: of every I always get this number. I want to
Speaker 3: get this right. It's like one out of every five
Speaker 3: or one out everyvery ten people seventy years or older
Speaker 3: has a threshold level of these mutant blood cells that
Speaker 3: have kind of just happened to accumulate over their lifespan
Speaker 3: that can double their risk of heart disease or double
Speaker 3: their risk of str So it's common. It's common, Like
Speaker 3: men don't know it, but like by the time men
Speaker 3: are in their seventies, like forty to fifty percent of
Speaker 3: them have a substantial number of their blood cells missing
Speaker 3: the Y chromosome or cells in their blood I should say,
Speaker 3: because red blood cells don't have a nucleus, but like
Speaker 3: other cell like white blood cells, like they're just they
Speaker 3: just tend to lose their Y chromosome as they get older.
Speaker 1: It's already so small, it's not a lot there to
Speaker 1: lose compared to the X.
Speaker 2: That's a sure.
Speaker 3: Yeah, I'm not gonna cry too many tears about this,
Speaker 3: but and it's interesting because people are like, so what well,
Speaker 3: loss of why? And also, by the way, there is
Speaker 3: loss of X two because women have two X chromesales
Speaker 3: and they do tend to lose an X chromosome as
Speaker 3: we get older, but it's less because we have like
Speaker 3: a backup. It's less fucky, less intensive. But we just
Speaker 3: don't know as much because of course they haven't studied
Speaker 3: women as much as they've studied men.
Speaker 2: Of course, shocker.
Speaker 3: But the loss of why, which has been better studied,
Speaker 3: is linked to like a whole host like risk of
Speaker 3: Alzheimer's is up, risk of cancer is up. But the
Speaker 3: thing is, it's not clear whether it's causal. It might
Speaker 3: there might be something upstream that's causing both loss of
Speaker 3: why and the risk of these other things. So, you
Speaker 3: know a lot of stuff happens as we age, you
Speaker 3: know with our DNA.
Speaker 1: Yeah, yeah, and our risk factors for most diseases increase
Speaker 1: as we age. But probably there's well, I mean this
Speaker 1: is just absolute conjecture, but probably the diseases that we
Speaker 1: have best linked to DNA damage and mutagens have a
Speaker 1: higher kind of increase in risk the older that we get.
Speaker 3: Well, the thing is is that they've actually started linking
Speaker 3: these increased DNA change, that the increase in mutation to
Speaker 3: the diseases of aging. Right, So it's not just that
Speaker 3: you have a higher risk of mutant cells linked to
Speaker 3: a higher risk of heart disease. They've now shown with
Speaker 3: like mouse studies and cell studies in the lab, that
Speaker 3: those mutant cells are like able to induce more inflammation
Speaker 3: or respond with a more inflammatory response, probably because of
Speaker 3: the mutation that they've acquired. It's often in certain genes
Speaker 3: like tettoo, and so heart disease is a disease of inflammation,
Speaker 3: like alphosclerosis. That's one like blood cells I SAR bloodvessels.
Speaker 3: It's like an inflammatory disease. So the idea is like
Speaker 3: the DNA change has gone haywire, kind of boost the
Speaker 3: inflammation in your body that then precipitates these diseases of aging.
Speaker 3: It's kind of right, it's somewhat speculative. I know, you're
Speaker 3: you're You've come from a data perspective, a skeptic perspective,
Speaker 3: So I'm careful here and saying none of this is definitive.
Speaker 3: But the evidence increasingly looks like it's it is. There
Speaker 3: are connections here.
Speaker 1: I mean, it does kind of make sense, even though
Speaker 1: it is a pretty intense, I guess paradigm shift for
Speaker 1: a lot of people to move into. But even and
Speaker 1: maybe it's because I don't have very specialized knowledge in
Speaker 1: these areas. I could see people who are like the
Speaker 1: most specialized being the most resistant sometimes to changing their
Speaker 1: gestalt thinking. But you know, anybody who has been studying aging,
Speaker 1: anybody who has been studying the relationship between these different
Speaker 1: diseases of aging, has probably noticed mutagens or mutations damage
Speaker 1: to DNA across the spectrum in the lab. But it's
Speaker 1: probably been kind of hard to put their finger on
Speaker 1: the relationship, right is it that the older we get,
Speaker 1: the more our DNA damages and that causes these diseases,
Speaker 1: or do these diseases cause downstream damage to or DNA.
Speaker 2: It's probably hard to know.
Speaker 3: I mean, there's definitely there's definitely that question. But because
Speaker 3: they can do some of this stuff in like mouse
Speaker 3: models now, and they can they can do functional essays,
Speaker 3: they can do tests that kind of show how to
Speaker 3: connect the dots. And also because there are people that
Speaker 3: are at the extremes of this. So, like I write
Speaker 3: in the book about Werner's syndrome, and so I mentioned
Speaker 3: in a particular case where I spoke to the son
Speaker 3: of Michael Prescott, and Michael Prescott he he's a fantastic individual.
Speaker 3: I never got a chance to speak with them directly,
Speaker 3: but his son told me how. Like, so, Michael Prescott
Speaker 3: got his first heart attack in his thirties. I think
Speaker 3: it was on his son's like fourth birthday, maybe I
Speaker 3: can't recall, on one of his thirties, Yeah, this thirties,
Speaker 3: and then he had like four other heart attacks in
Speaker 3: the same year, and then like all these health things
Speaker 3: started start getting cataracts, like his hair went gray. His
Speaker 3: son has said that by the time he was in
Speaker 3: his early forties, taking him to like baseball games, everybody
Speaker 3: assumed that Michael was his son's grandfather. He looked like
Speaker 3: in his sixties and his and this doctor think, we're
Speaker 3: at Vanderbilt, like not like a great and it was
Speaker 3: a great institution, not something not like a small small
Speaker 3: town like rural. Yeah, rural. You know, nothing against any
Speaker 3: small town hospital. But they couldn't figure it out. And
Speaker 3: so he would sit in this recliner in like the
Speaker 3: evenings in the living room, just like reading research papers.
Speaker 3: I'm sure it'd be different now, like you'd probably ask
Speaker 3: chat GPT and have an answer in two minutes. But
Speaker 3: he had to look through the research literature at the time.
Speaker 3: And he ultimately went to his doctors and he said,
Speaker 3: I think I have this thing, and they tested him
Speaker 3: and they're like, you're so right, like this explains everything.
Speaker 3: And what he had was Werner syndrome, where essentially you
Speaker 3: age super rapidly. Unfortunately, he died in his mid fifties,
Speaker 3: which is exactly what happens in most cases, and what
Speaker 3: happens in Warner syndrome is you have just like a
Speaker 3: rapid accumulation of mutation. So so there's all this evidence
Speaker 3: piling up that mutation and and aging as length. I
Speaker 3: also talk in the book about like zoo animals that
Speaker 3: have been like examined and like they looked at giraffes,
Speaker 3: everything from giraffes to zebras, and then also like mouse
Speaker 3: and cat and dog, you like human tissue, and they
Speaker 3: found that, like when somebody, when animals live to their
Speaker 3: life like maximum life span, it seems that like no
Speaker 3: matter how shorter long they live, they end up with
Speaker 3: like three thousand mutations in their in their gut cells.
Speaker 3: So so the idea is that like the animals like
Speaker 3: the mouse that lives shorter just mutate faster, and the
Speaker 3: ones that mutate slower live longer. So the maths math,
Speaker 3: I think it's as the young people are the math
Speaker 3: Did I use that right? I think I think so.
Speaker 2: I don't don't ask me. I'm not a young person.
Speaker 2: It sounds good to me, but it does.
Speaker 1: Kind of beg an interesting question that I've always wondered.
Speaker 1: And I don't know if there is an answer to
Speaker 1: this question. But you know, let's say we're talking about
Speaker 1: something as I don't want to say straightforward it as cancer.
Speaker 1: Cancer is in no way straightforward. But where the relationship
Speaker 1: between mutation and DNA damage and you know, cancer diagnostics
Speaker 1: and symptomatology is.
Speaker 2: I guess fleshed out pretty well.
Speaker 1: I've always wondered is it a threshold response? Like is
Speaker 1: it that because we know that there are people who
Speaker 1: have mutations to their DNA before they're ever born, like
Speaker 1: they have disrupted oncogenes or tumor suppressor genes that will
Speaker 1: cause it to be easier for them to get cancers.
Speaker 1: Why there's such a thing as childhood cancer. And then
Speaker 1: we know that there are people who are exposed to
Speaker 1: intense you know, mutagens like astronauts or people who smoke
Speaker 1: cigarettes their entire life, or you know, people who are
Speaker 1: exposed to environmental toxins who are just like experiencing large
Speaker 1: scale damage to their DNA. But of course we've all
Speaker 1: heard the story of the woman who smoked her entire
Speaker 1: life and never got cancer, and we've all heard the
Speaker 1: stories of people who were just like so unlucky. Is
Speaker 1: it about the load? Is it about all of these
Speaker 1: I mean, like algorithm for.
Speaker 3: The Rolling Stones? Why is my why is my mind blinking?
Speaker 3: I read his autobiography and it was amazing. This is
Speaker 3: embarrassing too.
Speaker 1: Oh I have to google that, so don't worry about that.
Speaker 1: Oh my Jagger, duh Jagger Keith Richards, Jagger, Keith Richards
Speaker 1: amazing autobiography.
Speaker 3: Like, wow, what a book. Uh, people don't want to
Speaker 3: read my book, they should read that book too. So
Speaker 3: I mean, how is he Like he's like the epitome
Speaker 3: right of like living a hard life, and he seems
Speaker 3: to be doing great right right, and so you know,
Speaker 3: drugs and rock and roll did pretty fine by him.
Speaker 3: So yeah, I mean it's funny because I'm also working
Speaker 3: on a piece right now for The Atlantic about how
Speaker 3: people with like mutations that should be fatal are still alive.
Speaker 3: Like there is some question that hangs about this. It's
Speaker 3: interesting they mentioned astronauts, by the way, because in my
Speaker 3: book I talk about how astronauts actually do have more
Speaker 3: mutant blood cells than the average person or the average
Speaker 3: person of their age.
Speaker 1: So yeah, they're like not shielded up there, right, They're
Speaker 1: they're getting hit. I mean, even flying in a plane
Speaker 1: is not great, and they're like extra flying elon musk.
Speaker 3: Maybe that would be a wait again, I'm thinking about
Speaker 3: living on board.
Speaker 2: No, let's just get him to go to make that
Speaker 2: can be the guy. I'll be fine.
Speaker 3: Totally that too.
Speaker 2: But yeah, I have always wondered, is it is there
Speaker 2: a threshold? Is there an unwritten threshold?
Speaker 1: And maybe it's different for different people where you know,
Speaker 1: they cross into the rubicon and all of a sudden, Okay,
Speaker 1: now it's Alzheimer's, now it's cancer, and now it's these
Speaker 1: other things, but up until then.
Speaker 3: It's not. It's a really it's a really profound question.
Speaker 3: It's like a very deep question. So I think that
Speaker 3: it's like pause and appreciate how how important it is.
Speaker 3: Because even people, for example that you know, I said,
Speaker 3: one to two out of every ten people in their
Speaker 3: seventies have these specific kind of like mute cells in
Speaker 3: their blood that are linked to heart disease and linked
Speaker 3: to cancer. But not everybody is getting heart disease and
Speaker 3: cancer that has these mute blood cells. I think maybe
Speaker 3: scientists might suggest that, like there is a certain amount
Speaker 3: of vigilance in like fromadian system about like clearing out
Speaker 3: cells that seem to be bad actors. I don't know
Speaker 3: if that's the reason why. I mean, some of it
Speaker 3: just could be bad luck. Good luck luck is kind
Speaker 3: of a tricky term in biology, right, because there's always
Speaker 3: something determining it, Like there's mechanism, but it just might
Speaker 3: be so small scale that we'll never really find out.
Speaker 3: But you know, like on the larger scale of things.
Speaker 3: I know, I personally, after having written this book, have
Speaker 3: changed some behaviors just because it's it's kind of like
Speaker 3: at the end of the day, you can you might
Speaker 3: not be able to determine your health, but you can
Speaker 3: stack the odds more in your favor. So sleep is
Speaker 3: extremely It's like it seems to be very well established
Speaker 3: to like lower the prevalence or risk of mutant cells
Speaker 3: in your blood mutes. And of course I keep talking
Speaker 3: about the blood because it's easy to sample, like it's
Speaker 3: kind of hard.
Speaker 2: Right, because that's what you're going to see in research studies.
Speaker 3: Yeah, right, yeah, I mean I don't want someone coming
Speaker 3: to take my brain cell, like, you know, I got
Speaker 3: my right level check. They could took my arm and
Speaker 3: took my blood, like I don't really want them to
Speaker 3: take my brain cells. Who knows how many I have left,
Speaker 3: you know.
Speaker 1: So oh yeah, I was just talking to my neurologist
Speaker 1: about that the other day, you know, like I take
Speaker 1: prozac and it works really well for me. But I
Speaker 1: also have this like weird neurological sleep disorder called IH,
Speaker 1: and I actually have these crazy meds so that I
Speaker 1: like am awake enough during the day. It's like similar
Speaker 1: to type two narcolepsy. And I was talking about how
Speaker 1: once these or rex and drug this is so.
Speaker 2: Yeah about her here north arap But yeah, okay, so
Speaker 2: anybody listening this may apply. If not, don't worry. Just
Speaker 2: I'll be past this in a second.
Speaker 1: But once these new ORX and drugs are on the market,
Speaker 1: I'll be so curious to see how well I respond
Speaker 1: to them, because ultimately it's anybody's guess. Why you know
Speaker 1: I have IH? Is it that I don't make enough
Speaker 1: or rex and is there something wrong with my gabba?
Speaker 1: The only way to know is for somebody to do
Speaker 1: like a spinal tap, And I'm like, not worth it.
Speaker 3: I mean, I just nuture where you'd be, you'd be
Speaker 3: able to get better diagnostics. Like I don't know exactly how,
Speaker 3: but like I do think that as we get better
Speaker 3: on like eavesdropping on cells, even with cancer, right, there's
Speaker 3: like yeah, circulating tumor DNA that the people can just
Speaker 3: get like pick up all.
Speaker 1: My patients are doing that now. It's amazing how many
Speaker 1: even since I started in this field to now how
Speaker 1: many more patients are using these They're like these startup
Speaker 1: companies where they can detect the tiniest amounts of DNA
Speaker 1: and their blood and see if their tumor markers are
Speaker 1: going up or down long before they see anything on scans.
Speaker 3: And so yeah, for people that are listening that might
Speaker 3: not know what's circulating, tumor DNA like to tumor cell
Speaker 3: DNA is about it's like it's it's like not necessarily
Speaker 3: not going for a biopsy into the tumor. You're just
Speaker 3: picking up what they're spewing out into the blood when
Speaker 3: they die, you know. So on cells die, they they
Speaker 3: release their DNA and you can just eavesdrop. It's like
Speaker 3: almost like looking gosh, I sound like I don't do this,
Speaker 3: but like if you want to find out what's going
Speaker 3: on at your neighbor's house, you can lose look through
Speaker 3: their trash. They're just like spewing it out there, right.
Speaker 2: That's a good way to put it.
Speaker 1: Or like the environmental DNA research where people are like collecting,
Speaker 1: you know, from an elephant footprint to see what ecologically
Speaker 1: is living in there or like you.
Speaker 3: Know, than like looking through your neighbor's trash. But yes, so,
Speaker 3: but going back to what we were talking about, trying
Speaker 3: to trace this back to we're talking about the brain.
Speaker 3: Oh yeah, I do think that, Like, and the thing
Speaker 3: about the brain is like oftentimes the things you're talking about,
Speaker 3: like sleep regulation, these are like very small clusters of
Speaker 3: neurons having this kind of like weight like stuff. Like
Speaker 3: I'm so fascinated always with the there's a theory about
Speaker 3: our weight is kind of we have a set point
Speaker 3: in our brains that like tells our body like how
Speaker 3: much to weigh. And we're talking about like clusters of cells,
Speaker 3: like we're not talking about like giant golf ball sizes
Speaker 3: of tissue. So it's hard. The reason I'm saying that
Speaker 3: it's like it's much harder to sample. I don't want
Speaker 3: someone going and biop seeing these cells because they can
Speaker 3: that's too small a region. But maybe we could figure
Speaker 3: out a way to eavesdrop on what mutations are happening there,
Speaker 3: or do some imaging that's like informed by some mouse
Speaker 3: studies that show when you have mutations there's a certain
Speaker 3: structural distinction, like who knows.
Speaker 1: And precision medicine is like such an obvious outcome of
Speaker 1: this type of sampling which we're seeing, you know, kind
Speaker 1: of starting in research settings definitely, Like in the cancer
Speaker 1: world we mentioned there are these these uh, I guess
Speaker 1: surveillance approaches that allow for the tiniest amount of genetic
Speaker 1: material to be found in the blood. But think about
Speaker 1: like psychiatry for example, like why does prozac work on
Speaker 1: me when like cetallogram makes me feel like shit?
Speaker 2: Right, we might be able to figure that out later.
Speaker 3: Like if I take Allegra, I'm like, probably I should
Speaker 3: be in Allegra sales. If anyone's sort of Allegra listening,
Speaker 3: I will be like, you're sales promoter or whatever. But
Speaker 3: if I take a Zertec or you know, like I'm
Speaker 3: just done. I can't function for weeks. And there's certain
Speaker 3: people that are like more sensitive to Zertech than and
Speaker 3: so yes, I do hope that one day we'll be
Speaker 3: able to have more of like the pharmacogenetic insight. But
Speaker 3: I guess that strays a little far from my main
Speaker 3: message here, which is like, even if I'm not sensitive
Speaker 3: to something today, my immune system might change because I
Speaker 3: mutation and I might be sensitive heat tomorrow. So part
Speaker 3: of the thing I want to emphasize is like we
Speaker 3: have to give ourselves grace. Like a lot of the
Speaker 3: time we're trying to figure out like who we are,
Speaker 3: like what our bodies are doing, and then all of
Speaker 3: a sudden, I don't know, you find out you're allergic
Speaker 3: to something, but you could eat it before, Like what's
Speaker 3: going on? Well, our bodies change, like cells turnover, DNA changes,
Speaker 3: And my message is like we got to kind of
Speaker 3: get our arms around that whole concept.
Speaker 1: And so you know, this maps really well, I think
Speaker 1: in a lot of ways to the research that we're
Speaker 1: constantly talking about on another podcast I work on, the
Speaker 1: Skeptics Guide the Universe, Will Well, you know, we covered
Speaker 1: different science stories every single week, and very often we'll
Speaker 1: be saying, oh, you know, based on the you know
Speaker 1: whatever uk Biobank data, new researchers have you know, gotten
Speaker 1: into this big database and they've learned that this is
Speaker 1: how many steps you want to walk a day, or
Speaker 1: they've learned that like this is how many vegetables you know,
Speaker 1: on average people would eat, and then it has this
Speaker 1: downstream effect on what we always are calling all cause mortality, right,
Speaker 1: because it's like the broadest way to measure people who
Speaker 1: did this died, you know, later than people who did that. Yeah,
Speaker 1: and so what are those things that helped me not
Speaker 1: die as soon? And obviously when you drill into research
Speaker 1: like that, there are a million nuances and a thousand variables.
Speaker 1: But it does make me wonder how much underlies you know,
Speaker 1: how much of this really is what's going on with
Speaker 1: our DNA, with all of these behavioral changes that have
Speaker 1: all cause mortality effects.
Speaker 3: Yeah, And by the way, I was just gonna I
Speaker 3: was just gonna say, although I love me a good
Speaker 3: uk Biobank study that out as the example, all roads
Speaker 3: lead back to this uk Biobank, which of course is
Speaker 3: like right, okay, like decided to get really serious about
Speaker 3: getting like DNA sequences from a bunch of people in
Speaker 3: they're just like, you've got a huge repository analysis. But yeah,
Speaker 3: your question about like how much of variants in our
Speaker 3: fate is due to d our DNA and also the
Speaker 3: DNA mutation that happens in us, And I think the
Speaker 3: answer is like a lot more than we have appreciated
Speaker 3: in the past. And and Yeah, Like when I keep
Speaker 3: going back to that thing I mentioned about how like
Speaker 3: a single blood cell from a centenarian has three thousand
Speaker 3: mutations that aren't found in other parts of the body. Like,
Speaker 3: I just feel like we're going to be talking a
Speaker 3: lot more about how our behaviors do affect our mutational
Speaker 3: rates and like in different ways. So one thing I
Speaker 3: found out as I was wrapping up the book that
Speaker 3: I was able to include is that, you know, so
Speaker 3: first of all, let me just back up and say,
Speaker 3: we've gone from not understanding how much a person mutates
Speaker 3: in the course of LIW life, Like fifteen years ago,
Speaker 3: twenty years ago, we didn't even talk about this, right,
Speaker 3: We've gone from like basically not a lot of data,
Speaker 3: zero data, to like too much data, like data that
Speaker 3: computers will have to crunch to make sense of. Because
Speaker 3: what happened is in two thousand and nine, scientists developed
Speaker 3: ways to get the genetic sequence from individual cells. So
Speaker 3: no longer were they're kind of looking at the bulk
Speaker 3: DNA of the body and making like a general assumption
Speaker 3: about the DNA of a person. All of a sudden,
Speaker 3: you can do like a census and be like, well,
Speaker 3: these cells have this mutation in this person, but these
Speaker 3: cells don't have this mutation in this person. Hmm, like
Speaker 3: something something happened at some point like that is all
Speaker 3: in the last decade really that labs have been able
Speaker 3: to adopt the technology. And so going back for a second,
Speaker 3: like just to say, as I was wrapping up the book,
Speaker 3: they had crunched all of this like almost noisy data,
Speaker 3: Like it's almost noisy, it's so much and found that
Speaker 3: there's actually a different DNA mutation signature in people who
Speaker 3: smoke tobacco versus chew Like the people that chewed tobacco
Speaker 3: have a different mutational pattern than those who smoke it.
Speaker 3: So like we are going to get more granular insights
Speaker 3: into how our behaviors affect our DNA like and that
Speaker 3: is so profound to me, like to us just to
Speaker 3: know that, like what we choose to do. So it's
Speaker 3: kind of like adding a layer like you're talking about,
Speaker 3: like you know, you have a bunch of people, you
Speaker 3: look at their DNA, You've all caused mortality. Now I
Speaker 3: think we're going to have this extra layer that's like Okay,
Speaker 3: they have that baseline genome, but then they're doing these
Speaker 3: behaviors that these are the mutations are finding and that
Speaker 3: that's linked to their mortality.
Speaker 1: Yeah, and like, here's the thing that I'm going to
Speaker 1: start getting a little like philosophical psychological about this, because
Speaker 1: again I'm seeing this through my lens as a health
Speaker 1: psychologist in a large metropolitan cancer center. One of the
Speaker 1: biggest struggles that I have with my patients is the
Speaker 1: why me? What could I have done to prevent this?
Speaker 1: Is it because I didn't eat more vegetables? Is it
Speaker 1: because I wasn't you know, I didn't take that class
Speaker 1: that you know would have kept me more active? And
Speaker 1: so much of the work that we are doing often
Speaker 1: is grappling with the randomness of cancer, the fact that
Speaker 1: cancer is not terribly selective, and that some people like
Speaker 1: you mentioned before it's a loaded term, but are just
Speaker 1: kind of like genetically unlucky. And I'm always worried about.
Speaker 1: While on the one hand, learning more about how our
Speaker 1: behaviors can affect these our DNA downstream I think will
Speaker 1: be very empowering for making choices, I sometimes worry that
Speaker 1: it maps back to the sort of power of positive
Speaker 1: thinking movement, the secret all of this, like, well, you
Speaker 1: manifested this because of some of the choices you made.
Speaker 3: I'm already worried, like I'm or as I was writing
Speaker 3: about this DNA and cigarettes and tobacco and things like that.
Speaker 3: M M, I was already worried about like the first
Speaker 3: paper linking microclastics to mutations, which is it's gonna come right,
Speaker 3: like all the thousands of tiktoks that will launch, Like
Speaker 3: I do. I do think that like what you're saying
Speaker 3: is true, that there's a lot of danger here in it.
Speaker 3: This is walking a super fine line. There's a danger
Speaker 3: that we're going to try to be overly prescriptive in
Speaker 3: like behavioral change based on like very early studies linking
Speaker 3: certain behaviors to certain mutational patterns.
Speaker 1: And judgmental and also prey on people with a lot
Speaker 1: of pseudoscience.
Speaker 3: Well, there's a lot of It's a treacherous where you
Speaker 3: have a lot of people looking to say something about
Speaker 3: biology when it's got to be careful at the same time.
Speaker 3: Like it's funny because I actually wrote my book in
Speaker 3: part to address this y N question, because I did
Speaker 3: want to introduce the idea of randomness to people and
Speaker 3: and for people to make peace with mutation, Like we
Speaker 3: should talk about how it's good for you, because I
Speaker 3: think that's really important. But I also say that, you know,
Speaker 3: the in the two decades I've been reporting on genetics,
Speaker 3: a lot of it has been on rare disease families
Speaker 3: affected by like these genetic mutations that are rare, and
Speaker 3: I feel like there's an other ring of people that
Speaker 3: have really obvious mutations, and I want to make a shirt.
Speaker 3: I should make a shirt this summers like I am
Speaker 3: a mutant because we're all mutants, and I think that
Speaker 3: part of what I'm trying to do is just get
Speaker 3: people to accept that, like living to live is to mutate.
Speaker 3: To mutate us to live. And so what I want
Speaker 3: to say about immunity is like you have to If
Speaker 3: your immune cells don't mutate, you can't make antibodies to
Speaker 3: fight the pathogens you encounter in your life. The engine
Speaker 3: of our immune system is mutation. So I don't know
Speaker 3: if you want to talk about that, but that's a
Speaker 3: super important flip side of all the negative things we've
Speaker 3: been talking about.
Speaker 2: Yeah, I think that one hundred percent that segue is.
Speaker 1: Necessary, especially right now because the way I plan to
Speaker 1: get into it, which God, it just makes me realize
Speaker 1: how old I am, and how long it's been since
Speaker 1: I've been well, I actually did recently finish my PhD.
Speaker 1: But how long it's been since I took a biology
Speaker 1: class because that was in psychology. But I was going
Speaker 1: to bring up how like you know sickle cell, Like
Speaker 1: that's always the example, right, Like sickle cell is like
Speaker 1: this horrific disease and it can cause so much pain
Speaker 1: and so much disability for so many people, but it
Speaker 1: happens kind of as an outcome of good mutations that
Speaker 1: a lot of people are caring that help prevent them
Speaker 1: from pretty debilitating malaria infections. Right, So there's like often
Speaker 1: we do see like two sides of the same coin,
Speaker 1: even within similar genetic mutations. But what I'm hearing from
Speaker 1: you is that, like we got to stop thinking about
Speaker 1: mutation as like putting a moral judgment on it anyway
Speaker 1: or as somehow.
Speaker 3: I mean, it's interesting that earlier question we're like, oh,
Speaker 3: not to get philosophical. I'm like, this is all philosophical.
Speaker 3: It's all like it's all philosophy, Like it's not. It's
Speaker 3: not like it's just like hard science. Like I really
Speaker 3: try to approach this topic through stories like history, stories,
Speaker 3: patient narratives and like, uh and really like the deeper
Speaker 3: philosophy at what all this means? So everybody here remembers
Speaker 3: the COVID pandemic, right.
Speaker 2: We all know, so when was that totally black?
Speaker 3: That so so when our bodies had never seen COVID before,
Speaker 3: Nobody on Earth, no human being on Earth had like
Speaker 3: encountered COVID before. And yet you know, despite the tremendous
Speaker 3: humans human loss, many of us got it and our
Speaker 3: bodies could fight it off. How could they fight a
Speaker 3: disease they had never seen before? How could my immune system?
Speaker 3: And you're I'm assuming you got COVID your immune three times? Yep?
Speaker 3: Oh man, I'm on two, so they're not so uh
Speaker 3: how could our bodies fight it? And the answer is
Speaker 3: our immune cells have something a weird function where their
Speaker 3: DNA can shift around and change a lot. And what
Speaker 3: they do is they they kind of pull a lever.
Speaker 3: You never like the vaguest style like slot what they
Speaker 3: call slot machines that you know, you pull a lever
Speaker 3: and the things spin around and then like you get
Speaker 3: different combinations. That's going on inside our immune cells all
Speaker 3: the time with our DNA. Just imagine the cell like
Speaker 3: pulling a lever, not like an actual lever, but just
Speaker 3: there's functions that switch around the DNA, and what happens
Speaker 3: is you get a different instruction from that sequence, and
Speaker 3: it makes an antibody with a different shape. And so
Speaker 3: it's just constantly making different mutations hoping one will make
Speaker 3: an antibody that's necessary. It's just playing the odds if
Speaker 3: you will, and so much so, so much so that okay, well,
Speaker 3: anytime you get sick, it's like doing this process, right,
Speaker 3: But when you get a vaccine, it also does it.
Speaker 3: So these researchers in New York I write about looked
Speaker 3: at people who had gotten like a booster shot, which
Speaker 3: again further causes more mutation, hence like more benefit. Like
Speaker 3: mutation is good in this instance. There are people that
Speaker 3: can't mutate their immune cells, and they have to live
Speaker 3: in like sterile bubbles or get transplants so that they
Speaker 3: can have like a reset of their immune system from
Speaker 3: somebody else that then gives them the ability to mutate.
Speaker 3: And so even people that got like these booster shots
Speaker 3: had cell immune cells that could make antibites about against
Speaker 3: versions of COVID that had not yet even existed. Like
Speaker 3: those variants that had not yet come along, which was
Speaker 3: miraculous if you ask me, So that's a good side
Speaker 3: of mutation. I don't know if I explained it well.
Speaker 1: Absolutely, I mean it's it's it's a weird moralization that
Speaker 1: we do from a scientific perspective, I think, because we
Speaker 1: are the center of our own universe, and when we
Speaker 1: think about biological processes, very often we think of them
Speaker 1: from a sort of anthropocentric perspective, So we're like, does
Speaker 1: it make me sick? Does it let me feel good
Speaker 1: in my body?
Speaker 3: The sickness is easier to see though, Also, like I
Speaker 3: think some of the meaning we give the term is
Speaker 3: because like there's mutations that every time we got a drink,
Speaker 3: like of alcohol, Like our livers are getting insulted. The
Speaker 3: scientists say, a doctor say insulted. I mean, it's a
Speaker 3: nice way of putting it maybe, And they've found evan
Speaker 3: that like even in healthy people, when livers get damaged
Speaker 3: when they're they're around, like if you have too many calories,
Speaker 3: if you end up like going towards fatty liver disease,
Speaker 3: you're the immune cell, sorry, not the emune cells, the
Speaker 3: liver cells that regenerate in your liver oftentimes pick up
Speaker 3: mutations that help them process extra calories better, like like
Speaker 3: sequester the extra ones they don't need better. So so
Speaker 3: there's and like we would never know that's going on
Speaker 3: until this age of DNA sequencing. So some of this
Speaker 3: stuff's been like the good side of mutation has been hidden.
Speaker 3: We just take it for granted. And and I do
Speaker 3: think that, uh, maybe if part of it's also that
Speaker 3: we're not super comfortable with change. We're like, this is
Speaker 3: my body, Like I don't need the DNA to change,
Speaker 3: but sometimes we it helps us well.
Speaker 1: And I think it's also why there's this ever difficult struggle.
Speaker 1: And I wish somebody would tell this to all of
Speaker 1: the billionaire investors out there, But there's this sort of
Speaker 1: push pull and this difficult struggle between I don't want
Speaker 1: to say between because it makes it sound like it's diametric,
Speaker 1: and it's not. It's more complicated than that, but between
Speaker 1: sort of like aging research and anti aging research and
Speaker 1: cancer research, like the very things that we could do
Speaker 1: sometimes to our bodies to make us live longer could
Speaker 1: be very dangerous because they can like induce cancer in
Speaker 1: us and vice versa, and I think we're always yeah,
Speaker 1: like there's always this like, oh, if we just like
Speaker 1: drink you know, this potion, or we just you know,
Speaker 1: change ourselves so that they don't do this thing anymore,
Speaker 1: I'll just live forever. And I'm like, yeah, and you'll
Speaker 1: just be loaded with more mutations and you'll have way
Speaker 1: more diseases. You'll be fighting off the whole.
Speaker 3: Yeah, Like I don't have time. Like I think if
Speaker 3: people really want to know the full story, they should,
Speaker 3: they should read the book. But one of the things
Speaker 3: I'll mention is that like even antioxidants, it's like I
Speaker 3: was like, oh, they must be great, but as I
Speaker 3: looked into it, it's like more like a little bit
Speaker 3: can be good, but like too much is actually linked
Speaker 3: to worse outcomes. So so it's like what your grandmother's
Speaker 3: all said about like moderation so true, so necessary, and like, yeah,
Speaker 3: it's interesting because not just not just cancer that like
Speaker 3: anti aging stuff doesn't just necessarily increase risk of cancer.
Speaker 3: It's also like if you think about it, because there
Speaker 3: are companies now starting up that I write about that
Speaker 3: are trying to like slow mutation from happening in the body,
Speaker 3: as as on the premise that like mutation is what
Speaker 3: causes frailty and aging and all these things. But of course,
Speaker 3: as we just talked about, like if you can't mutate,
Speaker 3: you're not going to make new, better antibodies. So is
Speaker 3: the compromise of slowing mutation going to be a weakened
Speaker 3: immune system? Yeah, gb D I.
Speaker 2: I'm not such an important point.
Speaker 1: We talk about this a lot on the SDU kind
Speaker 1: of going back to the overarching point that you know,
Speaker 1: you see all of this pseudoscientific bullshit online about like
Speaker 1: we want to boost your immune system.
Speaker 2: Well that's good to a point until.
Speaker 1: It becomes until you get an autoimmune disease, right, and
Speaker 1: like you want to exactly you want to take these
Speaker 1: antioxidants or you know, like reduce oxidative stret Well that's
Speaker 1: good to a point until and everything is like that,
Speaker 1: like everything is toxic and large enough or small enough,
Speaker 1: you know, depending quantities are.
Speaker 3: Lacked there, Like you know, going back to the immune
Speaker 3: system again, not that I'm hung up on it, but
Speaker 3: I did write a lot about COVID. You know, during
Speaker 3: the pandemic, a lot of discussion on Twitter was about
Speaker 3: how to boost your immune system, and there was a
Speaker 3: lot of people saying like, oh, the vaccines like like
Speaker 3: five G gonna like change your DNA, and of course,
Speaker 3: like the mRNA vaccines do not directly change your DNA,
Speaker 3: like nothing is getting inserted into your DNA, Like let's
Speaker 3: just be absolutely clear about that. But you do need
Speaker 3: like it is going to mutate. It's going to cause
Speaker 3: mutational processes in your DNA to make better antibody. So
Speaker 3: instead of saying like I would say, a strong immune
Speaker 3: system is a diversified one, and that diversification is really
Speaker 3: helped by vaccines. Like if you're not taking vaccines, you're
Speaker 3: not diversifying your immune system. So it's not going to
Speaker 3: be as ready to like it doesn't have that antibody
Speaker 3: it needs in place at the get go. You're going
Speaker 3: to be trying to make it on the fly and
Speaker 3: like good luck, because you might not take it in time.
Speaker 1: It's why I always get my flu shot every year,
Speaker 1: even if it turns out that it's not that effective
Speaker 1: that year. My assumption is if I'm doing it every
Speaker 1: single year, I am developing immunity to all these different
Speaker 1: strains of flu.
Speaker 3: I need to be very clear that I was vaccine
Speaker 3: hesitant and I'm a reporter for twenty years on. You know,
Speaker 3: I did not. I did not get the flu vaccine,
Speaker 3: despite the fact of living with somebody he would always
Speaker 3: get the flu vaccine and I'd be like, I don't
Speaker 3: need the flu vaccine.
Speaker 1: So you were secondarily protected by him.
Speaker 3: Maybe so maybe so so uh But I got it
Speaker 3: one year not that long ago, less than a decade ago.
Speaker 3: And about a month later, I had like a really
Speaker 3: mysterious lethargy, went to two doctors, like couldn't figure it out.
Speaker 3: They tested me for CMV, which is like cytomegalovirus, because
Speaker 3: I had already had mono Like uh uh. Turns out
Speaker 3: I had subacute hyroiditis. And the only reason they found
Speaker 3: out was I walked. I was like really so like
Speaker 3: I was very tired to the point where I was
Speaker 3: I was drinking maple syrup from like like a glass,
Speaker 3: like and eating double hamburgers and going to spin class
Speaker 3: like six times a week. It was like things were
Speaker 3: weird and I was still very tired and yet like
Speaker 3: like jacked up in terms of like I was talking fast.
Speaker 3: So so finally I went to this like eronos and
Speaker 3: throat doctor because I had like a my neck was weird,
Speaker 3: and it was the kind of appointment you don't want
Speaker 3: to have where the doctor walks into the room, looks
Speaker 3: at you and then it's like yeah, I'll go get
Speaker 3: somebody else. And you're like wait, wait, don't you want
Speaker 3: to diagnose me? And he's like no, no, no, I
Speaker 3: just diagnosed you. I just looked at you. So I
Speaker 3: had a lump on my thyroid and it was because
Speaker 3: it was like die, it was like bursting. Now why
Speaker 3: do I bring this story up? Because sebakit thyroiditis is
Speaker 3: often a post viral effect. Ah, so this is a
Speaker 3: very so like you know, you lose your thyroid tissue.
Speaker 3: It's like not great. But if I had gotten the vaccine,
Speaker 3: I probably wouldn't have had as severe a flu and
Speaker 3: I probably wouldn't have had But then, like who knows,
Speaker 3: going back to like the whole thing we're talking about,
Speaker 3: like why me? You know, maybe I would still have
Speaker 3: had the mutation that I would have precipitated that whole thing,
Speaker 3: So who knows.
Speaker 1: We do what we can with the tools that we
Speaker 1: have available, and I feel like the responsible thing is
Speaker 1: to find balance in your life and to utilize the
Speaker 1: tools when they are uh, you know, when you have access,
Speaker 1: when you are in a privileged enough position to do them.
Speaker 1: I think where things get irresponsible, right, it is where
Speaker 1: people have access to tools that are evidence based and
Speaker 1: they refuse to utilize those tools, not because of a
Speaker 1: legitimate risk, but because of an imagined or a agenda
Speaker 1: driven description of risk that's not actually you know, based
Speaker 1: in science. That's when things are worrisome for me living
Speaker 1: in a country where there are people at the helm
Speaker 1: and giving global health advice or national health advice who
Speaker 1: do not have the expertise that they need to be.
Speaker 3: I would going to say the whole irony of the story,
Speaker 3: the long story I told you is I was drinking
Speaker 3: makeup sup before I even lived in Canada where I
Speaker 3: am mouse, and I called it my allergies are acting up.
Speaker 3: So if I'm like sniffling a bit, that's that's me
Speaker 3: in June.
Speaker 2: Basically that's your DNA.
Speaker 1: Man.
Speaker 3: Well, you know allergy is probably linked to immune cell's
Speaker 3: gone wrong, so anyway.
Speaker 2: Probably everything. I mean, that's the It's like whenever.
Speaker 1: I talk on the show about patriarchy or I talk
Speaker 1: about intersectionality, and like it's one of those things where
Speaker 1: where you start. Once you see it, you can't not
Speaker 1: see it everywhere.
Speaker 3: I imagine patriarchy has like mutation. And I was like,
Speaker 3: let me under that one a little bit more.
Speaker 2: I'll figure out how it is.
Speaker 1: No, But like probably once you start thinking in terms
Speaker 1: of you know, like we started thinking in terms of
Speaker 1: cell turnover itself. Once we realize that your cells are
Speaker 1: not permanent, it changed the way we thought about biology.
Speaker 1: Now that we realize that your DNA is not permanent,
Speaker 1: that it's constantly changing throughout the lifespan, it probably does.
Speaker 1: It's it's the water that these researchers and these you know,
Speaker 1: these biomedical scientists but also practitioners are probably starting to
Speaker 1: swim in, and it has explanatory value.
Speaker 3: Yeah. Yeah, And like I feel so glad that I
Speaker 3: did this book because now I'm like, well, I told
Speaker 3: you so, like I said it, and the you know,
Speaker 3: like you know, during the pandemic I wrote about I
Speaker 3: was the first journalist to write about COVID being airborne.
Speaker 3: And I did it at a time where a lot
Speaker 3: of my friends who are science journalists were like, don't
Speaker 3: say that, Rock sannem like it's you know, just wash
Speaker 3: your hands and I was like, no, no, I like,
Speaker 3: know these virologists, I know these aerobiologists, like you know,
Speaker 3: I think this is something I need to say, and
Speaker 3: I said it, and I felt so good after I
Speaker 3: said it, even though it took like six months for
Speaker 3: people to like robout you to come along and be like, oh,
Speaker 3: actually also wear a mask. I don't know if it
Speaker 3: was six months, but it was several. It wasn't right away.
Speaker 3: But I feel the same way about this. I feel
Speaker 3: the same way. I feel like I said it, and
Speaker 3: now I can relax because I let other people kind
Speaker 3: of like catch up to it and like feel the
Speaker 3: consequence of it. But I do think it's a really
Speaker 3: important thing for people to grasp. Well.
Speaker 1: Gosh, speaking of relaxing, that I have to ask, are
Speaker 1: you back to your your nonsense? You know? Are you
Speaker 1: just finding really interesting stories within these fields and continue
Speaker 1: to report on that. Do you have any new obsessions
Speaker 1: that you're chasing down now?
Speaker 3: I mean, interestingly, when I was writing this book, people like, oh,
Speaker 3: so you're writing about epigenetics, and I was like no, no, no, no, no,
Speaker 3: no no no. Like so, epigenetics refers to like the markers,
Speaker 3: these chemical tags that end up on DNA to like
Speaker 3: turn it on or turn it off, but it doesn't
Speaker 3: actually change the DNA sequence itself. And these tags can
Speaker 3: change through behavior, so like again like going back to
Speaker 3: smoking or exercise or all these things. Like it can
Speaker 3: modify like which genes are turned on and off by
Speaker 3: the addition or subtraction of these these epigenetic tags. So
Speaker 3: I've actually I've gone back to actually writing about that,
Speaker 3: and I have a cool story coming up about that
Speaker 3: in Nature and Nature Magazine. So yeah, like I'm back
Speaker 3: on my stuff. As you could say, amazing.
Speaker 2: I love it well, everybody.
Speaker 1: The book is beyond Inheritance, are Ever Mutating so and
Speaker 1: a new understanding of health. It's been such a pleasure
Speaker 1: to chat with you today and there's so much in
Speaker 1: here that we did not get to. So guys, pick
Speaker 1: up the book because I know you're going to love it.
Speaker 1: Thank you, Thank you, Thank you so much to Roxanne Camsey,
Speaker 1: Thank you for being here.
Speaker 3: It was just a joy. Yeah, that was so much fun.
Speaker 3: I'm so glad we talked.
Speaker 1: Thank you me too, and everybody listening. Thank you for
Speaker 1: coming back week after week. I'm really looking forward to
Speaker 1: the next time we all get together.
Speaker 3: To talk to Artie