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