Speaker 1: My name is Nikki and I was diagnosed with multiple
Speaker 1: sclerosis in two thousand and seven, when I was twenty
Speaker 1: seven years old. The silver lining to my diagnosis is
Speaker 1: that I was lucky enough that my GP found it
Speaker 1: when she did, because it was by complete peer accident.
Speaker 1: Had she not discovered it when she did, I probably
Speaker 1: wouldn't have shown any symptoms for about a decade later,
Speaker 1: and my condition would have been obviously worse than it was.
Speaker 1: At that time. I was just having horrible headaches, which
Speaker 1: is not has anything to do with MS. So she
Speaker 1: sent me for an MRI and I did the test
Speaker 1: and she called me the very same day. And the
Speaker 1: fact that she called me the very same day, I
Speaker 1: was like, Oh God, what's happening. Something really bad is
Speaker 1: going on. And she's like, you know, best case scenario,
Speaker 1: you might have migraines. She goes, worst case scenario, I
Speaker 1: think you might have multiple sclerosis. So now I'm really
Speaker 1: panicking because I'm twenty seven years old. I don't know
Speaker 1: anything about multiple sclerosis. I know it exists, you know
Speaker 1: from the media and the famous people that you here
Speaker 1: have it. Now I'm thinking I'm going to die and
Speaker 1: I'm twenty seven I haven't lived the life that everybody
Speaker 1: gets to live. I am I going to get be
Speaker 1: able to get married?
Speaker 2: Am I?
Speaker 1: You know what's going to happen.
Speaker 3: So then to determine whether or.
Speaker 1: Not I really had multiple sclerosis, I went through a
Speaker 1: battery of tests over probably the next four or five months.
Speaker 1: And if you've never had a spinal tap, let me
Speaker 1: tell you they are the world's worst creation. There's nothing
Speaker 1: positive I can say about spinal taps. I hope nobody
Speaker 1: ever has to have one. But after all that was
Speaker 1: said and done, it was pretty much one hundred percent
Speaker 1: certainty that I had multiple sclerosis, and so I kind
Speaker 1: of had to digest that and face my own mortality.
Speaker 1: It's hard to kind of grasp the concept that your
Speaker 1: lifespan is going to be shortened. We all know we're
Speaker 1: going to die, but we it's off in the far future.
Speaker 1: We don't think about it on the day to day.
Speaker 1: We don't grasp it. It's not something we worry about.
Speaker 1: But at that point, my death seemed to be right
Speaker 1: around the corner, and it was very scary, and feelings
Speaker 1: of depression and helplessness kind of took over, and I
Speaker 1: was just not in a good place in my head
Speaker 1: just thinking about how all of this was going to
Speaker 1: play out. But I did end up finding a fabulous
Speaker 1: multiple sclerosa specialist, and he is the best thing that
Speaker 1: I could have ever hoped or and honestly I can
Speaker 1: say without him, I would not be here talking with
Speaker 1: you today. So over the next nine years, it took
Speaker 1: that long to find a medication that I would respond to.
Speaker 1: We tried everything. My body will either reject or not
Speaker 1: respond to lots of different medications, So with the choral medications,
Speaker 1: I just went into complete allergic reactions on every single
Speaker 1: one and it was just not going to be able
Speaker 1: to happen to stay on it. So then there's the
Speaker 1: self injectable medications, but they would burn when they would
Speaker 1: go in, and I ended up creating a lot of
Speaker 1: scar tissue around my body from where I had to
Speaker 1: inject because there's only so much skin areas you can
Speaker 1: put them into. But when we were doing MRIs, because
Speaker 1: each drug that you go through you have to wait
Speaker 1: about six to eight months to see if they actually work,
Speaker 1: the self injectable medications did not stop any of the
Speaker 1: progression of the disease. At this point, Like I said,
Speaker 1: it had been nine years and I was just still
Speaker 1: progressing and falling down this horrible hole, and my prognosis
Speaker 1: was really grim. At that point, we didn't really know
Speaker 1: if I was going to respond to anything or if
Speaker 1: I was just needed to prepare myself and get my
Speaker 1: affairs in order type of thing. But God loved my
Speaker 1: specialists because you did not give up on me. And
Speaker 1: there are infused medications. So I've actually been on an
Speaker 1: infused medication now for five years and it is working,
Speaker 1: which is fabulous. It really has slowed the progression of
Speaker 1: the disease. The downside of my infusions one is the cost.
Speaker 1: My infusion is about seventh dollars a month, and had
Speaker 1: I not had insurance, there would be no way for
Speaker 1: me to receive this medication that would save my life.
Speaker 1: I would have to just die because you can't afford
Speaker 1: seven thousand dollars a month. Also, with my medication, I
Speaker 1: get very tired, like the day before and the day
Speaker 1: of I'm tired, and sort of the day after I'm tired.
Speaker 1: So it's good like forty eight hours to seventy two
Speaker 1: hours where I'm kind of just have to be still
Speaker 1: and relax. My body just doesn't function. And the last
Speaker 1: thing that's kind of scary about my infusions is it
Speaker 1: interacts negatively with something called the JC virus, which we
Speaker 1: all have, most of us have in our brains, but
Speaker 1: nothing really happens with it because it's never really activated.
Speaker 1: But this drug will activate it. And when it is
Speaker 1: activated and you're on this medication, your risk for PML
Speaker 1: goes right up, which is a really long medical term,
Speaker 1: but basically it's a brain infection that can cause death.
Speaker 1: So that's kind of scary. Every time I sit in
Speaker 1: the chair once a month, going is this the day?
Speaker 1: I don't know. Since it took such a long time
Speaker 1: for me to find the medication that would help me,
Speaker 1: I had gone from the beginning stages of MS to
Speaker 1: the secondary stages of MS. What that means is I
Speaker 1: don't have flare ups anymore. My conditions and my symptoms
Speaker 1: are with me every day, all the time. Nothing changes.
Speaker 1: So my motor nerves are what's mostly affected, and so
Speaker 1: my coordination's off, my balance is off. I trip and
Speaker 1: fall a lot, and a lot of people get.
Speaker 3: Uncomfortable when that happens, because I don't think a lot
Speaker 3: of people are.
Speaker 1: Used to seeing someone just fall flat on their face
Speaker 1: and start laughing. So I'm definitely was a klutz before MS,
Speaker 1: but now have really shined in that area. I also
Speaker 1: have a lot of numbness and tingling in my hands
Speaker 1: and my feet they shake sometimes. Sometimes the numbness gets
Speaker 1: so bad I have to look down at the ground
Speaker 1: to actually make sure that I'm standing i can't feel it,
Speaker 1: or I have to look down at my hands to
Speaker 1: see if I'm holding something because I just can't feel
Speaker 1: the nerve endings at the end of my fingers. It
Speaker 1: just isn't there. I get tired a lot.
Speaker 3: I lose motivation to do things just because my body
Speaker 3: is so exhausted. Recently, I've started slurring my speech a
Speaker 3: little because my tongue just can't keep up with my
Speaker 3: brain impulses. So it sort of sounds like I'm drunk
Speaker 3: and trying to explain to people that I'm not drunk.
Speaker 3: When they think I am, they don't really listen because
Speaker 3: they're like, yeah, no, you're just wasted. I'm like, no,
Speaker 3: it's two o'clock in the afternoon. I'm just trying to
Speaker 3: explain to you what's happening. But I would have to
Speaker 3: say the most humbling symptom that I have with my
Speaker 3: multiple sclerosis is the loss of bladder control. That is
Speaker 3: an incredibly embarrassing, sort of dejecting thing to experience because
Speaker 3: it makes you feel like you're incapable as an adult.
Speaker 3: You know, you've gone back to being a child and
Speaker 3: not being able to make it to the bathroom on time. Recently,
Speaker 3: my short term memory is evading me. I need sticky
Speaker 3: notes to get through my day. Otherwise I don't know
Speaker 3: where I am. Sometimes I'll be in the car, I'll
Speaker 3: be driving and I have completely forgotten where I'm going.
Speaker 3: But even after all of that, I'm still one of
Speaker 3: the lucky ones who have multiple sclerosis because at this point,
Speaker 3: I don't need any assisted devices to move around. I
Speaker 3: don't need a cane yet or a walker. I do know, though,
Speaker 3: that in the future I will most likely be confined
Speaker 3: to a wheelchair. I'm not thrilled about that, obviously, but
Speaker 3: I'm sort of resigned to it. My worry is that
Speaker 3: as my disease progresses, I'll become a burden on my
Speaker 3: loved ones that will have to take care of me
Speaker 3: because I won't be capable of doing that. And I'm
Speaker 3: scared as to how my final days will play out,
Speaker 3: because multiple sclerosis won't kill me, but the fact that
Speaker 3: I don't have an immune system will kill me. So
Speaker 3: I don't know if it'll be pneumonia or some sort
Speaker 3: of sepsis or at this point COVID. It's like a
Speaker 3: grab bag. And so that sort of fear of the
Speaker 3: unknown really just overwhelms you at times, and you just
Speaker 3: want to sit on the couch and say, well, what's
Speaker 3: the point. But at the end of the day, you
Speaker 3: just have to do your best and get up and
Speaker 3: try to.
Speaker 2: Keep going.
Speaker 1: And see the lucky side, the bright side that I
Speaker 1: still can walk on my two legs and I still
Speaker 1: can have a full life where I walk my dogs
Speaker 1: or drive a car. So as much as the dark
Speaker 1: thoughts want to take over, I have to try and
Speaker 1: really stop and remind myself that it's a day by day.
Speaker 1: You can't focus.
Speaker 4: On what could be coming.
Speaker 1: You have to just take every day as it is
Speaker 1: and be thankful that that's where you are at that moment.
Speaker 2: And that's my story.
Speaker 4: Wow, it's just there's just there's just so much. Yeah,
Speaker 4: thank you so much, so much, Nikki for taking the
Speaker 4: time and being willing to share your story with us.
Speaker 5: Yeah, thank you. We really appreciate it.
Speaker 4: Yeah, we do. Hi.
Speaker 5: I'm Erin Welsh and I'm Erin Alman Updike.
Speaker 4: And this is this podcast will kill.
Speaker 5: You Today we're talking about multiple sclerosis.
Speaker 4: We are This is a very complicated topic. It is.
Speaker 5: It's complicated in so many ways, and I want to
Speaker 5: say thank you again Nikki for sharing your story. I think,
Speaker 5: especially for a topic like MS, it's so important to
Speaker 5: be able to hear from people that are living with
Speaker 5: this disease, because, as I think we'll kind of see
Speaker 5: in the biology section, as much as you can learn
Speaker 5: about the specific biology of what underpins this, it just
Speaker 5: doesn't fully encompass the experience of someone who is living
Speaker 5: with this, you know.
Speaker 4: No exactly. That's something that I came across a few
Speaker 4: times too. And the history research is that like MS,
Speaker 4: like many other diseases, are described by a series of
Speaker 4: signs and symptoms, but those signs and symptoms vary from
Speaker 4: person to person, and they don't capture the feeling of
Speaker 4: someone like how does it feel to, you know, experience
Speaker 4: this symptom or this sign, And so it just I
Speaker 4: think that it really shows how inadequate. Are you know,
Speaker 4: diagnostic criteria are not even diagnostic criteria, but how inadequate
Speaker 4: our definitions of disease really are.
Speaker 5: Yeah, and our and our measures of things too, because
Speaker 5: you know, we can measure like life years lost or
Speaker 5: disability scales and things like that, but that doesn't encompass
Speaker 5: like so many other parts of your life.
Speaker 4: Yeah, no, absolutely so.
Speaker 5: Yeah, I think that's very true for a lot of
Speaker 5: the chronic diseases that we've covered on this podcast, like
Speaker 5: sickle cell I feel like that a lot. With cystic fibrosis,
Speaker 5: I felt like that a lot. So I very much
Speaker 5: appreciate you, Nikki, Thank you so much. Yeah.
Speaker 4: Well, is it quarantin any time?
Speaker 2: It is?
Speaker 5: After that, it's quarantin any time.
Speaker 4: What are we drinking this week?
Speaker 5: We're drinking Sylvia's Sour.
Speaker 4: This is named for Sylvia Lowry, who I'll talk a
Speaker 4: lot more about her later, but basically, she was an
Speaker 4: incredible person who essentially like founded the National Multiple Sclerosis
Speaker 4: Society and also helped found the Multiple scleros Is International Federation.
Speaker 4: It's just like she did such an incredible amount of
Speaker 4: work to raise awareness and research funds and support funds
Speaker 4: for people living with MS, so we wanted to honor
Speaker 4: her with a quarantine drink.
Speaker 5: So, Aaron, what is in Sylvia?
Speaker 4: Snour It is orange and mango and rum and limejuice
Speaker 4: and some mint and yeah, I don't remember fully, but
Speaker 4: I will post the full recipe on our website this
Speaker 4: podcast will Kill You dot com, along with the non
Speaker 4: alcoholic place eber Rita recipe, and I will also post
Speaker 4: both on our social media pages Twitter, Facebook, Instagram, et cetera.
Speaker 5: So check it out there on our website This podcast
Speaker 5: will Kill You dot com. You can find anything that
Speaker 5: you've ever wanted to find in relation to this podcast
Speaker 5: Will Kill You. You can find our merch, which we
Speaker 5: have some pretty incredible merch. You can find a bookshop
Speaker 5: dot org affiliate account. You can find transcripts of all
Speaker 5: of our episodes. You can find links to the sources
Speaker 5: that we've used in every single episode. You can find Bloodmobile,
Speaker 5: who provides our music. You can find a Patreon page.
Speaker 5: You can find everything, anything.
Speaker 4: Lots and lots of stuff. I actually wrote it down
Speaker 4: on a post at this time, but I left it upstairs.
Speaker 5: Well, there you have it.
Speaker 4: Do we have any other business or should we get
Speaker 4: into the episode, I think.
Speaker 5: We should get into the episode right after a short break.
Speaker 5: Multiple sclerosis or MS is an autoimmune inflammatory, chronic demyelinating,
Speaker 5: neuro degenerative disease of the central nervous system.
Speaker 4: That's a lot of adjectives.
Speaker 5: There's a lot of words I know, and we'll get
Speaker 5: into all of them and what all of those things mean.
Speaker 5: But there are basically two major processes at play in
Speaker 5: the pathology of MS. Demyelination which occurs in an autoimmune fashion,
Speaker 5: so our own immune system attacking our nerves along with inflammation,
Speaker 5: and then scar formation or gliosis that then results in
Speaker 5: nerve damage. So those are kind of the two big
Speaker 5: picture things that are happening.
Speaker 4: Okay.
Speaker 5: MS has several different classifications, and will go through them
Speaker 5: all in a bit, but the relapsing remitting form of MS,
Speaker 5: which is often called RR or RMS, is the most common.
Speaker 5: I think most sources I found sent up to ninety
Speaker 5: percent of cases are the relapsing remitting form. And then
Speaker 5: there's the primary progressive form or PPMS, which is less
Speaker 5: common about ten percent, and then a secondary progressive that
Speaker 5: can result from the relapsing remitting form. So in terms
Speaker 5: of the pathology at its core. What's happening in MS
Speaker 5: is that our neurons become demyelinated. We've talked about myelin
Speaker 5: I think before on this podcast, but I can't remember
Speaker 5: what episode, and I tried to look through my notes
Speaker 5: and I couldn't find it. But anyways, myolin is the sheath.
Speaker 5: It's the outer layer of our nerve axons. It's like
Speaker 5: an insulating layer that surrounds our nerve fibers. You can
Speaker 5: think of it as like the insulation around an electrical wire.
Speaker 4: That's exactly how I was thinking about it.
Speaker 5: Yeah, that's how it's most often described. Oh yeah, so
Speaker 5: without this, you know, insulating sheath, nerve impulses can't travel.
Speaker 5: Either they can't travel as quickly as they're supposed to,
Speaker 5: or they can't travel the way that they're supposed to,
Speaker 5: or sometimes they can't travel at all. They just simply
Speaker 5: can't make the jumps they need to make. So as
Speaker 5: this process of demyelination, which literally just means like the
Speaker 5: myelin sheath is going away. As this myelin sheath becomes destroyed,
Speaker 5: nerve impulses aren't traveling from our brain to whatever target
Speaker 5: organ they're supposed to. And then this can lead to
Speaker 5: any and all different kinds of neurologic symptoms because of
Speaker 5: this lack of signal transduction. And so that's what the
Speaker 5: kind of symptoms can look. What does that actually mean
Speaker 5: in terms of disease, Let's talk about it.
Speaker 4: Anything and everything.
Speaker 5: Anything and everything is the real answer. So MS often
Speaker 5: starts with what is called a clinically isolated syndrome or
Speaker 5: a CIS. This is, and I think like eighty five
Speaker 5: percent of cases, the very first manifestation of MS, and
Speaker 5: it can be almost anything that's neurologic, and it just
Speaker 5: depends on where in the brain or the spinal cord
Speaker 5: this demyelination happens. So let me give you an example.
Speaker 5: One relatively common presentation that happens in about twenty percent
Speaker 5: of people as the first sign of MS is something
Speaker 5: called optic neuritis. This is when the demylination and this
Speaker 5: inflammation happens to affect the optic nerve, which is our
Speaker 5: second cranial nerve. Optic neuritis, when it's like this, presenting
Speaker 5: sign of MS usually happens as a pretty abrupt onset
Speaker 5: of blurry vision or loss of color vision, or complete
Speaker 5: loss of vision in one eye or sometimes the presence
Speaker 5: of like a black spot or a scotoma in the
Speaker 5: middle of your vision and pain with eye movement because
Speaker 5: of this inflammation that's happening in the nerve.
Speaker 4: Oh okay, why is this one of the first signs?
Speaker 5: Great question. It's just a common place that MS affects,
Speaker 5: is the optic nerve in your brain, and so it's
Speaker 5: a it's just a common place that you will then
Speaker 5: have MS presenting. And I know that's not a very
Speaker 5: satisfying answer.
Speaker 4: Well, there's not a lot of satisfying answers in I
Speaker 4: think this episode.
Speaker 5: Probably yep, yeah, But this optic neuritis doesn't occur exclusively
Speaker 5: in MS. It can occur in other disorders as well,
Speaker 5: but usually MS it happens just on one eye rather
Speaker 5: than both eyes, though in theory it could happen in
Speaker 5: both and in other disorders it might be more common
Speaker 5: to happen in both eyes at the same time, but
Speaker 5: that is sort of just one very small example. This
Speaker 5: type of demyelination and inflammation can happen in any part
Speaker 5: of the white matter, which is where the myelin containing
Speaker 5: nerves are in our brain or our spinal cord. So
Speaker 5: some other common presentations of this clinically isolated syndrome or
Speaker 5: this first time presentation of what will then be MS.
Speaker 5: Could be weakness in one or more of your limbs.
Speaker 5: It could be spasticity on the flip side, which is
Speaker 5: where you know the muscles become very either flexed or
Speaker 5: they get stuck in an extended position and that can
Speaker 5: be very painful. You can have abnormal sensation like numbness
Speaker 5: or tingling in the arms or legs, or even one
Speaker 5: that kind of comes up commonly is like a band
Speaker 5: like sensation of like a squeezing band feeling around the
Speaker 5: rib cage.
Speaker 4: Hmm.
Speaker 5: If the autonomic system, the autonomic system parts of your
Speaker 5: brain are what's affected, you can have bladder or bowel
Speaker 5: incontinence or loss of function. If it's the cerebellum or
Speaker 5: parts of the brain stem that are involved, then you
Speaker 5: can have difficulties walking like we've talked about on this
Speaker 5: podcast before, a taxia where you just can't coordinate your
Speaker 5: movement so you have gait difficulties. So the list of
Speaker 5: possible symptoms is very, very very.
Speaker 4: Long, and it just depends on like where the demyelination
Speaker 4: and inflammation is happening exactly right, So I have a
Speaker 4: question about the demyelination.
Speaker 3: What is that?
Speaker 4: Like how fast of a process is that? And I mean,
Speaker 4: and maybe this is like way looking ahead to the future,
Speaker 4: but it is like when does myolination in general happen?
Speaker 4: And is there any possibility for like remielination.
Speaker 5: Yeah, yes, we'll talk all about that, okay, Yes, So
Speaker 5: in general, to be classified as like a clinically isolated syndrome,
Speaker 5: these symptoms come on anywhere from over a matter of
Speaker 5: hours to a few days, so they happen kind of gradually.
Speaker 5: So this demilination is like it's a process. It's not
Speaker 5: just like and all of a sudden the myolin's gone.
Speaker 4: Okay, it's like an unraveling, all right, Yeah, but it
Speaker 4: does happen relatively quickly, so they come on, you know, within.
Speaker 5: Hours to a few days. To be classified as a
Speaker 5: clinically isolated syndrome, the symptoms have to last for at
Speaker 5: least twenty four hours. So we're not talking about like
Speaker 5: numbness that comes on and lasts just a few hours
Speaker 5: and then disappears. This is something that comes on lasts
Speaker 5: at least a day, but usually from days or weeks
Speaker 5: and then does resolve. And generally, especially with a clinically
Speaker 5: isolated syndrome or a first time presentation, people do tend
Speaker 5: to recover to about eighty to one hundred percent capacity.
Speaker 5: So in the case of something like optic neuritis, you
Speaker 5: have loss of vision or drastic change in your vision,
Speaker 5: it lasts for at least twenty four hours, and then
Speaker 5: it gradually improves back to pretty close to or at
Speaker 5: your baseline level of vision. And that happens with essentially
Speaker 5: remyelination of oh of your nerves.
Speaker 4: And then how does that happen?
Speaker 5: Oh, Aaron will Well, we'll have to get into all of.
Speaker 4: It, Okay, Okay, I'm sorry, You're.
Speaker 5: Okay, it's good questions, it's just too much, okay. But
Speaker 5: so that's the symptoms, right, One of the key things
Speaker 5: because obviously all of those symptoms are incredibly broad and
Speaker 5: it's not just MS that can cause any of those symptoms, right,
Speaker 5: They're not specific in and of themselves to MS necessarily.
Speaker 5: So one of the key things to discern, especially with
Speaker 5: a first time presentation of an isolated neurologic symptom, is
Speaker 5: whether or not there are associated MRI changes. So MRI
Speaker 5: magnetic resonance imaging is a type of imaging that's really
Speaker 5: good at looking at soft tissues and our nervous system.
Speaker 5: And there are a number of different MRI changes that
Speaker 5: you can see on different types of MRI imaging, which
Speaker 5: I'm not a radiologist, so I'm not about to get into,
Speaker 5: but there are a number of different findings on MRI
Speaker 5: that can be relatively specific two MS. Right, So if
Speaker 5: you have these symptoms consistent with a cis a clinically
Speaker 5: isolated syndrome, and you have these typical findings on MRI,
Speaker 5: you are very likely to then go on to develop MS. Okay,
Speaker 5: and with new diagnostic criteria, if you find more than
Speaker 5: one of these MRI findings that are separate in time
Speaker 5: and space. So either like two symptoms with two different
Speaker 5: lesions on MRI, or maybe you have lesions without symptoms,
Speaker 5: but you have lesions in different stages of healing in
Speaker 5: different places in your brain and spinal cord that together
Speaker 5: can lead to a diagnosis of MS even with a
Speaker 5: first time presentation. Does that make sense?
Speaker 4: I think so. So Basically, like if you go to
Speaker 4: a doctor and you say, okay, I have a loss
Speaker 4: of vision in one eye and I have tingling in
Speaker 4: my hands, and then you get an MRI and they
Speaker 4: see two separate lesions associated with those two symptoms, then
Speaker 4: you get a diagnosis potentially.
Speaker 5: Potentially Yeah, but it even could be that if you
Speaker 5: just had loss of vision and that was your only symptom,
Speaker 5: you could still have brain findings on MRI even without
Speaker 5: having clinical symptoms, right, okay, right right, And that is
Speaker 5: kind of a really big deal because for a really
Speaker 5: long time, it was the case that you could really
Speaker 5: only make the diagnosis of MS if somebody had a
Speaker 5: recurrent CIS, and that would then lead you to the
Speaker 5: diagnosis of the relapsing remitting type of MS. There are
Speaker 5: other things that you can do. You can do lumbar
Speaker 5: punctures to look for findings that are indicative of MS.
Speaker 5: So there's a lot of different, you know, kind of
Speaker 5: things that you can put together to try and make
Speaker 5: an earlier diagnosis of MS now than we ever used
Speaker 5: to before, which is a big deal, as we'll talk
Speaker 5: about later when it comes to like starting early treatment.
Speaker 4: Right.
Speaker 5: So, but then, what tends to happen with MS, especially
Speaker 5: without treatment in the most common form, the relapsing remitting form,
Speaker 5: is that after this first cis this first presentation, there
Speaker 5: are recurrent relapses or attacks, and generally, especially early on
Speaker 5: in the course of disease, between the relapses, people tend
Speaker 5: to not have symptoms. But over time, as these relapses occur,
Speaker 5: and remember, each one of these could be any of
Speaker 5: those neurologic presentations. One time it might be my hands
Speaker 5: are tingling, another time it might be I can't move
Speaker 5: my legs at all. Another time it might be I
Speaker 5: go blind in one eye. It could be any of
Speaker 5: those or any combination there. And over time, as these
Speaker 5: relapses recur, they result in progressive worsening of disability, progressive
Speaker 5: loss of neuronal function. Because what happens is that every
Speaker 5: time this demyelination process occurs, not only do you have
Speaker 5: acute inflammation and a lot of immune reaction in that area,
Speaker 5: but then there is damage to the underlying nerves and
Speaker 5: that's difficult to repair. So our brains and spinal cord
Speaker 5: can repair the milin sheath. We have cells. That's their
Speaker 5: job is to make myelin, and they can do that,
Speaker 5: but as part of our body's natural repair process, they'res
Speaker 5: scarring that happens in the brain. We call this gliosis,
Speaker 5: and this scarring then leads to progressive disability over time.
Speaker 4: Right, So is that just because like the myelin sheath
Speaker 4: can't be fully repair or can't function the way it
Speaker 4: used to, or.
Speaker 5: It's both a process of damage to the underlying nerves
Speaker 5: underneath that mielin sheath. Right, So you have direct damage
Speaker 5: to the nerves, you also have inflammation causing damage to
Speaker 5: the cells that are repairing the miolin right to the
Speaker 5: cells that are responsible for making the myolin. And then
Speaker 5: as part of our repair process, like there's different kinds
Speaker 5: of repair in our bodies. There's regeneration and then there's
Speaker 5: like repair with fibrosis and scar formation, and that's part
Speaker 5: of our body's natural repair process. But that scarring then
Speaker 5: leads to neuronal damage.
Speaker 4: I see.
Speaker 5: So you can kind of think of it as sometimes
Speaker 5: the statistics say that every attack results in like eighty
Speaker 5: to one hundred percent recovery. So if you think of
Speaker 5: it as eighty percent recovery and scar formation, and then
Speaker 5: eighty percent recovery and eighty percent recovery, as these relapses accumulate,
Speaker 5: the recovery is further and further from the initial baseline.
Speaker 5: So over time, especially without treatment, relapsing remitting MS can
Speaker 5: lead to what's called secondary progressive MS, which is where
Speaker 5: instead of seeing these discrete relapses of like new symptom
Speaker 5: onset and then recovery, you just now have like a
Speaker 5: progressive accumulation of neurologic dysfunction and disability.
Speaker 4: Gotcha, I have a question about one of the symptoms
Speaker 4: that's often reported. Yeah, and so you know you talked
Speaker 4: about how well the symptom that you feel is related
Speaker 4: to where the demyelination and inflammation is happening, which completely
Speaker 4: makes sense, But fatigue seems to be reported, So like
Speaker 4: what is the what is the basis of fatigue? Like
Speaker 4: obviously it's a very real thing, but like where does
Speaker 4: that happen and how is that happening?
Speaker 5: It's such a good question. I don't know. I don't
Speaker 5: think we understand at all. Fatigue. It's a huge part
Speaker 5: of MS, especially as it progresses, but it can also
Speaker 5: just be an initial presenting sign, right, Okay, And we
Speaker 5: don't know, we don't understand I think enough about fatigue.
Speaker 5: And because it's not it's not like a tinkling in
Speaker 5: your hands, right, it's not one specific nerve. And so
Speaker 5: I think, like I said, how you can have radiologic
Speaker 5: findings on MRI that maybe don't correspond to a specific symptom,
Speaker 5: but maybe lots of little demyelination events in various areas
Speaker 5: can then result in these more generalized symptoms like a
Speaker 5: fatigue or et cetera.
Speaker 4: Right, it's like many different signals are getting lost or
Speaker 4: being slowed down rather than one specific one.
Speaker 5: I do know that there is some I saw paper,
Speaker 5: but I didn't have time to read through the whole
Speaker 5: paper that was trying to get at more specifically the
Speaker 5: mechanisms of MS related fatigue. So I'll put that on
Speaker 5: our website so if people are interested they can read more.
Speaker 4: Yeah, I mean it seems like it would have huge
Speaker 4: implications for many other rates, like aic fatigue syndrome. There's
Speaker 4: like so.
Speaker 5: Much of MS that is applicable to so many other things.
Speaker 4: But yeah, yeah, I digress.
Speaker 5: So the other form of MS is when this progressive
Speaker 5: worsening of neurologic function happens initially rather than the relapsing
Speaker 5: remitting happening first. And this is called primary progressive MS
Speaker 5: and happens in about ten percent of cases. Interestingly, this
Speaker 5: type of MS tends to be diagnosed in older individuals
Speaker 5: over age forty, whereas relapsing remitting tends to be diagnosed
Speaker 5: between ages twenty and forty most commonly, so they seem
Speaker 5: to be a little different. But there's also so much
Speaker 5: overlap between these two that there's also some question whether
Speaker 5: they truly represent two different, you know, phenotypes of this
Speaker 5: disease or not. So when it comes to MS, there's
Speaker 5: a lot of questions, but there are two big, kind
Speaker 5: of separate but very related questions that full disclosure, we
Speaker 5: don't fully have answers to, and that is what is
Speaker 5: the ultimate cause of MS and what is the underlying
Speaker 5: mechanism of damage? So the underlying mechanism of this damage
Speaker 5: is still not entirely clear. There are a number of
Speaker 5: papers that I will point listeners to with a lot
Speaker 5: of like really immunology geek heavy details on like what
Speaker 5: specific immune mediators, inflammatory markers, et cetera. Are involved. We
Speaker 5: know that especially B cells and to a lesser extent,
Speaker 5: T cells and self reactive antibodies aka autoimmunity is heavily
Speaker 5: involved in the in the mechanistic underpinnings of MS. And
Speaker 5: we know that it's a combination of this immune response
Speaker 5: and inflammation that results in the destruction and damage to
Speaker 5: the mielin sheath and then those cells that produce it,
Speaker 5: and then that's what makes it more and more difficult
Speaker 5: to recover, et cetera.
Speaker 4: Right, Right, because if it's an autoimmune thing where your
Speaker 4: cells are attacking your YOURSELFLF, then it's just going to
Speaker 4: be better and better at recognizing it and it's going
Speaker 4: to be more and more damage accumulates. That makes sense, Okay.
Speaker 5: Yeah, So now to the question of what ultimately causes MS,
Speaker 5: and this is one that has been up for debate
Speaker 5: for I'm guessing you'll tell us how long.
Speaker 4: Erin's to be one hundred and sixty years or something, right, Hey,
Speaker 4: have you not quite that?
Speaker 5: Yeah? Yeah. The bottom line is we technically still don't know,
Speaker 5: but we know a lot. So there are a number
Speaker 5: of different genetic polymorphisms genetic changes that have been associated
Speaker 5: with an increased risk of MS. Most all of these
Speaker 5: are either near or in regions that are in some
Speaker 5: way involved in our immune response, which makes sense since
Speaker 5: this is an immune regulated disease. And there is some
Speaker 5: good evidence that some of these regions overlap with other
Speaker 5: autoimmune diseases, which isn't that surprising.
Speaker 4: That's very interesting.
Speaker 5: I didn't know that. Yeah, like type one diabetes and
Speaker 5: lupus and others. There is some like mediocre evidence that
Speaker 5: some environmental risk factors like decreased sun exposure or low
Speaker 5: vitamin D levels might increase the risk of MS, like mediocre,
Speaker 5: not super strong evidence. And there's some decent evidence that
Speaker 5: smoking does increase the risk of MS.
Speaker 4: Does that also include secondhand smoke? I assume I believe.
Speaker 5: So that's what I have read, okay, And currently MS
Speaker 5: is also about three times more common in those assigned
Speaker 5: female at birth, although that wasn't always the case, which
Speaker 5: I think is fascinating in and of itself.
Speaker 4: I'll talk about that great.
Speaker 5: Can't wait. But none of these genetic or environmental factors
Speaker 5: tell the whole story. And there is another piece that
Speaker 5: for a very long time has been thought to play
Speaker 5: a big role in terms of a causal factor of MS.
Speaker 4: This is such a big lead up, I know, I
Speaker 4: am so excited.
Speaker 5: Can you tell?
Speaker 2: So?
Speaker 5: Just recently? Literally, Aaron's me this paper weeks two weeks
Speaker 5: prior to recording this episode.
Speaker 4: We're recording this in January.
Speaker 5: By the way, we're recording in January. This paper came
Speaker 5: out literally like two weeks ago.
Speaker 4: I was excited about it.
Speaker 5: I'm thrilled. Some very strong evidence has been published in
Speaker 5: support of this particular risk factor, which.
Speaker 4: Is no no, no, no, no, no no no no.
Speaker 5: Drum roll Epstein bar virus EBV okay for listeners. EBV
Speaker 5: or epstein bar virus. This is a human herpes virus.
Speaker 5: We've touched on a lot of different herpes viruses on
Speaker 5: this podcast. We've covered HSV one and two. We've covered virusicella,
Speaker 5: which is human herpes virus three. EBV is human herpes
Speaker 5: virus four. There's a lot of other ones. They're DNA
Speaker 5: viruses that are very highly co evolved with humans, and
Speaker 5: they have these latent analytic phases, so they're really really
Speaker 5: good at hiding out in our immune system. Now. EBV
Speaker 5: is a virus that preferentially infects and replicates within a
Speaker 5: certain subset of our white blood cells. Are b lymphocytes.
Speaker 5: These are cells that, if we think all the way
Speaker 5: back to season two, are vaccines part one episode. If
Speaker 5: you remember that far back, barely b lymphocytes are responsible
Speaker 5: for producing antibodies. That's their number one drop. So EBV
Speaker 5: is a virus that preferentially replicates in our antibody producing cells,
Speaker 5: and it is an incredibly ubiquitous virus. It infects ninety
Speaker 5: five percent of the human population. By the time we
Speaker 5: reach adulthood, all of us have it, and most of
Speaker 5: us will never ever even know that we were infected.
Speaker 5: Some of us might have been unlucky enough to have
Speaker 5: gotten mono infectious mononucleosis that's EBV. That's an acute EBV
Speaker 5: infect if you get it as like a teenager or
Speaker 5: young adult, but most of us get it as kids
Speaker 5: and we never even knew that we had it. ABV
Speaker 5: has been known for a really long time to be
Speaker 5: implicated in the development of a whole bunch of different
Speaker 5: cancers Hodgkins lymphomas, B cell lymphoma's, nasopharyngial carcinoma, like the
Speaker 5: list goes on. So why am I talking about it?
Speaker 4: About MS?
Speaker 5: Okay, For a very long time, people thought, because of
Speaker 5: some of the findings, especially on lumbar puncture on CSF fluid,
Speaker 5: that it is very likely that there is some kind
Speaker 5: of viral component to MS, some kind of viral precursor.
Speaker 5: Because of the type of immune response that we see
Speaker 5: in the cerebral spinal fluid. So people thought for a
Speaker 5: long time there's something viral going on here, and EBV
Speaker 5: has long been thought to be one of the main
Speaker 5: contenders to be the virs potentially associated with MS. And
Speaker 5: there have been a lot of papers throughout the years
Speaker 5: that provide evidence of kind of epidemiological support for this,
Speaker 5: and a lot of them had pretty solid links showing
Speaker 5: that infection with EBV puts you at higher risk of MS,
Speaker 5: especially symptomatic infection. So infection that results in infectious mononucleiosis
Speaker 5: or MONO is a substantially greater risk factor than just
Speaker 5: asymptomatic EBV infection. I think people are two or three
Speaker 5: times more likely to develop MS after infectious mononucleiosis compared
Speaker 5: to asymptomatic EBV. But back to this new paper. This
Speaker 5: new paper that just came off the press lends even
Speaker 5: more support to this idea. This paper, which was published
Speaker 5: in Science on January thirteenth, twenty twenty two, showed that
Speaker 5: infection with EBV increases year risk of MS by thirty
Speaker 5: two times. Thirty two times. Some of the early studies
Speaker 5: of lung cancer and smoking showed like a twenty five
Speaker 5: times increase in risk of lung cancer from smoking. But
Speaker 5: the other thing is that so this paper, and I
Speaker 5: just encourage everyone to read it because I'm not going
Speaker 5: into as much detail because I would talk for too long.
Speaker 5: But they used serum samples from over ten million active
Speaker 5: duty military personnel that spanned over a decade, and they
Speaker 5: looked at eight hundred and one people who were diagnosed
Speaker 5: with MS during their time in the military and compared
Speaker 5: them to like twice as many matched controls. And from
Speaker 5: this study they were able to establish a very causal
Speaker 5: association between first EBV sero conversion that came first, then
Speaker 5: markers of axonal degradation, degradation of the axons. They were
Speaker 5: able to find markers of that in the serum, and
Speaker 5: then later diagnosis of MS, so a causal relationship first EBV,
Speaker 5: then symptoms of neurons starting to degenerate, then a diagnosis
Speaker 5: of MS.
Speaker 4: It's a big deal, a.
Speaker 5: Very big deal. And they also did further studies on
Speaker 5: these serum samples that showed a disregulated antibody response that
Speaker 5: was specific to EBV, epstein bar virus and no other viruses,
Speaker 5: and they tested against a whole number of other viruses
Speaker 5: to look at like levels of antibody and dysregulation of
Speaker 5: antibody response and found a disregulated antibody response only to
Speaker 5: EBV in people who developed MS, and not for any
Speaker 5: other virus.
Speaker 4: So why EBV? What's it doing?
Speaker 5: Oh gosh, erin great question. We still don't know. But
Speaker 5: and even further support of this, yet another paper came
Speaker 5: out erin thank you very much for sending me this
Speaker 5: one too. This came out two days before we recorded.
Speaker 5: It found antibodies that were produced in people with MS
Speaker 5: that bind to a specific ABV viral antigen and cross
Speaker 5: react on a specific human cell surface protein that is
Speaker 5: associated with autoimmune demyelination. And that's a lot I know,
Speaker 5: But basically this second paper that came out provided at
Speaker 5: least one possible mechanistic link that basically says, hey, this
Speaker 5: anigen that ABV has looks a lot like one of
Speaker 5: our cell anigens, right, like something on our human cells,
Speaker 5: And in people with MS, they're making antibodies that are
Speaker 5: cross reacting.
Speaker 4: It's so interesting and it makes me wonder Like EBV
Speaker 4: has been around for a long time. It infects everyone
Speaker 4: everyone essentially, so like, what's the trigger? What? What is
Speaker 4: the sequence of events.
Speaker 5: Right, Yes, it's so fascinating, and it's also it's why
Speaker 5: in only some people, right, right, And that's the question
Speaker 5: we truly really we don't know.
Speaker 4: But EBV is necessarily a part of MS.
Speaker 5: It seems, based on the most recent papers, that EBV
Speaker 5: is a necessary precursor to the development of MS. It
Speaker 5: is not sufficient EBV. Infectional loan does not cause MS,
Speaker 5: but EBV is necessary for the eventual development of MS,
Speaker 5: which is an amazing thing to be able to say
Speaker 5: it really is. Maybe someone else's like two months from now,
Speaker 5: is going to say no, no, But as of now,
Speaker 5: I mean, this is pretty amazingly strong evidence.
Speaker 4: Yeah, I mean, and it also has a lot of
Speaker 4: implications for treatment and.
Speaker 5: Prevention and prevention, yes, speaking of treatments, there are thankfully
Speaker 5: a lot of different treatments that are now available and
Speaker 5: that did not use to be the case. And today
Speaker 5: there is much more of a push towards early detection
Speaker 5: like I mentioned, and early initiation of what is called
Speaker 5: disease modifying therapy or DMT. And these are therapies many
Speaker 5: of them target B cells since we know that B
Speaker 5: cells are so involved in this dysregulated immune response. Or
Speaker 5: other components of our immune system inflammatory system that are
Speaker 5: directly targeting the mechanisms of DAMA image trying to prevent
Speaker 5: this damage, prolong the time between relapses in relapsing remitting MS,
Speaker 5: and prevent the development of disability. There unfortunately aren't as
Speaker 5: many therapies for primary progressive MS. So in both primary
Speaker 5: progressive and in relapsing remitting MS, there's also a lot
Speaker 5: of other therapies that are more towards whatever the symptoms
Speaker 5: are rather than treating the underlying disease. So there's always
Speaker 5: like a multifaceted approach to treatment. Right, that was long winded,
Speaker 5: But that's MS.
Speaker 4: There's I mean, there's a lot there, and it's still
Speaker 4: like it's so complicated, and I have so many questions
Speaker 4: about how myelination works and what actually.
Speaker 5: Is I I'm sorry, I'm not a neurologist and it's
Speaker 5: not my strong suit, aarin, So tell me listen. M hm,
Speaker 5: you said one hundred and sixty years. Yeah, like it's
Speaker 5: got to be around for longer than that, So like,
Speaker 5: what's up with it?
Speaker 4: All right? I will try to get at that just
Speaker 4: after we take the short break, all right. So usually
Speaker 4: you ask me something like where did this thing come from?
Speaker 4: And obviously, like you know, we can't necessarily do that
Speaker 4: with this disease, right normally I can, right like I
Speaker 4: can at LEAs tell you what's commonly accepted to you know,
Speaker 4: for the evolutionary origins, or I can at least like
Speaker 4: take a guess or something. But multiple sclerosis I can't.
Speaker 4: I can't do that. I don't because we don't know,
Speaker 4: like you said, what exactly causes it still, the mechanism
Speaker 4: of disease, and I can't even really make a guess
Speaker 4: because we just lack that knowledge. If it is caused
Speaker 4: in part by EBV, then you know, it seems as
Speaker 4: though EBV, like most herpes viruses, has been co evolving
Speaker 4: with humans, so it's been infecting humans since before humans
Speaker 4: were humans. If it's caused by EBV plus genetic predisposition
Speaker 4: or EBV plus genetic predisposition plus adolescent vitamin D exposure
Speaker 4: or other environmental exposures, then we still don't know, like
Speaker 4: I said, how all of those things interact and what
Speaker 4: that means from an evolutionary perspective. I did read, though,
Speaker 4: one paper that discussed typothetically, why humans spontaneously get MS
Speaker 4: whereas other primates don't seem to, although it can be
Speaker 4: induced experimentally, which I think is really interesting. Yeah, And
Speaker 4: in this paper it was suggested that it might have
Speaker 4: something to do with the fact that humans have big
Speaker 4: brains with a lot of myelination, so it's just like
Speaker 4: a lot of myelination and that's a costly thing, and
Speaker 4: that the peak onset of MS typically occurs around the
Speaker 4: same time that myelination kind of like ends or starts
Speaker 4: to decline or something.
Speaker 5: Yeah, like we're not making more like your brain is
Speaker 5: still growing until you're like twenty five. Yeah, so after
Speaker 5: that point you're just losing brain.
Speaker 4: Yeah, yep, and so and so that's seems like it
Speaker 4: coincides that transition sort of seems like it coincides with
Speaker 4: the typical age of onset for M. But I think
Speaker 4: one of the biggest challenges faced in trying to understand
Speaker 4: the potential evolutionary origins of this or any other disease
Speaker 4: whose ideology isn't well worked out, is trying to sort
Speaker 4: through which epidemiological data are actually meaningful and which are
Speaker 4: spurious or just red herrings.
Speaker 5: Yeah.
Speaker 4: For instance, you mentioned that over the past one hundred
Speaker 4: years there's been a shift in the ratio of who
Speaker 4: is most often diagnosed with MS.
Speaker 5: Yes.
Speaker 4: At the beginning of the twentieth century, the disease was
Speaker 4: diagnosed either fairly evenly in people assigned male at birth
Speaker 4: and people assigned female at birth, or it was diagnosed
Speaker 4: slightly more often in people assigned male at birth. But
Speaker 4: since the middle of the twentieth century or so, people
Speaker 4: assigned female at birth began to be more commonly diagnosed,
Speaker 4: and the ratio today, like you said, is around three one.
Speaker 4: So is this an indication that people assigned female at
Speaker 4: birth are developing MS at higher rates today than they
Speaker 4: have historically or could it be partially an artifact from
Speaker 4: how difficult to diagnose diseases were viewed differently between men
Speaker 4: and women, especially in the days when hysteria was considered
Speaker 4: a valid diagnosis, Like this is all pre MRI, right,
Speaker 4: like before you could see a physical sign of MS
Speaker 4: as a physician.
Speaker 5: Oh, that's such an important point, Aaron.
Speaker 4: Yeah, So that I think is really important to consider,
Speaker 4: and it sort of is commonly talked about in the
Speaker 4: narrative of MS, like this is an increasing disease, it's
Speaker 4: increasing more in people assigned female at birth. Is that
Speaker 4: actually the case. Has there been something that changed over
Speaker 4: the past one hundred years or so, and if there has,
Speaker 4: like we shuld we'd obviously look for it. We should
Speaker 4: absolutely try to find out what that is, but we
Speaker 4: should also examine other reasons that might have led to
Speaker 4: that shift. Okay, So that's all like a very long
Speaker 4: winded way of saying, I don't know the evolutionary origins
Speaker 4: of this disease because we don't know enough about it. Yeah, okay,
Speaker 4: fair enough, Okay, so what do we know. Let's go
Speaker 4: back to what are commonly reported as the earliest recorded
Speaker 4: cases of MS. The first is Saint Ludwina of schidem
Speaker 4: In Holland, who was born in thirteen eighty. Around the
Speaker 4: time she was fifteen, Ludwina went out to do some
Speaker 4: ice skating and while she was skating, she lost her balance,
Speaker 4: she fell down, and she broke a rib. She never
Speaker 4: fully recovered from this, and for the rest of her
Speaker 4: life she experienced difficulty moving around, paralysis, pain, and visual deficits,
Speaker 4: all of which would come and go, but time got
Speaker 4: progressively worse until she died at the age of fifty two.
Speaker 4: Throughout her life, Ludwina felt that she was sent to
Speaker 4: accept this suffering for the sins of others, and this
Speaker 4: was taken to be a sign of a miracle. So
Speaker 4: after she died, she was canonized and is the patron
Speaker 4: saint of ice Skaters and the chronically ill.
Speaker 5: Wow.
Speaker 4: Yeah, she does it all. It's still kind of debated
Speaker 4: whether or not it actually was MS the Ludwina was
Speaker 4: experiencing and how much is truth versus how much is
Speaker 4: myth or exaggerated over time or you know, certain bits
Speaker 4: are picked out to support you know, this was MS,
Speaker 4: but it does seem a lot more like MS than
Speaker 4: another early story that's commonly mentioned, which is that of Halla,
Speaker 4: a woman who was written about in the Icelandic Saga
Speaker 4: of Saint Thorlax. So, sometime between twelve ninety three and
Speaker 4: thirteen twenty three CE, Halla suddenly lost her sight and speech.
Speaker 4: She prayed for them to recover and they did. MS
Speaker 4: could be something else, could be that, Yeah, but that
Speaker 4: was it. It was just that, just essentially. I mean,
Speaker 4: I think there was like a little bit more to it,
Speaker 4: but that was the gist.
Speaker 5: Okay, Yeah, so you know the first.
Speaker 4: Case of what definitely seems like MS takes place much
Speaker 4: more recently. Augustus dest was a grandson of King George
Speaker 4: the Third, who began experiencing symptoms of MS in his twenties.
Speaker 4: In a diary entry from eighteen twenty two, when he
Speaker 4: was twenty eight years old, he described being at the
Speaker 4: funeral of a close friend. Quote, I attended the funeral,
Speaker 4: there being many persons present, I struggled violently not to weep.
Speaker 4: I was, however, unable to prevent myself from so doing.
Speaker 4: Shortly after the funeral, I was obliged to have my
Speaker 4: letters read to me and their answers written for me,
Speaker 4: as my eyes were so attacked that when fixed upon
Speaker 4: minute objects, indistinctness of vision was the consequence. Soon after,
Speaker 4: I went to Ireland, and without anything having been done
Speaker 4: to my eyes, they completely recovered their strength and distinctness
Speaker 4: of vision. For most of his life, Dest kept a
Speaker 4: journal describing his symptoms, the way he felt about them,
Speaker 4: and his experiences with the doctors he saw. And it's
Speaker 4: a really valuable and interesting insight into this disease and
Speaker 4: how it was perceived, and it kind of shows in
Speaker 4: some ways how far we've come, but also in other
Speaker 4: ways how some things haven't really changed very much at all.
Speaker 4: So I want to read another quote from Desk from
Speaker 4: eighteen forty three, about twenty one years after that other entry.
Speaker 4: I read quote. What I complain of now is that
Speaker 4: sitting produces a numbness all down the back part of
Speaker 4: my thighs and legs, and gives me a curious numb
Speaker 4: sensation in the lower region of the belly. When standing
Speaker 4: or walking, I cannot keep my balance without a stick.
Speaker 4: I sleep well when I am not annoyed with little
Speaker 4: nervous twitching in my legs and feet. For the first
Speaker 4: time in my life, I was attacked by giddiness in
Speaker 4: the head, vertigo, sickness, and total abruption of strength in
Speaker 4: my limbs. I was able to drive to my own house,
Speaker 4: but totally incapable of getting out of the phaeton. I
Speaker 4: was carried up to my bedroom, where I was sick
Speaker 4: as a dog and broke out in the most profuse perspiration.
Speaker 4: And so some of these descriptions, even though they were
Speaker 4: from the early eighteen hundreds, they may sound completely familiar
Speaker 4: to people living with MS today. But hopefully what will
Speaker 4: not sound familiar are the treatments that doctors prescribed for
Speaker 4: dest here's the selection. Leeches, beef steaks with wine twice
Speaker 4: a day, back rubs with alcohol, opium and oils being slapped,
Speaker 4: extremely hot baths, strychnine, quinine, nitric acid, ammonium carbonate, mercury, cinnamon, rhubarb,
Speaker 4: horseback riding, and a little bit of light electrotherapy. It's
Speaker 4: like getting shocked. Yeah, extremely hot baths, Like we didn't
Speaker 4: talk about this in the bio, but that's that would
Speaker 4: have exacerbated the symptoms so much it would have felt horrible.
Speaker 5: Yeah.
Speaker 4: So yeah, yeah, And there's a huge variety in those
Speaker 4: treatments that he was prescribed, which I think speaks to
Speaker 4: the fact that doctors clearly had no idea what was
Speaker 4: causing the disease and that no one single therapy seemed
Speaker 4: truly helpful for symptom control, let alone as a cure.
Speaker 4: And this didn't change once MS was formally described as
Speaker 4: a disease. Throughout the first half of the eighteen hundreds,
Speaker 4: several different anatomus described lesions in the brain or along
Speaker 4: the spinal cord while doing an autopsy, which, if you
Speaker 4: remember from our pupil fever episode, had become quite popular
Speaker 4: around this time. Pathology had grown greatly as a field,
Speaker 4: and many people wanted to make a name for themselves
Speaker 4: by identifying a new disease. One of these was Jean
Speaker 4: Martin Sharco, whose name may be familiar from our endometriosis episode,
Speaker 4: or because of a genetic disorder that bears his name
Speaker 4: Charkson Marie tooth disorder, or just because he's kind of
Speaker 4: a big figure in the early history of neurology. He
Speaker 4: played a role in the identification of many neurological disorders.
Speaker 5: Yeah, he's a big deal.
Speaker 4: Big deal. Charco was a French neurologist and pathologist who
Speaker 4: worked at a huge teaching hospital that was built to
Speaker 4: treat the poor women of Paris. His approach was to
Speaker 4: follow his patients for a long period of time, and,
Speaker 4: when they died, perform autopsies on their bodies to see
Speaker 4: if he could identify any pathological basis for the signs
Speaker 4: or symptoms that they reported. The story of Charcot and
Speaker 4: MS begins when he hired a woman who had some
Speaker 4: motor problems to be his housemaid. He thought she had neurosyphilis.
Speaker 4: He kept iran until her disease progressed to the point
Speaker 4: where he was like, you can't really clean anymore, so
Speaker 4: you're going to this hospital for poor Parisian women. And
Speaker 4: he shipped her off there, oh gosh, and that's where
Speaker 4: she lived until she died, at which point he performed
Speaker 4: an autopsy and he noticed some plaques scattered throughout her
Speaker 4: nervous system. And within a few years he had seen
Speaker 4: several more of these plaques in several more of the autopsies,
Speaker 4: and so he was thinking, hmm, okay, I think I
Speaker 4: might have a new condition here, because a lot of
Speaker 4: the people that had these plaques had reported things like numbness, vision, parlbs,
Speaker 4: movement difficulties, speech problems, et cetera. And he noticed too
Speaker 4: that these signs and symptoms tended to relapse and roomIt
Speaker 4: and so yeah, he was like, this has got to
Speaker 4: be a new disorder, and I'm gonna go describe it.
Speaker 4: So in eighteen sixty eight, Charco gave a series of
Speaker 4: lectures that named the disease, although they didn't he didn't
Speaker 4: use the name multiple sclerosis. That would really only be
Speaker 4: settled upon in like by the nineteen fifties or so, like,
Speaker 4: there was disseminated sclerosis. There were a ton of different
Speaker 4: names for this, but he also drew like boundaries around it.
Speaker 5: Right.
Speaker 4: He described the pathological anatomy, the symptomatology, pathophysiology, ideology, which
Speaker 4: he described as being anything from unknown infections, moist cold,
Speaker 4: or trauma, and treatment which he said there wasn't any
Speaker 4: He hadn't come across anything that seemed to work. And
Speaker 4: he also noted that the disease seemed to be more
Speaker 4: common in women than in men. Does this mean that
Speaker 4: Charcot was ahead of his time, because, like I said,
Speaker 4: that's something that really only in since the mid nineteen
Speaker 4: hundreds or so people recognized and kind of yes and no.
Speaker 4: If he was ahead of his time, it wasn't for
Speaker 4: the right reasons, because let's hear why he thought people,
Speaker 4: especially women, developed ms oh yeah quote long continued grief
Speaker 4: or vexation, such for instance, as might arise from illicit
Speaker 4: pregnancy or the disagreeable annoyances and carking cares which a
Speaker 4: more or less false social position entails. This is often
Speaker 4: the case as regards certain female teachers. Having said so
Speaker 4: much with respect to women, the question of the male
Speaker 4: sufferer arises. These are, for the most part, persons who
Speaker 4: have lost caste and who thrown out of the general
Speaker 4: current and too impressionable, are ill provided with the means
Speaker 4: of maintaining what in Darwin's theory is called the struggle
Speaker 4: for life.
Speaker 5: Oh de end quote, Yeah, oh okay. I feel like
Speaker 5: these early descriptions have probably progressed into some of the
Speaker 5: thinking that has taken a long time to overturn, because
Speaker 5: there was a lot of like earlier studies that were like,
Speaker 5: is it stress that causes MS?
Speaker 4: Right? And like, it couldn't possibly be that someone's disease
Speaker 4: caused them stress, right, couldn't possibly be that?
Speaker 2: No?
Speaker 4: And obviously, if you listen to the endometrios this episode,
Speaker 4: Charcot was involved in hysteria like he you know, was
Speaker 4: a huge influence of Freud, And there was so much
Speaker 4: much in this time that built this foundation for the
Speaker 4: disease becoming a part of someone's identity, right, or someone's
Speaker 4: identity influencing what disease they were thought to have. And
Speaker 4: it's still a big problem today and it's taken decades
Speaker 4: to even try to undo. But anyway, for decades, Charco's
Speaker 4: description of MS from these lectures basically remained unchanged, with
Speaker 4: just a little refinement here and there not because no
Speaker 4: one was studying the disease. Charko's lectures kicked off a
Speaker 4: huge amount of interest in MS. But just because the
Speaker 4: general outline of the disease remained the same, that doesn't
Speaker 4: mean that the way it was perceived also was unchanged.
Speaker 4: So going back to dest and his journals, I think
Speaker 4: reading through them, as well as other people's accounts of
Speaker 4: their experiences with MS in the late eighteen hundreds and
Speaker 4: early nineteen hundreds, it helps us to better consider this
Speaker 4: disease through the lens of history. Pick any point in
Speaker 4: the history of MS from the mid eighteen hundreds and
Speaker 4: ask what else was going on in biomedical science at
Speaker 4: the time, what new discoveries have been made or technologies developed,
Speaker 4: and you'll see how that historical context affected not only
Speaker 4: the diagnosis of this disease, but also how it was
Speaker 4: treated and what was thought to be the cause. So
Speaker 4: improvements in microscopes and the autopsy trend that led to
Speaker 4: this disease being defined because it allowed people to see
Speaker 4: the connection between these lesions and the symptoms of MS,
Speaker 4: and since germ theory was in full swing around the
Speaker 4: time MS was first fully characterized, researchers proposed microbe after
Speaker 4: microbe responsible for the disease, and even produced some MS vaccines,
Speaker 4: none of which was able to be repeated or panned out. Really,
Speaker 4: and this focus on a microbiological cause of MS so
Speaker 4: early on it was surprising to me initially, but it
Speaker 4: also makes sense in light of the ability of syphilis
Speaker 4: to cause neurological disease. Until a lot of people were like, oh,
Speaker 4: if syphilis can do this, then you know, we see
Speaker 4: neurological disease. This could be caused by another pathogen. Yeah,
Speaker 4: And more recently, you know, one of the current trends
Speaker 4: is the gut microbiome in general, and what are microbiota,
Speaker 4: how that influences our health and other diseases, and so
Speaker 4: there has been attention more recently regarding what role that
Speaker 4: has to play in MS. So we don't, you know,
Speaker 4: we don't know. Maybe we'll learn more, and I think,
Speaker 4: you know, we've now with this EBV super robust study,
Speaker 4: we've kind of come full circle, and maybe some EBV
Speaker 4: vaccines in the works. Yeah. A quote from the early
Speaker 4: nineteen hundreds by Pierre Marie, a student of Charcot, may
Speaker 4: soon seem very prophetic. Quote. I have little doubt in fact, gentlemen,
Speaker 4: that in the employment of such a substance as the
Speaker 4: vaccine of pasture or the lymph of cook, the evolution
Speaker 4: of insular sclerosis will someday be rendered absolutely impossible.
Speaker 5: Wow, And hopefully that's true, fingers cross.
Speaker 4: Yeah. And the prevailing medical thought at various times also
Speaker 4: affected treatment. So like with the development of salvarsan for
Speaker 4: syphilis and penicillin, people attempted to treat MS with antibiotics,
Speaker 4: And the same happened when like anticoagulant factors were developed
Speaker 4: or other types of treatments right that were effective for
Speaker 4: other diseases.
Speaker 5: Right, any new treatment does it work for MS? Right?
Speaker 4: And that's a completely reasonable approach. I think it also
Speaker 4: just speaks to like people where like, we don't know
Speaker 4: what is causing this. And I also think it's important
Speaker 4: to talk about how diagnosis was impacted by common bios
Speaker 4: or trends in medicine. And I've talked before about the
Speaker 4: difference between signs and symptoms and how advancements in medical
Speaker 4: technology and measuring devices led to the shift in physicians
Speaker 4: relying more on signs than symptoms for many diseases. So like,
Speaker 4: signs are things that are observable detectable by someone who's
Speaker 4: not the person experiencing them, and symptoms are only able
Speaker 4: to be described by the person experiencing them, and so
Speaker 4: this switch from focusing more on signs rather than symptoms
Speaker 4: that also applied for MS. In the days before MRIs,
Speaker 4: diagnosis was often described as being difficult, or maybe it
Speaker 4: was that a proper diagnosis required that a physician had
Speaker 4: to listen to and believe their patient difficult, difficult, and
Speaker 4: people with MS were often diagnosed with a variety of
Speaker 4: other conditions. In the seventeen hundreds and eighteen hundreds, that
Speaker 4: was often paraplegia. This is what dest was diagnosed with,
Speaker 4: and paraplegia was this umbrella term under which a lot
Speaker 4: of diseases that included partial paralysis or movement disorders were thrown.
Speaker 4: And then when the spira keet that causes syphilis was
Speaker 4: identified in the late eighteen hundreds, it was common for
Speaker 4: a person living with MS to get a diagnosis of neuisiphilis,
Speaker 4: which is what another couple of people in the eighteen
Speaker 4: hundreds or early nineteen hundreds were diagnosed with formally or
Speaker 4: just suggested to have the German poet Heinrich Heiney and WNP. Barbellian,
Speaker 4: pen name of Bruce Frederick Cummings, who wrote a book
Speaker 4: describing his life with MS titled The Journal of a
Speaker 4: Disappointed Man. So they were both thought to have neurosiphalis,
Speaker 4: but more likely MSMs, but doctors also suggested to Barbelian
Speaker 4: that it was all in his head. And in that
Speaker 4: same vein, Margaret Gaddi, who was a Victorian novelist and
Speaker 4: naturalist who also had MS, was told by her physician
Speaker 4: that her illness was quote caused by her tendency to
Speaker 4: use excessive physical effort in gardening, using heavy tools in
Speaker 4: the manner of a man.
Speaker 5: Oh, how dare you?
Speaker 4: I want to see her garden. But it was incredible.
Speaker 4: But all of that sounds familiar, right, because the history
Speaker 4: of MS shares a lot of parallels with that of
Speaker 4: endometriosis and other quote invisible diseases, which is a term
Speaker 4: often used to describe diseases where doctors or other people
Speaker 4: may look at someone and go, oh, you don't look
Speaker 4: sick to me because there are no outward signs of
Speaker 4: the disease. And I don't love this term because I
Speaker 4: think it can be misused to undermine or discredit the
Speaker 4: very real things that people with one of these diseases
Speaker 4: are experiencing. If I can't say you're sick, then you
Speaker 4: must not be sick, or those things you say you're
Speaker 4: feeling are just not real, like you're exaggerating them, right,
Speaker 4: And this is the kind of logic that led to
Speaker 4: hysteria being diagnosed for all manner of diseases, including MS.
Speaker 4: As Maya Dusonberry puts it in her book Doing Harm quote,
Speaker 4: perhaps one of the clearest examples of an autoimmune disease
Speaker 4: carved out of the waste basket of hysteria is multiple sclerosis.
Speaker 4: That phrase is so excellent, the waste basket of hysteria,
Speaker 4: because it's like, how many things were misdiagnosed as hysteria?
Speaker 4: And this was even commented on in the early twentieth century.
Speaker 4: Doctors were like, MS is not that difficult to diagnose,
Speaker 4: but there are a lot of misdiagnoses, with doctors most
Speaker 4: commonly confusing it with hysteria, and people living with MS
Speaker 4: were diagnosed with hysteria well into the nineteen fifties. It
Speaker 4: happened at such a high rate, in fact, that it
Speaker 4: drove the definition of hysteria to change in the early
Speaker 4: twentieth century to distinguish it from MS.
Speaker 5: Wow I did not know that.
Speaker 4: Yeah. But although MS remained underdiagnosed for many people, especially women,
Speaker 4: in the first half of the twentieth century, rates of
Speaker 4: diagnosis did in general go way up, and a big
Speaker 4: part of that was due to the fact that there
Speaker 4: were simply more neurologists. By the nineteen tens the nineteen
Speaker 4: twenties or so, there had been a substantial rise in
Speaker 4: trained neurologists in the US, and not just restricted to
Speaker 4: cities but also to smaller towns and rural areas, and
Speaker 4: by the nineteen fifties, what had once been thought to
Speaker 4: be a rare disease was now considered one of the
Speaker 4: most common illnesses of the central nervous system. And with
Speaker 4: this rise of neurologists there also grew to be more
Speaker 4: focused at ten, specifically on MS wider scale studies such
Speaker 4: as you know, the one that was able to be
Speaker 4: done with soldiers from World War One and World War Two,
Speaker 4: where we had a lot more medical information about thousands
Speaker 4: and thousands of people readily available. Which is kind of
Speaker 4: funny that this twenty twenty two paper is mirroring the
Speaker 4: same thing, but from the data from World War One
Speaker 4: and World War Two. That's where it sort of paved
Speaker 4: the way for these large scale epidemiological studies looking at
Speaker 4: geographical trends where it seemed to be occurring at higher
Speaker 4: rates or more often diagnosed in people from more northern areas,
Speaker 4: northern regions that I want it like. I'm very excited
Speaker 4: to hear you talk more about that, because I know
Speaker 4: it's like a more complicated story than that. But this
Speaker 4: pattern where MS seems to be more frequent in not
Speaker 4: as you go farther away from the equator, but just
Speaker 4: more northern climates and northern hemisphere has led some people
Speaker 4: to suggest that this disease has Viking roots, as in
Speaker 4: the frequent travels of Vikings in history essentially disseminated that
Speaker 4: MS predisposition around certain places. Yeah. I don't know how
Speaker 4: much evidence there is to support this, but my guess
Speaker 4: is that as better and better genetic tools are being
Speaker 4: developed all the time, maybe we will be able to
Speaker 4: tease out some sort of historical story for why we
Speaker 4: see what we see. By the mid nineteen fifties, there
Speaker 4: was much more awareness about multiple sclerosis among the medical community,
Speaker 4: and scientific advancements had helped to understand more about what
Speaker 4: was going on inside someone living with MS, which helped
Speaker 4: in the development of some treatments to manage the signs
Speaker 4: and symptoms of the disease. But this growth and awareness
Speaker 4: was not just limited to healthcare workers working directly on MS.
Speaker 4: One of the biggest turning points in the history of
Speaker 4: MS happened on May first, nineteen forty five, when a
Speaker 4: woman named Sylvia Lowry, whose brother Bernard had MS, and
Speaker 4: Sylvia had gotten so frustrated by the lack of clear
Speaker 4: information and adequate treatment from her brother's physicians, and so
Speaker 4: she posted an ad in The New York Times with
Speaker 4: the following request quote multiple sclerosis, Will anyone recovered from it?
Speaker 4: Please communicate with patient? And she got dozens of replies,
Speaker 4: like way more than she expected, and so she thought, Okay,
Speaker 4: I can't be the only person who could use this information.
Speaker 4: I'm going to bring all of these people together. And
Speaker 4: in nineteen forty seven she brought over twenty leaders in
Speaker 4: the field of neurology together to try to set objectives
Speaker 4: for an organization that was dedicated to understanding the disease
Speaker 4: and finding a cure. Wow, and Sylvia, like I said,
Speaker 4: didn't stop at founding the Multiple Sclerosis Association, which was
Speaker 4: later changed to the National Multiple Sclerosis Society. She also
Speaker 4: helped found the Multiple Sclerosis International Federation, and for the
Speaker 4: rest of her life she campaigned incredibly hard to raise
Speaker 4: awareness of this disease and bring in more funds for
Speaker 4: research as well as supporting people living with the disease,
Speaker 4: and her efforts were hugely successful. Her work and the
Speaker 4: work of these and other MS organizations show once again
Speaker 4: how incredibly important it is for people to share their
Speaker 4: story and how much of a positive impact patient advocacy
Speaker 4: groups can have on bringing awareness to a disease and
Speaker 4: providing support and resources to those who need it. Within
Speaker 4: ten years of the National MS Society being founded, there
Speaker 4: were one hundred and twenty thousand members. She brought in
Speaker 4: celebrities and politicians, including Shirley Temple, which I'm now realie
Speaker 4: would have been a great quarantine. But that's okay, I
Speaker 4: would have been.
Speaker 5: I love a Shirley Temple.
Speaker 4: Me too, Me too? And Shirley Temple and other celebrities.
Speaker 4: They use their incredibly powerful platform for good and they
Speaker 4: turned like talk into action, right Like, instead of just
Speaker 4: being like, hey, we should you know, raise awareness for MS,
Speaker 4: it was like, no, we are raising awareness for MS,
Speaker 4: we are getting funds, we are you know, providing resources.
Speaker 4: And this is also still a common theme today, which
Speaker 4: I think is wonderful, with celebrities like Jamie Lynn Siegler
Speaker 4: who plays Meadow on The Sopranos, which I'm finally watching
Speaker 4: right now, and former US Representative Donna Edwards and many
Speaker 4: others raising funds and awareness for the disease. I would
Speaker 4: also just like to encourage anyone who is interested in
Speaker 4: learning more to check out the National MS Society website
Speaker 4: because it's an amazing resource for seeing the latest news,
Speaker 4: finding support, understand the signs and symptoms of the disease,
Speaker 4: and so much more.
Speaker 5: I was also going to shot them out because I
Speaker 5: found their descriptions of symptoms and everything to be honestly
Speaker 5: so much better than most of the papers that I read.
Speaker 4: Yeah, it was a great website. Yeah. The second half
Speaker 4: of the twentieth century saw a few more big advancements
Speaker 4: in multiple sclerosis. Outside of this huge growth and awareness,
Speaker 4: the development of clinical trials combined with better guidelines for
Speaker 4: staging the disease really helped to evaluate whether certain medications
Speaker 4: were helpful, harmful, or did nothing, something which previously had
Speaker 4: been really difficult to assess because of the relapsing, remitting
Speaker 4: nature of this disease. And finally, the development of the
Speaker 4: MRI in the late nineteen seventies meant that you could
Speaker 4: finally visualize this disease, which helped not only with understanding
Speaker 4: more about it, but it also lent edence to the
Speaker 4: people who had had their symptoms repeatedly dismissed. Kind of
Speaker 4: reminiscent of the way that laparoscopic surgery was used to
Speaker 4: legitimize endometriosis, just parallels. But it's true that the MRI
Speaker 4: revolutionized diagnosis, especially early diagnosis for people with MS, which,
Speaker 4: like you said, has been tremendously helpful for coming up
Speaker 4: with a treatment and management plan for people living with
Speaker 4: a disease, as well as being able to evaluate which
Speaker 4: medications might have an impact. There is so much more
Speaker 4: that I could have included in this history in terms
Speaker 4: of like the specific medical developments and who discovered what,
Speaker 4: and who wrote this paper and who found this sign
Speaker 4: or whatever. Over the past one hundred and sixty years
Speaker 4: and that information is out there if you're interested in
Speaker 4: learning more. I recommend the book multiple Sclerosis, The History
Speaker 4: of a Disease, but I'm going to leave off with
Speaker 4: the history here where Since them, we have many medications
Speaker 4: that seem to be very helpful in managing symptoms, and
Speaker 4: we are now so much better than we used to
Speaker 4: be in our knowledge about multiple sclerosis. But at the
Speaker 4: same time, there are still so many unanswered questions why
Speaker 4: first and foremost, because without a why, it's going to
Speaker 4: be nearly impossible to find a cure right or it's
Speaker 4: going to be very difficult. And I also think that
Speaker 4: we still have a long way to go in terms
Speaker 4: of understanding how much of the criteria that we use
Speaker 4: to define multiple sclerosis actually captures the experience of someone
Speaker 4: living with it. So, Aaron, can you tell me more
Speaker 4: about where we stand today with MS?
Speaker 5: I will try my best right after this break.
Speaker 2: So.
Speaker 5: MS is the most common demyelinating disease. It is the
Speaker 5: most common inflammatory neurodegenerative disease in young adults. It's the
Speaker 5: most common non traumatic cause of neurologic disability in young adults.
Speaker 5: It has a lot of most common designations in terms
Speaker 5: of the overall prevalence which has been increasing, and there's
Speaker 5: kind of a lot of factors that might be going
Speaker 5: into that. In the Global Burden of Disease study, which
Speaker 5: looked at data from nineteen ninety to twenty sixteen, it
Speaker 5: was estimated that in twenty sixteen there were over two million,
Speaker 5: two hundred thousand prevalent cases of multiple sclerosis globally.
Speaker 4: Okay, how was that distributed.
Speaker 5: Great question, Very unevenly across the globe. So the highest
Speaker 5: prevalence by far is in North America with one hundred
Speaker 5: and sixty four cases per one hundred thousand people, closely
Speaker 5: followed by Western Europe at an estimate of one hundred
Speaker 5: and twenty seven cases per one hundred thousand people, Australasia
Speaker 5: only ninety per one hundred thousand, in Subsiharian Africa between
Speaker 5: two and three cases per one hundred thousand, Oceania two
Speaker 5: cases per one hundred thousand, So it really does vary
Speaker 5: across the globe. You mentioned, Aaron, there is some kind
Speaker 5: of question where sometimes people say it's it's closer to
Speaker 5: the equator is less, or northern latitudes is greater. And
Speaker 5: there's even been some studies that have tried to look
Speaker 5: at even within countries, whether there are like north to
Speaker 5: south gradients in cases, and part of that is why
Speaker 5: the idea of sun exposure and vitamin D has some
Speaker 5: support as in more northern areas where you have less
Speaker 5: sun exposure is where you have higher rates of MS.
Speaker 5: But it also doesn't hold true like one hundred percent,
Speaker 5: because there are specific indigenous populations and areas that actually
Speaker 5: have very low rates of MS, even though they live
Speaker 5: in very northern areas. So it's not the whole story,
Speaker 5: like a north to south gradient isn't the whole story,
Speaker 5: but there does seem to be at least some associations.
Speaker 4: So what if somebody moves, like for instance, from an
Speaker 4: area of high risk to low risk or low risk
Speaker 4: to high risk, what does their risk profile look like?
Speaker 5: Yeah, it's a good question. I read in at least
Speaker 5: one paper that, for example, migrants from low risk areas
Speaker 5: let's say Africa, to a high risk area let's say
Speaker 5: North America, those migrants still have low risk of development
Speaker 5: of MS. They came from a low risk area. When
Speaker 5: they moved to a high risk area, they still have
Speaker 5: a low risk of development of MS. But children of
Speaker 5: those migrants tend to have higher risk of development of MS,
Speaker 5: which is really interesting.
Speaker 4: That's very interesting.
Speaker 5: Yeah, Now, in terms of prevalence, it is interesting to
Speaker 5: look at the prevalence being increased, which it has in
Speaker 5: twenty sixteen. That prevalence rate is ten percent higher than
Speaker 5: the estimated prevalence in nineteen ninety, for example. But we
Speaker 5: are diagnosing MS earlier, which could contribute. We also have
Speaker 5: such better treatments that people are living longer with MS,
Speaker 5: so globally, the age standardized death rates decreased significantly in
Speaker 5: that time period, by about eleven percent. So those things
Speaker 5: combined might explain some of this increase. So there's still
Speaker 5: a question as to whether an increase in prevalence means
Speaker 5: also that there is a true increase in MS, or
Speaker 5: if we're just diagnosing it better and people are living
Speaker 5: longer with it, which is always going to increase the prevalence.
Speaker 4: Of RYS and has like the age specific rate or
Speaker 4: like incidents changed.
Speaker 5: It's hard to get a handle on incidents, and so
Speaker 5: most all of the studies just really look at prevalence. Okay, Yeah,
Speaker 5: but it's a good question. In twenty sixteen, in this
Speaker 5: same study, it was also estimated that there were over
Speaker 5: eighteen thousand deaths due to MS in that one year alone,
Speaker 5: as well as over one million, one hundred thousand disability
Speaker 5: adjusted life years. And we've talked about how that's not
Speaker 5: a perfect measure of the impact of a disease, but
Speaker 5: it is at least a measure that we have that
Speaker 5: this is something that is significantly impacting people's lives, right.
Speaker 4: For a long part of their lives.
Speaker 5: Right, exactly like diagnosis at between twenty and forty and
Speaker 5: you know, this is something that's lifelong and progressive.
Speaker 4: Yeah.
Speaker 5: So the good news, and I do feel like we
Speaker 5: get to end with pretty good news in terms of MS,
Speaker 5: is that there is an incredible amount of research being done. Like, yeah,
Speaker 5: two papers that came out in the last week that
Speaker 5: are a big deal. Yeah, And like we kind of
Speaker 5: really highlighted a lot in this biology section. There is
Speaker 5: just so much that we don't know. And I think
Speaker 5: that what's especially exciting about research on MS is that
Speaker 5: the kinds of studies that are being done are incredibly
Speaker 5: important not just for MS, but also for our understanding
Speaker 5: of neurodegeneration and cell regeneration, right, and this can help
Speaker 5: in the treatment of so many different diseases and neurodegenerative disorders.
Speaker 5: This is also what has led to so many new
Speaker 5: treatments for MS and related disorders as we better understand
Speaker 5: these kind of mechanistic underpinnings of this damage. Right, this
Speaker 5: kind of basic science is phenomenally important. And then there's
Speaker 5: also so many questions as to, you know, the genetics
Speaker 5: of why does one person develop MS after an infection
Speaker 5: with EBV and another person doesn't, Like, what is it
Speaker 5: about those immune responses? And and that is important not
Speaker 5: just for MS, but also for so many other immune disorders, right,
Speaker 5: Understanding what these triggers are, what these predispositions are, and
Speaker 5: like what we can actually do about them. Yeah, And
Speaker 5: these new studies really showing that EBV is likely, in
Speaker 5: fact a necessary precursor to the development of MS, meaning
Speaker 5: that MS is like viral sequelae of infection with this virus.
Speaker 5: That means that we could prevent MS, right, Yeah, if
Speaker 5: we could prevent infection with EBV, And it also means
Speaker 5: we could prevent so many other things that EBV also causes, right, brickets, symphoma, mono,
Speaker 5: like so many other things, right, and moderna of COVID
Speaker 5: vaccine fame just started. Like literally, this press release also
Speaker 5: came out within the last couple of weeks. They just
Speaker 5: started phase one trials of an mRNA vaccine targeting EBB.
Speaker 4: Oh my gosh, it's so thrilling.
Speaker 5: It is, And this technology has been able to happen
Speaker 5: so quickly because of the research that was done on COVID.
Speaker 5: So like, it's just it's one of these things that
Speaker 5: the interplay between the basic science research on one aspect
Speaker 5: of a disease can have implications for so many others.
Speaker 5: I just think it's really fascinating.
Speaker 4: Yeah, so totally.
Speaker 5: I think there are really exciting and promising things to
Speaker 5: come when it comes to MS treatment and possibly prevention.
Speaker 4: Yeah, it really does feel like we're on the edge
Speaker 4: of having like a firm complete picture for what causes
Speaker 4: some people to develop MS, and hopefully that'll lead to
Speaker 4: better treatments or cures or tools for prevention.
Speaker 5: Yeah.
Speaker 4: And if it turns out that the epstein bar virus
Speaker 4: is a good way to focus those tools even better
Speaker 4: m h. And if you want to know more about
Speaker 4: EBV and all the tricky ways that it acts to
Speaker 4: cause disease or predisposed to disease. Make sure you tune
Speaker 4: in for next week's bonus episode. I am so thrilled
Speaker 4: to get to chat with doctor Mika Luftig, Associate Professor
Speaker 4: and Vice chair in the Department of Molecular Genetics and
Speaker 4: Microbiology at Duke University.
Speaker 5: It's gonna be so good.
Speaker 4: I am so excited. Doctor Luftig has worked on the
Speaker 4: epstein bar virus for nearly his whole career and he
Speaker 4: is going to be subjected to my many many questions
Speaker 4: on the how, the what, and the why of EBV infections.
Speaker 4: And I also want to get into some bigger picture
Speaker 4: questions about like grad school and academia, good stuff, bad stuff,
Speaker 4: all the stuff in between. I think it's I think
Speaker 4: it's going to be a good one. So make sure
Speaker 4: you mark your calendars.
Speaker 5: Okay, tune in, don't miss it.
Speaker 4: Sources sources, Okay, So I have several, but I'm just
Speaker 4: going to shout out one in particular, and that is
Speaker 4: a book by Jock Murray called multiple Sclerosis, The History
Speaker 4: of a Disease. And then there I have more about
Speaker 4: like evolutionary history and so on that I'll post.
Speaker 5: I had a number of papers on the kind of
Speaker 5: general biology and a lot more on the specifics and
Speaker 5: mechanisms of the damage in MS. Specifically, I want to
Speaker 5: shout out the Science paper and the Nature paper that
Speaker 5: we're really looking at EBV and MS. Those were both
Speaker 5: very exciting, published January twenty twenty two. And like I
Speaker 5: also said, I do want to give a special shout
Speaker 5: out to the National MS Society website because I think
Speaker 5: that it is just such a helpful breakdown of so
Speaker 5: many different aspects of MS, but especially like different symptoms
Speaker 5: of MS, because I think that's something that most of
Speaker 5: the papers just don't do a good job of explaining.
Speaker 4: Yeah. Yeah, thanks again so much Nikki for taking the
Speaker 4: time to chat and sharing your story. It honestly means
Speaker 4: so much to.
Speaker 5: Us, so much. Thank you. Thank you also to Bloodmobile,
Speaker 5: who provides the music for this episode and all of
Speaker 5: our episodes.
Speaker 4: And thank you to you listeners. We hope you liked
Speaker 4: this episode. We hope that you found something new that
Speaker 4: you didn't know about and that you take a little
Speaker 4: tidbit and share it with somebody else.
Speaker 5: Yeah yeah, tell your friends. Yeah, And a special shout
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Speaker 5: the world to.
Speaker 4: Us, it does okay, well, until next time, wash your
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Speaker 5: You filthy animals, U.