Dr. Svetlana Mojsov: The Unsung Ozempic Hero

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Ozempic and Wegovy are everywhere, but there is one scientist who has been left out of all the news articles. Arpita tells the story of a female immigrant scientist whose discoveries were the key in creating these wonder drugs. 

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Episode Transcript

Aarati (00:11):
Hi everyone, and welcome back to the Smart Tea Podcast,
where we talk about the lives ofscientists and innovators who
shape the world.
Good morning, Arpita.

Arpita (00:20):
Good morning, Aarati.
We are recording this on aSaturday morning, and I'm
surprised Aarati's awake.

Aarati (00:29):
I am so not a morning person.
It's pretty early for me to betalking to people.

Arpita (00:35):
I want to state for the record that 9 a.
m.
was Aarati's idea.
I did not push that, and I wasvery surprised.
I was like, oh shit, like I willdefinitely be awake, but I

Aarati (00:46):
was,

Arpita (00:46):
am

Aarati (00:47):
I was also like, okay, she wants to know what time I
will be awake, so what time isnot embarrassing for me to say.
Like, Is it really embarrassingif I say like 10 o'clock, 11
o'clock?
It's not morning anymore.
So

Arpita (01:05):
was, that was really funny for me.
I was like, oh, okay, like, wow,okay, let's do it.

Aarati (01:09):
Yeah.

Arpita (01:11):
Like on a Saturday, Like, I'll wake up, but I
usually have, like, a slowmorning, you know, I'll, like,
wake up, I'll, like, make somecoffee, I'll, sit on the couch,
read my Kindle.

Aarati (01:21):
Yeah.
Just relax.

Arpita (01:23):
if you can see what's happening here.

Aarati (01:25):
Oh wow.
Oh my goodness.
Is that Poppy?

Arpita (01:29):
This is Poppy.
Poppy, you wanna say hi to thecamera?
Um,

Aarati (01:32):
Yeah.
I can tell by the orange fur andbeautiful green eyes.

Arpita (01:36):
Can you hear her purring?

Aarati (01:38):
Yeah, she's so cute.
Oh my goodness.
So content

Arpita (01:42):
she does this every day.
And so usually most of my dayworking from home is sitting in
this chair with this blanket,this cat.

Aarati (01:51):
God, that sounds amazing.

Arpita (01:53):
And I'm like, at one point, like if I ever get a new
job in which I actually have togo into work, like, I don't know
if I'm going to be able tohandle that

Aarati (02:01):
Yeah,

Arpita (02:02):
Like, it's going to be a downgrade, right?

Aarati (02:03):
I have the same exact thing.
Just, do we really have to meetin person cause then I have to
get all dressed up...

Arpita (02:09):
That's what I mean, much effort.

Aarati (02:12):
And also I think part of it is my brain, like, I need to
work on tasks half an hour at atime, like, so need to do work,
and then I need to go cooksomething, and come back and do
work, and then go make tea orsomething, and like, you know?

Arpita (02:26):
I'm fully with you.

Aarati (02:27):
It makes me so productive.

Arpita (02:28):
I agree with you.
I don't know if I would do wellin an office setting at this
point.
I'm also just like, do I knowhow to talk to people still?

Aarati (02:37):
Same.

Arpita (02:38):
Do I know how to have like a deskmate?

Aarati (02:41):
Yes.
Do I know how to have aconversation?
Do I know how to like

Arpita (02:45):
be a normal coworker?

Aarati (02:46):
Yes.

Arpita (02:48):
I don't know if I can.

Aarati (02:49):
Yeah, I don't think, I don't think I can either mm god.
I've been, um, waking up earlyanyway this week a lot because
I've been putting together thisworkshop, for tech people and.
anyone else who's interestedabout science communication
basically.
Um, so we've been like planningthis, these workshop sessions
and then we've been having themearly in the morning because

(03:12):
some people are like from Europeand some people are from the
east coast and so we want tofind a time that everyone is
kind of available and can attendand it's been pretty good.
It's been like we've had prettygood turnout and everything but
yeah, partly because I'm like,yeah, okay.
I've been Recently

Arpita (03:28):
You can wake up early.
Yeah.

Aarati (03:30):
anyway.
Get going.

Arpita (03:32):
That's funny.

Aarati (03:33):
Yes.

Arpita (03:34):
Well, I'm very proud of you.

Aarati (03:35):
No, thank you so much.
Anyway, I wonder who you'retalking about today.
Are they a morning or nightperson?
Do you know?
Mm

Arpita (03:43):
wow.
Great question.
If I had to hypothesize, I wouldsay this person is a morning
person, but you know what?
I could be wrong.
A lot of really intelligentproductive people are night
people.
So who knows really?
Today we're talking aboutSvetlana Mosjov.
Um,

Aarati (04:00):
Another Russian?

Arpita (04:00):
She is Macedonian.

Aarati (04:01):
Oh, Macedonian,

Arpita (04:05):
Yeah, another Eastern European.
But I am very excited to talkabout her she is one of the
scientists who was involved indiscovering GLP-1, which is
Semaglutide, which is Ozempicand Wegovy and all of these like
weight loss medications, whichare huge

Aarati (04:24):
Mm hmm.

Arpita (04:24):
you know, guess like current events because it's
created a ton of revenue forpharmaceutical companies and all
these like celebrities aretaking it.
And I just find it veryfascinating in general because
it started out as something tohelp people with diabetes and
then turned into this likeweight loss, wonder drug.

(04:47):
Um, but this is a reallyinteresting story about how this
came to be.
So I'm really excited to talk toyou about her.

Aarati (04:54):
I'm excited because last year I was working with Boston
Medical University and I made aseries of videos with them about
GLP 1 medications, like Ozempic.

Arpita (05:08):
Oh, cool.

Aarati (05:08):
Yeah, And so we just made a bunch of videos
explaining to patients how touse it basically, just like, you
know, how to store it and how toinject yourself and things like
that.
It was a lot of fun, but it wasIt was, it was cool.
Yeah.
So I'm excited to hear about, I,I know kind of like, now I know
how to inject yourself with themedication...

Arpita (05:30):
Ok yeah, that was not of my research.

Aarati (05:32):
Yeah.
I don't, I don't know anythingabout how it got started or
Svetlana herself.
So I'm excited to hear about it.

Arpita (05:39):
Great.
Okay.
Let's hop it.
So Svetlana was born in Skopje,which is in Northern Macedonia,
and she was born when it wasformerly Yugoslavia.
So she grew up in the 50s inEastern Europe and loved, you
know, going out in nature andwas very scientifically curious,

(06:01):
her family moved to Belgrade andshe loved physics and chemistry
and loved lab class andexperiments where, you know,
you've got to combine twodifferent things to create a
third thing that was brand new.
Um, and so Yugoslavia aftertheir war, uh, had a really

(06:22):
great education system wherethey encourage students to.
Get an education regardless oftheir gender, which was pretty
great for how early this was.
So she got a degree inchemistry, from the university
of Belgrade.
So she had a very good earlystart.
Um, I should caveat by sayingthis, that Svetlana is very much

(06:46):
still alive.
So in terms of like biography, alot of like this early stuff was
fairly limited.
So a lot of the things about herpersonal life and, um, I don't
know, the way you would, like,read a biography about

Aarati (07:01):
Mm hmm.

Arpita (07:02):
someone who is no longer with us is a little bit
different.
Yes.
So, yeah,

Aarati (07:07):
That makes sense, yeah.
The research will be different,um, people won't have written,
like, a whole thing about herlife and commemorating her and
remembering her yet, you

Arpita (07:17):
Yet, exactly.
She's very much alive, very muchwith us.
And so, um, yeah, so like theresearch is a little bit
different.
The bulk of this focuses on, youknow, her adult life and her
work.
So just caveating the fact thatwe are very quickly barreling
through our youth Okay, so thenShe immigrated to the U.

(07:39):
S.
for graduate school atRockefeller University, and once
she got here, she was very drawnto Bruce Merrifield's lab, and
she joined as the first femalegraduate student.
And Bruce would later go on towin a Nobel Prize for his very
efficient method of synthesizingpeptides.

(08:01):
And so she was basically in achem lab.
So during her graduate work, shefocused on glucagon.
So glucagon is a hormone that isreleased by your pancreas as a
check on insulin.
So when you eat, you experiencean increase in blood glucose,
and then your pancreas releasesinsulin to help lower it.

(08:22):
Glucagon does the opposite.
So when your blood glucose dipstoo low, your body uses glucagon
to then release glycogen storesin your liver and other parts of
your body to make sure that yourblood glucose doesn't drop too
low.
Did you learn the, um, did youlearn the, uh, mnemonic for that
in grad school where it's like,glucose is gone, so it's gluca

(08:43):
gone, and sometimes that's whyit releases?

Aarati (08:46):
Oh no! I don't think I've, I don't think I learned
that one.
I think I've kind of associatedglucagon as like the hunger
hormone kind of you know, but Ididn't, I didn't have like a
pneumonic device that would havebeen so helpful.

Arpita (09:00):
Glucose is gone, glucagone.

Aarati (09:02):
That's so useful.
Yeah.
I don't know why I didn't thinkof it myself, too.
It's like right there.

Arpita (09:09):
I know, it's literally right there.
It's like barely a mnemonic.
It's like actually the word.

Aarati (09:13):
wonder That's how they came up with it.

Arpita (09:15):
I have no idea.

Aarati (09:16):
That like the amount of creativity that scientists have.

Arpita (09:20):
That's actually fact.
Like, um, god, this is escapingme.
What is the green stain we usefor everything?
The, um,

Aarati (09:27):
GFP?

Arpita (09:27):
GFP?
yeah.
Where it's like literally greenfluorescent protein.
It's like, we couldn't think ofanything.
We were just like, it's greenand it's fluorescent And it's a

Aarati (09:38):
have RFP for red fluorescent, and then YFP, and
then we have all the FPs.
All the fluorescent proteins,yeah.
But then, you know, on the otherhand, I, we, like, I read
science papers, but, I readscience papers where they're,
like, literally making stuff up.
They're just like, oh, we'recalling this behavior, like,
rotating to left, or R T L, andthen they use R T L for the

(10:04):
entire paper, and I'm like, isthat really necessary to
abbreviate that or create awhole separate word for
something that already exists,you know?

Arpita (10:13):
I feel like a lot of times in papers, maybe this is
not true.
I also get really grumpy whenlike unnecessary things are
acronymized.
I don't know.
That's not a real word, but likewe do not need an acronym for
everything.
Um, because if you're likeskimming a paper and you miss
the part where they define it.
You're like, what is R T like,what does that mean?

(10:37):
Like, and then you have to like,then you have to exactly, they
need to like, command F and likefind where they'd mentioned it
the first time and then go backup.
It's so dumb.
But I wonder if papers do thatbecause a lot of journals have
word count limits.

Aarati (10:50):
Probably! Which I also think is stupid, because I'm
like, everything is online,like, what is the

Arpita (10:58):
Why do you care?

Aarati (11:00):
Why does it matter, everything's online now, it, it
literally doesn't matter,

Arpita (11:05):
It literally doesn't matter.
And then they.
They link all like thesupplementary information
anyway.
So I'm like, if the table that Ineed is in supplementary
information, like, why do younot just like put it all in one
place so I can just scroll tothe bottom and find your tables?

Aarati (11:20):
Yeah.
Or just link it somehow.
I mean, we're so behind thetimes in some of these cases.
I don't know.
It's just so frustrating andthen it just impedes people
accessing that kind of knowledgebecause you don't want to read
the paper then if it becomes toofrustrating to read, you're just
like, it's such a barrier tounderstanding and learning.

Arpita (11:42):
And like no one, most normal people are not out here
reading an entire paper start tofinish.
Like that is

Aarati (11:51):
Yeah.

Arpita (11:51):
point of a paper.

Aarati (11:52):
Abstract conclusion, maybe a little in the

Arpita (11:54):
Right, like, maybe and also, like, usually I have a
specific question.
If I'm looking at a paper.
I have a specific thing that I'mtrying to understand.
I don't care about your methods.
I don't care.
I don't care.
I just want to know.
I'm looking for this one datapoint.

Aarati (12:09):
Yeah you're looking for like, Figure 3b...

Arpita (12:12):
Exactly.
I'm like, I your Table 2, like,row three.
Like that's what I need.

Aarati (12:17):
what I need.
I need that one data point

Arpita (12:20):
And if I have to scroll up looking for all your damn
acronyms, like I'm going to be

Aarati (12:24):
yeah, yeah, you've made this whole job, like, half an
hour when it should have beenfive minutes.
It's

Arpita (12:30):
Oh,

Aarati (12:31):
so frustrating.
Anyway, we've gotten on a verybig tangent.

Arpita (12:34):
Now that we've gone on our big soapbox about how

Aarati (12:37):
we

Arpita (12:37):
hate journals.
Um, now I have to find my placeagain.

Aarati (12:40):
Yeah.
How did we get on this topic?

Arpita (12:42):
I don't know.
Glucagon?
Oh yeah, glucose Yes.

Aarati (12:46):
Glucose is gone.
That's so far back.

Arpita (12:50):
We, yeah, we were, we're on page, we're on page one of
this

Aarati (12:54):
Oh my God.
Okay.
See like in the mornings youhave all this energy and I'm
grumpy and it's like not a goodcombination.

Arpita (13:03):
I know maybe we should go back to post lunch recording
when both of us like, you know,like leveled out.

Aarati (13:11):
Yeah, where you're tired and I'm happy.
Oh my God.
Oh, God.

Arpita (13:15):
Okay.
Let me, Let let me find my placeagain.
Yes.
Okay.
So in people with type twodiabetes, their blood glucose
levels get too high because theyhave insulin resistance.
So that means that when insulinis released, their blood glucose
levels actually don't reallyrespond that well.
So then it remains high insteadof being lowered by insulin.

(13:36):
So There's this hypothesis thatif you suppress glucagon, and
then you prevent increasedlevels of blood glucose, this
could actually help withtreating type 2 diabetes.
However, this was difficult tostudy because synthesizing

(13:56):
glucagon was pretty challenging.
However, in this lab, in BruceMerrifield's lab, he was really
focusing on synthesizingpeptides and synthesizing
proteins and Svetlana in thislab finally got it to work.
So she was able to synthesizeglucagon.

Aarati (14:13):
Oh, nice.
And this when she's still a gradstudent or postdoc or something.

Arpita (14:18):
She's a grad student.

Aarati (14:19):
Okay.

Arpita (14:20):
So while she's a grad student.
Svetlana met her future husband,um, an immunologist.
Nussenzweig.

Aarati (14:29):
Good job.

Arpita (14:30):
Thank you.
Uh, and so he was, um, workingon an MD PhD, uh, at NYU, and
then he was doing his PhD atRockefeller as well.

Aarati (14:42):
Wait, he's doing an MD, PhD at NYU?

Arpita (14:45):
Sorry, he, just his MD and then his PhD at Rockefeller.

Aarati (14:50):
Okay, because I was just like, oh my god, I've heard of
MD PhD, which I think is alreadyamazing and incredible, but is
he doing an MD PhD PhD, like adouble PhD?

Arpita (15:01):
no, no.
No, sorry, MD

Aarati (15:03):
MD

Arpita (15:03):
PhD, and he's studying at both NYU and Rockefeller.

Aarati (15:08):
Got it.

Arpita (15:08):
That's how they met.

Aarati (15:09):
Got it.

Arpita (15:10):
So he was very cute.
And when she would be stressedwriting her dissertation and
working on experiments, he wouldcome to her office and lab and
bring her food and hot cups oftea.
And

Aarati (15:22):
Oh my amazing.
Adorable.

Arpita (15:25):
And so by the end of her PhD in 1978, she wrote her
thesis on glucagon synthesis,and then she stayed in Bruce's
lab as a postdoc to like refinethese techniques a little bit
more.
And then a few years later inthe early eighties, her husband,
Michel started residency at MGHin Boston.
So they both relocated to Bostonand Svetlana joined the

(15:48):
Endocrine Department as anadjunct instructor.
So in this new role, she becamethe head of a new facility that
would specifically synthesizepeptides for the endocrine
scientists.
So, that was really her job wasto synthesize these peptides,
which then she would send off toall the labs that were using
these for their experiments.

(16:09):
So though this was like reallyimportant work, it wasn't very
time consuming.
So it gave her a lot of freedomto pursue her own research.
So she had one lab bench and shedidn't really have a lot of
funding.
She had pretty limited funding.
So she was only able to hire onetechnician but with these
limited resources, she knew thatshe wanted to study this

(16:30):
mysterious peptide that wascalled Glucagon-like peptide 1,
which we now know as GLP 1.
So GLP-1 had been recentlydiscovered in another MGH
endocrinologist lab, JoelHabener and he and his lab were
studying key hormones, includingglucagon in anglerfish

(16:51):
pancreases.
And they apparently like pulledthese anglerfish out from the
Boston Harbor.

Aarati (16:56):
Wait, they pulled the anglerfish out of Boston Harbor
to study in the lab?

Arpita (17:01):
Correct.

Aarati (17:02):
Whose job is that?
Is that the scientist's jobalso, to go trap fish?

Arpita (17:06):
You would know that it was some like undergrad, like
some unfortunate like child whowas forced to go out onto the
docks.

Aarati (17:14):
Some intern.

Arpita (17:15):
Literally.

Aarati (17:16):
Like high school intern, who's like, we need more fish
for the lab, go catch them atsix in the morning.

Arpita (17:22):
Literally.
So they dissected and froze thefish pancreas islet cells.
So those are like the specificcells that produce insulin and
glucagon.
And they were searching for theDNA inside and then they
ultimately cloned a gene calledproglucagon which they thought
was actually the thing that wassynthesizing GLP 1.

Aarati (17:46):
I wonder why they were using anglerfish?

Arpita (17:48):
I don't even know.
Anglerfish aren't really a modelorganism.

Aarati (17:52):
Yeah.
Yeah.
It's an interesting choice tostudy glucagon also, like
insulin and glucagon in a fish,like, I don't

Arpita (18:03):
know.
I don't even know what the modelorganisms are for studying like
pancreas or like endocrinerelated stuff.
Like, I don't, I don't know.
I don't know what modelorganisms are.
It's a good question.
Are you Googling it?

Aarati (18:16):
Yeah.
I see a lot of stuff aboutzebrafish.

Arpita (18:20):
So then why didn't they just buy some zebrafish?

Aarati (18:22):
Yeah, because we had the I'm just wondering, because
like, I studied worms, right?
Like, nematodes, and we had thiswhole list of reasons as to why
they're the greatest modelorganism ever.
Like, they're transparent andthey have, like, these little
tiny brains, which makes themreally easy to study, um, and
they self replicate basically,which is fantastic if you find
one mutant, you can makethousands more without having to

(18:46):
breed them and like do all thesecross genetic stuff.
It's pretty amazing.
So, yeah, I'm sure, I'm sure theanglerfish community is also
like, anglerfish are thegreatest model organism ever.

Arpita (18:57):
Are anglerfish a model organism though, or are they
just like fish that exist?

Aarati (19:01):
Are they just fish that exist?
And we, and this lab justdecided to study them.

Arpita (19:07):
Yeah.

Aarati (19:07):
Yeah.
I'm sure there must be a reason.
Somebody tell us.
Somebody tell us the reason whyfish are the greatest model
organism.

Arpita (19:14):
This like lab went on to win like a buttload of prizes,
which is like really not aspoiler.
I feel like we kind of knew butlike clearly they did something

Aarati (19:23):
Yeah.
Yeah.
Okay.
Sorry.
yeah.
There's, they're usinganglerfish to study islets,
right?
Islets and pancreas, in thepancreas.

Arpita (19:32):
The islet cells in the pancreas.
Yes.
So in 1982, just before Svetlanagot to MGH, they reported that
this gene, proglucagon, encodeda large precursor protein that
the body then cleaved to formglucagon.
So this kind of reaction ispretty common in protein

(19:53):
synthesis in the body.
You have like a much largerpeptide that is synthesized and
then gets kind of broken downinto these smaller things that
then go on to have effects onyour specific cells.

Aarati (20:04):
Yeah, it's almost like refining it in a way this really
big thing and then it just youshave it down a little bit to
make it the perfect fit likewood cutting.
or something.

Arpita (20:13):
Exactly.
That's a great analogy.
So GLP-1's amino acid sequencealso shares some features with
gastric inhibitory peptide orGIP.
which at the time, GIP was theonly known member of a distinct
category of hormones calledincretins.
So Incretins are produced by thegut and they kind of kickstart

(20:35):
the pancreas into releasinginsulin.
And because they do that,scientists thought that it could
make them really useful forstudying and then even maybe
like treating or curing type twodiabetes.
But in the studies for GIP, itended up being kind of
disappointing.
Using it in humans resulted invery little effects in changes

(20:58):
in insulin levels.
And this ended up being kind ofa bust for Joel Habener's lab.
So Joel and Svetlana wonderedwhether GLP-1 would be different
and if it actually would end upbeing an incretin.
So one step towards finding outwhether or not this was true was
to see where in the body theactive form of this peptide was

(21:21):
being made.
So this is the portion of theprotein that when cleaved or cut
off from the parent proteinwould become biologically active
or actually have an effect onyour cells.
So Svetlana looked at the stringof 37 amino acids that made up
the mammalian GLP 1 sequence.
And based on the similarity ofthe sequence to glucagon, she

(21:45):
hypothesized that a stretch of31 amino acids between the spot
seven to 37 within the largerGLP-1 peptide might be an
incretin.

Aarati (21:57):
So the GLP 1 peptide has like, how many did you say?
Um, 37 similar amino acids toglucagon?

Arpita (22:08):
37 amino acids total.
And then.

Aarati (22:11):
amino acids total.

Arpita (22:12):
And then because she was looking at the sequence, and she
was like, these 31, so spots 7to 37, um, seem similar to
glucagon.
And so she was like, this mightbe, like, she's just
hypothesizing that this might bethe sequence that is most
interesting.

Aarati (22:30):
Right.
Okay.
And so because of that, it ispossible that GLP 1 will act in
a similar way to glucagon torelease sugar stores from the
body.

Arpita (22:40):
So, she had this hypothesis that it was spot 7 to
37, and then she had to provewhether or not that was true.
So, to see whether the 7 to 37fragment was present in the
intestines, she used an antibodyto search for it.
So she first made a lot of GLP 1like the protein itself and

(23:01):
injected rabbits with differentsegments of her GLP 1 peptide.
And then she waited two monthsfor the antibodies to
proliferate in their blood.
So she basically, the antibodieshere are kind of functioning as
a tag or a marker to help yousee whether or not that's
present in the blood.
So she's kind of chopping upthis bigger peptide into smaller

(23:22):
segments and testing differentparts of it, even though her
hypothesis is 7 to 37 and seeingwhich tags are present and which
bits of this biologically activeprotein are present in the
blood.

Aarati (23:33):
Oh, so she made like a range of antibodies that all
recognized different parts ofthe peptide.
It wasn't just one antibody.
Oh, okay.

Arpita (23:43):
her.
So she has an idea that it'sthis specific segment, but as a
good

Aarati (23:48):
as a good

Arpita (23:48):
scientist...
She,

Aarati (23:49):
yeah, she's gonna test, she's gonna test all the
regions.
Yeah.
Good job.
Okay.
Very thorough.

Arpita (23:57):
Very thorough.
Um, and so she then collects,uh, so she's doing this in
rabbits.
I don't know why we moved fromanglerfish to rabbits, no idea,
but she

Aarati (24:09):
At least it's a mammal, so I'm happier with rabbits, or
like, not happier, but you knowwhat I mean.
Like, it makes more sense.

Arpita (24:17):
This next part made me laugh.
Um, so she collected blood fromone of the neck arteries in the
rabbits and then isolated theantibodies.
And she said in an interviewthat this experience working
with the rabbits made herdislike working with lab animals
because it made her feel likeshe needed to go home and take a
shower.
And I was like, Literally, yes.

Aarati (24:36):
Yes.
yes.
Yeah, that's, that's why Ialways stopped at worms.
Worms are like, microscopic Ican't even touch them.
I never got to even flies.
I was like stuck, stuck at theworms.
Oh my gosh.
I can't imagine rabbits.
They're so cute too.
I mean, she was just withdrawingtheir blood, right?

(24:57):
So

Arpita (24:59):
There's no sacking, but I mean, I'm, I'm sure she
eventually sacks them, but Imean, I You

Aarati (25:03):
to, but yeah.
Oh yeah.
But I totally get that.

Arpita (25:07):
I totally get it.
It made me laugh.
So two floors below her, Joeland his team are beginning to
look at the biology of GLP 1.
So in 1984, the lab got a newpostdoc.
His name was Daniel Drucker, whowas looking to identify which
specific cell types wereproducing GLP 1.

(25:29):
Um, so like looking at the isletcells, but like which one
specifically.
Um, and Daniel was an MD and anendocrinologist.
He had never worked in a labbefore, so he struggled a little
bit when he got there.

Aarati (25:43):
Yeah.
It's, I think people actuallythink that doctors know a lot
more science than they do, like,you know,

Arpita (25:51):
Or like

Aarati (25:52):
very,

Arpita (25:52):
bench research.

Aarati (25:53):
Yeah, like, bench research and stuff, and it's
like, it's very different,that's why our whole field
exists of, like, medicalcommunications, because doctors
don't have the time to go intoall the research, And they need
something, like, really quick,and easy to digest on the
limited amount of time theyhave.

Arpita (26:10):
Yeah, it's, it's true.
So he struggles a little bit.
Um, and Daniel then asksSvetlana if she wants to
collaborate.
And Svetlana told him that she'dalready produced antibodies to
different stretches of GLP 1and, like, she has a specific
way to detect its presence inthe intestines.

(26:32):
So Joel's lab and Daniel, uh,joined forces with her to use
her detecting methods to trackdifferent stretches of GLP 1
peptide in various rat tissues.
So they've somehow moved on torats.

Aarati (26:46):
Okay.
Just across all the modelorganisms.

Arpita (26:48):
know.

Aarati (26:49):
model organisms, the better.

Arpita (26:50):
So Svetlana found that the 7 to 37 stretch of GLP 1 was
the active portion, which isexactly what she had
hypothesized, which was in rats.
So this data, uh, were publishedin a joint paper, um, that
listed Svetlana first and Joellast, and it's now considered a

(27:13):
landmark in the field of GLP 1s.
So the next question was whetherthe 7 to 37 form of GLP was
biologically active.
So that means, does it actuallytrigger insulin release in the
pancreas?
So we know that this is like thesegment of GLP 1 that's actually

(27:33):
doing the work, like there'sancillary proteins around it,
like we know now this is the bitthat we really care about.
But is it the actual peptidethat is now triggering the
release of insulin in thepancreas?

Aarati (27:45):
Oh yes.
Is it actually doing the thing?
Yeah.

Arpita (27:48):
actually doing the thing?
Yeah, exactly.
I know I was trying really hardnot to get into the weeds of
protein research.
Hopefully this is making sense.

Aarati (27:58):
Yeah.
I think it is.

Arpita (28:00):
so using Svetlana's synthesized GLP 1, Daniel led a
study showing that GLP 1 didactually prompt insulin
secretion in a line of ratpancreatic islet cells.
So now that they've shown this,they want to test its effects in
a whole organ.

(28:21):
So Joel contacts a friend, anendocrinologist named Gordon
Weyer, who developed a ratpancreas model.
And this is an organoid.

Aarati (28:32):
Oh, okay.
Yes, you're going to explainthis more.
Cause it sounds, I'm likeimagining a pancreas floating in
a little jar or something.

Arpita (28:39):
That is in fact, exactly what it is.
So it isn't an actual, so, okay,let's reverse.
Okay.
So now that they've shown thatthis happens basically in vitro,
that this is, so that's thecells are kind of like by
themselves in a vacuum, they arereleasing the insulin that we

(29:03):
are hypothesizing.
So we're like looking at thecells by themselves.
Now we're trying to see if thisis happening in real life,
basically, like, actuallyhappening in the organs?

Aarati (29:13):
Yeah.
So we proved it in the petridish.
Yeah, we have a little Petridish with cells.
It's doing the thing.
When we put GLP 1 in, oractivate GLP 1 in these cells,
they release insulin and we cantest that because we can take
the, you know, solution of cellsand see how much insulin has
been produced in the Petri dish.

(29:33):
And now let's see if it actuallyhappens in real life in a, in a
animal.

Arpita (29:39):
Exactly.
So really they're like sequenceof events.
You can think of like startingvery, very small.
They're getting bigger andbigger and bigger.
And so now they are in anorganoid.
So this friend, Gordon, hasdeveloped a three dimensional
cluster of cells that aredeveloped from pancreatic stem
cells designed to mimic thefunctions of an organ.

(30:00):
So it's not like an actual ratpancreas that was like excised
and put into a dish.
It is a cluster of cells thatfunction together kind of like
an So it's a, almost like asimulation that is manufactured.

Aarati (30:17):
So he like, took pancreatic stem cells and kind
of made them differentiate intonot a full

Arpita (30:24):
pancreas,

Aarati (30:25):
but like..

Arpita (30:26):
A, quote unquote, pancreas

Aarati (30:28):
A glob of cells that kind of act like a pancreas.

Arpita (30:31):
Correct.
Exactly.
Correct.
So if you think about if youwere to just remove the entire
pancreas, it is relying on, youknow, nearby structures and
other cells.
It requires blood flow.
It requires all of these thingsin order to function properly.
So if you actually dissected arat and put it, put their

(30:52):
pancreas in a dish, it wouldkind of just be like tissue that
doesn't really do anything.

Aarati (30:56):
Yeah, Makes sense yeah.
There's no arteries.
There's no, yeah, yeah, thatmakes sense.

Arpita (31:02):
So you're basically creating like a simulated little
bit of it that you canmanipulate in a dish.
It's like one step above like abunch of cells in a dish.
Okay, so the organoid is storedin a plexiglass box, so you were
right, and it's oxygenated atbody temperature, and it's like

(31:22):
this very controlled environmentwhere researchers could measure
the insulin levels minute byminute.

Aarati (31:28):
Mm hmm.

Arpita (31:29):
So Gordon injects the rat organoid with the
synthesized GLP 1 and insulinoutput increased.
So they started putting less andless peptide in, and they
learned that even tiny amountsof GLP 1 had an effect.
So Svetlana measured how muchGLP was administered to confirm

(31:50):
that the peptide aligned withthe insulin response, and the
two hormones go exactly up inparallel.
So Administering GLP 1 releaseto a one to one release of
insulin.

Aarati (32:03):
So the more GLP 1 you administer, the more, insulin
will be released, and the lessGLP you administer, the less
insulin will be released.
Oh wow, so you can like exactlytiter how much insulin, if you
want this much insulin to bereleased, you have to put this
much GLP in.
That's really cool because Ifeel like that rarely happens in
science, like it's always thishuge mixed box of like 10

(32:26):
different factors that are...
you know?

Arpita (32:29):
And then you have to do some crazy stats to figure out
what the relationship is.

Aarati (32:33):
Exactly.
That's so cool though.
That's like so nice, the one toone ratio.
Beautiful.
I would be so excited.

Arpita (32:41):
It's beautiful.
So.
Uh, she says in an interviewthat it was a beautiful
experiment.
She agrees with you.
And the paper that theypublished in 1987 in the Journal
of Clinical Investigation listedjust three scientists.
So Svetlana was first, Gordonwas second, and Joel last.
This work confirmed that GLP 1was one of those very long

(33:03):
sought after incretins.
The MGH group was the first tostart testing GLP 1 in humans.
So Joel teamed up with a youngMGH diabetes specialist, David
Nathan, who infused the peptideinto healthy people and people
with diabetes.
And GLP 1 prompted insulinrelease.

(33:25):
just like it did in theorganoid, um, when glucose
levels rose.
So for example, after you eat.
So by the time David Nathan'spaper was published in 1992,
Svetlana had moved back to NewYork City.
So she and her husband, Michelhad moved two years earlier when
he received a job at RockefellerUniversity.
So they came back and atRockefeller Svetlana joined the

(33:48):
lab of an immunologist, and alsoa future Nobel laureate, Ralph
Steinman as an assistantprofessor.
And so her life is changing alittle bit at this point.
She has two young kids and isbalancing being a working
mother, but regardless as anassistant professor, she still
is studying GLP-1 biology.

(34:09):
Back in fish, unclear of fish,um, and she has funding from the
National Science Foundation todo this work.
So, meanwhile, back at MGH, workon GLP 1's effects in humans was
moving forward with manydifferent investigators.
So we have a few new charactersin the nineties, Jens Holst

(34:32):
found out that unlike GIP, whichwas the failed peptide, GLP-1
could normalize blood sugarlevels in people with diabetes.
So just remembering that peoplein diabetes have very
uncontrolled levels of bloodglucose and normalizing that can
be really huge for theirtreatment.

Aarati (34:49):
Yeah.
So GLP-1 is not just releasinginsulin, but the insulin is
actually working to normalizethe blood sugar levels.
Very, very important.
Because what's the point ofreleasing insulin if it doesn't
work for some reason?

Arpita (35:01):
Exactly.
And they also very interestinglyfound that in rat studies, GLP 1
also caused appetite loss.

Aarati (35:10):
Yes.
Now we're getting to, now we'restarting to get to the
beginnings of

Arpita (35:17):
Okay, so put a pin in that we're going to come back to
that.
So though Svetlana was now atRockefeller, and she's in New
York.
She took a lot of pride in herwork that she did on GLP-1 at
MGH so she was starting towonder whether any patent
applications had been filed.
So she sent a few emails toJoel, which he never responded
to.
And a few years later in 1996,she mentioned this to a friend

(35:39):
who worked at a biotech companywho then looked it up and told
her that there were actually afew patents that had been
granted a few years earlier.
So she looked these patents upand she found two 1992 patents
was when the paper got publishedon a quote unquote fragment and
quote unquote derivatives of GLP1 that had the ability to prompt

(36:00):
insulin secretion.
And these are all the peptidesthat she had developed.

Aarati (36:04):
But she's not the one with the patent.

Arpita (36:06):
All of these patents listed Joel as the sole
inventor.

Aarati (36:11):
Oh my gosh, no way.

Arpita (36:13):
Yeah.
And so then Svetlana hired apatent law firm to help her
fight for co inventor creditbecause Joel is not responding
to any of her emails.

Aarati (36:22):
Oh my gosh, he knew he did something shady.

Arpita (36:24):
This is really interesting.
So patent law is really tricky.
So inventorship can be a reallygray area since contributions
are not always like very welldefined.
So for example, if you did anexperiment that's like kind of
different, and then it inspiresme to invent something, do you
get credit for that?
Um, it's like unclear, but thelaw requires making a quote

(36:48):
unquote, not insignificantcontribution to the concept of
the claim invention rather thansimply carrying out the
experiments.
So it's really kind of whereintellectual property law and
patent law sort of overlaps.
Like who actually gets thecredit?

Aarati (37:03):
Right.
Yeah, because if my professorhad the idea, and then I just
carry out the idea, and I'm justlike the pair of hands who did
the actual experiment becausethey're the professor, you know?
They get the patent because itwas their idea.
That makes It makes sense.

Arpita (37:21):
To be clear, that is not what is happening in this
situation.
Svetlana absolutely the personwho had the idea behind this,
but that is kind of why thiswhole situation is tricky with
her lawsuit.
Um, so the fight with MGH'spatent office went on for years.
So, while this was happening,patents for the GLP 1 peptides

(37:42):
were licensed to apharmaceutical company, Novo
Nordisk.
Novo Nordisk immediately begandrug development using this
technology.
So finally, this is almost likea decade later, between 2004 and
2006, MGH agreed to amend fourpatents to include Svetlana, and
the United States Patent andTrademark Office accepted this

(38:03):
change in inventorship, and nowthat she had patent in name, MGH
agreed to award her one third ofdrug royalties with Joel getting
the remaining two thirds.

Aarati (38:13):
Good for her, for fighting for it for that long.
Like, over a decade, that takesdedication,

Arpita (38:19):
A long time.

Aarati (38:20):
good for her.
Like, yeah, get, get yourcredit, get, get your money.

Arpita (38:25):
No, literally.
Um, so a few years later, nowwe're in 2010, FDA approved the
first Novo Nordisk GLP agonistdrug called liraglutide, and it
was sold under the brand nameVictoza for diabetes.

Aarati (38:41):
Yeah.
I did four videos on Victoza.

Arpita (38:45):
So she started getting some royalties, but then they
stopped after just over a yearbecause her first patent
expired.
So it took her so long to gether name on it that she actually
didn't get to collect that manyroyalties on it.

Aarati (38:56):
That sucks.

Arpita (38:57):
And just like you, just like your sigh, I think she
agreed with that.
She was exhausted by this patentdispute.
She was like, I just want to putall of this behind her.

Aarati (39:05):
Yeah, screw this.

Arpita (39:07):
In an interview, Joel mentions that he has regrets on
how this patent story playedout.
He didn't think it would reallymatter that much or become this
consequential or lucrative whenhe filed the patent.

Aarati (39:17):
Then why didn't you tell her?

Arpita (39:19):
I call bullshit.

Aarati (39:22):
Like, you don't a big deal, then you should like, be
like, Hey, I'm this thing.
Do you just want to get in onit?
Because it's no big deal.

Arpita (39:31):
Yeah, I call BS that, but regardless, here we are.
So as much as Svetlana was likeready for this GLP 1 story to be
over, even though she reallycared about the science, as we
now know, GLP 1 was just gettingstarted.
So new versions of GLP-1agonists were approved for
diabetes.
In clinical trials, insulinlevels increased, which helped

(39:53):
control diabetes symptoms.
But as we found in rats, it alsocaused appetite loss.
So whether it was desired or notparticipants these clinical
trials began losing considerableweight.

Aarati (40:05):
When I was doing the videos, I think I read that the
mechanism of action for GLP 1 issuch that it causes like nausea
and that's kind of what leads toappetite loss.
And so then if you take too muchof it, you can actually induce
vomiting and all these likereally negative side effects.
And so that's like one thingthat patients who are taking GLP

(40:29):
1 medications kind of need to beaware of is that you can't just
like take a whole bunch andexpect like, Oh, I'm going to
get these fantastic resultsbecause it might actually become
more dangerous..

Arpita (40:41):
I'm not sure about vomiting and nausea, I'm
interested in that, but Ididn't.
I was trying to find out theokay.
Let me just read this part

Aarati (40:49):
Yeah.
Talk about the mechanism ofaction.
Yeah.
Talk, talk about how it works.

Arpita (40:53):
So in just to back up a little bit in obese individuals,
or even in type 2 diabeticindividuals, the fat in your
belly or visceral fats, thisisn't the fat that's like right
under your skin this is likedeep fat that's around your
organs.
can cause inflammation inside ofyour body, which can contribute
to the insulin resistance.

(41:14):
And excess fat can accumulate inyour liver and other tissues,
which then interfere with thebody's ability to respond to
insulin signals after eating.
As a result, if there are excessnutrients floating around and
insulin isn't being producedadequately to bring this down,

(41:34):
the body stores all these excessnutrients as lipids in adipose
tissues.
And then this causes a viciouscycle.
So a GLP-1 agonist directlycounters these effects.
So GLP-1 agonists are used as,how do you say this word?
S A T I E T Y.
Satiety?

Aarati (41:55):
Satiety?

Arpita (41:56):
Satiety?

Aarati (41:57):
I always said satiety.

Arpita (41:59):
I don't actually think I like said it out loud.
I was just reading this

Aarati (42:02):
Hang on.
I'm Googling it.

Arpita (42:04):
I feel like it's satiety.

Aarati (42:05):
Satiety.

Arpita (42:06):
Okay,

Aarati (42:07):
Satiety.
That's what Google says.

Arpita (42:09):
Great.
So GLP 1 agonists are used as asatiety hormone in humans.
So they act on the brain, whichcauses food from the stomach to
empty slower than normal.
So with more insulin in theblood from GLP 1 and less food
leaving the stomach, overallblood glucose after eating is
reduced.
So in more recent research, GLP1 agonists go far beyond

(42:33):
satiety, may also change foodpreferences to become more
healthy and even reduce aperson's interest in alcohol,
tobacco, and even opioids.
And it was quickly apparent thatthe potential for this class of
drugs is enormous and may be aparadigm shift, not only for the
management of obesity, but forseveral other conditions.

Aarati (42:54):
Wow.
I didn't know all about alcohol,tobacco.

Arpita (42:57):
That was a really recent paper that I read.
I was honestly just a few monthsago.
But I also just wanted tomention that we think about
hormones a lot of times asaffecting just the organs around
them, really hormones affectyour entire body, including your
brain.
So it does make sense that whenyou think about a hormone like
insulin, it is affecting yourentire body.
So it does make sense that it'sacting on your brain and your

(43:19):
brain telling your body thatit's hungry.

Aarati (43:22):
Yeah.

Arpita (43:23):
Um, so I'm not sure about the nausea.
I didn't read about nausea, butit really is also like, it's
mostly focused on gastricemptying is what I read about.

Aarati (43:31):
Oh, interesting.
Yeah.
Cause that was just one pointthat I remember making in the
video that the, just the waythat it works can induce nausea.
And so you have to talk yourdoctor about, you know,

Arpita (43:44):
doctor

Aarati (43:44):
Yeah, because it was very much like a patient video.
So it's like, talk to yourdoctor about finding the right,
dosage and just be aware thatthese could be the side effects.
Like,

Arpita (43:53):
Exactly.
Exactly.

Aarati (43:55):
those commercials that have like, Yeah.
like go on for like a minute

Arpita (44:00):
okay.
So now that we know what themechanism is, uh, drugs like
Wegovy and Ozempic have becomereally household names.
Um, like mentioned, they havecelebrity users and they have
generated billions of dollars inprofit for pharmaceutical
companies and have resulted ininternational scientific acclaim
for the researchers creditedwith discovering GLP 1.

(44:23):
So, in 2017, Jens Holtz, Joel,and Daniel Drucker Jointly won
the Harrington prize forinnovation in medicine given by
the American Society forClinical Investigation and the
Harrington Discovery Institutefor their discovery of incretin
hormones and for the translationof these findings into
transformative therapies.

Aarati (44:44):
Wait when was this?

Arpita (44:47):
2017.

Aarati (44:47):
2017.
It's so recent.
Oh my gosh.

Arpita (44:48):
I know this is all very recent In 2020, the Warren
Alpert foundation prize wasawarded again to these three.
And it's a very prestigiousaward that's given for
biomedicine by Harvard.
And Svetlana was again, leftout.
She got this news and she wasincredibly hurt and
disappointed.
And especially scientificcommunity awards are a really

(45:10):
big way that credit is given inscience, and they're often
chosen based on nominations.
So there is, I was reading likea press release on this and it's
like, it's possible.
That, and this doesn't make itokay, but it's possible that
Svetlana, she continued to workon GLP 1, but because she didn't
have her own lab, she didn'thave her own funding, her, like,

(45:32):
didn't have, like, those highprofile publications the way
that Joel did, for example, it'spossible that she was just,
like, simply less conspicuousthan the three, and, like,
wasn't immediately thought of.
It doesn't make it okay.
But it is just like a thoughtfor like, because these are done
by nominations.
It was like the most highprofile scientists in the field

(45:52):
were the ones that were chosen.

Aarati (45:54):
Yeah.
But that's why I was asking youlike, when did this happen?
Like 2017 is so recent because Ifeel like now even more, there
is such a push for acknowledgingthe women in STEM.
And this seems like such anobvious way to do it.
Like, you know, if a woman hasmade a great contribution, who
cares the size of her lab, like,acknowledge that.

(46:16):
Please give her her credit.
Don't just leave her out becausethat's such a blow to not just
her because she did so muchwork, but all women in STEM who
are just like, okay, so if Imake some great discovery some
man's just gonna get, all thecredit and all the patents and
all the acknowledgements likecome on, we're past that.

Arpita (46:34):
I hate to tell you that this story gets worse.
So, uh, then in 2021 theGairdner award was given again
to the three men.
Um, so now we have three awardsthat were given just to them and
Svetlana was left out.
So at this point, GLP 1 was verymuch part of the zeitgeist and
many Americans vocabulary.
There was press conferences,interviews, and global

(46:55):
recognition to those three withSvetlana left off very
consistently.
So any commentaries thatjournalists published, then
aligned with the scientificprize winners, again, only
listing Joel, Jens and Danieland heavily exaggerated their
contributions, right?
Like now you have journalistsbeing like, look at these people
and look how like, blah, blah,blah.
We're like talking about Ozempicand Wegovy.

(47:17):
And Svetlana wasmischaracterized as a quote
unquote scientist in Joel's lab,even though she was in fact an
independent researcher with herown funding who made this work
and discovery possible.

Aarati (47:28):
Okay.
Now I'm also mad at the men too,because before I was just mad at
the people who are giving outthese nominations and these
awards, but now I'm mad at themen too, for not like setting
these journalists straight andbeing like, Hey, you should
really be talking to Svetlanaalso.
She did a lot.
This wouldn't be a thing withouther.
And like, it's on them too tobring her into the fold, right?

(47:49):
If they see that someone's beingoverlooked, like men do better
too.
I'm getting mad.

Arpita (47:54):
So she also gets mad.
Um, and she is an intenselyprivate person.
She had this whole badexperience with like the patent
situation.
She does not want to deal withthis.
Um, so she didn't actually starttrying to get the story
rectified until just last yearin 2023.
Other scientists at Rockefellerat Weill Cornell and MGH all
spoke up and submittedcorrection requests to

(48:15):
publications and press releasesabout her absence.
So one of her close colleagues,Francis Barney said quote,"This
is a story that has happenedover and over again in science.
There are no villains.
You do not have to say thatsomebody hogged credit, but
rather that she isn't gettingthe recognition that she
deserves.
End quote.

Aarati (48:32):
Mm hmm.

Arpita (48:33):
So though these corrections had the right
intentions, they brought themistake to the forefront of the
public eye.
So Joel, Daniel, and Jens allconfirmed that Svetlana had
important contributions and feltvery sympathetic.
And Joel said he, quote, wishedthat there was something that he
could do, end quote.

Aarati (48:52):
You literally could have, Like, what does that even
mean?
Like, you literally could havejust opened your mouth and
brought her name into thediscussion.

Arpita (49:03):
Understandably, Svetlana was very upset by this saying,
quote, Of course they will say Ideserve more recognition, but
then they take the recognitionthat belongs to me and they
assign it to themselves, endquote.

Aarati (49:14):
Yeah.
Oh my god.

Arpita (49:16):
So Svetlana is very like, um, she's like very, um,
Level, she's like, not rufflableand so this is like very outside
of her personality, but she saidin an interview with science
magazine, quote,"It's fine.
Let's just move on." Endquote.
So, however, her colleagueFrancis said her attitude is
always pragmatic.
If everybody else is gettingrecognition, why not her?

(49:40):
So finally, just last year, Celland Nature issued a revised
narrative of GLP 1's discoveryto include her name.
And later that year, the journalScience and the news outlet Stat
published two lengthy profileson her that finally told her
side of the story.
And just a few weeks ago, inthis year, 2024, she was ordered

(50:01):
the Tang Prize in biochemistryand was listed as one of 2024
Time Magazine's 100 MostInfluential People.
And since then, she's receivedan outpouring of support,
especially from femalescientists who similarly feel
like their work has beensidelined.

Aarati (50:17):
Yes.

Arpita (50:18):
This all happened like literally just a couple of
months ago when she's finallylike, I, I, the reason I picked
this story is because I saw acouple of articles about her and
it was this female scientist whowas left off of this amazing
discovery that has like, reallychanged the way that think about
this huge disease, diabetes, andalso weight loss.

(50:40):
And it's just become this whole,like, this almost like entity of
like, Ozempic and Wegovy youknow, like, we're hearing about
this all the time.
And the fact that something thatis generating so much revenue,
so much recognition has verypointedly left her off, I
thought was crazy.
And to your point in the year ofour Lord 2024, like that is...

Aarati (51:01):
Yeah.

Arpita (51:01):
crazy.

Aarati (51:02):
I'm so glad that we've moved that, that far, though.
Like, 2017 doesn't seem thatlong ago, but at least, like, in
those last seven years, we'vemade a lot of progress, it
sounds like.
So I'm happy about that, andhopefully we just continue from
here on.

Arpita (51:18):
I know it's like interesting though.
Like if she hadn't actuallyspoken up for herself and said
anything, like nothing wouldhave changed.
Because this narrative went onfor several years and it was
really just, you know, like lessthan a year ago that she was
like, Hey, I actuallycontributed to this and you
should include my name on this.
And it took that long for thechange to be affected and it

(51:39):
took her speaking up forherself.
So if she hadn't saidanything...

Aarati (51:42):
Especially when you said was, like, on all the papers,
she was, like, the first authoron all these papers, like, did
no one do their research?
And say, oh, who's the firstauthor on this paper?
Who's this Svetlana person?
Maybe we should talk to her.

Arpita (51:56):
I know.
It's, it's really crazy.
Um, and yeah, that kind ofbrings us up to today.
So Svetlana is alive and well,she's in her mid seventies and
she continues to live in NewYork with her family.
But yeah, that's her story.
And there's like, been some veryinteresting interviews with her
where, you know, she talks abouthow she doesn't really get

(52:17):
any...
she doesn't get any revenue fromany of its pharmaceutical
companies because it is notactually GLP1 because they've
done their own drug developmentbased on that patent.
So that's why we havesemiglutide.
Semi glutide is a analog of GLP1because they've done their own
proprietary, whatever.

(52:38):
Um, it's extremely similar, butit's.

Aarati (52:41):
Yeah.
But they've modified it enoughthat it's

Arpita (52:45):
Exactly.
So she doesn't get any moneyfrom that.
And her patents have allexpired, but she maintains that
she wasn't in it for the money.
Like, she didn't really careabout the money.
What she cared about was beingrecognized adequately for the
work and being represented tothe equal extent that her male
colleagues were so that shecould set a precedent for, like,
women who came after her.
Like, that was what she reallywanted.

(53:07):
Wasn't in it for the money.
Yeah,

Aarati (53:09):
But still, the money would be nice.
you know?

Arpita (53:12):
I totally agree with you.

Aarati (53:14):
Yes.

Arpita (53:15):
The other thing that I found very interesting was, so
her husband, Michel, is a also avery prominent scientist who
does not really show up in thestory very much.
And looking him up he is a,like, a very accomplished
scientist in his own right.
But she very pointedly does notrely on him to throw his support
behind her to be like,"Hey,like, I have a lot of clout in

(53:36):
this academic community and yoube paying attention to this
person, Svetlana." Like, shevery much wanted to do this on
her own.
she does not lean on him.
Academic support, if that makessense.
Um, which is very interesting.
And she mentions that she wantsto make sure that their academic
achievements and their workremains independent and they're

(53:58):
not conflated with each otherbecause then I think she becomes
known as like, Michel's wife.
And that's not wanted at all.
Um, so obviously he's herhusband and her partner and all
of these things, but in terms ofacademic clout, she's not
leaning on his, On hisinfluence, which is very
interesting.

Aarati (54:16):
Yeah.
And there's so many people outthere also who are just like,
whenever a woman makes it big,they always try to kind of
equate her success, to a man,and be like, oh, the only reason
she made it big, is becauseShe's dating him or she's
married to him and it's always aman It's always so I totally get
that.

Arpita (54:36):
Simone, Simone, Biles husband who plays in the NFL.
He's not even very good.

Aarati (54:43):
Yeah, exactly that.
It's it's like she's thisamazing amazing person in her
own right.
Let's not You know, include theman in this at all.

Arpita (54:53):
Yeah.
Um, but yeah, that's Svetlana'sstory and how GLP1s came to be.
And they had quite aninteresting story of trial and
error.
And she finally got therecognition she deserves.

Aarati (55:05):
That's a great story.
I'm so happy.
It had somewhat happy ending.

Arpita (55:10):
A somewhat happy ending.
yeah, Yeah, Yeah, yeah,

Aarati (55:11):
yeah, yeah Yeah, hopefully it becomes happier as
the years go on.
yeah, more and more recognitionand, you know, um, but yeah,
that was a great story.
I didn't know any of that frommaking the videos last year.
I hadn't really gone into thewhole history of GLP great
story.

Arpita (55:28):
Thank you.

Aarati (55:31):
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(55:53):
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