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March 14, 2022 28 mins

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Episode Transcript

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Matt Boettger (00:00):
You're listening to the pandemic podcast.
We equip you to live the mostreal life possible.
And the face of these crises.
My name is Matt Bodecker.
I'm joined with a great friend,Dr.
Steven Kisler and epidemiologistat the Harvard school of public
health.
Good day.
Do you find

Stephen Kissler (00:12):
sir?
Good day.
Good, good payday day, Matt.
It's wait, wait, is it really?
Yes, it is 3 1 4.
And so this is a, this is aholiday in which mathematicians
unite so great.
This

Matt Boettger (00:24):
is, so this is the exclusive reason why we
delayed.
That's been damaged.

Stephen Kissler (00:30):
That's right.
That's great.

Matt Boettger (00:32):
So I do apologize for those who were probably
looking forward to a podcast twoweeks out in that three weeks
out, Steven had a lot going onlast week and he still is
crushing it, but he's still madetime to put out a relatively
quick episode today because weonly have.
30 minutes or less right now,before he has it on the median.
So we're kinda really quick.
If you want to donate greatpandemic, I don't even know how
to say, oh, patrion.com/benefitpodcast.

(00:54):
I'm not trying to go so quicklyright now.
Like we've got to get Steven

Stephen Kissler (00:57):
all these questions here on here.

Matt Boettger (01:00):
I know we did that so badly for the intro and
outro.
So if you want to do that, youcan do that in the show notes.
One-time gift in the show notes,Venmo, PayPal.
Great.
It is now two years since we'vebeen going on for the pandemic
podcast and the pandemic aswell.
So this is a big milestone forus.
One year seemed normal.
Two years seems outrageous forus to be together.
Like, I don't know what happenedto.

(01:21):
Thank you for all those who'sleft reviews.
One quick one, I'll leave onFebruary 25th where there's a
couple as we near the two yearanniversary of COVID exploring
exploding in the U S I want toexpress my gratitude for the
pandemic podcast.
You've been and continue to be asteady source of information I
can trust.
Thanks guys, for all yourefforts.
So pretty all those.

Stephen Kissler (01:42):
Yeah, totally.
And real shout out for peoplewho have like been barren with
us for this entire time.
It's I know, it's yeah,appreciate it.
And glad that we've gotten toconnect with many of you over
the course of the pandemic.
So

Matt Boettger (01:53):
yeah, it would be great someday in person and the
guys are in wherever Boston,Denver feel free to send an
email, Matt living in thereal.com.
We'd love to connect with youguys in one way or another.
So thank you for all thosereviews.
So let's get going.
And is there anything else onthe show notes I need to talk
about for intros?
I feel like I'm missingsomething, but not that
important.
We have less than 30 minutes.
So let's start with the outlineright now.

(02:14):
Stephen, the first thing I wouldtalk about is policy and
guidelines.
Things are changing.
Things are rapidly changing andthings have changed and so much
so that like I went to thegrocery, no, not the grocery
store, but I've been to otherplaces and had been unmasked.
Going into restaurants.
Now, things are really kind ofnormal.
Hospitalizations are so low nowthat I feel comfortable that
going in and just kind ofstarting to live a normal life.
Now you'd have policies andguidelines trying to keep up.

(02:37):
I know Hawaii is going torelease.
There's finally in in March 26.
So no more, you don't need tohave quarantine, that kind of
stuff.
Airlines have continued theirmask mandate.
Just I think for up until thesecond week of April, but could
change rapidly.
I think they're consultingreally powerful people like you
and other people to figure outwhat the heck they're they need
to

Stephen Kissler (02:56):
do.
And so that's, yeah, that's agenerous description for,

Matt Boettger (03:01):
so they're figuring that out.
So everything's changing.
One thing that changed is theCDC guidance.
I want you to inform us in me,particularly because I'm with
you, I'm like what's going onwith the change of the CC
guidelines, because apparentlyit was one thing.
And it was like the cases per ahundred thousand and an article
mentioned, I'll put this in theshow notes that the new
transition to the guidelines ornot the guidelines, but the

(03:21):
measurements the initial one hadlike 75 in the country being at
high risk or whatever, that,whatever that level was, the
new.
Guidelines or the new way theymeasure criteria for COVID
infections, but to down alonglike 15% of the U S at high,
high risk.
So can you help explain what'sgoing on and how we use this and
that going

Stephen Kissler (03:39):
forward?
Yeah, totally.
I mean, I think this reallyfolds in nicely to a lot of
conversations.
Previously about just thecomplexity of making decisions
and changing guidelines aroundthe pandemic.
It is, it is, it is not an easyjob.
And I, I can't say that I amexcited about every, all of the
updates to the CDC has made, butI also kind of understand.
Where a lot of it is coming fromand what it's been motivated by.

(04:01):
So, the, the, I think the, thethe biggest thing that has
caught people's attention isthis big shift in the U S map,
right?
Where it's like places turn fromred to green where it's like
high risk versus low risk.
And it's like, what the heck?
Like, somebody just decided tochange the rules and then, and
that, and that again, plays intothis notion of like that.
And I think there's this falsenotion that that good faith and

(04:24):
honest communication impliesconsistent unchanging
communication, right?
Because the context isconstantly changing too.
And it's changed hugely in thein the context of increasing
vaccination rates and a lot ofunderlying immunity from
previous infections.
So now the same number of casesthat we saw a year ago does not
mean the same thing as the samenumber of cases that we're

(04:44):
seeing today because due to thatunderlying immunity and due to
our improvements in our abilityto treat COVID, we have, we have
drugs now that are effective ateach stage of infection.
Like it's, it's just a differentball game.
And so it's not that, eh, Justthat, someone decided that the
pandemic was over and we needto, change, but it's like this,

(05:04):
this also reflects to a largedegree, the reality of the
situation, which is that therisk of severe outcomes given
infection is, is hugely reduced.
Now, thankfully in this countrydue to all of the, everything
that we've been through andeverything that we've done to
try to make it that way.
And so that's really what theguidelines reflect.
The, I think there is still roomfor criticism in that.
They're they've really scaledback a lot on surveillance and

(05:26):
have made the triggers forchanging these guidelines tight
to mainly tied tohospitalizations.
Nope.
On the one hand, that makessense because the that's by far
the sort of the most stableindicator of how much.
COVID is, is circulating at agiven time because there are so
many idiosyncrasies withtesting.
Like it's really hard to knowwhat case counts mean in one

(05:47):
place versus another.
I think those people get testedfor all sorts of different
reasons, but of course thedifficulty is that
hospitalizations are hugelydelayed.
And so by the time you see a bigrise in hospitalizations there's
a good chance.
There's already a lot of COVIDspreading Too late to really
turn around a major event.
So something we're gonna have towatch this closely.
I do think this is sort of a, awork in progress, defining what

(06:08):
these guidelines should be.
But yeah, hopefully that, thatgives a little bit of nuance to
what's going on.

Matt Boettger (06:14):
So w guess would probably be to be expected then
if it's still an, a kind of anevolving situation that we could
probably see a series of changeswithin the CDC, as it grows and
understands and reflects and,and kind of finds its stable
ground for this new endemicit's.
This is not the final say of howwe're going to measure going
forward.
Cases and

Stephen Kissler (06:30):
how to respond to it.
Exactly.
Yeah.
I mean, this is, this is thescientific and political process
and I, and I don't meanpolitical here as a dirty word.
It's like, it's, the CDC hasmade their guidelines and then
there's been a lot of responsefrom other government
institutions, from otheracademics, from other, just even
lay people who are responding tothese guidelines and maybe even
pointing out things that the CDChadn't considered, despite their
good faith efforts to considerall possibilities.

(06:52):
And then Nope.
Factor that in.
And then if it is, changes needto be made, then I am confident
that they'll be.

Matt Boettger (06:58):
Okay, sounds good.
All right.
We're going to, we're going todo a lot of speed rounds here.
So next being around variantlet's touch base on this.
I was really not thinking muchof B2 still don't but there was
one article that kind of raisedmy eyebrows a little bit about
how maybe New York has seen alittle bit of a sub variant
spread.
Not sure how accurate that is.
I haven't got a chance to kindof chase this down to see, but a

(07:19):
particular line in this article.
I'll put in the show notes.
And that is that a, this B2variant is up to 30% more
infectious.
Last I heard this was, it waslike three to 6% more
infectious.
And I was like, oh, well,that's, that seems about right.
30% of an already outlandish,like crazy variant.

(07:40):
What are you hearing?
Whereas B2 on your radar rightnow.
And are these, are these kind ofWell, is the

Stephen Kissler (07:45):
accurate, yeah, so there's, I mean, there's a
huge amount of uncertaintyaround these statistics and a
big part of that is because,again, the context is changing
hugely.
And so, as, as we've talkedabout, and I think there's been
a lot of discussion about thissort of in the media as well,
that that an increase ininfectiousness can be due to a
whole bunch of different things.
Maybe that's increased intrinsicinfectiousness, but a lot of
times it's actually an interplaywith previous immune exposure

(08:09):
which vaccines you've gotten,how recent they've been, which
various strains have infectedyour community, how recent those
outbreaks have been.
And that can create a hugeamount of variation in the
infectiousness of a givenvarious.
In a given population.
So I think part of the reasonwe're seeing these like vastly
different estimates of theinfectiousness of BA two
relative to BI one is, is justdue to that because it's
spreading in differentpopulations.

(08:30):
I mean, I think it's worthnoting that we've, we've had BA
two circulating at low levels inthe U S for months now, and it
hasn't really taken off in mostplaces.
So that's kind of confusing too.
So there's, there's a lot goingon here besides just sort of a
baseline difference ininfectiousness.
It seems like it really needs toget to get lucky in a way in a
given population before it canreally take hold.
And it just hasn't been able todo that.

(08:50):
So, so at least in the U S itseems to me like that 30% is
probably, as, as just a baselinefigure.
I think that that's a littlehigh, because I think if that
were the case as.
Every every BA two is 30% moreinfectious than BI one.
We would have seen hugeoutbreaks of BA two already at
this point, but in somecommunities, I'm sure that's the
case that that 30% is, is, isaccurate.
And so it's just a matter offinding the right communities.

(09:12):
And then once it gains afoothold, it can spread.
Okay,

Matt Boettger (09:15):
great.
Anything else that we should beconcerned about or on our radar?
Because I've been kind of out ofthe loop.
I've been snipping articles hereand there, but I haven't seen
anything about variants ofconcern besides B this B2, is
that a proper kind of reflectionright now?
Nothing bigger

Stephen Kissler (09:28):
than that.
It's pretty much all that rightnow.
We we've seen some upticks incases, for example, in the UK
where they've already had alarge BA one wave and, and some
of that seems to be driven by BAtoo, but there's so far in all
of the increases in cases thatwe've seen around the world
there aren't any new variantsthat have been implicated in
that.
And it also doesn't seem likefrom what we've seen, there's
really any difference inclinical severity between BI one

(09:48):
and BA too.
So I think that's a big reasonwhy, that's, that's pretty much
all we've heard about and thatseems to reflect what I'm seeing
too.

Matt Boettger (09:55):
Okay, great.
So let's hit now the vaccinebooster situation, there's a few
articles here and there.
Talking about the second boosteris, is this something that's
going to be coming down thepipeline for us relatively soon?
Maybe not.
Where did you guys thinkingabout.
This booster in some articleswill say that, ah, it's been
tested.
It's a very marginal boostcompared to the original booster

(10:16):
for the Omicron, particularly.
So maybe it's not something isgoing to be on our, the
forefront of our radar.
Come this fall.
What are you guys talking about?

Stephen Kissler (10:25):
Yeah.
So, at this point it that's,that reflects my understanding
too, that there especially forpeople who are who have.
Normally functioning immunesystems and I've gotten a
booster, it seems like getting abooster booster.
Doesn't really it doesn't giveyou a huge improvement in
protection against severedisease.

(10:47):
We're still gathering thatinformation because again, one
of the, probably the biggestelement of this.
Rate at which protection fromthe vaccine declines.
And we just haven't had peoplewho have been vaccinated and
boosted for long enough toreally know what that rate is
and, and what the floor might bein that reduction in immunity.
No, that said, one of the bigpromises and boosting was that

(11:10):
it would give you much longerterm immunity.
And so my hope is that it'sholding up better over time.
We'll have to wait and see, butthat's so far I haven't seen any
data that suggests that anotherbooster is, is.
Makes sense at this point.
Great.

Matt Boettger (11:22):
And that, it's good to hear.
That's probably mostlyspeculation cause their number
articles are saying that, oh, itlooks like the booster could
last for months and months andmonths, if not years and years
and years.
And that's really, at this pointin time, people just probably
speculating on what little datawe have right now, but this
doesn't take time before.
Okay, so this one, you said youdon't know too much about, but I
want to put it on the radar forpeople who might be interested

(11:45):
because this article wasfascinated me and I haven't
heard anything about this untilthis one article.
And this is about this fromAstraZeneca and I'm probably
going to blow the name, but it'slike Abu shelled or something
like that.
And for those of you who areimmune compromised and have
received your vaccine and yourbooster, and then maybe got
tested and realized, man, I hadno antibodies surface from this.
This is a promising reality.
I do know it seems incrediblyscarce and that people who

(12:07):
actually desperately need it areon huge waitlist.
So, I'm hoping, I'm hoping thatby just even putting this out
here and making it more peoplecan be aware of it, then it
might push for more readilyavailable, but this has ever
shelled AstraZeneca.
I think it's a.
And then, or maybe a vaccine, Icouldn't quite gather that, but
whatever it is, you take itbeforehand and it's kind of
vaccine specifically for immunecompromised and it should prompt

(12:28):
promising results of those whohad zero antibody.
From two vaccines and a boosterthat people received antibodies
and felt a lot more confidencein going out and even doing
basic stuff in life.
So huge check to up in the shownotes, read about it.
Okay.
Last few things when we'll talkabout it.
Yeah.
That are that are kind ofpressing for me.
COVID side effects.
So I've been reading about thisnow.

(12:49):
I know you you've, you've punteda couple of the, one of these
things to mark needs a chime in,on some of this clinical stuff.
But we have long covet.
We've been seeing this foryears.
We talked about from the verybeginning.
And now for me, a new thing onmy radar, clearly probably not
for the scientific community isthis Epstein-Barr thing has been
really, I've been seeing this alot lately in the news and now

(13:09):
seeing connections towards maybelong covet and Epstein BARR.
And I'm out of live on this.
So maybe you can start withthis.
What is this EBV thing that 95,apparently 95% of us carry.
And a few of us, it can raiseits ugly head and do something.
Terrible things like Ms.
Which my cousin has even cancerand other times it just doesn't

(13:30):
do anything kind of sounds likeCOVID itself.
Right.
Where sometimes you're justescaped completely and otherwise
you're in the hospital and neardeath.
So in fill this in and wherewe're at might be in its
relationship to long COVID andother things.

Stephen Kissler (13:42):
Yeah.
So this is, this is great.
It's, it's an area that I'mpersonally and scientifically
really interested in as well.
And I think it, it folds intothis broader discussion of like,
w w how is it that we have somany infectious diseases and yet
we know so little about the sortof long-term outcomes from them.
So for a bit of background,you're right.
This Epstein-Barr virus isextremely common.

(14:04):
As you said, most of us havebeen infected by it, or will be
infected by it at some point inour lives.
And, and in the vast majority ofcases, it seems like it doesn't
really do much.
But in some it's, it's beenimplicated by an, different
cancers.
There's a recent really paper inscience that really did
convincingly link theEpstein-Barr virus to Ms.
And so, but again, I think thereally important thing from that
is that getting infected withEpstein-Barr does not mean you

(14:26):
will get Ms.
It just means that it's one ofthose.
Important conditions amidst anentire backdrop of genetic and
environmental conditions aswell, that could lead to the
development of Ms.
And so the difficulty inunderstanding these things is
really related to anotherphenomenon in medicine and
science that I hear people talkabout a lot, which is like,

(14:48):
about nutrition.
So like, why do we know solittle about how, what we eat on
a day-to-day basis?
Affects our health and thelong-term.
We do know a fair amount, but,but like, what's, what's the
deal there?
Like how is it that something ascommon as eating is something
that we have so littleinformation about, and that's
really because the of two thingscoming together, which is that
the results, the health outcomesof different diets are subtle.

(15:12):
And delayed.
So usually, the differencebetween, taking in, a certain
number of grams of red meatversus half as many grams of red
meat.
The impact of that is probablythere.
But it's relatively small and itonly accrues over a long period
of time.
And so that's, that's, that'sthe sort of question it's really
difficult to studyscientifically.

(15:34):
And so with infections, it'svery similar because usually you
have, you have very high ratesof infection that might lead to
a slight difference in risk fora given infectious disease or
for a given health outcome.
And oftentimes they're delayedhugely.
I mean, the development ofcancer, the development of Ms is
going to be vastly delayed fromthe point of infection.
And so it's really difficult togo back in that causal chain and

(15:56):
say this thing.
Is what caused this downstreamserious effect.
And so that's part of why we'restill learning about this, but
there are ways that we'rebeginning to get a lot more
information about this.
So I do think that there arethere's probably a lot of links
that we don't yet know thatwe're just beginning to
understand between infectiousdiseases and more long-term
chronic and outcomes.
Things that we understand to bechronic.

(16:18):
And one of those is this linkbetween Epstein-Barr and various
other health conditions.
I think it's certainly the casewith COVID.
We don't really know what thelongterm effects of COVID
infection are, but it does seemlike certainly, long COVID
certainly exists isdebilitating.
And we don't really know howlong.
Certain cases of long COVIDmight last that's related to
other things, we had mentionedmano, which Epstein-Barr can,

(16:40):
cause there are somesimilarities between mono and
long COVID.
There's some similaritiesbetween lung COVID and other
types of inflammatory diseasethat can be triggered by other
sorts of viruses that lasts forlong periods of time.
And I think really what a lot ofthis comes down to is that we
don't have a really clearunderstanding of how viruses
interact with our with ourimmune system.

(17:00):
Because really what a lot ofthese things are is that an
infection has perturbed the waythat our immune system responds.
And usually, at best the immunesystem has a short.
Intense response that clears thevirus and then returns to
normal, but sometimes aninfection can prompt the immune
system to have a longer lastingresponse and it doesn't ever
really return to that normalstate.
So, so that, that seems to bepart of what's happening here

(17:21):
with with these differentviruses.
So genetically, Epstein-Barr andCOVID are very distantly
related.
SARS cov two is a RNA virus,meaning that it uses RNA to
encode its genome Epstein-Barris a DNA virus.
So it actually uses a genomethat.
More similar in some sense, atleast molecularly to ours.
That may also be part of thereason why Epstein-Barr can

(17:42):
cause some of these downs longlong-term outcomes is because
it's it is just a little bitmore close to our actual genome
and so can integrate into ourgenome in in ways that is a lot
harder for something like SARS,cov two to do.
So there are a lot of importantmicro biological differences,
certainly at the clinical level.
And, and thinking about.
The outcomes of these things.
I do think there are somesimilarities that we have a lot

(18:03):
to learn from.

Matt Boettger (18:04):
Great.
A couple of things before youhad the last thing before we get
going in about 10 minutes, thisreminds me, I read an article
about how I think some countrieslike Sweden and stuff, how they
did their first wave, it didn'tget much of any kind of impact.
And there are Tracy and some ofthe things I, I don't know if
Epstein-Barr was part of thisequation that this might be kind
of a tangent reminded me of likea series of reasons why.

(18:24):
And you were saying that I thinkthe reason why I was triggered
by this, cause he would saythere might be a distant
relationship between Escobar andCOVID.
I mean, there was some, but notreally, but they mentioned that
how, when they were trying totrade.
Like maybe why some peopledidn't get infected in Sweden.
They saw a relationship betweeneach one and N one and the
Corona virus.
There was like some similaritiesin its, in its like molecular

(18:45):
just enough similarity thatmaybe somehow that H one N one
outbreak, blah, blah, blah,helped the protect them just
enough, a serious of people.
Have, did you see much aboutthat, of this connection
between.
You

Stephen Kissler (18:56):
know, I didn't see much about the connection
between certainly, differenttypes of viruses.
I've heard some, someconversation about previous,
previous coronavirus outbreaksthat might've given some amount
of protection, but it is truethat know, one of the other
examples that comes to mind is.
We do know that flu and RSV giveyou some amount of immunity
against one another.
So if you have a really big fluoutbreak that can push the

(19:17):
spread of RSV, which is usuallya childhood respiratory illness
and it can move it around andit, and it's, they seem to
interact with each other throughthis sort of broad spectrum
immune response.
And so it wouldn't be surprisingto me that a, the, an outbreak
of a virus that does ramp up theimmune system's response could
actually provide some short-termprotection against infection
from another virus.
Yeah, it's I, I haven't seen alot of data on it, but it's
totally plausible.

Matt Boettger (19:38):
Okay, great.
For those of you just, I'm goingto keep a close eye.
We'll keep a close eye on thiswhole kind of EBV thing.
It's been passing to me andwhere am I go in the future?
The questions I had also, I waslike Pimms and em, and Missy,
which I w that Stephen'sdefaulted to mark.
I'm curious about this.
So, it will have mark I knowmark, if you're listening, get
back on or submit yourresignation.

(19:59):
Okay.
Last part before you get going,the endemic, what does the
future hold for us now?
This is we only about 10 minutesor less.
I'm really curious of what doesit look like going forward for
us handling one great articlecame out from the Atlantic.
Why America became numb tocupboard.
You have to read this, if youhaven't.
So please open the show notesfor those of you.
One of the things they talkedabout is this kind of like
bifurcation of direction, whereare we going to go now?

(20:21):
Is it, we do, do we desire goingback to normal?
Is that what we're trying to do?
Or do we want to build backbetter?
Right.
And so it was a great articleabout how most people actually
truly do want to build backbetter, but they perceive as if
the rest of the world just wantsto go back to normal, probably
because we're just so desperate,right.
To just go back into ourhabitual lives.
But we do.
On a large sense, want to buildback a better.

(20:43):
So I want to kind of throw itback to you and you had some
insights with potentially withUkraine, this kind of stuff that
I haven't heard yet.
So I'm fascinated about how,what the future holds for us as
we move forward to this, livingwith this and what, what
direction we ought and should,and shouldn't be going.

Stephen Kissler (20:56):
Yeah.
So I mean, one of the thingsthat I'm thinking about a lot
with us is how there's The theCOVID pandemic has really I
think in, in many wayshighlighted our collective
relationship with mortalitybecause it's been a long time
since we've had such a newprofoundly impactful.
Event that globally has causedan increase in mortality on the

(21:20):
scale that COVID-19 has.
And so, I think it's interestingbecause prior to the pandemic we
had become numb to all sorts ofdifferent types of death.
And so now there's thisquestion, we're starting to see
this phenomenon with COVID-19where it's like, okay.
So at some level we're going tohave to start to accept a
certain amount of death, but nowthere's there's.

(21:42):
There's this there's this sortof recognition and
intentionality about it, whereit's like, well, Hey, wait a
minute.
Like what w what other thingshave we been doing this with?
But we didn't even realize it.
And I think that that's really,one of the big motivations for
like, how do we build backbetter?
Like, we've been using flu as abaseline.
We accept X number of flufatalities per year.
But then that raises thequestion like, that's, that's a
choice too, to a large extent,there w we can never, we can

(22:05):
never eliminate all, I, I don'tthink that will ever be immortal
in the, on this world, but like,we won't be able to remove all
of our risks of death.
I, I think that in many waysthat's a fool's errand, but a
lot of these things are, arewhen.
Get right down to it, theirchoices, right?
We're in many ways, they're likechoices about who lives, who
dies and how many, and and.

(22:28):
It's you know, that, that is,that does simplify it to some
extent, but that, I think thatthinking about it in those terms
is really useful because we dohave a fair amount of agency in
some of these things.
And we do have to ask, w what,what is acceptable and what does
it mean to build back better?
And so folding this into sort ofanother area is that, we're,
we're thinking a lot aboutbuilding back better returning
to normal.

(22:48):
But I think it's also easy toforget that this idea of
normalcy is a little bit of anillusion to that our lives both
individually and collectively asa society operate as a as, as
this movement from crisis tocrisis in a way, right?
Like we're all dealing with one,I don't think that.
Any of us can probably honestlysay that when the COVID-19

(23:10):
pandemic hit, that everything inour life was perfect, everything
was good.
We were at a tournament, totallynormal state.
We were in like this perfectequilibrium, Zen, whatever.
And then the COVID pandemic camethrough and messed everything
up.
Right.
We were all dealing with allsorts of stuff before it hit.
And our experience of thepandemic has been a layering of
this new crisis over the top ofall of the other crises that we

(23:31):
had been dealing with on apersonal and community and
social level.
And so I think a big part ofwhat we need to think about as
we're thinking about thisendemic relationship with
COVID-19 is this recognitionthat it's not, we can't just
think about it in isolation, butwe need to think about it in the
context of the messiness oflife.
And so that's where you're mythinking about the conflict in
Ukraine was also coming in,which is that we're, we've,

(23:53):
we've been talking all about thepandemic and shifts and variants
and And, and what it looks liketo return to endemicity, but,
but the return to endemicitylooks very different when you're
in a country, who's at peaceversus when you're in a country
at war similarly the sorts ofconcerns that we have.
And, and again, so I'm anepidemiologist.
So I'm dealing with, with a lotof the infectious disease

(24:14):
outcomes here, but of course,the biggest issue right now is,
is in, in Ukraine is not reallycoming from pathogens.
It's coming from bullets.
And and that's, that's, that's adifficult reality too, but
that's, what I want to note hereis that there is also a lot of
issues with.
Here to where people are unableto get care for their chronic

(24:34):
illnesses.
Women are having to deliverbabies and bomb shelters, and
that's not good for anyone'shealth.
And infectious diseases arespreading as well.
So thankfully we're at a placewith COVID-19 where if this
conflict were to have happenedtwo years ago, COVID-19 would
have been.
An absolutely awful layer overthe top of this, it's still not
good.
But certainly, as people arecrowding, as people are
displaced, there's going to be alot more spread of COVID-19.

(24:56):
Actually one of my biggestconcerns is actually with other
infectious diseases as well.
It turns out that the rates oftuberculosis and Ukraine as some
of the highest of anywhereacross Europe.
And so again, crowding peopleindoors and close proximity and
the sort of mass migration outof Ukraine could also create a
really big issue there.
So there are a lot of infectiousdisease outcomes that we need to
think about.
And I think that the biggestupshot from all of this is that

(25:17):
there, there really is nonormal.
It really is just this sense ofhow do we manage this?
Crisis and issue that that isbecoming more familiar and more
predictable in the midst oflives that are unfamiliar and
unpredictable at every singleturn.
And, and I think that that's,that's the much bigger question
that I don't know how to answer.
I mean, I'm just raising all ofthese points that all of, and

(25:40):
like, you know, we all know thatlike that's our tagline, right.
Life is complicated and it willcontinue to be.
But I think that it's importantto think about how we.
Develop our relationship withCOVID-19 and other infectious
diseases against this backdropof realizing that everything
else is also going to bedifficult and complicated at the
same time.

Matt Boettger (25:57):
That's great.
I mean, yeah, I mean so much inmy mind, I only have like a few
minutes left.
I think this has been a biglearning lesson for me.
And I think for the whole girl,I think in some sense, we're in
our infancy in dealing with likeglobal connection.
We're not, we haven't reallyreached maturation in this
reality because I think hundredsof years ago, we lived in, we
lived in a small village or acommunity, and that became our
world.

(26:17):
And then because of technology,our world expanded and became
large, so much larger than mymind and my heart and my soul
can grasp.
Right.
I can easily get overwhelmedright now.
My problems exist beyond mycommunity.
I see them, I read them on thenews.
They're bigger.
And so then chances for greateranxiety.
And I feel like the gift here isthe pandemic is expedited
expedite in our maturation,right?

(26:39):
Of like, okay.
The fact of the matter is welive in a global community.
We learn very much that we cannot be siloed.
Even if we try, we Americans tryto be a silent in our small
little bit.
It's.
The COVID taught us that there'sno way we can actually fully
eradicate the outside world andlive in our bubble of utopia,
which doesn't really existanyway.
And so just now trying toregroup together, understand how

(27:01):
do we actually live in a worldthat can be joyful, can be
peaceful in some level, but alsowithout, without becoming siloed
and realizing that there's aworld out there that's in
constant crisis and we're inconstant crisis in one way or
another.
And how do we incorporate allthe.
And still live a fulfilled life.
And I think that's, that's thecomplication right?
Where it never was utopia.

(27:22):
And this is, this is the nextstep of us, of our, of our
growing of how do we still livelife, move forward, be hopeful
without ignoring the thingsaround us and keeping our eyes
open.
And I ended up for me.
That's probably it for those ofyou who are like living the
real, that's my whole concept oflike, that's kind of what it is
like, how do we actually likelive in a complicated.

(27:43):
And respond simply withouthaving to, silo the rest of the
world from us.
That's a hard task.
I don't have an easy solution,but that's the awakening.
Right.
So, thanks for that.
That's really, that's reallyawesome.
Okay.
We've got to go.
He has a meeting in eightminutes and he probably needs at
least two and a half minutes toprep.
So.
Thank you all for listening onthis episode, you can reach out
to me mad@livingthereal.com.

(28:04):
Please email me, let us knowwhat's going on at four.
It to mark and Steven always.
If you want to support uspatrion.com/pandemic podcast
Elizabeth$5 a month or one-timegift PayPal, Venmo all in the
show notes.
If you want to reach out toSteve.
S T E P T N K I S S L E R inTwitter.
It's an awesome place to followhim and get a lot information, a

(28:25):
lot of information epidemiology,and what's going on in virus,
the virus studies and all thatkind of stuff, which is beyond
my pay grade, but I li I read itanyway.
Okay.
I have a wonderful two weeks.
We'll see you for sure.
Well, hopefully God willing intwo weeks.
Take care and have a wonderfulcouple of weeks.
All right, bye.
Bye.
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