This Podcast Will Kill You - Ep 45 Hepatitis C: Hepatiti?
Episode Date: March 3, 2020From its discovery only 30 years ago to the recent development of an effective treatment, the short life of the Hepatitis C virus certainly has been action-packed. This week, we take you through the b...iology of this deadly virus by exploring its cancer-causing qualities and pondering the plural of hepatitis. Then we take a stroll through the often bizarre and disturbing history of blood technology, discussing how a lack of sterilization and screening allowed for the proliferation of the Hepatitis C virus around the world. Finally we ask, “what’s going on in the world of Hepatitis C today?” Spoilers: it’s not all bad! As long as you can afford the treatment of course... See omnystudio.com/listener for privacy information.
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In 2005, my life changed forever.
My mom had just been diagnosed with hepatitis C
and advised me to get tested.
When my doctor told me I also had it,
the room went dark.
All my thoughts stopped
and I didn't hear anything else being said.
I worried that I'd given my kids a deadly disease.
The next day, I scheduled my family to be tested.
Everyone's results were negative, but this didn't end my personal nightmare with the disease.
I was witnessing hepatitis C ravaged through my mom's body.
A liver transplant would only buy her time.
She ultimately chose not to undergo a dual organ transplant and passed away on May 6, 2006.
My liver began to deteriorate quickly.
I went from stage one to stage four in less than five years, which terrified me.
I saw no hope.
After years of unsuccessful treatments and being unqualified for clinical trials, I was finally
accepted for a clinical trial in early 2013 and began the treatment later that year.
My viral load started at $17 million.
I went back for a blood draw in three days and it had dropped to $725.
At day five, I was at 124, and in seven days my viral load was undetected.
This trial drug had destroyed the very thing that killed my mother seven years earlier.
Today, I've managed a sustained virologic response for four and a half years, but it's been a long road.
One thing I always tell people who contact me is that nobody's hepatitis C journey is the same.
We may have the same symptoms, but how our bodies respond to treatments is unique.
Don't hide in shame about having hepatitis C.
It doesn't matter how you contracted it.
What matters is that we get tested and treated.
That was from Kimberly Morgan Bossley and her story with hepatitis C that we found on Healthline.
Hi, I'm Aaron Welsh.
And I'm Aaron Elman Uptake.
And this is, this podcast will kill you.
Today we're talking about hepatitis C, as you may have guessed.
It's kind of like in the firsthand.
bunch of times. Yep. Yep. So, what are we drinking this week? We're drinking live and let liver.
And what is in live and let liver? Well, of course there's alcohol, which is, you know,
take it easy on the alcohol on this one, guys. Or just make yourself the placebo,ita.
That too. But in the quarantini, we have gin, grapefruit juice, lime juice, and grenadine.
Yeah, it's delicious.
we will post the recipe to our alcoholic quarantini as well as our non-alcoholic placebo
rita on our website this podcast will kill you.com and our social media pages so Twitter
TPWKY Instagram this podcast will kill you and Facebook yep cool cool I'm excited for this episode
I know you are I know you are but what am I also excited you're such a nerd I know
I can't believe that's the first time I've ever said that joke, actually.
That was a good joke.
I was a good joke.
Thank you.
Let's take a really short break and then dive in to hepatitis.
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Quince.com slash this podcast. So hepatitis literally just means inflammation of your liver. Okay.
Makes sense. So we probably most often, at least many of us, think of viral hepatitis when we hear the
word hepatitis. But do keep in mind that that's not by any means the only thing that can cause
inflammation of your liver. What else can cause inflammation of your liver? Oh my gosh.
bacteria can cause it.
You know that was like asking me to ask that question.
I know. Parasites can cause hepatitis. You can have autoimmune hepatitis. You can get
like hepatic involvement if you have things like lupus, blah, blah, blah. It's so many things
can cause inflammation of your liver. But often acute hepatitis is very commonly caused by viruses.
I would argue that, in fact, we are just very uncreative in naming viruses because the viral hepatitises are named hepatitis A, B, C, D, and E.
I mean, to be honest, like, it's not a bad way to do it.
It's not bad, you know.
But one thing that makes it very confusing is that all of these different hepatitis viruses have nothing to do with each.
did you just say hepatiti?
Yeah.
It's terrible.
All of these viral hepatitis, mm-mm-mm-hmm.
All of these viral hepatite, mm-mm.
Hepatiti?
I think is the word that you're looking for?
No.
Not hepatiti, Aaron.
Is that not the plural?
It's not the plural.
We'll see.
Okay.
We'll see.
By the end of the episode, it will be.
All right.
All of these viral hepatitis viruses.
They have nothing to do with each other, Aaron.
Hepatitis B is not closely related to hepatitis C, etc.
Okay.
They just all are viruses that happen to affect the liver.
What?
That's wild.
It is.
It is wild.
So these are not even the same type of viruses?
Oh, heck no, Aaron.
Okay.
So that part is where I disagree with the naming then.
Thank you.
Okay.
I'm glad that you're finally on my page.
So we're only discussing today one of these hepatitis viruses, and that is hepatitis C.
Okay.
And it turns out, actually, that TPWKY listeners are very familiar with this family of viruses that hepatitis C belongs to.
Hepatitis C is a flava virus.
I was bold over when I saw that.
I know. It's very exciting.
Yeah. So if you, like if these words like flava virus are confusing to you, don't worry, you're not alone.
Flavaviruses include dengue, the one we just talked about a few weeks ago.
Also, yellow fever, etc.
Okay.
If you remember yellow fever is called yellow fever because it is a fever.
because it is a favor that turns you yellow because of its effect on your liver.
Right.
Okay.
So, like the other flavavaviruses, hepatitis C is an RNA virus.
Hepatitis C, like many RNA viruses, has a huge amount of what we call antigenic variation.
So it has a lot of different antigens on its surface, like the flu does, okay, influenza.
So that means it's really hard to target from a vacancy.
vaccine perspective because it has a lot of variation. There's a whole bunch of different targets.
It's hard to get them all. They're constantly changing. RNA viruses also have really high
mutation rates. So they evolve very quickly. Hepatitis C is one of those. So spoilers, we don't
have a vaccine. But unlike many of the other flabaviviruses, you don't get hepatitis C from
mosquitoes. Which I find very interesting also. But there's
There are also tick-borne and non-vector-borne flaviviviruses.
Yeah, there are, absolutely.
And you do get hepatitis C from blood, which ultimately is where mosquitoes get flavavaviruses
from anyways.
So you're just missing the vector.
So hepatitis C, it invades your liver cells, your hepatocytes.
That's where it tends to replicate.
and then it bursts out into your bloodstream and circulates in your blood.
So it's transmitted person to person when you come into contact with that blood.
So in the past, when blood products weren't screened properly, and I know, Aaron, you're going
to talk a lot more about that, right?
Oh, yeah.
Yeah.
Blood products were a very big source of infection prior to screening.
In some areas of the world, blood products are still a source of infection, if it's very
difficult to screen or if there's not access to good screening tools. But hugely important
are actually medical tools used in things like surgeries, injections. That's actually one of the
most common sources of infection today is medical injections using not properly sterilized
needles or glass syringes. And then the other big source of infection today is injection
drug use. It is possible to get infected via sexual transmission, but it's honestly very rare. It's not
like hepatitis B, which is much more likely to be transmitted sexually. Okay. Okay. So, Erin, I think I
told you last week, like, oh yeah, hepatitis C is going to be so easy for me to research. It's like
really straightforward. We know a lot. Yeah. You were like, oh, it'll take me no time. Yeah. And then you
texted me today and you were like, oh, God.
It took me forever, and Erin, I'm not going to have answers to any of your questions.
Ah, Aaron.
Okay.
So let's talk about how you get sick from hepatitis C.
Okay.
While it can and often does cause an acute hepatitis, which we'll talk about the symptoms of in just a second,
the biggest issue and most dangerous part of hepatitis C is that in between 50 to 85% of cases,
it results in a chronic infection that can eventually result in liver failure and or liver cancer and
death.
First question.
Oh, God.
Okay.
Sorry.
50 to 85 is quite a big range.
What determines whether someone is going to become chronically infected or not?
Excellent question.
There's a number of different things.
Comorbidities, so things.
So things like having diabetes can increase your risk of chronic infection.
Heavy alcohol use, especially more than 50 grams of alcohol a day, which is like four
alcoholic beverages a day, can increase your risk of chronic infection.
Being immunocompromised, for example, co-infection with HIV definitely increases your risk for
chronic infection.
So, yeah, things like that.
The amount of virus that you're infected with is not actually a virus.
associated with whether or not you develop a chronic infection, which is different than a lot of
other viral diseases that we see. Okay. If you get infected with hepatitis C and then you do not
develop chronic infection, can you get reinfected and then develop chronic infection? Okay, so you're not
like immune, which I guess is then the struggle with creating a vaccine. Yep. Okay. Good question.
Okay, so chronic infection means in this case that even though a person might not have any symptoms,
the virus stays in their body, continues to replicate, and many, many years, we're talking like
10, 20, 30 or more years down the line can result in serious disease.
So then the question that I always like to try and answer on this podcast is how does this virus
actually cause disease.
Yeah.
Aaron, we don't know.
What do you mean?
I mean, we don't know.
So here are the things we do know.
Okay.
When hepatitis C invades your liver, it does stimulate an immune response.
So your innate immune system, which I think we talked about the innate versus adaptive
immune system in the first vaccines episode, if you want like a really nice intro to your immune
system. But basically, the very non-specific first immune response is triggered when you get
infected with hepatitis C. However, for some reason that is unclear, the downstream effects of that
don't really happen in a lot of people infected with hep C. So what that means is,
You know, you have your first-line defenders like macrophages and stuff that come in, release a bunch of chemical signals to trigger things like natural killer cells, which we talked about in the vaccines episode, that are supposed to come in and kill any viral infected cells so that that virus doesn't continue to replicate.
Something doesn't work right in that response when you get infected with hep C.
So we know that people who develop chronic infections with hepatitis C, which again is the majority of people who get infected, they don't have a good T-cell response.
So their T-cells aren't responding well to fight down this infection.
But that's all we know.
We don't know why.
We don't know how to predict who is going to do a good job of fighting off the infection versus who isn't.
And we don't know what the virus is doing specifically to.
cause these changes in people's immune response.
It gets worse. It gets worse, Erin. Okay, okay. I'm just shocked that we can treat this.
Dude, this is why I thought we knew the answers to these questions, because the amount of advances
that we have made in treatment for hepatitis C over the last like five years is bananas.
Yeah. So I was like, of course we know. Yeah, we got tons of treatment. We can cure it now.
deal. So, I mean, not a big deal, but, you know, I thought we knew, Aaron, we don't know.
And the other thing is, like, the whole cancer thing, which we're going to talk in more detail
about, actually, we're not, because we don't know. We don't know how hepatitis C causes cancer.
We don't know. That's the title of this episode, Hepatitis C. I don't know. We don't know.
Wow. Okay. There are six different genotypes of hepatitis C.
overall, they're not associated with different risks of ultimately liver failure, but
genotype 1B is one of the most common genotypes, and that one is associated with an
increased risk of liver cancer.
Okay.
But it's not because we don't know why.
It's not clear why.
Of course.
Yeah.
Oh, my gosh.
Who knew?
I didn't.
Well, let's talk about what we do know, and that is the signs and symptoms.
So in an acute infection, the incubation period, so the time from when you first get infected to when you first show symptoms, is actually quite long.
It's usually like around seven weeks, which is pretty long.
Only about 30% of people infected with Hep C will actually have acute symptomatic infection.
And generally this presents with malaise, so feeling fatigued and feeling.
crappy. You often get nausea, which isn't surprising since your liver is very involved with
your GI tract, you know, and right upper quadrant pain. Your liver is in the right upper quadrant
of your abdomen. Okay. So your liver hurts. Okay. And then what you also get is dark colored
urine, and that's because you get an increase in bilirubin, which is basically a breakdown product
of your red blood cells that your liver is supposed to get rid of, but your liver's not working
right. So then bilirubin builds up and you have to pee it out. Huh. So instead of your poop
being poop colored, your urine is kind of poop colored. And then as that bilirubin continues
to build up, that's when you see things like jaundice. So that's literally your skin turning yellow
from how much bilirubin is circulating in your system. Right.
Another huge thing that you see in acute hepatitis infections are if you test your blood to look at specific enzymes that your liver produces, they will be off the charts high, like thousands of times or at least tens of times elevated on what they normally are.
And that's a really big sign that you have an acute.
That means first time shortly after you get infected hepatitis infection.
Okay.
But for the most part, acute infection, even when it's symptomatic, is self-limited.
So with hepatitis C, you are very unlikely to die from what we call fulminant, which is like very rapidly progressive, acute liver failure.
Okay.
The real risk comes in the chronic infection.
Exactly, exactly.
And in general, disease symptoms are pretty long-lasting.
You can be sick anywhere from like two to 12 weeks.
weeks, but for the most part, people do recover.
Okay.
In the case of hepatitis C, however, up to 85% of infections become chronic.
And for the most part, during this chronic infection, a person won't necessarily have that
many signs or symptoms.
If you were to test their blood, they might still have slightly elevated liver enzymes,
but you can see these elevations and liver enzymes from a number of different things.
So it's not like that specific to chronic hepatitis infection.
But progressively, as this infection kind of goes along its course, the biggest symptom that people tend to experience is fatigue.
Like really bad fatigue.
Just never really feeling fully energetic is kind of one of the biggest symptoms.
But as we'll talk about there are some other.
symptoms that you start to see, especially as the disease progresses. Because basically what's happening
inside your liver is fibrosis. So fibrosis is the result of chronic inflammation in the liver that
leads to scarring. Very mild fibrosis can be reversible. But what happens with fibrosis,
especially when it's a chronic infection, is that it progresses to what we call cirrhosis, which is
kind of the end stage of fibrosis.
Huh.
Okay.
I didn't realize that.
Yeah.
I didn't either.
I had to double Google it to make sure I was saying it correctly.
I should know these things, Aaron.
I'm going to be a doctor.
That's what Google exists for.
Yeah.
I checked Dr. Google too.
Oh, oh, good.
So cirrhosis, which is kind of the end stage fibrosis.
It's like your liver is so fibroatic.
It's all, it's like your liver is supposed to be nice and red and beefy looking.
But when it starts to get progressed from fibrosis to cirrhosis, it gets hard.
It doesn't move as much.
It can't.
The blood flow is really bad.
And this happens in about 20 to 30% of people with chronic hepatitis C infection.
Wow.
That's a lot.
It's a lot.
Yeah.
And cirrhosis itself can lead to liver failure and eventual death.
But in the case of hepatitis C, it's also associated with an increased risk of hepatocellular
carcinoma, aka liver cancer.
Okay.
So what are some of the symptoms that we see when you progress all the way to cirrhosis?
I don't know.
What are they?
Let me tell you.
So the symptoms, they can be severe.
depending on how bad, you know, how bad the fibrosis has gotten if it's truly cirrhosis at this point.
Fatigue is still a big one.
Muscle weakness is another because basically just like your liver is in charge of doing a lot of things to make products that the rest of your body uses.
And if your liver can't do that, then your muscles and things can't work the way that they're supposed to.
Gotcha.
When you eat food and you absorb nutrients, all of the,
those nutrients get absorbed into your bloodstream. All of the blood from your whole GI tract,
for the most part, travels to your liver through one big vein called the portal vein. Okay. So all of the
blood from your GI tract, for the most part, is going to your liver, and then your liver is going to
process all of that. Okay. As your liver starts to become serotic and hardens, that closes off
that blood vessel. And so it basically puts increased pressure on that portal vein and it backflows it,
if that makes sense. Oh, that sounds terrible. It is terrible. It's like squeezing the end of a garden hose,
right? Yeah. And that garden hose that goes to your liver, when it backflows, it backflows into your
GI tract. And so this can cause all of the veins associated with that to then start to dilate. So this can cause
what we call varices or varicose veins.
You've heard of those in like your legs?
Yeah.
Well, you can get those associated with your GI tract.
So around your belly button, you can get huge amounts of varicose veins.
You can get them in your esophagus because even your blood flow from your esophagus goes to that portal vein.
And those, if they're under too much pressure, can burst.
Oh, my gosh.
And then you can bleed out and die because of it.
What?
Mm-hmm. Mm-hmm. Yep, that can happen. Another thing that can happen, if you think of closing off the end of a garden hose, how much pressure you can build up in that garden hose. Eventually, that hose is going to start to leak from the sides, right? Uh-huh. It's going to like spew liquid out, water out from the sides. The same thing can happen in what we call your portal tract, in that portal vein, which can cause the fluid that's supposed to be in that vein to start leaking in.
your abdomen. So you can get a huge amount of fluid in your abdomen. That's what we call ascites.
Oh my gosh. I have seen people in liver failure, not necessarily from hepatitis C, but from cirrhosis,
that we've drained eight liters of fluid from their belly. Where is that liquid coming from?
It's from your bloodstream. Like you retain it. I know, but eight liters? Eight liters. It's bad. It's not good.
Gosh. That's like really bad. So yeah, you can imagine that that can cause a lot of complications, right? A whole bunch of fluid just in your abdomen that can be anitis for infection. So you can get abdominal infections because of it. It also is just putting a lot of pressure on all of your organs. All this pressure in the veins can lead them to burst, like I said already. So in general, liver failure is not good news.
Well, yeah.
And then some of the other signs and symptoms that we see are similar to what we see in acute liver disease.
So things like jaundice, weakness, itching is a really big one because as Billerubin builds up, it actually causes a really intense itching.
Why?
I don't really know.
I'm not really sure, but it does.
It just makes you itchy.
Interesting.
And then hepatitis C can actually also have extra hepatic.
so outside of the liver manifestations, especially by increasing abnormal proteins in your blood,
which can have issues like making your blood too thick, blah, blah, blah.
Hepatitis C is not a good disease.
Well, it's horrible.
It's horrible.
And the big C in Hep C, cancer, I mentioned already, it's generally only associated with cirrhosis.
So cirrhosis becoming cancer in people with hepatitis C.
That's not true for liver cancer that's not associated with hepatitis C.
Like you don't have to have cirrhosis to get liver cancer.
But in people with hepatitis C, they generally have cirrhosis first and then liver cancer.
And so are there differences in the types of liver cancer that you get?
Like is the hepatitis C associated liver cancer different than alcohol associated liver cancer
or just like...
Good question.
There are different types of liver cancers.
What's associated with hepatitis C is called hepatocelular carcinoma.
That's the same type of liver cancer that you would get associated with very heavy drinking
or with hepatitis B, which is another major cause of HCC,
hepatocellular carcinoma.
But in general, HCC is actually a pretty rare complication of hepatitis C infection.
it's about 1.5%, 1 to 3% I've seen overall of people with chronic infection will go on to develop
HCC. How exactly this chronic infection results in cancer? I really thought we knew, Aaron.
I mean, cancer is associated with high levels of inflammation, and we know that this causes
chronic inflammation. Right. So maybe it's as simple as that. But the true, like, mechanism,
the way that we know it for like HPV, we don't know in this case.
Okay.
So, yeah.
The good news is that there is treatment.
That's great news.
It is great news.
And it's fascinating and amazing to me because we've made massive advances in treatment in the last few years.
So it wasn't until, I believe, 2013, that the first what we call DAA, direct acting antiviral.
So that's an antiviral that directly attacks and blocks the replication of hepatitis C virus was put on the market in the U.S. at least was in 2013.
Prior to this, there was still treatment, but it was a combination of something called interferon, which is actually one of those mediators of immune response that our body uses naturally.
And another antiviral called ribavirin.
this was used before we had these DAAs, and it did result in like 40 to 60 percent of cases being cured,
but treatment took forever, like almost a year, if not more, and there was a ton of side effects,
and it was really difficult to tolerate.
So the introduction of all these new, I think there's at least eight now, direct acting antivirals,
DAAs, has been massive because now treatment usually only should.
takes eight to 12 weeks. It could be up to 24, depending on how severe disease is to begin with.
But cure rates are above 90%. That's really cool if you can afford the medication. Yep, that's
the asterisk. The cost of these medications, it varies hugely. It's dependent both on whether
there's a generic formulation. And since a lot of these drugs are super new, there might not be
generics yet. And also what country you're looking at. So these can vary anywhere from 15
dollars to $2,500 for a one-month supply of some of these drugs.
Can I guess which country is the $2,500?
It actually, none of these were in the U.S. actually.
What?
Yeah.
Okay, so the U.S. is $25,000 a month?
Maybe.
I didn't see numbers for the U.S., but yeah.
But yeah, but it is, that's one of the biggest challenges now that we have a way to cure it
is both identifying disease because there are so many people living with hepatitis.
C that don't know that they're infected and actually getting this drug or these drugs to people
who are infected.
So there's a lot of people who are infected and know they're infected but haven't yet had access
to these curative treatments.
Right.
So, yeah.
That's the biology of hepatitis C.
So much we don't know.
So much.
Do we know anything?
I don't know.
So tell me, Aaron, what?
what's up with this? How did it get here? Why are we so bad at screening blood? Or are we?
Great questions. Let's take a quick break.
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As you mentioned, the hepatitis C virus is a pretty recent discovery. And so the history of it is
pretty short. The virus itself was only discovered or named in 1989, but researchers knew of a
non-A, non-B hepatitis virus for a little over a decade before that, so around 1975 was when it was
kind of first recognized to exist. But before we get into too much of the medicine,
medical history side of things, I want to talk about the evolutionary history of hepatitis C.
Please.
For a long time, researchers assumed that hepatitis C virus had its roots in a non-human
primate hepasca virus.
Okay.
But then they discovered hepatitis, like a hepatitis C-like virus in horses and dogs, which
suggests that these viruses might be more widespread throughout mammals than previously thought.
Okay.
So where did they come from? Okay, looking at the genetic diversity of hepatitis C virus,
there seems to be the most diversity in sub-Saharan Africa and in Southeast Asia.
And so that's probably where it had been circulating for a really long time in humans,
for who knows how long.
But by the way, how it's circulated in these populations is not clear.
because as you mentioned, it's blood-borne.
Right.
So there are a bunch of hypotheses ranging from mosquitoes,
it actually being vector-borne.
Fascinating.
To sexual transmission, having it play more of a role
or like circumcision practices or other things like that.
Interesting.
Yeah, so it's kind of unclear.
It's the theme of this episode.
But how long did it circulate?
And that is also a really hard.
question to answer. Shockingly.
Listeners. Sorry. We're sorry. There are models based on the genetic diversity of the virus
that put the origin of hepatitis C no more than a thousand years ago. Okay. Which doesn't
really seem possible given the hugely widespread nature of the virus, which we know is a more
recent thing, but the fact that it exists in different genotypes in isolated,
populations, like geographically isolated populations.
Yeah.
And so maybe we're missing something about the replication of the virus itself,
about how mutations accumulate, this sort of thing.
I mean, the short answer is we don't know.
So.
That's the title, Aaron.
Let's get into the stuff that we do know.
And that is how it became global over the past 100 years.
And by global, I mean, like, really.
global. I know this is maybe preempting you a little bit, but how many people are estimated to be
infected with hepatitis C worldwide? Do you mean estimates from today or like four years ago? Because I've
seen very different estimates. I've seen very different estimates too. And I can't tell whether it's like
super optimistic. At least 71 million. Let's say that. Right. And then the higher estimates are around
170 million. Yeah. Exactly. So up to
to two and a half percent of the world's population.
Yep. Episection over. What the heck?
What the heck? I mean, that's an enormous number of people.
Yeah, it really is.
And the reason that I wanted to mention those numbers now is because a big part of the story
of hepatitis C is not just in the history of its discovery and medical advancements and
treatments and so on. I mean, those are really important. But I think it's really important
also that we understand how we got here.
Mm-hmm.
How on earth did 70 to 170 million people become infected with this virus?
Yeah.
How?
I mean, it's a complicated question to answer, because there are many different parts of it.
But a big part of that answer is, as you mentioned, through blood transfusions and other blood products.
And so even though the history of hepatitis C is a short one, the history of blood and blood technology is not.
And those histories are intertwined.
So I decided for this episode.
to focus on the blood transfusion side of the story.
Awesome.
And holy cat, what is so much more interesting than I thought it was going to be?
I had a really fun time researching this.
Okay, blood is a precious resource.
The cost of a barrel of crude oil as of January 2020 is about $58.
Okay.
The cost of a barrel of blood would be about $63,000.
And I estimated that based on the cost of like a gallon of blood.
I'm sorry. Yeah. What? Yeah. Wow. Uh-huh. But even more than the monetary value of blood is, of course, it's life-saving qualities. From blood, whole blood, you can get white blood cells, plasma, clotting factors, antibodies, and then there's, of course, blood itself for transfusions. It is vital. It is a life-giving liquid. And as you might expect, this quality of blood,
has led to it being revered for millennia. It's impossible to give a history of blood itself and how
it's been viewed throughout history because the scope would be enormous. Like which cultural
lens are you going to look through? Which myths are you going to write about? So let's pick this
story up from where this life-given quality of blood first started to be tested. Blood had long been
recognized as one of the four humors of the body. This was like the presiding medical theory. So it was a
with phlegm, collar, and bile.
I like that flam makes the cut.
I know.
Bring back phlegm.
Then this whole, like, humor theory of the body dates all the way back to ancient Greece,
because I have to mention that in an episode contractually.
But how blood traveled throughout the body, its circulation, wasn't discovered until 1628.
Whoa.
Yeah. The first attempts at transfusions followed shortly after, mostly using animals, and they were unsuccessful, as you might expect.
Like animals into humans?
Animals into animals. Oh, okay, okay. Okay. We'll get there. We'll get there.
So in 1666, the first known successful blood transfusion was performed.
Whoa.
An English doctor named Richard Lower took two dogs, and from one, he drained as much blood as possible,
without killing it.
I do remember this, actually.
I knew this story.
I'm going to keep telling it anyway.
Do it, please.
With the other dog, he sewed a reed to one of its neck arteries
and attached the other end to the jugular of the barely alive dog.
And he allowed the blood to flow from one dog to the other
until the one that was giving the blood died
and the other one that was receiving the blood revived.
He stitched him back up.
And then the dog essentially came back to life.
He like, within a few minutes, he was back on his feet.
He was running around and seemed perfectly happy, even with his dead comrade next to him.
I was going to say the other one was dead.
Cool.
Yeah.
But this, even though it was a very gruesome experiment, it cracked open the world of possibilities
to both physicians and philosophers.
How could this be used to save lives?
By transferring blood from one animal or one person to another, would the recipient take
on the qualities of the donor.
Can you make a tame dog vicious by the transfer of blood?
Could you change your personality by getting someone else's blood?
And so while the philosophers were busy debating the ramifications of blood transfusion,
the scientists were busy refining the technique.
Soon it was possible to conduct small transfusions, enough to keep both the donor and the recipient
dogs alive.
But it wasn't all good news, not just because probably, you know,
many, many dogs died along the way.
Because people almost immediately started experimenting on humans, transferring blood from a cow
to a human, for example.
Oh, no, bad idea.
Yeah.
He survived.
Wow.
It was also done on, like, he was, he was forcefully volunteered.
Of course.
You know.
Nobody volunteers for those, quote, experiments.
No.
They did this to him because they were like, oh, he's a, he's a drunk.
He's mean to his wife.
wife, let's see if we can make him more docile with the blood of this gentle cow.
And so he did seem to be, you know, a little bit calmer after that, probably because he was
like exhausted and had been close to death.
Yeah.
And then a couple, like a year later or a few months later, he shows back up.
His wife is dragging him there.
And she's like, you got to do it again.
He's back to his, you know, normal state.
and so they did it and then he dies.
Yeah.
Turns out in the trial, she had been poisoning him all along.
And so he actually died of arsenic poisoning.
No way.
Isn't that great?
I love that.
Oh, my God.
So anyway.
That's really funny.
Okay.
But even though, you know, not all of these transfusions were successful by any means,
people started to see the possibilities in this.
People were still dying by the bucket load from infectious diseases like smallpox, plague, cholera, you know, the ones.
What if these physicians wondered, people could be cured of such illnesses by transfusing healthy blood, like from lambs, into sick people?
What if?
What if?
Lams specifically.
Yeah.
So they tried it.
Didn't work, Karen?
I mean, you know, to read the reports of some of these experiments,
you'd think that they'd discovered a miraculous cure-all.
Wow.
They started making claims that not only could fresh lambs blood be used to cure leprosy and scurvy and so on,
but also unfavorable personalities or the other thing that they tried,
and this was human-to-human, was to resolve marital conflicts by swapping the blood of wives and husband.
Just do a little tradies with my herbs? Wow. I should ask him if he'd be into that.
You should try it. Transfusing spouses, I love it. Wow. And by no means were these new transfusions
widely accepted. Some people believe them to be the work of Satan, or at the very least,
completely useless in curing any of the diseases that they were supposed to. Okay. In this bad press,
in addition to a couple of deaths following transfusions and a wrongful death trial,
led to the premature end of blood transfusions.
In less than five or six years after the first successful transfusion,
blood transfusions involving humans were banned in France and England,
and the Pope banned the practice in the rest of Europe.
Wow.
Five years.
It was like a real 180.
Flash in the pan.
Mm-hmm.
And it would be more than 150.
years before doctors experimented again with blood transfusions in humans.
Huh.
Uh-huh.
So in 1818, an obstetrician in London decided that he had to try something to reduce
the enormously high mortality rate of people bleeding out after giving birth.
Ah.
So he tried a few transfusions with varying degrees of success.
It's like 50%.
Okay.
But even with this low success rate, what this did was get scientists interested in transfusions again.
and they gave themselves license to experiment as they wished.
And experiment they did.
While there were some milk transfusions, for instance,
most doctors restricted the material to human blood.
Sorry, time out.
How, what?
Yeah, something about the proteins and fattiness and milk would be good.
But where do they put the milk?
In the blood stream.
No, mm-mm, no.
It didn't. That one didn't last long. It wasn't super popular. I don't know if that experiment was repeated.
Okay. Okay.
Most people fortunately just used human blood.
Okay.
But even then, there were many ways a blood recipient could die.
Physicians didn't know anything about blood groups, clotting factors, sterile technique, et cetera, et cetera.
So about 56 of 100 blood transfusions during the 1800s ended in death.
That is more than not.
It is more than not.
And it's probably likely that at least some of these people were going to die anyway.
Okay.
But, you know, despite these not so great numbers, people didn't abandon the procedure altogether.
And that's probably fortunate because the discovery of blood groups was just around the
corner. The guy who discovered blood groups like A, B, A, B, O, etc.
Right. Okay.
Whose name was Carl Lansdiner made some seriously impressive predictions about how different
blood types could behave when introduced to one another and suggested that this knowledge
would be really useful in increasing the success of transfusions.
Huh.
And that would win him the Nobel Prize.
But even still, nobody really paid much attention for a while.
to this? Yeah, kind of strange. Eventually they did. So throughout the early 1900s, they refined the
technique a little bit, but doctors would just sit by their patient's side and kind of guess by intuition
alone when their patient had received enough blood. You're looking pinker. I don't do. Yeah, seriously,
that was basically it. Okay. They didn't always guess correctly. And then there was a huge issue of
blood doing what it does, which is clotting.
So it would gum up the works like very rapidly until sodium citrate was discovered as a non-toxic
anticoagulant.
And then the world of transfusions was open to basically everyone.
Like it was as long as there was a willing donor, you could get the job done.
Doctors weren't yet storing blood for later transfusions.
They typically needed someone then and there, like a donor on the hoof, I think is what they
called it. So you would just like go into the surgery or go into the whatever and be the donor at that time?
Yep, exactly. And this could be a lot to ask of someone. And so arose the practice of selling or buying
blood and the field of professional donors. And remember, this is the early 1900s when microbiology
as a field was just a few decades old and the causative agents of many diseases were unknown.
And the decades that followed saw the creation of the earliest blood banks and improvement in storage techniques,
but arguably the biggest progress came, as you might expect, during World War II.
It's no coincidence that this is also when Hepatitis C began its global spread.
Ah, World War II.
World War II.
So millions upon millions of people were dying or getting seriously injured, both military,
and civilian and also traveling all around the world and then returning home, hopefully, at the end
of the war. So with all of these injuries, there was not only a huge need for blood, but also a need for
improvement in blood technology. And we've talked before about how much antibiotics revolutionized
medicine during the war. People weren't as likely to die from infection from a minor wound
or major wound after the discovery of penicillin. But before during this episode, I didn't realize
just how much of an impact freeze-dried plasma made on survival as well. Yeah, that makes sense. I
wouldn't have thought of that either, but like, yeah. Oh, it was remarkable. Yeah.
It, like, so freeze-dried plasma was just add water, I guess, was a field-ready way to reduce
shock and restore blood volume. And this alone probably saved thousands of lives. Wow.
blood, whole blood was less of a focus because it was much more difficult logistically to store and
handle and so on.
Yeah.
And so military doctors looked on the plasma as a miracle.
Soldiers would be going into shock with severe wounds and then they would bounce back from
death with the injection of some plasma.
Wow.
But these doctors also recognized plasma's limitations.
So the positive effects were often short-lived and the wounded appeared to be starved for oxygen
unable to get warm and then would sometimes slip back into shock.
Since there was no red blood cells.
Exactly.
To carry oxygen.
And so although plasma was pretty awesome, it was no replacement for whole blood.
And the problem was where to get it.
During the war, there was a shift from paid donors to volunteer donors
because there just wasn't enough blood coming in.
And so they were like, oh, you know, support the troops, campaign like for community,
that sort of thing.
But at least in the U.S., this blood wasn't.
wasn't being shipped overseas because the logistics of keeping blood cold during transport was
difficult. As a result, there was a constant shortage of blood, and some doctors had to resort to
being impromptu donors. Oh, gosh. Yeah. Or employing the whole donors on the hoof method
as had been used previously. After the war ended, and the pressing need for blood decreased,
the blood banks and blood donor organizations didn't fade. They actually grew enormously.
The threat of nuclear war between the U.S. and the USSR kept people running to blood banks to donate.
Because if a nuclear attack happened, the immediate need for blood would be greater than maybe like the entire war combined.
People recognize the problems with paid donors, though, and the American Red Cross, along with smaller blood banks across the country,
focused on convincing the public to donate blood out of a sense of community.
But there was a darker side to this.
racism in blood donation had existed since the modern history of blood transfusions and it didn't stop after the war
even though scientists repeated over and over again that blood was blood and you couldn't tell a person's race
based on their blood the red cross and other blood donation centers still practice the racist
regulations of only allowing white people to donate or when that rule was overturned they forced people to label
blood so that a recipient could then see or choose whether they wanted to receive that blood.
Are you, I shouldn't be surprised by this, Erin.
It was probably less of the patient and more of the hospital.
Yeah, of course.
Yeah.
There could have been the patient too, but.
But just the fact that it, that, like, that was the Red Cross practice.
Mm-hmm.
Mm-hmm.
Eventually, these racist practices died out, not soon enough, and then they would later be
replaced by still screening blood based not on the blood but on the person who's giving the blood.
Yep.
Which is really problematic.
To say the least.
Yeah.
But ethical and legal issues surrounding blood donation continued to pop up or reemerge,
mostly focusing on whether blood could be considered a commodity.
So around the world, different countries had debated whether or not to pay donors for their
blood or to rely on volunteers.
And the U.S. was one of these countries that was sort of caught between those two things.
And the ethical issues with paying for blood were obvious to everyone.
There was exploitation of poor people who were literally selling pieces of themselves as a way
to make money, which is an issue that continues to be a problem in paid medical studies,
but we're not going to get into that.
It's a different episode.
It's a different episode.
Yeah. And then the fact that there was still no good testing for certain infections, such as hepatitis, even though hep C was not yet known.
And then came the legal and moral ramifications of whether blood was considered a commodity, because if it was, it was then subject to federal trade and commerce laws in the U.S.
And if it were considered a product, it was subject to the uniform product code, which was a regulation that stated that anything sold as a product of commerce carried an employer.
warranty. Huh. But blood banks, both nonprofit and commercial, couldn't easily guarantee the safety
or quality of the blood they were peddling. So they sought and gained an exemption to this by getting
blood to be labeled a service, which is why it was so difficult for anyone to sue blood banks
after being infected with contaminated blood. Fascinating. Wow. And in the U.S., prisons were a huge source of
plasma for a very long time and outrageously unsanitary conditions in at least one group of prisons
in Oklahoma owned by a physician. Yeah, he owned six prisons. What? It was a site of enormous
hepatitis infections in the 1960s. And so I should point out that at this time, so throughout the
60s and 50s, basically, and even before then, hepatitis, like as you mentioned, hepatitis as a condition,
inflammation of the liver was recognized.
Right.
And it was even known to be associated with blood transfusions.
Okay.
But no one, of course, knew what the causative agent was for a long time, and I'll get there.
And so usually the hepatitis was diagnosed based on clinical symptoms.
So, like, the jaundice and the inflammation and all of that, not on finding a virus.
Yeah.
Even though hepatitis was a known problem in blood transfusions, people in the blood business looked at it as, well, it's better to live with hepatitis than die of not getting blood.
So it's an unfortunate but necessary risk.
During the 50s and 60s as well, injection drug use also started to really pick up and become widespread.
And so the combination of a massive increase in blood donation and blood transfusions and injection drug use really also help to spread hepatitis and other blood-borne pathogens.
And hemophiliacs were one population that experienced extremely high rates of hepatitis C and, of course, HIV, as we discussed in that episode, due to their need for multiple transfusions or factor 8, which was made from.
plasma. In the early 1970s, the CDC put transfusion-related hepatitis deaths at 3,500 per year.
Whoa. Wait, in what year again?
1970s, early 1970s. Wow. Just transfusion-related hepatitis deaths.
Well, and many physicians actually argued that that number was 10 times that.
Holy guacamole.
Mm-hmm. And this wasn't just a problem in the U.S. This was a problem in the U.S. This was
a global problem. I'm focusing on the U.S. because that's where a lot of the book took place.
But anyway, Europe, who relied solely on unpaid volunteers, condemned the U.S. practice of using
paid donors, but they constantly bought plasma from the U.S.
They had a constant plasma shortage. And so, yeah. And when a test for hepatitis B was finally
developed in 1975, which was only 40% effective, actually, better than the 15% effective test
from 1972. The people could finally start screening blood. And what they found was that paid
donors were three times more likely to be infected with hepatitis compared to unpaid donors.
This is hepatitis B. Hepatitis B. Yes. And then there were arguments over whether to
completely eliminate paid donors until the FDA said in 1978,
hey, let's let the market decide.
And they forced blood banks to label blood as being either from paid or unpaid donors.
Almost immediately, the practice of paying donors for blood was over.
Wow.
Like they did not.
Nobody, no hospital bought paid donor blood.
Huh.
Plasma was another story.
Yeah.
You can still get paid for that.
Yeah.
I remember in college, I had friends who would go donate plasma for-
beer money. And then they would be like, oh, it's great. Like you get so much drunker
faster because whatever. That's a terrible practice. Nobody do that. Nobody do that.
So a few years after this ruling by the FDA, rates of hepatitis B dropped. But people were still
getting hepatitis from transfusions. An investigation revealed that 90% of transfusion-related
hepatitis was not caused by hepatitis B, but by something they couldn't test for.
Ooh.
They called it non-A, non-B hepatitis.
Yeah.
Non-A, non-B, I'm guessing it's C.
Yep, easy.
In 1984, five years before the new virus would get a name and a test, it infected an estimated
180,000 blood transfusion recipients, killing about 1% of them.
Is that in the U.S. alone?
I think that's global.
Okay, because that seems whoa high.
Yeah, I think that's global.
Because that's just in one year.
In one year.
That's a massively huge number of people.
So in 1989 and beyond, once researchers could identify hepatitis C cases,
they started to get a better sense of how the virus behaved and what they saw was super
concerning because of all of the things that you said.
And whereas hepatitis had previously been seen as this unfortunate risk of blood transfusions,
this new information about hepatitis C was like, okay, no, there's an increased urgency for a clean,
uninfected blood supply.
And that coincided also with the AIDS pandemic beginning.
Those two things combined, particularly urged on by the AIDS pandemic, really led to a
complete reform of blood screening and blood transfusions. But even though blood donation regulations
really changed to decrease risk of any sort of blood-borne infections, damage had been done in a lot
of ways. Over time, the positive effects of these new regulations, in addition to the
introduction of things like needle exchange programs, really did start to slow this,
hepatitis C pandemic down, within 30 years.
Like the virus was discovered in 1989.
30 years ago.
30 years ago.
It was discovered.
Wow.
A test was developed for it.
And an effective treatment was created.
That's so, I'm just so interested in that.
Like, is there a story like that for any of the diseases that we've talked about?
30 years to go like that rapidly. I know that it's because we discovered it so recently,
you know, like, whereas just diseases that were discovered so long ago, of course it took
them longer to figure things out. But I just think that's so, so fascinating. I mean,
HIV is, is along those lines. That's true. It's not, it's not the death sentence it once was.
Absolutely. But, you know, in terms of hepatitis C, we're still far away from elimination or eradication.
Yeah. There are still, as we mentioned, millions and millions of people infected with the virus around the world, and new infections continue to occur.
Erin, tell me about hepatitis today and what's being done.
We'd love to. We'll take one more quick break before we jump in.
This section is actually going to be very short. We kind of already talked about these numbers, so let's just repeat them for everyone.
It's unclear to me exactly, I'm sure it's unclear to the globe, exactly how many people are currently living with hepatitis C.
But we know it's at least 71 million, which is what the WHO, the World Health Organization estimate is based on 2015 numbers.
Okay.
However, if you look at numbers from just a couple of years previously, it could be as high as 170, 180 million people.
Yeah. What caused the drop of 100 million people? I think it's just depending on what model people
were using and what years of data they were using. So if they were using data from like the 80s and 90s and then modeling out from their infections were higher than if they used numbers from the early 2000s. And it's because of those blood transfusion screenings and things like that. So at least that's from what I understand. That's what it seems like. But here's where, I mean,
either way, 71 million people, that's 71 million people living with hepatitis C. The WHO also
estimates that there's over 1.75 million new infections every year. Oh my gosh. And they estimate that
400,000 people die every year as a result of hepatitis C. How many? 400,000 people. Wow. And this is now a
curable disease. So nobody in theory should be dying from hepatitis C. Right. And the biggest issue
is twofold. One, it's estimated that only 19% of all people who are living with hepatitis C actually
know their diagnosis. Wow. That's very low. It's very low. And of those diagnosed, only about
5 million people. So it's estimated that 13 of those 71 million people, 13 million know their diagnosis.
Only 5 million of them have been treated as of 2017. So there's a huge amount of work that needs to be done
to get those people, the treatment that they need. Yeah. What is what's being done?
Well, the World Health Organization has a huge hepatitis initiative and they have a number of different
ways that they're trying to increase access to these drugs and also increase access to screening.
Because one of the issues is while initial screening tests for hepatitis C, which are antibody-based,
so we can basically just take your blood and see if you have any antibodies to hepatitis C,
those tests are pretty easy and pretty cheap, like less than $2.
But they're not specific.
So while they'll tell you, yes, you were exposed to hepatitis C, remember that 85% or less of people actually go on to develop chronic infection.
So it might just mean that you were exposed to hepatitis C, but you've cleared the infection.
The tests to actually know whether you are currently infected chronically with hepatitis C are more expensive and often require expensive equipment and specialized technicians to be able to.
to do those tests because they're often PCR-based tests or antigen-based tests.
So looking for the actual virus itself in your bloodstream.
Right.
So that's one of the things is developing better diagnostic tools that are cheaper, easier to use,
things like point-of-care testing, which means you can, when you have somebody there and
you want to test them, you can actually do it right then and there.
That's huge, not just for hepatitis C, but for a number of different infections people
are working on.
And then the other thing is treatment.
So while we have treatment, it's very expensive in a lot of cases.
And so getting people access to these drugs is difficult, even though it's hugely important.
And so that, honestly, it takes money and it takes pharmaceutical companies being willing to sell their drugs for cheaper.
Okay.
So let's find something else because that's never going to happen.
Yeah.
The other thing is the vaccine.
I actually don't know how much progress has been made on a vaccine thus far.
It's very difficult because of how much variability there is in hepatitis C and how quickly it mutates.
It's really difficult to develop a vaccine.
The other issue is, since we don't know a lot about how it interacts with our body,
we don't know how good of an immune response we'd be able to generate with a vaccine, if that makes sense.
So it's unclear if we can develop a good vaccine.
at this point. But I'm sure there are people working on it because this is a human-specific disease.
I'm not sure that I even mentioned that. But with any human-only disease, it is theoretically possible
that we could eliminate it. But at this point, that's not even an option. And so one thing I would
like to say is that while in the U.S. and much of Europe, Australia, other places, blood products
are very, very, very, very safe at this point. They're very well-screened. That's not true everywhere.
So in some places, it is still difficult to test blood products for every possible infection.
But overall, they are much better tested than they were in the 80s and 90s. And because blood
transfusions are generally rare, blood transfusions itself are not a huge risk on a population level
for hepatitis C infection today.
Okay.
The two largest sources and risks for infection, the biggest one is unsafe medical procedures.
So using glass syringes, not properly sterilizing them, using, reusing needles for medical injections.
Right, which used to be common practice.
Yes, yeah.
And is still common practice in a lot of places where they don't have access to disposable syringes and
disposable needles.
It's expensive.
It's super expensive. And so that's a huge source of infection. And the other is injection drug use. So like you mentioned, harm reduction practices like needle exchanges, distribution of sterile needles. This can be hugely effective in helping to reduce the spread of disease, including but not limited to hepatitis C.
Mm-hmm.
So that brings me to what I really want to talk about in terms of hepatitis C, and that is that this is, like HIV, a disease that is highly stigmatized.
Right.
Because of its associations with injection drug use, and it's, I think a lot of people still associate it with sex, even though that's not a huge source of infection, but in our Puritan culture, sex is bad, so, you know, sexually transmitting.
In fact that's the word I'm looking for?
Stigmatized.
Stigmatized?
Yeah.
And so one thing that I think is really great that has become a recent recommendation in the U.S. by the CDC
is universal screening for everyone born between 1945 and 1965.
Huh.
Yeah.
It is now the recommendation that if you were born in those years between.
1945 and 1965 and you haven't yet been screened for hepatitis C, you should absolutely go get
screened. No matter what you think your quote unquote risk might be, even if you never used injection
drugs, even if you never had blood products, it doesn't matter, you should get screened.
And that's because hepatitis C was so common that any type of medical procedure could have
potentially put people at risk.
But what I think is great about things like universal screening is that it helps to reduce that stigma.
Everybody should be screened because anybody could have been exposed to hepatitis C.
Yeah.
But the thing about screening, I think screening is really awesome.
And we haven't sort of talked about what diseases make sense to screen for.
Like when would you screen versus when would you not screen?
So I wanted to talk really quickly about what makes a disease a good candidate for screening
and why hepatitis C has only recently been a good candidate for screening on a large scale.
First of all, to be a disease that it makes sense to screen for, you have to have an effective
screening tool, right?
Yeah, which makes sense.
Seems pretty basic.
For there to be an effective screening tool, that means it has to be inexpensive so that it's cost-effective to
do this test on everyone who comes into your office, basically. And it has to have a good enough
sensitivity and specificity that it's actually useful. So we know that we're getting the majority of
cases of this disease, and we don't have a lot of false positives or false negatives. Secondly,
you have to have a disease that's at a large enough prevalence in the population for you to actually
pick it up. Since no screening tool that we use is perfect, there's always going to be some false positives
and some false negatives, if a disease is really, really rare,
then your false positives and false negatives are going to be out of whack,
and there's not really a point to screening in that case.
Does that make sense?
Okay.
And third of all, and this one is where hepatitis C is only now makes sense to screen,
you have to be able to do something about it,
because there's no real point in screening whole groups or populations
if there's nothing you can do except tell them,
hey, you have a horrible disease.
End of story.
So now that we have such effective treatment tools,
and of course screening tools are always getting better,
screening is a really good recommendation for something like hepatitis C.
That's cool.
Yeah.
I really love that.
Yeah.
My little epi nerd in me.
So yeah, that's basically hepatitis C.
The biggest sort of obstacles that we have going forward are access to treatment.
and better screening tools and getting everyone who has hepatitis C to actually know their diagnosis
so that they can get access to potentially life-saving treatment.
I mean, it's amazing the enormous strides that medicine has made.
I know.
And science has made in the past 30 years.
Yep.
Good job.
Good job.
But also, like, bad job on a lot of other things.
Oh, yeah.
Oh, so sources.
Sources. So I got most of the information about the history of blood transfusions from book called
Blood and Epic History of Medicine and Commerce by Douglas Starr. And I recommend this book. It has
more of the discussion about the racism surrounding blood transfusions, which I didn't talk much
about, but there's a really dark history to that. And screening blood by the identity of the person
rather than what's in the blood has also remained a huge issue.
Yeah.
But read more of that book to find out more.
Another book that I relied on also was hepatitis C virus from molecular virology to
antiviral therapy.
Cool.
If you'd like to know more about what's being done for hepatitis C worldwide, you can
check out the Global Hepatitis Report by the World Health Organization.
That was in 2017, I think is the most recent one.
And then there's a number of different articles that I have on just the clinical disease and
epidemiology.
We'll post all of our sources on our website.
This podcast will kill you.com under the episodes tab.
Thank you to Bloodmobile for providing the music for this episode and all of our episodes.
And thank you to all of you for listening as always.
Yes.
We appreciate you.
We love you.
Thank you for letting us do what we love to do.
It's unbelievably fun to talk.
about horrific diseases with my best friend and have so many people listen.
It's the dream, really.
Well, with that, wash your hands.
You filthy animals.
And hepatitis, see you later.
This is Bethany Frankel from Just Be with Bethany Frankel.
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