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