Epidemiologist Steve Deppin explains COVID-19’s unique threat—7.7 billion people unexposed to SARS-CoV-2—with Alpha, Beta, and Delta variants three times deadlier than flu, while Omicron spreads faster but retains lethality. Age and comorbidities like obesity or cancer treatments drive severe outcomes, including long COVID cases requiring lung transplants, such as a 25-year-old athlete. Early ICU failures worsened survival rates; vaccines now reduce hospitalization/death risks but don’t block infection entirely. Healthcare disruptions (e.g., Tennessee’s 20% positivity in August, U.S. kidney transplants plummeting from 300 to 30 monthly) caused indirect deaths. COVID will endure as an evolving pathogen balancing transmission and host survival, defying herd immunity through immune evasion. [Automatically generated summary]
Before we go into that, I just want to remind everyone, I have an email address for any thoughts, concerns, gripes, complaints, criticisms.
I welcome them all, especially the things you have to say that you wouldn't say to my face.
That's truthunrestricted at gmail.com.
I have a very special guest today.
As I said, we're going to be talking about COVID-19 and all of its aspects.
I mean, not all of them, but the ones that seem most important to everyday people, I think.
So without further ado, I will allow him to introduce himself.
So my name is Steve Deppin.
I am an epidemiologist by training.
My specific areas of expertise are actually in cancer and diagnosis and treatment of cancers and improving the outcomes with respect to that.
Like many epidemiologists, I had to take a crash course in infectious disease epidemiology as COVID-19 struck out.
And so some of my early work last year was in that space looking at public health and under what circumstances we need to stop doing some essential surgeries and sort of the effects of some of that, some of those decisions.
So that's where I come from.
What I bring is the mindset of what does evidence look like as a researcher and as a scientist, and in some cases, how that plays out in the public health domain from my relatively narrow and specific perspective.
So anything that I say are in during this time are me and mine.
Any mistakes are mine and my own do not reflect that of either any of my employers, my collaborators, or anyone else.
So it's all on me.
Great.
With all that out of the way, let's get right into it.
So we started this from my perspective.
It started with the news, with Facebook, with all the mentions of a thing going on somewhere else in the world.
You know, at first it was China and then it was elsewhere.
So from your perspective, how did we get into this?
Where were we before we started?
And how did we transition from a world that didn't have COVID to one that did?
So COVID, which is novel coronavirus or SARS-CoV-2, was a new coronavirus, which we now are very familiar with.
There's a bunch of other coronaviruses running around, right?
A number of them cause a common cold, which have interesting names like 229E and NL62 and et cetera, which you don't really hear about unless you're a coronavirus geek and researcher, because that's a common cold.
That's everyday, like get a little sniffles.
If you got a five-year-old, congratulations to the Petri dish that is kindergarten and daycare.
And that's what you're experiencing on a regular basis.
So coronavirus is just a virus with a specific physiologic set of tools.
And as we all now know, that's like that crown of proteins around this ball of stuff that makes the virus RNA and so on.
So yeah, when we started this, there was what two years ago, 7.7 billion people who were naive to this virus, which means they had no titers.
They had never experienced it before.
And like other viruses or bacteria that are truly novel, which are usually just a better engineered, a better, better evolutionarily engineered thing in our environment, because our immune systems can't recognize it, we are highly susceptible once it hits the human species mammalian pathway.
So that's that was the situation then.
A bunch of people who are highly susceptible.
Now we've had at least 5 billion individuals get at least a dose and or a billion who are cases who have either had the disease and recovered or had the disease and died.
So COVID is estimated, and this is again, alpha, beta, and delta, about three times more deadly than the common flu.
And Omicron is about as deadly as the above.
And just because of evolution is much more transferable, especially the newer variants.
Yeah, yeah, that's that about sums up everything I know.
Actually, I knew barely any of that, really.
I knew that it was widespread around the world, every continent, but the actual numbers are pretty staggering.
When we look at this situation, each one of us usually looks at it as to what's going to happen to me.
What does it mean to me?
Why do I care that there is a coronavirus?
Many of us, we hear that it's the elderly are more deeply affected by this.
They're much more likely to suffer mortality than those who are younger.
A lot of younger people are fairly cavalier about this whole situation.
How does that line up with your view?
Are younger people getting the vaccine at much less rates from your perspective?
Or is this, do you have any thoughts on that?
So speaking from the United States experience, vaccine rates and subpopulations is highly variable.
It varies from state to state.
It varies from age group to age group.
Many of the elderly, actually in the United States, fortunately, the elderly are among the highest vaccination rates compared to anybody else.
Other countries, the most recent data was actually from Japan, was that the elderly were actually had a lower vaccination rate because of vaccine hesitancy.
So there might be vaccine hesitancy is both age and locale related.
So you can't really say categorically what that looks like.
And that's part of the problem when we look at COVID and how much variation there is across populations.
The U.S. looks different from Southeast Asia, looks different from Canada, et cetera.
So with respect to the epidemiology and the evidence, age is a primary driver for susceptibility.
And by susceptibility, let me put that very specific.
Susceptibility is not whether or not you get the disease, whether or not you get the infection, but whether or not the infection puts you in the hospital or kills you, right?
So when we think about susceptibility, we really are thinking about that sort of endpoint.
And then every step along the way, so if you get infected, there might be comorbidities, long COVID, everything from losing your sense of taste and smell to major lung COVID, comorbidities, long-term.
Cardiomyopathy, right?
You're going to have heart failure at some point in your life.
And I look at it.
So long-term effects.
And then those things, those bad things that arise from a COVID infection increase their likelihood of occurring as you get admitted to the hospital and then as you get put in an ICU, right?
So, because those are each more extreme versions of what that disease is then looking like.
In the ICU, for example, we're not treating the disease per se.
We're treating the symptoms and trying to keep you alive long enough so that your body can, your immune system can recover enough to knock out the infection.
We're just trying to keep you alive.
We're trying to keep the oxygen exchange, literally, as your lungs fill up and other bad things happen.
In the terminology of fighting a war, it's logistics, not tactics, giving the resources to the body so the body's mechanism can affect the right.
And it's very, in many cases, very simple.
And certain drugs that you would use in an ICU, you wouldn't use elsewhere and so on.
And that's talk to, that's you need to talk to a pulmonologist, an infectious disease expert, or you can go online and it actually has guidelines for when you give methotrexate and so on.
So there's very specific drugs that you'd only give in an ICU situation or not.
And I'm sure there's other factors for each condition.
The patient has different conditions that might prevent certain.
Right.
So especially in the United States, other major risk factors are like BMI having being any sort of immunocompromisation.
So it could be lupus.
It could be rheumatoid arthritis.
It can be a cancer treatment.
It could be someone who is under long-term steroids, but in some cases, being under long-term steroids because of, again, the pharmacokinetics of the steroids, it actually might be protected.
So there's still a number of things we're not, we don't know about.
We're not sure about, I guess, but those are the biggies.
So where are we going?
What does this look like in two years, five years?
A lot of people would just like this to just go away.
There's a lot of people that would like this to be a world before we had COVID.
I don't think that's going to happen, right?
Like we got this forever now.
Just one of the other things that we have to worry about, right?
Yes, so it's especially in Canada, United States, it's hard to imagine, but in much the rest of the world, Tb is much more deadly right, malaria is much more deadly, right?
Yeah malaria yeah, Tb is back and and is, and is really nasty and and the vaccine, the vaccine for Tb, doesn't work as well in high temperature environments, for example.
So it really is going to be like that.
We're going to have this disease, which has a fair amount of morbidity and mortality associated with it, and we're going to be living with it for the rest of rest of our existence and our kids and our grandkids.
Unlike the other thing that's a big difference between now and two years ago is we know how to treat it.
Previously there were no treatments.
We didn't even know.
I mean, there were some instances in the early, early days where the things you would normally do in an ICU for someone who has pneumonia which is really the case were not effective.
I mean, in some cases made things worse, made it more likely to be septic.
We quickly figured those out and stopped doing that, learning that, the things and that, if you introduce that earlier or you do that thing earlier, before things get bad, it actually makes things worse.
For example, as we were just literally just trying to figure out how to how to do it, the timeline of the infection yeah right right right, because again that physiology change very much, changes quite a bit.
So the treatment regimens, both from just sort of what we do and how we handle mechanical ventilation, parts of the things to on that extreme, and ecmo and so on um, which are really crazy intensive treatments um, you're at death store.
It's not a few percentage of people who die, it's we're trying to get below 50 kind of thing when you go to that extreme.
So that's sort of the treatment pathways.
But then there are also antiviral drugs which are are now out uh, and things which are, and monoclonal antibodies, for example, which treat people to try and keep them out of the hospital who do have a covet.
I mean that's novel uh, did not happen before, and so that's efficacious for keeping people out of the hospital.
Um, and then other specific antiviral treatments which which are novel um, and those others that are coming out.
And then the biggest thing obviously is we've got a vaccine that still remains highly effective even in this Darwinian evolutionary race that we're now in with Covid.
Yeah, it's the best overall scattershot prevention technique is vaccines for as many as possible, right?
Well, it's actually.
It's not scattershot, it's actually very, very specific.
The Covid works with the spike protein and the vaccine, especially MRNA vaccines, are specific to that spike protein and until COVID figures out how to get around the spike protein approach to invasion, the vaccine is going to be pretty effective.
Now originally, the vaccine was so good at preventing infection that we went haha, we're done right.
Until it was too late because we couldn't get enough shots in enough people's arms quickly enough to prevent evolution from kicking in.
After how many hovering millions of infections.
It figured out how to make some mutations on the spiked protein and elsewhere so that it could still infect.
But like vaccines are intended to do I mean, the real purpose of vaccine isn't really to prevent infection.
It will do that some.
The big thing is it kicks your immune system so that it recognizes it and greatly reduces your likelihood of going to the hospital and dying.
And the vaccines as are as made currently or the versions currently, I guess the way to put it are very, still very effective in those in those instances.
So they're still the best thing, right?
So you mentioned that the virus figures out.
This is just A metaphor, right?
Obviously, the virus isn't being controlled by a conscious entity that's actually deducing anything logically.
What you're talking about is that the virus itself is mutating in steps with each new infection that it gets, and that mutation can lead to what we call variants.
We've heard a lot about Delta and Omicron and all these, and that's really what you're talking about, right?
Is that it slowly changes with each new person that it comes in contact with, and that is leading to a slightly different version.
And that different version might be able to get around a defense that we previously had, or maybe it doesn't.
It's just rolling dice like anyone.
If it gets snake eyes, just like anyone, then it wins and we lose.
Is that more or less the interpretation?
Yes, it really is just evolution 101.
And because it's something that evolution can happen not every generation, but literally every infection.
You got to remember: what is the virus doing?
The virus is trying to create it in such a way that it can pass on its genetic code into some other post, period.
And for example, generally, that's why some of the more deadly variants that we've had in the past have simply been overwhelmed by the variants that are better at infecting, right?
They need less viral load.
They stay in the air a bit longer.
They latch onto smaller particles.
It has some mutations of spike proteins so that even though the vaccine is blocking, it still can only need to make a couple of connections.
So when you think about evolution in the good old Darwinian classic genetic sort of senses, its job is to spread and mutate and live in its host so that it can live in a happy medium and constantly be existing within its host, which is why we now see it in white-tailed deer, et cetera.
So it's something that is highly adaptive now to mammals, sourcing in our domestic cats and so on.
But it's not trying to go out there and kill you because actually, if you kill the host, it's kind of a bad genetic pathway that you've gone down.
That's what they refer to as Ebola, it kills the patient so quickly that it doesn't have a chance to infect many new people.
Right.
Right.
And or it's most virulent on a dead body, right?
So the most virus available is once the body has died.
And so that's why the handling of the body, especially as the person gets near death, is so problematic.
That's why it wasn't, you know, pandemic.
Now, if it were a lightweight aerosol, that could be a, you know, think about what's been happening, right?
The variant, especially the current Omnicron variant, many more people are asymptomatic.
It's affecting multiple age groups.
It goes all the way down.
And it requires far less what's called a viral load.
So it takes fewer individual viruses.
If I'm talking or if I cough at you, fewer cells.
It takes far fewer viruses, individual viruses to get into you to then make you infected.
Fewer individual cells.
And it's called an inoculum, is the formal word.
So it's like that exposure.
Your exposure to that can be less and you'll get infected.
And so you think about it, well, if I'm a virus, that's what I want to do.
I mean, I want to hide, be asymptomatic.
I want to take less in order to get to you.
And then when I do get to you, I'm actually, if I can keep you alive and then make a bunch more, then I can go and then get into someone else.
That's the best of all possible worlds, especially just in your breath.
So, yeah.
So you've mentioned a couple of times about new things that we've learned.
And we're still, as I understand, still learning many new things about this infection.
I call this the fog of war.
I relate a lot of things to war, but I call this one the fog of war.
And it really is.
Two years ago, we were just kind of revealing the first parts of this.
And a lot of people mention this: the communication on this was very all over the place.
There was just so much information so quickly.
It overwhelmed a lot of people.
It overtook almost everyone who used Facebook at the time.
It overtook every post everywhere within a two-week span or so for most people.
It just went from almost nothing to everything in their whole world.
And all the information from even just the people who were legitimately attempting to tell the truth, there was just a great confusion on this.
What did you, from your perspective, I'm interested to hear what did you think of that time when there was this great swarm of voices trying to say things and some of them were contradicting each other.
And we got a very confused mass at that point.
What was your perspective on that as an epidemiologist?
So my perspective was actually very bunker-esque.
So I cannot spend my time on Facebook and worrying about what is churning out in that space, especially in an unregulated media space, because I simply did not have time.
So for me, what was very important at that, and when we think about that early, especially the earliest time period, when we think about, so it came to the U.S., February, January, it was case one, Seattle.
There were other cases, but that was the first certified case.
And so looking at that sort of timeframe between there and March.
So in March, and again, I work in this space, especially in thoracic surgery, and the surgical societies came out and said, we need to stop doing surgeries because we don't know what or how to do good testing, right?
Yeah, we didn't have any tests.
Back in the day, we didn't have PCR testing.
Actually, Vanderbilt was one of the first institutions, state of Tennessee, the Tennessee testing lab was one of the first five to actually have that.
So we actually were able to get in front of many of those questions.
But still, it's not like today where you can go in and you can have a plate of 20 and do a single run.
It's literally one human going through the reagents, running the test, walking it, walking it from machine to machine.
And so you can't do a thousand tests, you know, and we have hundreds of surgeries a day.
Each person would need to be tested before they came in.
So we, so until the infection control systems were in place so that we could feel safe that we wouldn't infect a patient, we wouldn't infect a healthcare group from a patient.
And then if we do something to this patient and it generates even a short-term immunocompromisation, can we keep them safe in quarantine?
What does that look like?
So all those procedures, people are going, how are we going to do this?
And until we do, we just kind of say, okay, we're going to stop.
And then we need to figure out under what conditions we can reopen and what does that infection rate looks like?
What does that, you know, which, which ones, which are the surgeries that we need to do first?
And on top of that, there was also, do we have enough mess?
Do we have enough PPE?
Can we even do the infection control that we know works?
Because we're used to having really nasty infections that we're having to deal with.
And we're used to isolation and keeping patients in isolation and, you know, negative air and so on.
Anyway, we know how to do that, but are we going to get overwhelmed?
Because again, what was happening is you're seeing things like Wuhan and you're seeing Lombardy, Italy, right?
Where the healthcare system got completely overwhelmed and hospitals actually became vectors for infection.
So people were stacked and packed in the hallways and healthcare teams were getting affected.
And on top of that, we didn't have effective treatment.
So it was really, really scary.
And so in that sort of a situation, you're just trying to, there was nothing to add to the conversation.
You let the folks whose job that is, which was a CDC, for example, and then the individual researchers, because I mean, people say, well, the vaccine is early and, you know, it's done, blah, blah, blah.
So, I mean, if you go online and look up a guy named Mark Dennison at Vanderbilt, this is somebody who's been studying coronaviruses for 30 years.
And there are vaccine groups who have been working in this space.
MicroRNA as a technology has been around for some time.
And it was just the innovation that someone said, hey, I think I can do this and this will have a big impact on viruses.
And it just so happened that spike proteins are important.
And oh, here's a virus that has a really important spike protein.
Boom.
And that guy probably didn't get the funding to try all the things you'd have to try until there was a need to put that funding in place.
Right.
Right.
So there, so there's, I mean, if you want to, it's all after the fact, but there were some people in the bunkers who were doing some just amazing science.
So Graham, Dr. Graham out of NIAID, out of the National Institutes of Health, there's another guy named James Crowe here at Vanderbilt who does this amazingly cool stuff, Dennison, who I mentioned.
So yeah, I'm fortunate to be at an institution that has some really cool toys and some really amazing people.
And so we could literally get weekly updates as to where they're at and what's going on.
And that's what it came down to.
I mean, every week we would have reports of infection rates, et cetera, how many people building the ICU because we were trying to figure out what that was looking like.
And in that early era, as I was recurring, this is something that's really important to think about because we think about just the infection, infection, infection.
When you do something like that, or when, like in August, when the state of Tennessee had the highest infection rates in the United States, positives were happening in 20% of the people that we tested.
So we had a raging infection and then the healthcare system was getting overwhelmed, quite simply.
And so what does that look like?
Well, you have that infection, but as more and more of those healthcare resources are being pushed toward taking care of those who are infected, we think about, oh, we're just going to get used to it.
Well, if you're taking care of those folks, that means that in some cases in that extreme, especially, we're not able to do surgeries because our healthcare teams are under quarantine, or usually that was the case.
And in the early COVID era, when we had shut everything down because we just didn't know, we went from, you know, an average of, I think, in the United States, 300.
These numbers may not be right, but the order of magnitude is right.
So we went from like 300 living donor kidney transplants a month in the United States and we went down to 30 during a month.
That's got to have some additional measurable death toll.
Right.
And so the WHO report that should come out about COVID deaths and COVID-related deaths, which means the people who didn't get their lung cancer treatment, who didn't get their, or people who had someone who had the flu, but they couldn't get in because they're in line with everybody else trying to get an ICU bed because we still have flu season.
So it's all of those pieces.
Someone with chronic heart failure who's in the ED and they're stacked and packed and so you see spikes in cardiac related deaths in the same time period that you see your spike in.
So every month you're going to have some number of cardiac related deaths.
But when you see that number of cardiac related deaths in month X go up, and then you also see that's also the month where you had your giant spike in COVID, those are still going to be two competing things for the same amount of resources.
And I imagine that like a major factor in cancer treatment is the radiation and that kills your immune system.
I would imagine a lot of those got delayed at the very least, right?
And yeah, we were really worried, especially in lung cancer.
I mean, your lung cancer resection, when we cut, when we cut out a chunk of your lung, right?
A lower lobe is about a third of a lung.
So you don't have much lung to go around.
Yeah, the cancer is not going to wait.
And that's you're really worried about going and doing that because if you wait, especially with lung cancer specifically, which is my area of expertise, cancer is not going to wait.
So we do know that if you have stage one cancer, so early detectable curable cancer, it's what we want, right?
You have a good chance, 80% plus survival, five-year survival.
If that doesn't get treated, the median survival for stage one, untreated stage one lung cancer is 16 months.
So half the people who don't get treated will die from it in 16 months.
So it's not something you just sit around.
Now, there are other diseases that you obviously don't want to sit around either and some that you can.
But so that's that's sort of the those are all determinants when you're in that sort of an extreme situation.
But there's no reason to get in that extreme situation between infection control and vaccination, basically.
So I have hundreds of questions, quite literally, but I have one in particular that comes up again and again in conversation with people about COVID.
There's a notion that some people have.
I think it's among people generally who have accepted that COVID is real, but just are anxious to just get it over with.
I think it's almost like the idea that, you know, when one child in the neighborhood gets the measles, everyone invites their child over because they can arrange their life around dealing with the measles right now and they don't have to worry about it some other time.
And once you know that you should get it or you are going to get it, you just plan for it.
And I think the idea is that we should try to just get everyone this infection all at once so that we can all just have it pass through our system and it'll be gone.
But one factor in this is the obvious one that some percentage of us will need hospitalization.
There will be not enough beds to cover that many people and that that's a problem.
But aside from that obvious one.
Is there the idea that what I think, and I've said to other people in other conversations, is that this isn't a fire that's going to burn across the forest and then we'll be only trying to burn ash after that point.
There will be too many variants that will again be able to reinfect no matter what we do.
And you'll essentially get a fire that can change to a new fire that can again burn across the same forest multiple times.
Is that really the case?
Or what does that look like from a professional epidemiological standpoint?
Right.
So the Omicron variant laughs at your alpha and beta titers.
So new variants are going to, and that's, that's also part of that evolution thing, right?
If I do it once and I kick in your immune system and that now becomes a burnt wasteland, genetically, it makes sense for the next variant to be slightly different so that it evades your immune, those old immune system titers.
And if you get enough infections, if you can roll the dice enough, you're going to find one that works.
99.999, you know, it's, you know, one in 100,000, one in a million, right?
Yeah, it's a very small percent chance, but there's 7 billion of us now.
Right.
And you have tens of millions out of India that could then become, you know, one of those is going to mutate into something that's more interesting.
And that marching thing, because it is so efficacious, is going to spread in even other things, which are one of those factors that I talked about, right?
If I can be asymptomatic, if I can be a little more virulent, if I can require a little bit less energy, if I can last a little bit longer, if I can evade some aspects of the immune system and not necessarily be more deadly, but all those pieces, then I'm going to be more effective as a genetic variant.
And you got to remember, too, one of the reasons why we keep thinking, oh, well, Omicron is not as bad, especially new variants are not as bad.
Well, you're right.
But is it because of the genetics or because we're better at dealing with and treating COVID?
This is a real question in like even the cancer space.
Is the issue we're better at diagnosis or is it because of screening, for example?
Is it the reason why we see the outcomes improve longer life, et cetera?
Is it because we have better drugs?
Well, it's usually a bit of both.
But in many cases, what we're seeing is this variant is not as bad.
I believe the data is still under review, but I believe because we are better at treating it, we're seeing those mortality rates for COVID go down and down and down.
And that's sort of the classic curve.
That's a classic learning curve, basically.
Yeah, we know more about how to treat it in all the various circumstances.
Right.
So the long and short of it is the assumption is, is that you do it once and then you're good.
So in this environment, that is a false assumption.
That's a false dichotomy.
That's a false belief.
The other thing is, is that the squaly from it are not that bad.
So using your measles example, measles is highly virulent.
If you have one person in a measles, we actually did this experiment was actually done tracking a measles superinfection, which arose from someone who came from Israel into New York.
You have one measles variant and within 45 minutes, every single person on the plane is going to get exposed because measles is the most virulent infection that we know of.
One person gets it, it spreads.
It's crazy.
If you have no immunity to it, it's also rather deadly as such diseases go.
So it's not like chickenpox where it's like, eh, it's bad, but you know, get it over with.
We have a fair number of deaths arising from it.
And those tend to be deaths and kids, which are the ones that we really focus on and worry about.
Chickenpox is probably a better example of that than the measles.
Yeah.
Right.
Yeah.
But actually measles in some ways, although it's not as deadly or as virulent as Omicron, as COVID, it's still quite contagious.
It's a similarly contagious airborne saerosol.
So it has a lot of similarities to it.
And like measles, we have a really good vaccine.
The measles vaccine is pretty amazing.
You keep titers 20, 30 years later.
So we imagine that all vaccines are like measles or like tetanus or so on.
It prevents infection.
Even the measles vaccine, yes, it prevents infection because it's so good.
And it also prevents the more nasty aspects of measles because measles used to kill thousands of kids a year.
They go in the bad old days.
So there's that.
The other thing, the other big, big, big thing, which is really, really important, long COVID is serious.
Now, admittedly, we see in surgery, we see some of the worst cases because we see the worst of the worst.
And also because of the, I work at an academic medical center.
So long COVID is, you know, we see otherwise healthy young adults, 25-year-old male, otherwise healthy, an athlete, gets COVID, gets hospitalized.
It ravages his lungs.
His lungs no longer function.
And now he's on, now he's waiting for a lung transplant.
So when we talk about death or hospitalization, there's a lot of other quote unquote lesser, in other words, less than death, but you're trading one chronic disease for another.
Either one of those is going to kill you eventually.
So he's, you know, being able to see, being on a, on the, on the lung transplant list at age 25, hoping to see age 40 is actually a pretty long shot.
Right.
So we always knew that this wasn't going to end on a happy note.
So don't do it.
I think we're going to call the podcast there.
And any other questions, we'll have to wait for another time because I only have so much time each week to do this.
But it was a really great pleasure having you.
And I hope to have you on again, whether in this capacity or some other.