TRANSCRIPT

Eric Topol (00:00):

Hello, this is Eric Topol, and it's really a delight for me to welcome Hannah Davis who was the primary author of our recent review on Long Covid and is a co-founder of the Patient-Led Research Collaborative. And we're going to get into some really important topics about citizen science, Long Covid and related matters. So, Hannah, welcome.

Hannah Davis (00:27):

Thank you so much for having me.

Eric Topol (00:29):

Well, Hannah, before we get into it I thought because you had a very interesting background before you got into the patient led research collaborative organization with graphics and AI and data science. Maybe you could tell us a bit about that.

Hannah Davis (00:45):

Sure. Yeah. Before I got sick, I was working in machine learning with a particular focus on generative models for art and music. so I did some projects like translating data sets of landscapes into emotional landscapes. I did a project called The Laughing Room, where there was a room and you went in and the room would listen to you and laugh if it thought you said something funny, . and then I did a lot of generative music based on sentiment. So I, I did a big project where I was generating music from the sentiment of novels and a lot of kind of like critical projects, looking at biases in data sets, and also curating data sets to create desired outcomes in these generative models.

Eric Topol (01:30):

So, I mean, in a way again, you were ahead of your time because that was before ChatGPT in November last year, and you were ahead of the generative AI curve. And here again, you're way ahead in in the citizen science era as it particularly relates to the pandemic. So, I, I wonder if you could just tell us a bit I think it was back, we go back to March, 2020. Is that when you were hit with Covid?

Hannah Davis (01:59):

Yes.

Eric Topol (02:00):

And when did you realize that it wasn't just an acute phase illness?

Hannah Davis (02:06):

for me, honestly, I was not worried at all. I, my first symptom was that I couldn't parse a text message. I just couldn't read it, thought I was tired. an hour later, took my temperature, realized I had a fever, so that's when I kind of knew I was sick. but I really just truly believed the narrative I was going to get better. I was 32 at the time. I had no pre-existing conditions. I just was, you know, laying around doing music stuff, not concerned at all. And I put a calendar note to donate plasma two weeks out, and I was like, you know, I'm going to hit that mark. I'm going to donate plasma, contribute, it'll be fine. And that day came and went. I was still, you know, pretty sick with a mild case. You know, I didn't have to be hospitalized.

(02:49):

I didn't have severe respiratory symptoms. but my neurological symptoms were substantial and did increase kind of over time. And so I, I was getting concerned. Three weeks went by, still wasn't better. And then I read Fiona Lowenstein’s op-ed in the New York Times. They were also very young. They were 26 at the time, they had been hospitalized, and they had this prolonged recovery, which we now know as Long Covid. and they started the Body Politic Support Group joined that saw thousands of people with the same kind of debilitating brain fog, the same complete executive functioning loss, inability to drive, forgetting your family members' names who were all extremely young, who all had mild cases. and that's kind of when I got concerned because I realized, you know, this was not just happening to me. This was happening to so many people, and no one understood what was happening.

Eric Topol (03:49):

Right. extraordinary. And, and was a precursor, foreshadowing of what was to come. Now, here it is, well over three years later. And you're still affected by all this, right?

Hannah Davis (04:02):

Yes. Pretty severely.

Eric Topol (04:04):

Yeah. And I learned about that when I had the chance to work with you on the review. You were the main driver of this review, and I remember asking you, because I, I didn't know anyone in the world that was tracking Long Covid like you and to be the primary author. And then you sent this outline, and I had never seen an outline in all my years in academic medicine. I never saw an outline like this of the review. I said, oh my God, this is incredible. So I know that during that time when we worked on the review together, along with Lisa McCorkell and Julia Moore Vogel, that, you know, there, there were times when you couldn't work on it right there, there were just absolutely, you would have some good days or bad days. And, and that's the kind of, is that kind of the way is, how it goes in any given unit time?

Hannah Davis (04:55):

I think generally, I, I communicated as like 40% of my function is gone. So, like, I used to be able to have very, very full days, 12 hour days would work, would socialize, would do music, whatever. you know, I, I have solidly four functional hours a day. on a good day, maybe that will be six. On a bad day, that's zero. And when I push myself by accident, I can get into a crash that can be three to seven days easily. Hmm. and then I'm, then I'm just not, you know, able to be present. I don't feel here. I don't feel cognitively able, I can't drive. And then I'm just completely out of the world for a bit of time.

Eric Topol (05:35):

Yeah. Wow. So back in the early days of when you were first got sick and realized that this was not going to just go away, you worked with others to form this Patient -Led Research Collaborative organization, and here you are, you didn't have a medical background. You certainly had a data science and computing backgrounds. But what were your thoughts? I mean, citizen science has taken on more of a life in recent years, certainly in the last decade. And here there's a group of you that are kind of been leading the charge. we'll get to, you know, working with RECOVER and NIH in just a moment. But what were your thoughts as to whether this could have an impact at working with these, the other co-founders?

Hannah Davis (06:27):

I think at first we really didn't realize how much of an impact we were going to have. The reason we started collecting data in the first place really was to get answers for ourselves as patients. You know, we saw all these kind of anecdotes happening in the support group. We wanted to get a sense of which were happening the most at what frequency, et cetera. and it really wasn't until after that when like the CDC and WHO started reaching out, asking for that data, which was gray literature at the time that we kind of realized we needed to formalize this and, and put out an official paper which was what ended up being the second paper. But the group that we formed really is magical, I think like, because the primary motivator to join the group was being sick and wanting to understand what was happening. And because everyone in the group only has the kind of shared experience of, of living with Long Covid, we ended up with a very, very diverse group. Many, many different and I think that really contributed to our success in both creating this data, but also communicating and, and doing actionable policy and advocacy work with it.

Eric Topol (07:42):

Did you know the folks before? Or did you all come together because of digital synapses?

Hannah Davis (07:47):

Digital synapses? I love that. Absolutely. No, we didn't know each other at all. they're now all, you know, they're my best friends by far. you know, we've been through this, this huge thing together. but no, we didn't meet in person until just last September, actually. And many of them we still haven't even met in person. which makes it even more magical to me.

Eric Topol (08:13):

Well, that's actually pretty extraordinary. So together you've built a formidable force to stand up for the millions and millions of people. As you wrote in the review, 65 million people around the world who are suffering in one way or another from Long Covid. So just to comment about the review --you know, I've been working in writing papers for too long, 35 years. I've never, in my entire career, over 1300 peer reviewed papers on varied topics, ever had one that's already had 900,000 downloads, is the fourth most cited paper and Altmetric since published the same timeframe in January of all 500,000 peer-reviewed papers. Did you ever think that the, the work that, that you did and our, you know, along with Lisa and doing, and I would ever have this type of level of interest?

Hannah Davis (09:16):

No, and honestly, it's so encouraging. Our, our second paper to me did very well. and, you know, was, was widely viewed and widely cited, and this one just surpassed that by miles. And I think that it's encouraging because it communicates that, that people are interested, right? People, even if they don't understand what long covid is, there is a huge desire to know. And I think that putting this out in this form, focusing on the biomedical side of things really gives people a, a tool to start to understand it. And from the patient side of things, more than any other paper I've heard we, we get so many comments that are like, oh, I brought this to my doctor and, you know, the course of my care change. Like he believed me and he started X treatment. and that, that's the kind of stuff that just makes us so, so meaningful. and I'm so, so grateful that, that we were able to do this.

Eric Topol (10:16):

Yeah. And as you aptly put it, you know, a work of love, and it was not easy because the reviewers were not not all of them were supportive about the real impact, the profound impact of long covid. So when you now every day you're keeping track of what's going on in this field, and there's something every single day. one of the things, of course is that we haven't really seen a validated treatment all this time, and you've put together a list of candidates, of course, it was in the review, and it constantly gets revised. What are some of the things that you think are alluring from preliminary data or mechanisms that might be the greatest unmet need right now of, of getting some relief, some remedy for this? What, what, what's your sense about that?

Hannah Davis (11:13):

I think the one I'm most excited about right now are JAK/STAT inhibitors. And this is because one of the leading researchers in viral onset illness Ron Davis and that group believe that basically they're, they have a shunt hypothesis, and that means they, they basically think there's a switch that happens in the body after you've, you've had a viral illness like this, and that that switch can actually be unswitched. And that, to me, as a patient, that's very exciting because, you know, that that's what I imagine a cure kind of looks like. and they did some computational modeling and, and identified JAK/STAT inhibitors as one of the promising candidates. so that's from like the, like hypothetical side that needs to be tested. And then from the patient community, from some things we're seeing I think really easily accessed ones include chromolyn sodium.

(12:14):

So these are prescription antihistamines. they're both systemic. So Coen has been seeming to work for patients with brain fog and sleep disorders. And chromolyn sodium particularly works in, in patients with gastrointestinal mast cell issues. People are going on to kind of address the micro clots. I, for me personally, has been one of the biggest changers game changers for my brain fog and kind of cognitive impairment type things. but there's so many others. I mean, I think we, we really wanna see trials of anticoagulants. I'm personally really excited to start on ivabradine which is next up in my queue. And, and seems to have been a, a game changer for a lot of patients too. I V I G has worked for patients who are, have been able to get it, I think for both I V I G and ivabradine. Those are medications that are challenging to get covered by insurance. And so we're seeing a lot of those difficulties in, in access with a couple of these meds. But yeah, just part of, part of the battle, I guess,

Eric Topol (13:32):

You know, one of the leading of many mechanisms that in this mosaic of long covid is the persistence of virus or virus components. And there have been at least some attempts to get some Paxlovid trials going. Do you see any hope for just dealing, trying to inactivate the virus as a way forward?

Hannah Davis (13:54):

Absolutely. Definitely believe in the viral persistence theory. I think not only Paxlovid, but other a covid antivirals. I know that Steve deas and Michael Paluso at U C S F are starting a couple long covid trials with other covid antivirals that yeah, for sure. I think they all obviously need to be trialed A S A P. And then I also think on the viral persistence lens, ev like almost everyone I know has viral reactivation of some sort like EBV, CMV, VZV, you know, we obviously see a lot of chickenpox or shingles reactivations and antivirals targeting those as well I think are really important.

Eric Topol (14:41):

Yeah. Well, and I also, just the way you're coming out with a lot of this, you know terminology and, you know science stuff like I V I G for intravenous immunoglobulin and for those who are not, you know, just remember, this is a non-life science expert who now has become one. And that goes back again to the review, which was this hybrid of people who had long covid with me who didn't to try to come up with the right kind of balance as to, you know, what synthesizing what, what we know. And I think this is something the medical profession has never truly understood, is getting people who are actually affected and, and becoming, you know, the real experts. I mean, I, I look to you as one of the world's leading authorities, and I learn from you all the time.

(15:35):

So that goes to RECOVER. So there was a long delay in the US to recognize the importance of long covid. Even the UK was talking to patients well before they ever had a meeting here in the us, but eventually, somehow or other they allocated a billion dollars towards long covid research at the NIH. And originally, you know, fortunately Francis Collins, when he was director, saw the importance, and he, I learned bequeathed that 2 of the NIH institutes, one of the directors, Gary Gibbons visited me recently because of a negative comment I made about RECOVER. But before I go over my comment, you've been as he said, you, and Lisa McCorkell ,among others from the Patient-led Collaborative have had a seat at the table. That's a quote from Gary. Can you tell us your impression about RECOVER you know, in terms of at least they are including Patient-Led research folks with long covid as to are they taking your input seriously? And what about the billion dollars ?

Hannah Davis (16:46):

Oh, boy. tricky question. I don't even know where to start. Well, I mean, so I think recover really messed up by not putting experts in the field in charge, right? Like we are, we have from the beginning have needed to do medical provider education at the same time that all these studies started getting underway. And that was just a massive amount of work to try to include the right test to convince medical professionals why they weren't necessary. all that could have been avoided by putting the right people in charge. And unfortunately, that didn't happen. unfortunately recovers our, our best hope still or at least the, the best funded hope. so I really want to see it succeed. I think that they, they have a long way to go in terms of, of really understanding why patient representation matters and, and patient engagement matters.

(17:51):

I, you know, it's been a couple years. It's, it's still very hard to do engagement with them. it's kind of a gamble when you get placed on a, a committee if they are going to respect you or not. And, and that's kind of hard as people Yeah. Who are experts now, you know, I've been in the field of Long Covid research more than anyone really I'm working with there. I, I really hope that they improve the research process, improve the publication process. the, a lot of the engagement right now is, is just tokenization. you know, they, they have patient reps that are kind of like just a couple of the patient reps are kind of yes men you know, they, they get put on higher kind of positions and things like that. but they're, I think there's 57 patient reps in total spread across committees. we don't have a good organizing structure. We don't know who each other are. We don't really talk to each other. there, there's room for a lot of improvement, I would say, well,

Eric Topol (18:59):

The way I would put it is, you know, you kind of remember it like when you have gatherings where there's an adult table, and then there's the kiddie's table. Absolutely. Folks are at the kiddy table. I mean, yeah. And it's really unfortunate. So they had their first kind of major publication last week, and it's led to all sorts of confusion. you wrote about it, what did we, what did we glean from that, from that paper that was reported as a 10% of people with covid go on to Long Covid, and there were clearly a risk with reinfections. Can you kind of review that and also what have we seen with respect to the different strains as we go on from, from the Wuhan ancestral all the way through to the various lineages of omicron. Has that led to differences in what we've seen with Long Covid?

Hannah Davis (19:56):

Yeah, that's a great question and one that I think a lot of people ask just because it, you know, speaks to the impact of long covid on our future. I think not just this paper, but many other papers at this point, also, the, the ONS data have shown that that Long Covid after omicron is, is very common. I think the last ONS data that came out showed of everyone living with Long Covid in the UK. After Omicron, which was the highest group of all of them. we certainly saw that in the support groups also, just, just so many people. but people are still getting it. I think it's because it, most cases of Long Covid happen after a mild infection, 75 to 90%. And when you get covid, now, it is a mild infection, but whatever the pathophysiology is, it doesn't require severe infection.

(20:50):

And you know, where I think we hopefully have seen decreases in like the, the pulmonary and the cardiovascular like organ damage types we're not seeing real improvements at all in kind of the long term and the neurological and the ones that end up lasting, you know, for years. And that's really disappointing. in terms of the paper, you know, I think there were two parts of the paper. There were those, those items you mentioned, which I think are really meaningful, right? The, the fact that re infections have a higher rate of long covid is like ha needs to have a substantial impact on how we treat Covid going forward. that one in 10 people get it after Omicron is something we've been, you know, shouting for, for over a year now. and I think this is the first time that will be taken seriously.

(21:42):

but at the same time, the way RECOVER communicated about this paper and the way that you talked to the press about this paper shows how little they understand the post-viral history right, of, of like thinking about a definition. Why wouldn't they know that would upset patients? You know, that and the fact that they, in my opinion you know, let patients take the brunt of that anger and upset you know, where they should have been at the forefront, they should have been engaging with the patient community on Twitter is really upsetting as well. Yeah.

Eric Topol (22:20):

Yeah. And you know, I, when I did sit down with Gary Gibbons recently, and he was in a way wanting to listen about how could recover fulfill its goals. And I said, well, firstly, you got to communicate and you got to take the people very seriously not just as I say, put 'em at the Kiddie table, but, you know, and then really importantly is why isn't there a clinical trial testing any treatment? Still today, not even a single trial has been mounted. There's been some that have been, you know, kind of in the design phase, but still not for the billion dollars. All that's been done is, is basically following people with symptoms as already had been done for years previously. So it's, it's just so vexing to see this waste and basically confusion that's been the main product of RECOVER to date and exemplified by this paper, which is apparently going to go through some correction phases and stuff. I mean, I don't know, but whether that's going to the two institutes that it's, it's N H L B I, the National heart, lung and Blood, and the Neurologic Institute, NINDS, that are the two now in charge of making sure that RECOVER recovers from where it's, it's at right now. And yeah, so lack of treatments, and then the first intervention study that was launched incredibly was exercise. Can you comment about that?

Hannah Davis (23:56):

It's unreal. You know, it's, it, it just speaks to the lack of understanding the existing research that's in this space. Exercise is not a treatment for people with hem. It has made people bedbound for life. The risks is are not, the risks are substantial. that there was no discussion about it, that there was no understanding about it. That, you know, even patients who don't have pem who wouldn't necessarily be harmed by this trial deserve better, right? They still deserve a trial on anticoagulants or literally anything else than exercise. And there's, it just, it, it's extremely frustrating to see it, it would have been so much better if it was led by people who already had the space, who didn't have to be educated in post exertional malaise and the, the underlying underpinnings of it. and just had a sense of, of how to continue forward and, you know, patients deserve better.

(24:55):

And I think we're, we're really struggling because yeah, there's, there's going to be five trials as I understand it, and that's not enough. And none of them should be behavioral or lifestyle interventions at all. you know, I think it also communicates just the, the not understanding how severe this is. And I get that it's hard. I get that when you see patients on the screen, you think that they're fine and that's just how they must look all the time. But recover doesn't understand that for every hour they're asking patients to engage in something that's an hour, they're in bed, you know, that, that they're, they take so much time away from patients without really understanding like the, the minimum they should be able to do is, is understand the scope and the severity of the condition, and that we need to be trialing substantially more serious me treatments than, than exercise. right,

Eric Topol (25:54):

Right, right. And also the recognition, of course, as you know very well about the subtypes of long covid. So, you know, for example, the postural orthostatic tachycardia syndrome pots and how, you know, there's a device, so you don't have to always think about drugs where you put it in the back of your ear and it's neuromodulator to turn down your vagus nerve and not have the dizziness and rapid heart rate when you stand and all the other symptoms. And, you know, it costs like a dollar to make this thing. And why don't you do a trial with that? I mean, that was one of the things, it doesn't have to always be drugs, and it doesn't have to, it certainly shouldn't be exercise. But you know, maybe at some point this will get on on track. Although I'm worried that so much of the billion dollars has already been spent and no less the loss of time here, I people are suffering. Now, that gets me to this lack of respect lack of every single day we are confronted with people who don't even believe there's such a thing as long covid after all this time, after all these people who've had their lives profoundly disrupted.

(27:04):

What, what can you say about this?

Hannah Davis (27:07):

It's just a staggering, staggering lack of empathy. And I think it's also fear and a defense mechanism, right? People want to believe that they have more control over their lives than they do, and they want to believe that, that it's not possible for them personally to get a virus and then never recover and have their life changed so substantially. I really genuinely believe the people who don't believe long covid is real at this point you know, have their own things going on. And just, yeah,

Eric Topol (27:38):

It's kinda like how Covid was a hoax, and now this is, I mean, the, you, you just, of

Hannah Davis (27:44):

Course, but it's true, like it's happened with, it happened with me, CF s it happened with HIV AIDS. Mm-hmm. someone just showed me a brochure of, of a 10 week lifestyle exercise intervention for aids, you know, saying that you could positively think your way out of it. All that is, is, is defense mechanism, just, yeah. You know, it's repeating the same history over and over.

Eric Topol (28:07):

Well, I think you nailed it. And of course, you know, it was perhaps easier with Myalgic encephalomyelitis when it weren't as many people affected as the tens of millions here, but to be in denial. the other thing is the young people perfectly healthy that are those who are the most commonly affected. a lot of the people who I know who have been hit are like you, you know, very young and, and you know like Julia in my group who, you know, was a big runner and, you know, can't even go blocks at times without being breathless. And this is the typical, I mean, I saw in clinic just yesterday, an older fellow who had been in the hospital for a few weeks and has terrible long covid. And yes, the severity of covid can correlate with the sequela, but because of just numbers, most people are more your phenotype. Right, Hannah.

Hannah Davis (29:08):

Right, exactly. It's a weird like math thing for people to wrap their head around. Like, yes, if you're hospitalized, the chance of getting long covid is much, much higher than if you were not hospitalized. But because the vast number of cases were not hospitalized, the vast number of long cases, long covid cases were not hospitalized. but I think like all of these things are interesting clues into the pathophysiology. You know, we also see people who were hospitalized who recover faster than some of these, the neurocognitive mild, my mild encephalomyelitis subtypes for sure. I think all of that is, is really interesting and can point to clues about kind of what is, what is happening at the core.

Eric Topol (29:54):

Yeah. And that I wanted to get into before I wrap up some of the things that are new or added since our review in published in January. so I just recently reviewed the brain in long covid with these two German studies, one of which showed the spike protein was lighting up in the reservoir, the kind of initial reservoir, the brain, the skull, and the meninges. the, the, basically the layers covering the brain, the, particularly the skull bone marrow. And that's where all these immune cells are in high density that are patrolling the brain. And so it really implicated spike protein per se, in people who've had covid. and then the other German study, which was so striking in mild covid, the majority of people where they had it 10 months later, all this signature by m r i, quantitative, m r i of major inflammation with free water and this so-called mean diffusivity, which is basically the leaking and you know, the inflammation of the brain.

(31:01):

And so, and that's as long as they follow the people, you know, if they followed 'em three years, they'd probably still see this. And so there's a lot of brain inflammation that is linked to the symptoms as you've described. You know, the brain fog, the memory executive function. But we have no remedy. We have no way, how can we stop the process? How can we turn it around like, as you mentioned, like a jak stat inhibitor in other ways that we desperately need to get into testing. so that was one thing I, I wonder, I mean, I think people who have had the symptoms of cognitive effects know there's something going wrong in their brain, but here is, you know, kind of living proof that what there's sensing is now you can see it. thoughts about that?

Hannah Davis (31:52):

I mean, I think the research is just staggering. It's so, so validating as someone, you know, who was living this and living the severity of it, you know, without research for years, it's, it's wonderful to finally see so many things come out. but it's overwhelming research. And I, I don't understand kind of the lack of urgency. Those are two huge, huge studies with huge implications. you know, that the, that the spike would still be in the skull like that in the, in the bone marrow like that. and the neuroinflammation I think, you know, feels very obvious in terms of what, like the symptoms end up presenting. why aren't we trialing things like the, the, this is just destroying people's lives. Even if you don't care about people's lives, like it will destroy the economy. Like people are still getting this, this is not decreasing. these are really, really substantial tangible injuries that are happening.

Eric Topol (32:52):

Yeah, I know. And, and there's not enough respect for preventing this. The only way we know to prevented it for sure is just not to get covid, of course. Right. And then, you know, things like vaccines help to some extent. The magnitude, we don't know for sure, you know, maybe metformin helps but, you know, prevention and everyone's guard, not everyone, but you know, vast majority, you know, really let down at this point when there's not as much circulating virus as there has been. Now, another area where it has really been lit up since our review was autoimmune diseases. So we know there's this common link in some people with long covid. There's lots of auto antibodies and self-destruction that's ongoing. The immune system has gone haywire. But now we've learned, you know, this much higher incidence of rheumatoid arthritis and lupus and across, you know, every one of the autoimmune diseases.

(33:44):

So the impact besides the brain autoimmune diseases and then the one that just blows me away at the beginning of the pandemic, even in the first year there were starting to see more people showing up with type two diabetes and say, ah, well it must be a coincidence. And now there are 12 large studies, every single one goes through of a significant increase in type two diabetes and, and possibly even autoimmune diabetes, which makes sense. So this is the thing I wanted to clarify cuz a lot of people get mixed up about this, Hannah, there's the symptoms of long covid, some of which we reviewed, many of the long lists we haven't. But then there's also the sequela to organ hits like the diabetes and immune system and the brain and you know, also obviously kidney and heart and on and on. Can you help differentiate? Cause a lot of people get mixed up by all this stuff.

Hannah Davis (34:46):

Yeah, I mean I think, you know, we started out with symptoms because that's what we knew, that's what we were talking about. but I do think it's helpful to start, and I, I do think it would be helpful to do a big review on conditions and that does include ME/CFS and Diso but also includes diabetes, includes heart attacks and strokes are includes dementia risks. and yeah, I think the, the difficulty with kind of figuring out what, what percent of long covid are each of these conditions is really biased by the fact that for that, doctors can't recognize me CFS and dysautonomia that it doesn't end up in the EHR data. And so we can't really do these large scale like figuring out the percentage of what is what. but I think like, I, I saw someone describe long covid recently as like a, a large scale neurocognitive impairment emergency, a a large scale cardiovascular event emergency. I think those are extremely accurate. the immune system dysfunction is really severe. I really would like to see the conversation start moving more toward the, the conditions and the pathophysiologies based on what we're finding yeah, more than, more than just the symptoms.

Eric Topol (36:15):

Right. And then, you know, there's this other aspect of the known unknown, so with two other viruses. So for example, back in 1918 with influenza, it, it took 15 years to see or more that this would lead to a significant increased risk of Parkinson's disease. And then with polio, the post-polio syndrome showed up up to 30 years later with profound progressive muscular atrophy and, you know, falls and all sorts of major neurologic hits that were due for from the original polio virus. And so, yeah, some of the things that we're learning here with long covid hopefully will spill over to all these other post-infectious processes. But I think what's emphasizing in our discussion is how much more we, we really do need to learn how we desperately need some treatments, how we desperately need to have the respect for this syndrome that it deserves which still isn't there, it's just, it's unfathomable to me that we still have people dissing it on a daily basis and, and not, you know, a small minority, but actually a pretty strident group that's, that's not so small.

(37:35):

Now, before you wrap up, what have I missed here? Hannah with you, because this is a rarefied opportunity to have a sit down with you about what's going on in long covid and also to emphasize citizen science here because this is, if there's anything I've ever seen in my career to show the importance of citizen science, it's been the long covid story. you as one of the leaders of it. So have I missed something?

Hannah Davis (38:05):

I feel like we actually covered a pretty good bit. I would say maybe just for people listening, emphasizing that long covid is still happening. I think, you know, so many people that we see recently got long covid after getting vaccinated or having a prior infection and just kind of relaxing all their precautions and they're, they're angry. You know, the, the newer group of long Covid folks are angry because they were lied to that they were safe, and that's completely reasonable. you know, that it's still happening in, in one in 10 vaccinated omicron infections is a huge deal. and, and I think yeah, just re-emphasizing that, but overall that, yeah, you know, this is very serious. I think there's my, my MO for Twitter, really, honestly, despite all the, the accusations of fear mon mongering, I really don't put extreme stuff online, but I really do believe that this is this is currently leading to, you know, higher rates of, of heart attacks.

(39:08):

I do believe that we will see a, a wave of early onset dementia that is honestly is happening already you know, happening in my friend group already. and like you said there, there's a lot of unknowns that can be speculated about the fact that we see E P V reactivation in so many people. Are we gonna see a lot of onset multiple sclerosis mm-hmm. you know, lymphomas other E B V sequelae, like the danger's not over the danger's actually, like pretty solidly. there's pretty solidly evidence for some, some pretty serious things to come and you know, I keep saying we gotta get on top of it now, but

Eric Topol (39:55):

Well, I, I always the, unfortunately, some, some people don't realize it, but the eternal optimist that we will get there, it's taking too long, but we got to ratchet up the heat, get projects like RECOVER and elsewhere in the world to go in high gear and, you know, really get to testing the promising candidates. You so have aptly outlined here and in your writings. you know, I think this has been an incredible relationship that I've been able to develop with you and your colleagues and I've learned so much from you and I will continue to be following you. I hope everyone listening that if they don't already follow you and, and others that are trying to keep us up to speed, which you know, just this week again, there was a Swiss study, two year follow up showing that the number of people that were still affected significantly with long covid symptoms at two years was 18%.

(40:58):

That's a lot of folks, and they were unvaccinated, but still, I mean, they, in order to have two year follow up, you're going to see a lot of people who before the advent of vaccines. So this, if you look at the data, the research carefully and it gets better quality as time goes on, because we have control groups, we have matched controls, we have, you know, hopefully the beginning of randomized trials of treatment. we'll hopefully get some light. And part of the reason we're going to get there is because of you and others, getting us fully aware, keeping track of things, getting the research committee to be accountable and not just pass off the same old stuff, which is not really understanding the condition. I mean, how can you start to really improve it if you don't even understand it? And who are you going turn to to understand it? you don't, you don't just look at, you know, MRI brain studies or immune lab studies. You got to talk to the folks who, who know it and know it so well.. All right, well this has been hopefully one of many more conversations we'll have in the future and at some point to celebrate some progress, which is what we so desperately need. Thank you so much, Hannah.

Hannah Davis (42:19):

Thank you so much. Absolute pleasure.

Links

Our Long Covid review with Lisa McCorkell and Julia Moore-Vogel

https://www.nature.com/articles/s41579-022-00846-2

The Brain and Long Covid

https://erictopol.substack.com/p/the-brain-and-long-covid

Heightened Risk of Autoimmune Diseases

https://erictopol.substack.com/p/the-heightened-risk-of-autoimmune

Covid and the Risk of Type 2 Diabetes

https://erictopol.substack.com/p/new-diabetes-post-acute-covid-pasc

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Episode 49: Let’s Talk About Gambling