Episode 74: Nancy Klimas M.D. - Neuroimmunology

Dr Nancy Klimas, Director of the Institute for Neuro-Immune Medicine, Nova Southeastern University, is an immunologist internationally renowned for her work in multi-symptom illnesses.  In this week’s episode she explains her work, from HIV through ME/CFS and Gulf War Syndrome, that has led to her having insight and an amazing team to channel efforts into Long Covid research and treatment. 

In an insightful overview she describes her work in understanding the mechanisms (viral persistence, viral reactivation), impacts of (MCAS, cell dysfunction, T-cell dysregulation) and potential alleviation of the disease.  She has been involved in studies looking at clinical therapeutics such as LDN and has seen remarkable results with the use of MABs which she is hoping to replicate in a larger clinical trial in the coming weeks.

Living with Long Covid? How was your week?

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Transcript

Nancy Klimas - Neuroimmunlogy

SUMMARY KEYWORDS

MECFS, patients, people, virus, drug, LDN, trials, funded, immune system, study, mast cells, reactivation, years, reactivated, illness, brain, viral, money, treatment, week

SPEAKERS

Nancy Klimas, Noreen Jameel, Emily Kate Stephens

Noreen Jameel  00:00:04

Hi, my name is Noreen Jameel

Emily Kate Stephens  00:00:06

and this is Emily Kate Stephens.

Noreen Jameel  00:00:09

Both of us have been diagnosed with Long Covid 

Emily Kate Stephens  00:00:12

And we've created this podcast dedicated to the condition. Welcome to The Long Covid Sessions.  Hello love.

Noreen Jameel  00:00:24

Hello darling.

Emily Kate Stephens  00:00:25

 How was your week?

Noreen Jameel  00:00:26

Let's see. Not bad.. actually, for me, health-wise. This week hasn't been too bad. I'm recovering from whatever illness I had. I'm still not sleeping very well. I had some bloodwork done which shows I'm really low in iron. So hopefully I'll get an iron transfusion on the NHS because it's that bad, which would account for all my head falling out and various other symptoms like restless legs and all those kinds of things that you get palpitations, with the iron, low iron.

Emily Kate Stephens  00:01:00

Even the palpitations and things that's the that's the thing. And it's shocking, really that no one's taking this more seriously in you until now.

Noreen Jameel  00:01:12

As we know, it's really arbitrary whether the low iron is taken seriously or not.  If you're borderline or the low end, your GP will say no, you're fine.

Emily Kate Stephens  00:01:21

But that's also the thing, isn't it? It's done on the haemoglobin, whereas if your haemoglobin is okay but your ions through the floor as Dr. Klein explained - 

Noreen Jameel  00:01:29

 Yeah

Emily Kate Stephens  00:01:30

You've got all the symptoms. That's the crazy thing about you, you had all the symptoms, you've got huge blood loss... but I'm not a doctor Noreen so...

Noreen Jameel  00:01:40

You're my doctor! Yeah, apart from that, you know, I have to say though, those my kids are having really bad post-viral illnesses after getting glandular fever. And it's been quite shocking to see how post-viral -  because we're so we know what to look out for now, don't we? 

Emily Kate Stephens  00:02:01

Yeah. 

Noreen Jameel  00:02:02

So my daughter is now being tested for lupus. Waiting on bloodwork for that.

Emily Kate Stephens  00:02:07

Right.

Noreen Jameel  00:02:08

She's got all the classic signs. And my son who was hospitalised with mono two months ago, has now come out in a complete full body rash that none of the doctors can explain. It looks exactly like measles. But it's been eight weeks since he was hospitalised, eight weeks since he had any kind of medication.

Emily Kate Stephens  00:02:32

It's quite an interesting area, isn't it? Because I wonder what the instances of other post viral illnesses are, post Covid. And whether your children, had we not had the Covid, would have reacted to glandular fever in this way. I don't know. I don't know that we have stats on that because they don't know how you can separate it all out. 

Noreen Jameel  00:03:00

Yeah. And I think we are only aware of it because, you know, we're deep into the science of it, but I would I have put two and two together? My son's rash, you know, his very acute viral illness two months ago, probably not. Would I put EBV in my daughter eight months ago now down to potential lupus diagnosis with a bandaid across her face rash and joint pain and hair loss. Probably not. Anecdotally, doctors are telling me that this is really prevalent in children right now. Post viral, weird diseases. 

Emily Kate Stephens  00:03:37

Yeah, because our immune systems have taken such a hit, haven't they? 

Noreen Jameel  00:03:42

Yeah. 

Emily Kate Stephens  00:03:42

And it's really awful when you think about it being the kids who have been affected that way. Because this is their immune system for the rest of their lives. And we now need to work out how we can reverse this damage. 

Noreen Jameel  00:03:56

Yes. And how was your week my love?

Emily Kate Stephens  00:03:58

Well, so since we last recorded, I have had some great times. I've been skiing, I've done a birthday - not my birthday, my son's birthday - and I've been surfing and then in between each of those I have horrendous crashes. So right now I'm really really not good. I think it's..  I've had kids for three and a half weeks. This is day three of a pretty nasty crash. So I'm really not great. As I always say it's the mental impact of it that is the worst because you know I always tell you that I'm recovered and each time I go and do any of these things and feel properly alive and feel great, I say I'm not going to crash this time because I'm better, I'm recovered, look at the things that I can do. And then I go into a crash.

Noreen Jameel  00:04:55

Just by looking at you I can tell. You're a little bit shaky.

Emily Kate Stephens  00:04:58

Yeah, I'm in pain. Everything hurts. Everything hurts. I'm so shattered. My heart even hurts. I just had to walk the dog and now I'll walk about 300 metres, when I'm in the crashes, walk about 300 metres and I lose all of the blood in three toes on my left foot. They go white. I've taken a photo for you Noreen. 

Noreen Jameel  00:05:21

Fabulous.

Emily Kate Stephens  00:05:23

So, I don't know. I definitely feel better when I take aspirin and so I don't know if there's some kind of coagulation that causes the toe situation. I have also seen a cardiologist since we last spoke and I am actually being sent for a whole load of tests. 

Noreen Jameel  00:05:42

Wow, which ones?

Emily Kate Stephens  00:05:43

I'm having a lung function test, a stress echo, a VQ, lung scan and a PET scan of my entire body from my neck to my knees, which I thanked the cardiologist very much for organising this for me, but I did say that I really really would like if anyone out there can do it for me, I would like to see a neurologist and have some kind of scan of my head given that neurological symptoms have been my most prominent ones. I'm still waiting for that neurology referral from my GP. It's been submitted. I've not heard anything back. It was submitted around four months ago. Four years I've had this and I have not been able to get an appointment with a neurologist on the NHS. 

Noreen Jameel  00:06:32

Wow. Well, I'm slightly jealous I don't think I've had a PET scan or a VQ.

Emily Kate Stephens  00:06:38

Four years in,someone's decided to look at my body.

Noreen Jameel  00:06:42

 That's awesome. What's he looking for in the PET scan - full body inflammation?

Emily Kate Stephens  00:06:47

So I think it's they need to do an MRI of the heart or lungs but because I had such an adverse reaction to my prior MRI, he can't do it without the dye. And so it's just a different way of doing the scan. But because you're in the scanner, you get the whole of your body basically.

Noreen Jameel  00:07:09

Well that's really good. We see the same cardiologist he's sending me for another MRI because I did tell him that my heart is feeling much better than it was two years ago.

Emily Kate Stephens  00:07:19

Which is great news for everyone with heart pain, isn't it? 

Noreen Jameel  00:07:22

Yeah.

Emily Kate Stephens  00:07:23

To know that it can get better.

Noreen Jameel  00:07:25

Yeah, I've taken really very little medication in the last few years for it. So, here we go. Let's see. Maybe this is our on the up. 

Emily Kate Stephens  00:07:36

Yeah, but you know, but I'm on the app every week. I'm great, Noreen. I'm great. Oh, I'm really shit.

Noreen Jameel  00:07:47

Oh dear. I've been kind of slightly shit. Do you want I mean? It's just that a little bit more shit than what we consider just a normal shit? I don't know if you have a shitometer..

Emily Kate Stephens  00:08:00

Yeah, we do need we need a shitometer.

Noreen Jameel  00:08:03

Kind of our everyday shit, just level with all Covid. And then I've had that kind of 15% increase where I'm just not feeling 100%. And a lot of it has to do with my bad monthly cycle, which then puts me in a dip for a week or two and then I recover then it puts me in another dip, and obviously my lack of iron. But I'm hoping that once those things get sorted out, I'll just go back to the regular shit days.

Emily Kate Stephens  00:08:35

If there if anyone knows about this sort of multi systemic illness, it is this week's guest Dr. Nancy Klimas. She directs the Institute for Neuro Immune medicine which is at Nova Southeastern University in Florida.

Noreen Jameel  00:08:49

Surprising that so much good research is going on in Florida considering the state - the Surgeon General's quite a famous anti Vaxxer 

Emily Kate Stephens  00:08:57

Yeah. 

Noreen Jameel  00:08:57

What did you think of her? I mean, we've seen We've now spoken to so many doctors. I'm always interested in your take on a particular specialty, particular expertise and general knowledge.

Emily Kate Stephens  00:09:09

I thought she was great because she's this no nonsense powerhouse of this knowledge base, that has been built from HIV through all of the ME / CFS,  Gulf War Syndrome work that she's done and now putting that into Long Covid.

Nancy Klimas  00:09:32

My field for the longest time has been what happens to people after something like a virus or a toxic event that affects the brain, so neurotoxic injuries or post viral illnesses. And I have been in the field of ME / CFS for ever and - not quite that long, but 1987, that's a long time... And I had the opportunity to develop a research institute that was completely focused on those things in 2011. So I started at Nova Southeastern University this amazing research institute that has clinicians, basic scientists, computational biologists, all working together to try to find targets for therapy, and then translate that into clinical care. So it's a very exciting group of people I work with, I represent an amazing team. I think we have 17 faculty members in our group, it's a big group, maybe 50 or more of us all together doing.. doing research and clinical care in these areas. Since we were already doing ME / CFS all these many years, which is predominantly post viral or post toxic injury, Long Covid happened it sort of felt like one of those destined moments where we were in place doing that thing, and with a fair amount of expertise. And then a population that was just like our ME population desperately seeking knowledgeable care appeared and so we've been trying to segue or include, if you would, Long Covid into our research mission, in our care mission. 

Emily Kate Stephens  00:11:17

Well, I'm there's already so many questions to ask just from that introduction. I know that the department is... is neuro immune medicine. Are you initially coming at it from the point of view of a neurologist or an immunologist? 

Nancy Klimas  00:11:30

I'm a clinical immunologist, we have a lot of different types of expertise in our group, but our focus is in neuro inflammation. Well actually it's more than that because these diseases are far more complicated than that. But the basis of these diseases is immunology, inflammation, energy, oxidative stress and energy and perfusion. So if you think about the brain as a place that needs blood flow, makes energy, needs to clean that mess up again when it's done making free radicals, and if it doesn't, it triggers an inflammatory response. Then that's sort of the space of most of the ME / CFS science, throwing in a little viral reactivation just to keep things confusing. So there's a lot to sort of unpack in these illnesses and Long Covid is just as complicated, just touch more complicated maybe, than ME. So we use these computational biologists to deal with the fact that it's so darn complicated. When you use a group of people that can deal with a mass amount of data, just huge amounts of data, and make it fit together like the parts of a puzzle, basically, using math to figure it all out. I mean, it's pretty kind of cool, isn't it? But they're using essentially math, and then taking all these really complicated systems and figuring out the connections, the interactions time courses, and then providing to us perhaps very innovative ways to try to put it back together again.

Noreen Jameel  00:13:01

It's really interesting that you just said that Long Covid was more complicated than ME / CFS. MECFS seems extremely...

Nancy Klimas  00:13:07

In one major way. We're doing a big research study now that the CDC is funding to compare MECFS and Long Covid The results are not ready yet. But what you have in Long Covid s the instead of the original target - say you had Epstein Barr Virus, which is mononucleosis right and you had post-mono ME - well, the target of that infection was the immune system cells in the immune system. The target of Covid is your vascular wall, the ACE receptor, which just peppers the wall of the endothelial which is your blood vessels. So if you can imagine that the inflammatory site of acute Covid as it morphs into Long Covid is an inflammation of your blood vessels (and other things) but your blood vessels... That makes it a little more complicated. 

Emily Kate Stephens  00:13:59

Is that now agreed upon by the majority of people in the field that that is the path by which Covid impact the full system? 

Nancy Klimas  00:14:09

Well, we know that what did Covid bind to? What's the receptor that the virus binds to?

Emily Kate Stephens  00:14:14

The ACE2.

Nancy Klimas  00:14:14

The ACE2 receptor right? So there you go. Where's the ACE two receptor? Well, that's where the immune system is going to go. You know, excuse me, I have a virus hanging off this receptor target, right? And then the immune system goes after. So the big question, it's not a question in acute Covid whether or not the endothelial is involved. Why do you think you have all those micro clots and all the things that were killing people during the worst of it, but even are incredibly troublesome today? That's got an awful lot to do with the vasculature target for inflammation during the infection. So with Long Covid, you're saying okay, well, that was acute Covid, what's going on when it persists? What's happening there? And that is, of course, the million dollar question and the one that a vast amount of research is going on to try to answer.

Emily Kate Stephens  00:15:01

In terms of the research that you've done, in which direction do you think that we're heading towards the answer of that? Because I know that you have looked extensively at viral reactivation. 

Nancy Klimas  00:15:15

Yeah, and I don't want to discount all the elements and why it's going to be as complicated as ME to try to put that little puzzle back together again. I always say it's sort of like a quilt. You look at it through one window and you flesh it out. And then someone else is looking at it through another window and it's a completely different picture over there. But in fact, when you stand back, you put all the little pieces together, you're making a quilt and there's actually a whole landscape that's starting to emerge from all this different research. So one of the mistakes a lot of people make early in the field, and this is early in the field for Long Covid, is perceiving it is an either or situation or competition. And it's so not that. One of the ways we look at ME / CFS and of course now Long Covid: when you have a lot of interactive systems that communicate and are impacted by an illness, a good word to look at is homeostasis. So we think about what keeps a person healthy, what is well? What is healthy? What is the homeostatic networks, keeping everybody healthy? And I give lectures like this and I have a beautiful illustration. It looks like mountains and valleys. When you're in wellness, you're in this valley of homeostasis. If you have a cold or a flu, you get out of your happy space, your homeostatic niceness, and you start climbing up a mountain. But when you are over your infection, you drop back into the normal well. But if you're in the misfortunate space, of not getting over the infection and dropping into the right well, if you climb the mountain and drop down the other side, now your homeostatic network that's holding you there, it's stable.  It's not moving. And it's unwell. It's a sick setpoint. So one might think of chronic illness in terms of homeostasis, any chronic illness, but this one too, is what keeps a person in this sick space when wellness is really not very far away, but there's a mountain between wellness and chronic illness. So a lot of the math geeks that work with us, are are amazing computational biologists, their whole job is to try to figure out with their modelling systems, how to climb the mountain, make someone need to move out of their stable spot and drop back into the right, correct healthy homeostatic wellness spot. So all the math that our guys are doing when they're doing these computational modelling things they're saying, okay, I can describe what's wrong with you. I can figure out how these networks interact. That alone is amazing. If you're saying I can stand back from the big picture and tell you why the neuro-endocrine system, the immune system, the dysautonomia, the autonomic nervous system, and all those things are in this pattern, and they're not disperate individual observations, they're so connected, right? They're so networked. And I can describe that that alone is a big contribution to science. But if you can take that kind of information and model the illness, and then find targetable points for treatment, then what these folks are doing, at least in our group, and hopefully others, is doing insilico clinical trials. That means basically they're hitting random points in any direction, in any combination, in any time course, many hundreds and hundreds and hundreds of 1000s of clinical trials in a computer, and then coming back to us and saying "we could reset these networks, we can make this go back to normal or look a whole lot more normal if... you did x, y and z."

Emily Kate Stephens  00:18:51

So that's coming up with a theoretical science based on the computational data?

Nancy Klimas  00:18:57

Right! And then we take that and we say "ok, does it make any clinical sense?"  Like for instance they might tell me to use a drugs that the adverse events could be massive "ok, we're not doing that". But then we can say what was the target? Is there another drug that were to hit that target? And then with the way they model, they can actually look in a three dimensional way and say every single drug that hits that spot, whether we knew it did or not, they got that three dimensional structures and they say, well, here's your targetable spot. Okay, now, what's everything that touches that? So they'll give me a list of say 20 things and the first one is always some quarter of a million dollar monoclonal that fits that spot perfectly and has massive toxicity risks, right? Like, yeah, okay, that's great. It's perfect. Now when we get to less perfect what's going down the list? And I might have a nutraceutical on that list that's completely safe - like, okay, cool. Or there might be some pharmaceutical... 'Cause the other thing we want to do with these types of modelling works that we're doing is not waste a lot of time getting you to health. We don't want to take some theoretical thing and go through 25 years of research to prove that it's safe, and can be used, and get the FDA. If I can find a drug that can be repurposed that already exists and we know its safety record, then that's a lot lot faster than taking some "Here's the spot. Let's design a drug for that spot" which is what a pharmaceutical company would do. 

Emily Kate Stephens  00:19:03

Yeah. And this is what's really interesting about what you're saying about your team, because a lot of people that we have spoken to either on the science side of working out what it is or on the treatment side of working out what could help, whereas you're saying that you're trying to bring those two together.

Nancy Klimas  00:20:39

Yeah, we built this institute precisely to bring those two together. And it has tremendous rewards. First, when you have a bunch of computer guys over here, men and women doing their amazing modelling stuff, that blows my mind. And then over here in the laboratory, we got people who do assays all day long, and they're amazing scientists, and they're doing all this cool stuff - they never see a patient. But in our institute, right in the middle between those two people, is a clinic full of patients. And what happens - it has never happened in most of these types of scientists lives - is a patient walking up to them saying "thank you for the work you do that matters". Wow. Do you want to talk about an energised group when they can actually see the people that are trying to help? It's not theoretic is real here, these people and they're waiting, they're sick, they need something. So the energy in our team to try to move this forward, and of course, the clinical team is not just a clinical team, it's a clinical research team that does trials as well as take care of people. So we able to do translational science. So if I could segue to another disease that had a whole lot more money that allowed us a lot more latitude to move this kind of thinking forward, it was an illness called Gulf War Illness. The men and women that went to the Gulf were exposed to a tremendous number of toxins in one in three remain ill 30 plus years later theory was a neurotoxic injury. Acute, neurotoxic injury. They were exposed to organophosphates, oil, all kinds of nasty things and as it turns out, the one in three that remained ill were slow metabolizers. So they're the ones who couldn't detoxify as quick as everybody else and we figured out with lots of years of research, what the risk was, why these particular people got sick, but now they're still sick. 

Emily Kate Stephens  00:22:27

What was the risk? Was there an underlying autoimmune condition or something like that? That was just...

Nancy Klimas  00:22:33

Oh, no, no, maybe maybe some immunologic risk but the big risk was actually that they couldn't get the poisons out of their system as fast as the next person. So they were exposed to a lot of things. They don't detoxify quickly, and they accumulated toxins to the point where they were damaging. And remember, these people got Sarin exposed, they got organophosphates because of pesticides exposed. They were living in a cloud of oil fires that you couldn't see the whole country from a satellite for months, and that's what they were breathing and living in. So they had tremendous toxic exposures. And these same pathways that detoxified the pesticides in the Sarin gas are the same pathways to detoxify oil and gas. So they had this tremendous injury and then their brains were injured and there was neuro-inflammation. So we could discern, not too terribly long after they got back to the to their country, their states in this case, that there was a neuro-inflammatory condition. And now 30 years later, we can also see that they have, very similar to MECFS and Long Covid, that their bioenergetic system has been impacted. They've got inflammation. They've got oxidative stress and so on and so forth. Well in that group, which is very, very similar, but not exactly the same as Long Covid or MECFS, we did the same thing. The modelling work, the insilico trials, the hypothesis testing.. We had an animal model, which we do not have with these other diseases. To test our hypotheses, we cured a bunch of mice with our proposed interventions, then we were funded to move on to human clinical trials. So we were able to do this huge thing all the way through to human and where we are right now is in the Phase One trials in humans of the insilico projected intervention. Now, in MECFS. I have that same modelling all the way through to the thing I want to test then we actually finally got some donation money, thank goodness, some money. It's been just very hard to get funded in MECFS to do the translation piece.

Emily Kate Stephens  00:24:37

Even for a team like yours with that track record. 

Nancy Klimas  00:24:41

Yeah...

Emily Kate Stephens  00:24:42

You you are finding it difficult to get funded.

Nancy Klimas  00:24:44

Yeah. It's getting a little more plausible that we're going to find funding but we're talking about a decade of funding that was I mean, let's just say in ME / CFS there were seven years where the whole funding pot was not more than $3 million. It's not enough to do anything. And now there's a lot more but it's pretty well directed to the centres that were funded and unfortunately, we weren't successful in being one of those centres. So anyway, it doesn't matter. We just keep on applying, applying applying through other doors and we also do donation efforts to try to to fund some of this translation work. So anyway, in ME I actually have enough money to start a translational study and we're just actually now, right now, in IRB after a long pandemic pause, and we're finally getting that game off the ground. 

Emily Kate Stephens  00:25:33

I think you weren't concerned weren't you, obviously there are overlaps and some of the research that is being done will feed into ME, but I think you were concerned that the focus on Long Covid might move funding even further away from ME / CFS. 

Nancy Klimas  00:25:48

Yes, there's a risk of that.

Emily Kate Stephens  00:25:51

Does that mean that you think that is good funding going towards Long Covid? 

Nancy Klimas  00:25:55

Well, yes, because at least in the United States, the original pot of money was this $1 billion, $1.15 billion too Long Covid. I've been doing MECFS for more than 30 years, you couldn't add it all up and it wouldn't even come particularly close to that kind of money. It would be... I don't know...  it might be $200 million over... I mean I'm guessing but it's about right. probably... in 30 years, you know, divide by 30.

Emily Kate Stephens  00:26:19

So do you feel that funding has gone in the right direction? That 1 billion..

Nancy Klimas  00:26:24

Oh, I don't want to stick my foot to deep into that one.  They just put $500 million more to make sure the trials got done, so I will say Congress was paying attention to the advocacy voice to say "all well and good to spend all that much money on the basic science of it all but if it doesn't move to trial what are you doing", so there has just been a serious flush of money into their recovery network to fund the trials that they're proposing. So that's good news. I mean, that's really good news for Long Covid patients. And it's good news for ME patients because what we learned from Long Covid should be very meaningful in ME. Now, what I would love to see is if they would simply add an ME / CFS control group, another sick groups to the trials. If they're going to do a trial that makes sense to do an MECFS - I mean, it would be silly for instance, to use a Covid antibody and an MECFS patient, that's going to do it  - but it would not be silly to think that things through looking at immune viral reactivation, dysautonomia, all those types of targets, all those things could easily be used in ME / CFS patients and it would make tremendous sense, and good scientific sense, to have a comparator group, a sick comparator group when you're doing Long Covid studies. So I'm trying, maybe successfully or not but I'm trying to make the argument that as they're doing these well funded Long Covid studies to consider using an ME / CFS control group as a sick comparitor group.

Noreen Jameel  00:28:04

So when your patients come to you, they obviously come with a great deal of hope, given the centre and the work it's doing. When you say that it's taken 30 years to get to clinical trials for the Gulf War Syndrome. What are the timelines we're looking at for help with Long Covid for example?

Nancy Klimas  00:28:25

That's interesting... it hasn't taken 30 years to get to trials for Gulf War it's just that we're still doing them. Actually there has been just a lot of money for Gulf War and there've been clinical trials going on for 20 years. It's probably 35 trials going on right now for Gulf War because it's a well funded area that needs solid answers. And so that's good news. So I just want to say money matters, okay, that nothing happens without the investment and the ME / CFS patients are waiting 30 years to have clinical trials. I mean, they have things that you can compare to now.

Noreen Jameel  00:29:01

People affected by the Gulf War obviously had tremendous spotlights on them and Long Covid also has a spotlight but you know, when you sit in our position, Emily and I, were reaching four years of having Long Covid now... the idea that we have to wait huge amount of time to get treatment, or to have the work done I know that medicine takes time but..

Nancy Klimas  00:29:24

Yeah, and then again, I am completely committed to as much as one person can make a difference to say let's expedite, but you also have to be committed to doing it right. So I'm going to say that with ME, with so little money, we have all these tiny little trials and they're just giving you hints at what we should do but they're not definitive and they cannot be considered evidence-based enough to move the needle and provide guidelines for treatment that your primary care doctor could embrace and go and do. So people come to people like us because we're right on top of whatever is happening in the field. And we can try to individualise care as best we can with what we know. And maybe we know more because we lived and breathed this stuff. But it's not the same thing as having had Phase three clinical trial that can say 85% of this or that. So we need to move to Phase one to Phase two, Phase three trials as quickly as possible. And the commitment to do that would be ideally to repurpose drugs so that you don't have to wait the eight or nine years to get a drug to the point where it can be used in humans. That's a long delay to try to to avoid. And then as the RECOVERY network is trying to do, build its infrastructure so that it can roll out trials and multiple trials. Think about the AIDS network for a moment that ACTG - AIDS Clinical Trials Groups - from back in the day, before your time, but still in my time. That was amazing government effort. They said "okay, we're gonna build a network across the country. We're gonna have all these clinical trials groups. We can do 10, 20, 30 trials at one time, across all these things and we're going to move the needle as fast as we can". So we discovered it was a virus in 1984. We had our first intervention AZT in 1987, three years that was pretty impressive. By 1994, we had definitive treatments that changed everyone's lives. So it took 10 years from the discovery of the cause of the disease, to having a treatment that has saved many, many, many lives. So that's a fast path. 

Emily Kate Stephens  00:30:32

And do you think that we're moving at a similar speed with this? 

Nancy Klimas  00:31:32

I think that the investment at least in the United States is such that it could be. Okay. That this this network that is now... I know everyone thinks where are you? It's already been three years, but it takes three years to develop the infrastructure to get the team up. Who knew a lot about post viral illness three years ago? The MECFS people and that's about it. They had to build from from scratch. And they put an enormous carrot out there. This huge amount of money had every single university - there were two hundree applications from institutions, huge networks of people - to be able to join that network. That was pretty Wow. Basically, you put money out there, they will come. And they did they came and brought really really big people who are really sharp, are in this and they're trying to get to it. So I'm gonna say they're doing their thing. Meanwhile, those of us that aren't in that loop and that includes me, but we're so focused on the post viral illness. We also have our own path. We can apply independent of the network or into the network to try to move ideas forward. And so we are.

Emily Kate Stephens  00:32:45

Now one of those ideas that ties into that theory of repurposing drugs is you've done a lot of research into LDN - low dose Naltrexone - which is something that is of interest within the Long Covid community but that is a good example of something that you have been using with reasonable efficacy, am I right in thinking?

Nancy Klimas  00:33:09

Absolutely, yeah.

Emily Kate Stephens  00:33:10

In ME / CFS and then you are transposing that to long Covid.

Nancy Klimas  00:33:16

We are. Yeah, we're doing a lot of different things that we've learned from MECFS in our normal care of Long Covid, and then trying to develop trials. And so there is an LDN study that's underway right now. I think that Open Medicine is funding and if I remember rightly, so that's exciting. But LDN is a - low dose Naltrexone - is a very safe dosage of something called Naltrexone, which people will know because it's.. because it's related to the drug that we use when we reverse an opiate overdose. So there's just a lot of experience with that drug. And they've used it a lot at high dose to treat people with addiction. But all of that, that gives us tonnes of safety data. That's very helpful, but it's not what we're using LDN for because at the low dose it hits a completely different space, receptor, cell in the brain than the high dose. So I'm always warning people not to read everything there is about addiction medicine when they learn about LDN because it's not even talking about the right target. But it's instead affecting something called a glial cell, which is the source of a lot of inflammation in the brain, and it quiets glial cell activation, which we know to be over-activated and driving inflammation in the brain in these complex illnesses. So LDN is a nice drug but the problem with it is that it's very personalised, you have to have a little bit of a handle on how to use it because some people - Dr. Younger wrote the papers and fibromyalgia if you want to take out some papers Jarred Younger who's amazing guy, if you could get him on your podcast, you'd enjoy it - but he did all the early work when he was at Stanford on fibromyalgia and we have used the doses that he used because he was able to show in two back to back studies that were relatively small that he could reduce pain in fibromyalgia, significantly. And if you look at the amount of improvement he got, it was a little bit better than the FDA approved drugs that are out there for fibromyalgia. And it's just a much safer, easier drug to use them those drugs. 

Emily Kate Stephens  00:35:19

So that is something that you have been able to administer to the Long Covid patients who come to your clinic?

Nancy Klimas  00:35:25

 Absolutely.

Emily Kate Stephens  00:35:25

With effect?

Nancy Klimas  00:35:26

Yeah, and this is clinical experience, not a study, right? 

Emily Kate Stephens  00:35:29

Yeah.

Nancy Klimas  00:35:30

In experience, we use LDN in our practice all the time, and it's going to help most people - it's not going to help everybody. And like I say it's personalised because the dose that we pick, we start 1.5 milligrammes and move it to 3, and then 4.5, and remember that the opiate dose is like 100, so, this is very low dose.

Emily Kate Stephens  00:35:50

And then a similar vein, when I was reading about it, are you using amitriptyline alongside that LDN or is it that some of the patients received amitriptyline as well? Because that's another drug that is used for depression at high doses, but at low doses it has a different effect. 

Nancy Klimas  00:36:05

It is and it's anticholinergic. So amitriptyline is a messy, old fashioned drug with a tremendous history, it has been around probably 100 years, so we know a lot about it. And at low dose it's pretty good on pain. It's a pretty decent, antihistamine, and it's anticholinergic. So if you think about people with dysautonomia, that they're sort of cholinergically in hyperdrive, and so this counters some of that as well. Flipside, you can't use tricyclics forever because they have some risk, maybe too much to say based on the data that's out there, but I worry enough about using tricyclics for a long time because this might increase the risk for dementias or cognitive defects as you get older. So I use them sometimes just to get everything under control for a while and a while might even be a few years, but I try not to get into a lifelong dosage of something like that. LDN doesn't have as widespread a use. When you,  it's interesting, about these drugs where you worry about risk for this or that as you get older, because the way they're getting at that literature now is because you can dig into the entire electronic medical record of the National Health System, for instance, and you can say, "Well, look, this drug is associated with that." So in France, they did a study and said that the diagnosis of asthma was considered protective for neurodegenerative illness. Well, it turned out it wasn't the disease. It was the drug that we're using to treat the disease, -the puffers - that were hitting a neuroprotective spot in the brain and protecting. So when you say anticholinergic might not be good for you long term it could be the drug, but it could be the disease associated with drug or some other drug you also use when you use this drug

Emily Kate Stephens  00:37:56

And some of the drugs might actually have positive side effects. 

Nancy Klimas  00:38:00

Yeah, and some drugs do like the puffers for asthma apparently, that's that's a good idea. So that's interesting. 

Emily Kate Stephens  00:38:05

Are there other you have used clinically in the treatment of Long Covid that you have repurposed with good effect? Because there was a lot of talk here in the early days of antihistamines and - 

Nancy Klimas  00:38:18

There's so much important space and we do have our own blog, it's called "Hope and Help for Fatigue and Chronic Illness". We just released it in January we're in the top 2% internationally of all of all the podcasts. It's pretty exciting. 

Emily Kate Stephens  00:38:32

Wow. 

Nancy Klimas  00:38:33

We bust it up into pieces. Isn't that something? It's really cool, because we've gotten these real foremost authorities and we say, you know, in 10 to 20 minutes you need to tell us, how do you treat this aspect or that aspect of Long Covid or ME / CFS. So we've had some amazing people. Anyway, that brings me to what do you do? I bust it up into some of its pieces. Okay. So if you want to talk about say, antihistamines: with that we're talking about mast cells. Mast cells are your allergy cells. They're also the lineage cell for those glial cells I was talking about. Similar drugs affect them and mast cell activation is a major player in these illnesses and why you feel chronically lousy, because this over-activated immune system is driving a lot of things including your mast cells to degranulate and release a lot of nasty stuff. So if you can keep them from doing that, if you're not just mopping up the mess they're making, but actually stabilising the cell and keeping it from releasing things. That's a good we have a bunch of podcasts on this but our authority and our team is Theoharis Theoharides, whose got his own website called mastcellmaster.com. He's great. He's really great, clever guy, but he's done some some really amazing podcasts on our little series of podcasts about how to stabilise cells. Talk about it's an onion and you're peeling layers of the onion - I'm an immunologist. You'd think the very first thing I would do when I see a patient is take care of their immune system? It's not true. I can't make your immune system better until I've taken care of some other things first. So one of the things I take care of, the very first thing I take care of is oxidative stress. Oxidative stress is a great big player and it's part of the reason why energy levels are so poor.

Emily Kate Stephens  00:39:05

And the reason for PEM is it? For post exertional malaise?

Nancy Klimas  00:40:20

Yeah, it does drive the PEM because your cells are not making energy efficiently and they're not mopping up the mess that energy makes efficiently and once you drive too many... the mess, the free radicals and you don't mop up, it'll actually pop a cell open and kill it or at least drive it down to not function any further. So having enough of this stuff that mops up the free radicals is actually a critical player in trying to help people feel better and it's not so straightforward. It's not "here, have this magic formula of antioxidants, it's going to work" because you need some stuff. You needed to go across the blood brain barrier. That's a big thing. You know what crosses the blood brain barrier. Not everything that you pop in your mouth as a nutraceutical that crosses the blood brain barrier. So that matters. Then there are things that play more than one. So I talk about oxidative stress and I talk about mast cells. Some of the things that stabilise mast cells are powerful antioxidants. So that's a twofer, right. You don't have to take as many drugs if you get a twofer. So like quercetin, which is a terrific mast cell stabilisers, It's a terrific antioxidant. Luteolin. A terrific mast cell stabiliser, that also crosses the blood brain barrier and is an amazing antioxidant. But one of the other antioxidants that's a big player is NAC and N-acetyl cysteine. I don't know if you can get that in England. 

Emily Kate Stephens  00:41:41

Yeah, I just fought her. 

Nancy Klimas  00:41:42

Oh, you did? Excellent. Thank you, because it was controversial here. But now it's available again over the counter. But for a while they tried to pull it because of something - I think that is now resolved. But there's a neat study by Dr. Shungu, Dikoma Shung, that showed that NAC in ME / CFS patients and in Gulf War illness patients crosses the blood brain barrier and reverses to normal the imaging of oxidative stress in the brain. That's crazy cool. There's somebody that showed me with visual images that you can cross something into the brain and make something normal again. So we have all kinds of data that there's oxidative stress in the brain in MECFS and growing literature in Long Covid using the same kind of technology, but then here's an intervention that he's now funded to do a trial, a dose finding study, but, but I'm excited that he has this this dataset that he's been sharing that shows he got something to cross. So I start with antioxidants in my practice because if I don't do that, why would anything else work? If you can make the cells begin to work then then anything you do to jig them into action can make everything a lot worse. 'Cause cells hunker down because if it did anything more, it would die. Don't try to make it do more, fix why it's hunkered down. The point is the if you could correct as much as you can that would allow a cell to function normally, then you can try to make it work harder. So that's the immune system, so then here comes the immune system... What are we doing for it? Well, it's inflammatory. It's over-activated, and it's basically in hyperdrive. One of the 10 commandments of immunology is the immune system is antigen driven. It doesn't just turn on because it wants to is turned on because something pushed the on button. Okay. And the other thing about the immune system is there are only a few things that push a lot of different on buttons. Usually the immune system is just cleaning up the infection that's on board. Okay, got the flu, the cells that clean up the flu turn on,, clean up the flu and then there's a whole system to turn it back off again, right. But in the immune system, if everything's turned on, which this is a very over activated but in a poly funnel, so everything's turned on kind of way. There are only a few things that do that one is Epstein Barr Virus.

Noreen Jameel  00:44:03

On your quercetin / NAC. Just a quick thing. I mean, if you tell you a list of these things that people can buy just over the counter or - 

Nancy Klimas  00:44:13

Over the counter. Yeah, exactly. Yeah, they're they're usually in allergy combinations or individually. There's a lot of different products, what's called Di-hist like histamine, di - hist. One of my favourites are the ones that Dr. Theoharides tried to help to formulate that is called Neuro-protek. That's a good one. The Lutiolin you can buy straight up from that company as well. They're formulated specifically for mast cell stabilising things but they are powerful antioxidants at the same time, they cross the blood brain barrier. So for me it's all about getting stuff to the brain. Not that your body doesn't matter, your body does, but anything that gets to your brain is also in your body, it's the brain that's the hard target right? 

Emily Kate Stephens  00:44:56

Have you seen mast cells being prevalent in the majority of your patients? A mast cell issue?

Nancy Klimas  00:45:01

 Yeah, it's a very, very common, if not to the point where you can diagnose the actual condition mast cell activation. Which is hard to diagnose because you have to catch a moment in time when they're releasing histamine. It's very, very..

Emily Kate Stephens  00:45:14

And most people here don't understand this at all. 

Nancy Klimas  00:45:16

Yeah, yeah. It's really tricky to diagnose. So when you find it and you can diagnose it, yay. But if the blood tests are negative, and the patient looks like and responds to mast cell treatments, then then treat them, that's my my belief.. is make them better... 

Emily Kate Stephens  00:45:30

Yes, it's so Interesting. So the NHS here, they'll just send you for the, what is it - IgG - testing against specific allergens. Noreen and I have both been so allergic. We've both had that allergic reaction to so many different things. And if I have testing here, they say no, you're fine.  I can't even get an appointment and an allergy clinic. Let alone start dealing with the mast cell activation. 

Nancy Klimas  00:45:56

Yeah, I'm going to clue you onto another website. It's called "MECFSclinicianscoalition.org". That is a group of international physicians with a lot of experience in ME / CFS that got together and tried to write some helpful things for doctors to follow when they're trying to take care of ME patients. And there's a really good description of how to treat mast cell disorders in me. 

Emily Kate Stephens  00:46:25

Fabulous. 

Nancy Klimas  00:46:26

It's a very nice spot to go. Honestly, when you get a group of people together with many, many hundreds of years of experience combined. You say, okay, what's been the thing that helps your patients the most, one of the things we all agreed on was treating mast cell disorders. Mast cells really matter. 

Emily Kate Stephens  00:46:41

That's the same in MECFS as well. 

Nancy Klimas  00:46:43

Yeah, absolutely. Yeah. And the other thing with mast cells is that you don't have to have a positive allergy test to have a mast cell disorder. It's really important. 

Emily Kate Stephens  00:46:52

I understand that. 

Nancy Klimas  00:46:55

I mean, they can release with cold and with heat and with stress and with

Emily Kate Stephens  00:46:59

Yeah, with stress, particularly but yeah, I understand that but the clinical directive here does not understand... 

Nancy Klimas  00:47:07

I get that. I know you guys are dealing with some serious guidelines focused stuff and in the UK. 

Emily Kate Stephens  00:47:14

Yeah.

Noreen Jameel  00:47:15

Shall we talk about your work on CDA T cell dysfunction? 

Nancy Klimas  00:47:20

Oh, that's interesting. Yeah. 

Emily Kate Stephens  00:47:22

Because that's a very recent paper, isn't it? 

Nancy Klimas  00:47:24

Yeah. And that's with Liisa Selin who's a really excellent T cell immunologist, if you would, University of Massachusetts. She's really excellent. And her work is valid, there's other groups that are seeing the same thing. She has at the recent MECFS conference at the NIH in December, there was quite a bit on this. But the bottom line is that chronic immune activation is not good for your immune system. Let's just say that. And what it does is it wears it out to to basically... I mean, the word of T cell exhaustion rings true with people with fatiguing illnesses, but we're talking about not fatigued but exhausted, meaning they've depleted all the stuff they need inside that does the hard work of clearing viruses. So T cells, cytotoxic T cells, and natural killer cells, their job is to run around surveying for old viruses and keeping them from popping out as well as helping clear things that are going on right now. And if they are just constantly on guard constantly doing that job, they use up the preference and granzymes that they have inside that do the hard work and they shift to a sort of an early ageing phenotype that looks like the immune system of say an 80 year old in a 40 year - an older, more depleted immune system that can't jazz up and activate and GO GO GO GO GO.

Emily Kate Stephens  00:48:50

Your study saw this in MECFS and Long Covid patients. Is that right?

Nancy Klimas  00:48:55

That's exactly right. Yeah. That's definitely true. And then the other thing that's happening immunologically, when that happens is viruses reactivate. So if you go back to Long Covid, there's this really important observation that's in now multiple papers that says "what are the risk factors in acute Covid that makes someone more likely to have Long Covid?" And one of them is that if Epstein Barr Virus reactivates during acute Covid, you're more likely to have Long Covid and then a separate study that said, if Epstein Barr Virus is reactivated you're more likely to see that in Long Covid patients then recovered patients. So one of those observations is - at the time of acute infection EBV reactivates. And the other is three months later, six months later, if you have Long Covid, if you could get compared to people who have recovered, you're more likely to have Epstein Barr Virus reactivated. Okay, so now we bring up the ugly head of what is the role of viral reactivation in these diseases? Back to MECFS. We also see these viruses reactivated and while Long Covid hasn't had as much work in viral reactivation as MECFS has had, in MECFS we see the herpes family viruses in general, and EBV is a herpes family virus, but HHV6, CMV, but the big one HHV6 - HHV6 is the most common reactivated virus in ME patients and there hasn't been much focus on that yet, in Long Covid. And then there's another virus, it's got nothing to do with herpes family viruses, it's Coxsackie virus, it's an enterovirus and it reactivates in the gut. So this is the work of John Chia in MECFS, and it's a protected compartment - you can't see it in the blood, you actually have to have a biopsy of the stomach or the intestine to look for that viral reactivation. In John's work, which is extensive with many hundreds of patients, he showed (and I'm guessing but not too far off on the numbers), when he looked at people who had endoscopy for say GERD, for reflux, and he used the GERD as controls and the MECFS patients as the treated group, 80% of ME patients had reactivated enterovirus, and 20% of the GERD controls. So that's a very significant difference. I mean, that's very big. And then he's done a lot of work since then to to prove it.

Emily Kate Stephens  00:49:59

And that's something that's not being picked up on on any blood tests?

Nancy Klimas  00:51:28

Right. So we all focused on just one virus because it's the one they looked for Epstein Barr, but you got... when when the immune system is not behaving well, and it's letting viruses out it's going to let out the viruses that are latent whichever your viruses are. Now the most common of those will always be HHV6 because everybody has... something like 99% of adults has HHV6 virus. Same thing with EBV I think it's 98 or 97% have had acute EBV at some point. So these are very, very common, but enteroviruses are also common, so it complicates the picture of how do we treat, because the antivirals you would use for herpes family viruses are not the same as the ones you use for enteroviruses. And so it just becomes a little more dicey. We really don't have good treatments for enteroviruses. 

Emily Kate Stephens  00:52:17

Do we have good treatments for herpes viruses 

Nancy Klimas  00:52:20

No not really but they're better than... you know.  So we have acyclovir is the generic common one that is easy to get. Valacyclovir, acyclovir but there's another drug called valganciclovir, that one is toxic and hard to use, and we use it in patients that have life threatening viral reactivation when they have chemotherapy and things like that. But there has been a clinical trial with that more potent, more toxic, more efficacious but more scary antiviral in MECFS. Stanford did a study, Dr. Montoya, and he was able to show that the people who responded to that therapy were people that had high antibody titers for EBV that were suggestive of viral reactivation. So it gave us some of the information we feel better about using when we're looking during serology and saying, Are you reactivated or aren't you?

Emily Kate Stephens  00:52:23

So, reactivation aside, in terms of potential virus remaining in the system with Covid, you have tried monoclonal antibodies in, am I right in thinking, in three patients, 

Nancy Klimas  00:53:37

Three patients...

Emily Kate Stephens  00:53:38

Alleviating the Covid virus?

Nancy Klimas  00:53:41

Yeah. So let's do talk about that study. So a colleague of mine Dr. Pepe, who's the real guy that thought to do that, not me, he just came to me because he was so excited about what he saw and then we put our heads together and wrote that next thing... But he did a series of patients with monoclonal antibody to Long Covid.  He used in this case, was Regeneron, was the monoclonal that he used, in patients who had Delta or before. So these are people that were infected, like a year and a half ago or longer. And he was so excited he called me said "oh my gosh, these people are getting better". And he had this first series, now he's got a series of, I think he told me 18 ish patients, that he feels that he has been able to change their lives. So... And they are, if you saw this case series, they were they were better better. They weren't just...

Noreen Jameel  00:54:35

You see that so...

Emily Kate Stephens  00:54:37

Remission in a week. It's 

Nancy Klimas  00:54:39

Yeah, it's remarkable. So if you go to the literature and say, "Okay, why would that happen?". There's also these little small studies that look for Covid persistence. So here's that the brain bang on this one right... which is Covid is supposed to be a virus like a cold virus. It's in the same family, Corona viruses, that are cold viruses They come, they go, they come they go, they don't stick around. They're not latent. And they're not persistent, right. Latent means they go inside the cell cell and they hang out. And persistent means it never cleared it. Like Hepatitis C or B would be a persistent virus, right. And Epstein Barr would be a latent virus, something that went underground and you don't see it agains unless your immune system takes a hit. So, now we have this data to say people have found these Covid antigen, which is what you see when you do PCR, but some other data to say yeah, there's a whole virus is replicating in people that are sick three or six months and now maybe one paper that says a year out. So no one's really looked at you folks that are from 2020 2021 in enough case series to say Is it there or not? But here comes Dr. Pepe who treats some people with longterm Covid with a virus variant that was sensitive to the monoclonal that he used, right.  Remember that the variants keep changing and these monoclonals don't work on on the current variant. So much so that they've been pulled from the market. So these variants, Delta, Alpha, Beta variants, these monoclonals that were developed earlier in the pandemic game worked well on those. So he here he is he's got this case series that we reported and some more since then, that did it... that did the trick. You want to hear my long story that follows this. I'm so sorry to say this, but I will do this study. But it is not easy to do this study because the state of Florida is very excited Dr. Pepe called the Department of Health and Ken Sheppke, who's the first author of that paper, got excited to and we we wrote this pape. And then they found some money to allow me to do a phase one study, an open label phase one study with another 20 people. Now here is the problem. Those drugs were pulled from the market. Regeneron is expired, there's no current active bottle of Regeneron that you could legitimately give to a patient. The Glaxo product expires in about three weeks. But the Lilly product is good until August. So I want to do a Lilly product study, because that's the drug I'm allowed to use without everyone making new stuff.

Emily Kate Stephens  00:57:18

Which is effective on that same early strain?

Nancy Klimas  00:57:21

Yeah it's effective.  And in fact it even catches the early early Omicron. 

Emily Kate Stephens  00:57:25

Do you want Noreen and I to come and take part in your trial?

Nancy Klimas  00:57:28

So you can podcast me? Yeah, I've got a lot of volunteers. 

Emily Kate Stephens  00:57:33

I'm not surprised.

Nancy Klimas  00:57:34

I mean seriously. My process - I have to have an FDA IND which is in process, and then it goes to the IRB which is quick. But this FDA IND is a process. Right now I'm in that process. I am anticipating that I will be infusing patients I had hoped by now because honestly I got the funding in the beginning of February, six weeks ago, and so I thought I could roll through quickly in my optimistic rose coloured glasses kind of way of thinking and turns out, eah, that was funny. But we'll get there. If nothing else I'm in persistent bugger. So I get it through and I'll be treating people when I can't treat them. Earliest I could hope to treat them is...end of April, early May. That's probably where I'm really at in terms of starting this study. But then it's quick study, you know, because you only do two infusions or they're quick.

Emily Kate Stephens  00:58:34

And they're ready in a week. The people are done. 

Nancy Klimas  00:58:37

You can just line them all up outside the door. Get the number 20, go oop, sorry, stop.

Noreen Jameel  00:58:42

Is this is an expensive treatment?

Nancy Klimas  00:58:46

No, not right now. Because essentially, this drug is gonna get thrown away. So I didn't have to pay for the drug in this study. And you know, I don't know what the expense of this drug was during the pandemic because the country underwrote everything, right, everyone got this treatment for free, which is unusual here, very weird. But not weird where you are, but weird where we are. 

Emily Kate Stephens  00:59:06

Yeah. If it's effective, then someone would have to remake the drug.

Nancy Klimas  00:59:12

Oh, yeah. But you know if it's effective, wouldn't they want to, you know, so that's just it. So yeah, we're we're in communication with all of the companies that made monoclonals and they're waiting for me to get a publishable 20. So, I think that when we have that, and the state of Florida is very enthusiastic about this, and they're helping make connections that even if it's not funded by pharma, could perhaps be funded by private foundation, 

Emily Kate Stephens  00:59:39

I think we should all be quite excited about that. I do think that these people are amazingly placed, the way that they've turned their attention to long Covid. And the technology that they're doing this with, I just thought was was really fascinating. What did you think?

Noreen Jameel  01:00:06

I agree, she's this powerhouse of knowledge, but really, I would have loved for her to have been my headmistress at school. Do you know what I mean? She just gives off that and great no nonsense vibe.  Not even my headmistress please be the headmistress of my daughter's school . Right? 

Emily Kate Stephens  01:00:23

Yeah. Because she gives you a sort of faith in her, but not because she's trying to sort of bamboozle you with -

Noreen Jameel  01:00:31

The science - 

Emily Kate Stephens  01:00:32

With the science with her amazing. She's just so - 

Noreen Jameel  01:00:36

- solid, right? 

Emily Kate Stephens  01:00:38

Yeah. I want to go and see her.

Noreen Jameel  01:00:42

We say that about everybody. 

Emily Kate Stephens  01:00:44

Do you think we're just starstruck by these doctors? Because every one that we speak to...  and obviously we source these people, we do our research. We have the scientific papers backing us up, or sometimes it's anecdotal evidence, but we do build a bank of evidence before we approach these people to talk to them. Do you think that we then just get starstruck by the ones that we think actually have some weight in terms of the treatment of located patients? 

Noreen Jameel  01:01:17

Maybe, but I don't think we're easily starstruck and there have been people that we've interviewed that we haven't aired in the past - 

Emily Kate Stephens  01:01:24

That's true.

Noreen Jameel  01:01:26

Because it didn't fit with what we were looking for or didn't fit with the what's the right word here? 

Emily Kate Stephens  01:01:34

Our ethos?

Noreen Jameel  01:01:36

es. And it didn't pass the smell test some of it. Yeah.

Emily Kate Stephens  01:01:39

So people that we don't necessarily agree 100% with we have certainly aired because we have wanted to have that discussion on air. It is often being more to do with the people that we feel either are talking bullshit, or the people that are actually pretty condescending towards chronic illness sufferers.

Noreen Jameel  01:02:03

Yes. So there was a lot of due diligence in our work.

Emily Kate Stephens  01:02:07

Yeah, and this team at Nova Southeastern University have definitely passed our due diligence tests.

Noreen Jameel  01:02:17

We should have one of those get togethers you know that people have, well, we'll just put it out there and people in the area who listened to us can just come and meet us.

Emily Kate Stephens  01:02:26

Should we do that? A lunchtime thing, in central London? Yeah, somewhere in London. And we're just say we're going to be in this cafe. Let's not make it inaccessible. Come and meet us and meet other long Covidy people? 

Noreen Jameel  01:02:43

Yeah, 

Emily Kate Stephens  01:02:43

I think that's a really good idea. You know that I love my mindfulness group. Still, I still go to my mindfulness group and it's online, but just being with other Long Covidy people I find really reassuring sometimes.

Noreen Jameel  01:02:58

Yeah, we should do it. 

Emily Kate Stephens  01:03:00

Let's do it. If people would like to come, let's do it.

Noreen Jameel  01:03:04

Let us know in the comments. If you think this is a good idea, and we can arrange it unfortunately, we're in London, so it has to be London people.

Emily Kate Stephens  01:03:11

Yeah. Sorry to be capital-centric. But that's where we live. It's great idea Noreen.  Let's do it.

Noreen Jameel  01:03:22

Let's do it.

Emily Kate Stephens  01:03:31

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