Signs and Symptoms of Long-Haul COVID

Andrew: Yeah, let’s hope. Let’s first delve into the signs and symptoms of long-haul COVID. They differ slightly from the acute infection. But they are…you know, we’re seeing more and more of them. And they’re convoluted. Can you explain more about this, please?

Dr Brady: Yeah, you’re right. They do differ from acute COVID. And the predominant persistent symptoms in what we would call long-haul COVID or long-haul syndrome if you will, or post-viral or post-acute viral syndrome related to SARS-CoV-2, in descending order, there’s too many to list them all obviously, but fatigue has been shown to be the most prevalent followed by muscle and body aches, shortness of breath and difficulty breathing or air hunger, if you will, brain fog, difficulty concentrating, exertional intolerance like inability to exercise or be active, headache, difficulty sleeping, anxiety is a big one, memory and other cognitive issues, dizziness, tachycardia, joint pain, some GI stuff, diarrhea, sore throats, night sweats, on and on. There’s quite a lot of them. But those are probably the biggest ones.

Andrew: Okay, so when we have a post-viral syndrome of many natures, even just a flu when I say just a flu, even a flu, fatigue is one of the just common ones. Is there a difference in the type of fatigue that these people are experiencing? You mentioned air hunger. So is it a type of respiratory fatigue or more of a mitochondrial fatigue? That sounds really wishy-washy.

Dr Brady: Yeah, that’s a very good question. I think it’s probably a little bit of both. There is some evidence that there’s metabolic energy deficiency and difficulty in producing ATP. And people have, you know, talking about the NAD trap and many of those things. And I think that’s part of it. I don’t think that’s the entire picture. There is certainly a level of air hunger and dyspnea, and so forth. But I find that the long-haulers have significant fatigue, even if they’re not presently feeling short of breath or having air hunger. So I don’t think it’s one thing, and we’re not really sure. I personally think in talking to colleagues that there’s also a bit of just persistent difficulty in perfusing tissues and oxygenating tissues, probably because of small vessel dysfunction, endothelial dysfunction, and dysfunction of the glycocalyx. So, there’s a lot of stuff going on. Like I said, it’s still a little bit elusive. But it seems a little bit different and more complicated if you will, than a typical post-viral syndrome such as like an Epstein Barr virus, post-viral, or post-influenza fatigue.

The NAD Trap

Andrew: Right. Let’s delve into a little bit of this pathology. You mentioned something like the NAD trap. I have never heard of that before. Can you explain that for us?

Dr Brady: Yeah, many people with long-haul COVID seem to have mitochondrial uncoupling to some degree; they’re just having a hard time making enough ATP through aerobic respiration. And in more efficient energy biochemistry, they’re leaning back on anaerobic pathways and the Cori cycle; they’re having just difficulties in electron transfer. And that is really why some have seemed to do at least somewhat better on NADH precursors, NMN or NR, those types of supplements that replete that. And other mitochondrial nutrients, whether it’s CoQ10, or ribose, or carnitine, B complex vitamins, I mean, right on down the line, they do seem to help, but they don’t move the dial in a massive way in patients just doing them alone. And it doesn’t seem like this…at least in my opinion, this doesn’t seem like the core or root cause of the syndrome; it’s more of an effect, I think than it is a cause. It’s just part of the big ball of wax on the extended symptoms and metabolic perturbations that happen in long-haul COVID.

The Gut Connection

Andrew: Right. Okay. To delve in further as well, you also mentioned the glycocalyx. And you were talking about gut symptoms as one of the more common issues. And this is something I saw earlier on with some people, not a lot, not a great amount of experience by any means. But just some people who had COVID infections, they were complaining of gastrointestinal effects as the major effect for them instead of respiratory effects. Tell us what’s going on at the gut level. And are we talking about absorption and assimilation of nutrients as well?

Dr Brady: Yeah, it’s very interesting, the whole gut connection and the role of the gut in COVID-19, or just SARS-CoV-2 infection. You know, even though the gold standard diagnostic test, from the beginning and still, by and large, is a nasal pharyngeal swab of using quantitative PCR and looking at replication, cycles and things such as that to figure out if someone has a likely viable infection with SARS-CoV-2. And then COVID-19 is also really a clinical diagnosis when it comes down to it. But we have found in the laboratory with GI mapping and then doing actual SARS-CoV-2 stool testing that we find SARS-CoV-2 earlier in the GI tract than you can in the respiratory system in someone who even goes on to have full-blown acute COVID.

And you can find it persistent in the GI tract much longer than the respiratory tract, so long after it clears the respiratory tract. Even looking at lung aspirates and really is directed a sample as you can get in the deep airways and so forth, it will clear the respiratory tract, but it will still be persistent in the gut. And people who don’t go on to get acute COVID-19 symptoms from a respiratory standpoint but are exposed to SARS-CoV-2, we often can find high levels of SARS-CoV-2 DNA in the fecal material. And that is why, at least in the United States, and I think they were doing this in parts of Asia and probably many other countries, in order…particularly back more toward the beginning, in order to get, sort of, you know, kind of a handle on the penetrance of infection with SARS-CoV-2 in various locales, whether it’s at the municipal level, the county level, the state level here in the U.S. was to actually sample the sewer system, basically sample the waste and fecal material to look at the level of DNA for SARS-CoV-2.

So, really quite interesting. And there’s been a lot of correlations between, now that we’re seeing this, specific patterns in the microbiome of the gut and the likelihood of different outcomes in COVID-19 cases. So there’s been different types of connections made, but gut-related dysbiosis that seems to favor someone going down a bad path in COVID-19 include things that…not enough butyrate producers, number one. So if you don’t have enough butyrate producers, you would likely have an excessive Th1 immune response, which is part of COVID-19, and you would see things like interferon-gamma IL-2, IL-12, TNF-alpha, and IL-18 elevated, but also pro-inflammatory bacteria, like Morganella, Pseudomonas can also contribute to less favorable outcomes and more progression toward acute COVID. And then kind of low levels of beneficial bacteria that tend to act to attenuate the immune response like B. fragilis. So, and I’m sure there’s a lot more connections and interactions in the gut with the gut-immune, gut-lung axis, if you will, that we just don’t understand yet.

Andrew: Sure. You mentioned a few bugs there, and there’s obviously these other hero bacteria that there’s been some work done on, Akkermansia muciniphilia, Faecalibacterium prausnitzii. Is there any work being done on their actions? Because I think it was Faecalibacterium and prausnitzii, which was sort of like, we call it a pathobiont where it was mostly good, but sometimes you have to watch it. Maybe there’s other things that keep it in check. Is that…?

Dr Brady: I actually think there’s probably very few organisms that you don’t…you know, it’s about the dose, right, too little of anything is no good, too much of anything is no good. You need it right in the pocket, right. But in the case of Faecalibacterium prausnitzii, you were talking about, I believe, butyrate producers. So I did mention it, just less specifically. And then, in the case of Akkermansia, it’s really responsible for maintaining a good mucous lining along the mucosa of the GI tract, which has a lot to do with host defense and the behaviour of the mucosal immune response.

So I think, yeah, they’re both keystone species. And they’re both very important. But what we’ve been able to do in parallel at the lab at Diagnostic Solutions Lab in the U.S. is we were doing a tremendous number of quantitative PCR NP swabs for large hospital systems in various states. And we were also the only lab in the U.S.; I’m not sure if there was anyone else, anywhere else doing it commercially, we were offering a SARS-CoV-2 stool quantitative PCR. They were using it to screen fecal microbial transplant materials and things such as that. But we were also doing work for different municipalities and the like.

But we were able to get parallel samples in on clinical cases that we were aware of their COVID-19 status. So we had an NP swab on them, we had a quantitative PCR stool on them, and we had an antibody, we had IGg and IgM antibodies on them. So we were able to, very early on, try to find and triangulate on these different situations. And then we were trying to, and we were successful in quite a number of cases, of actually getting a GI map on them and being able to look at these different shifts that we were just talking about in the composition of the microbiota.

So early on, everyone was looking for how do you find a metabolic signature of COVID beyond just a positive NP swab with quantitative PCR? Because there’s issues of viral load and timing of when you take the samples. So we were trying to look at it more broadly. And we’ve been doing the same with long-haul. And I think there’s a big advantage in long-haul to look not just that direct markers such as, you know, what are the various cytokines doing, but what’s going on in the gut? I think if you can do those things in parallel, it probably adds a little bit of value, for sure.

Andrew: You know, it smacks of what we’re finding in Australia. Obviously, people are turning up for nasal pharyngeal swabs by the thousands; particularly there’s Sydney and Melbourne in lockdown, Queensland, we’re coming out. But what I think’s really interesting is when they’re looking at the sewage sampling, which bamboozles me when you’ve got tons and tons of fecal and urine refuse, excrement, plus other things in there, and yet they’re able to pull out viral fragments. Now, viral fragments, is this something that we can test for? And is it there in long-haul COVID? Are we talking about, not shedding, but remnants of viral particles left in the body?

Long COVID Theories

Dr Brady: Yeah, well, that’s the million-dollar question, right? That’s what a lot of people are working on. Is long-haul COVID in some way, shape, or form a manifestation of a low-level ongoing stealth infection? In other words, is there viable, replicating SARS-CoV-2 virus anywhere to be had anywhere in the body? Or is it simply ongoing, persistent immune responses to viral fragments or to spike proteins or whatever kind of peptides might be floating around the system after…post-infection? Or is it something different than both of those? Is it, for instance, a learned, somewhat imprinted locked-in dysregulatory, or over-exaggerated, or imbalanced immune response from having SARS-CoV-2 infection initially, and having some genetic susceptibility or uniqueness to go into an aberrant immune pattern and cytokine and chemokine expression that your body can’t release from, right? It becomes a persistent response. That’s number three.

And then a fourth kind of theory is that much of what you see symptomatically in COVID long-haul may be, in fact, a coming to the fore of opportunistic infections that were stealth, persistent infections that the person may have harboured prior to feeling ill, but their intact immune system was keeping them under wraps or in suppression, and they no longer can do that. It’s like Epstein Barr virus, cytomegalovirus. It I’m not sure in Australia, but certainly in the States, particularly in parts of the United States, a lot of chronic Lyme, chronic Babesia, Bartonella, Ehrlichia…I mean, a lot of the co-infections with Lyme are tick-borne. Tick-vectored pathogens have really flared and reemerged in long-haul patients, kind of in an opportunistic way. So at sometimes, it’s hard to separate out where are the symptoms exactly coming from in every individual with a multitude of potential reasons why that would be the case.

Andrew: Yeah, there’s extreme controversy in Australia. There’s continued denial that a tick-borne, like, let’s say, Lyme-like illness exists in Australia, despite them finding a relative, another species of that organism in an Echidna. But so it does exist, but it doesn’t exist.

Dr Brady: Yeah, well.

Andrew: Which…

Dr Brady: It’s not that much different here. I mean, despite overwhelming clinical evidence and presentation, and in many ways, laboratory evidence and every other way, there’s a general overall public health from a government regulatory standpoint, in my opinion, denial of the real level of problem with Lyme and other tick-borne illnesses past the acute phase, let’s say.

Andrew: Yeah. We could go off onto a whole tangent here about…you get the answer to the question that you ask. If you use the wrong, like an agar plate, you’re not gonna grow the organism that doesn’t grow on agar. So anyway, we’ll leave that one for another podcast.

Dr Brady: But we are concerned that long-haul COVID will be kind of handled in a similar way, similar to what we’ve seen in kind of these disorders that are, at least initially, not very well understood, a little bit fuzzy around the edges diagnostically. But we’ve seen historically what the medical response has been the things like chronic fatigue syndrome and ME, or fibromyalgia, chronic Lyme, and so forth. And there’s a lot of concern on the part of healthcare providers, but also obviously patients that long-haul COVID will be kind of dealt with in more formal conventional orthodox medical systems in the same way, which is denial and dismissal, and bad medicine as far as I’m concerned, for the patient.

Andrew: Yeah. Well, I tell you what, there is so much controversy, there’s so much to talk about just in that strain, would you be amenable to join us back on “Wellness by Designs” at another stage? Because you’ve got a lot of experience dealing with fibromyalgia. And that, again, is sort of along that vein. Would you mind joining us again for another episode concentrating on that and its treatment and that satellite of disorders treatment?

Dr Brady: Sure, I’d love to. I just figured everyone was sick of hearing me talking about fibromyalgia after putting out a book and doing 5 billion interviews. But yeah, I’m always happy to talk about it because it’s a big problem, and it’s mismanaged horribly. And a lot of patients out there are really suffering because it’s not managed right. And it’s not understood well at all by my healthcare colleagues, physicians and other types of providers. And it’s time that they do understand it better because there’s a lot of really good research and data out there, just they’re not aware of it, so.

Andrew: Yeah, right, right. Great. We look forward to welcoming you back on another episode. So getting back to long-haul COVID, is there any assessments…apart from the clinical signs and the history, obviously, is there any particular assessments that you find useful? Biochemical markers, for instance?

Assessments

Dr Brady: Yeah, I mean, there’s no gold standard, rock-solid…and, you know, there’s no binary referendum test, long-haul COVID test, right, that says, “Yes, no, you have it.” But a lot of people, a lot of really smart, good people have been doing a lot of work trying to come up with something that could potentially identify long-haul COVID sufferers, differentiate them from more acute COVID sufferers versus normal controls, and people with maybe other disorders that would alter the immune response.

In our lab at Diagnostic Solutions, we have a test called CytoDX; it’s basically a cytokine panel. So we look at pro-inflammatory versus anti-inflammatory cytokines. So cytokines on the Th1 side, cytokines on the Th2 side, and look at how they become imbalanced in different individuals. And as I said previously, in COVID long-haul patients, they don’t present with a, like, lit up like a Christmas tree cytokine panel like you would see in a cytokine storm, let’s say, in an acute COVID of a patient in the ICU. But they do have certain patterns where basically a lot of their Th1-related cytokines, like I mentioned before, you know, IL-2, and IL-12, and TNF-alpha and IL-18, and things like that tend to be elevated much more so than controls.

And there’s another laboratory in the U.S. also doing very excellent work called IncellDX. And it’s led by Dr Bruce Patterson, who is a very prominent virologist and pathologist from Stanford. And him and his group of researchers have done a lot of really good work looking at cytokine signatures and chemokine signatures in long-haul patients. And they’ve actually been able to study a fairly decent number of subjects who’d been classified as long-haulers versus normal controls and then looked at acute COVID patients as well. And used machine learning and a lot of big data analysis to try to ascertain what is the common signature that separates these different cohorts? And they’ve actually published on that on. I believe they have a patent pending on what’s called a long-haul index. So they’re looking at an index, if you will, of certain cytokines to sort of be a biological signature, not a binary test, you know, positive/negative, but sort of a constellation or a pattern of cytokines that are indicative of long-haul. And once again, they’re zeroing in on things like INF-gamma, IL-2, CCL4; they’re big differentiators in long-haul.

But it’s still in its early stages, but I would recommend people look up the work of Dr Bruce Patterson. He has a lot of interviews online. He has various publications in this realm, and they’ve actually…I have to give them a lot of credit. They’ve gone beyond that; they’ve actually developed a not only a research network but a physician network. And they’re treating a lot of long-haul patients, or they’re supplying information to, sort of, a network of doctors who are…almost like you have the Lyme literate doctors, now you’re getting the long-haul COVID-19 literate doctors, right, that understand this testing. They understand some of the more; I guess you can say forward-leaning tip of the spear type of therapeutic interventions that seem to be helping the long-haul patients.

Andrew: We’ll get into those in a tick. But I just wanna ask, you’ve got CASI coming up, which is the symposium put on to help practitioners learn the cutting edge that you’re talking about in the United States with Designs for Health. Is Bruce Patterson going to be one of the speakers there? I know Dr Elisa Song is speaking there. You’re speaking there.

Dr Brady: Yeah, Dr Patterson is not at CASI this year. I hope to have him at CASI next year, along with another expert in stealth infection and has done some of the best work in the world of anybody in chronic tertiary Lyme and co-infections and now in long-haul, which is Dr Richard Horowitz from New York. So the CASI, kind of, speaking panel and the topic and everything was set previously. And it’s a fascinating, unbelievable panel. I mean, the conference is mainly on healthy aging, and life extension, and health through the life cycle, senolytics and things like that. So we have some amazing people, including Dr Robert Naviaux from UC San Diego, talking about the danger response and really rewriting pathology. I mean, really looking at mitochondrial function in really novel ways, guys like Dale Bredesen on dementia and aging, and Edwin Lee on the latest therapeutic peptides in senolytic therapy. So it’s gonna be really cool, really cool show.

But I was supposed to have Dr Patterson, Bruce Patterson, Dr Horwitz, Tom Fabian, microbiome expert from Diagnostic Solutions, and actually a patient advocate about long-haul COVID in an expert panel that was going to be leading off the Integrative Healthcare Symposium, which is one of the largest symposiums in the integrative healthcare functional medicine space here in the U.S. in New York City in mid-September. And with the latest upticks in the Delta variant and the changes, immunization requirements indoors in New York City, and so forth, the event was actually cancelled. So the event was meant to meet again at its normal time in February in 2022. So I did just find out that they will be preserving my panel. And we will open the February 2022 conference with all of those great people and world experts really in COVID long-haul. And hopefully, they’ll know a lot more by then, and it’ll even be a more interesting panel.

Andrew: Great. Okay, so there’s two events that we’ve got to attend. They’re definitely a do not miss event, both of them. Okay, so back to long-haul. I have to ask about, are we seeing these individuals who are affected by long-haul? Are they that cohort that were just teetering on the edge of chronically stressed and nothing left in the tank, and then they’ve got no resilience leftover and bang? And I guess my question here is because there’s so much fear and anxiety around even “getting COVID” because of the sequelae, the whole treatment paradigm, everything to do with it even is stigma now. Are we seeing these people have just got nothing left in the tank?

Who is at Risk?

Dr Brady: I don’t think so. It’s not been my experience. It’s been a really counterintuitive situation, right, where the people who when they go onto clinical COVID-19, the vast majority of people that went on to really severe significant disease early on, went on respirators and things like that, or ventilators, and ended up dying, unfortunately, or just having really rough times recovering, they tended to be what you said. They had some co-morbidity, they were overweight, they had hypertension, they had diabetes, they had COPD, or they were massively stressed in some other way. COVID-19 long-haul patients, I see an inordinate number of people who prior to it would have been described as the opposite. They were the really healthy, vibrant people, marathon runners, triathletes, significant…

Like, my wife is one of the patients. It’s one of the reasons I have such an interest in this. My wife is a COVID long-haul patient, and she was a professional dancer and like an amazingly fit, strong, metabolically intact person, not overly stressed, you know, hey, living with me is stressful, right? But no, she was not overly stressed and happy and everything. And she was sick early, March of 2020, here in the Northeast of the U.S. And that’s when it was really raging here in kind of the first wave if you will, the wild type, we call it, viral wave.

And, by the way, the majority of people that have really significant, persistent, problematic long-haul syndrome, an inordinate number of them, not only are they these, kind of, fitter people you wouldn’t expect to go down that road, most of them had their acute COVID events early, like March 2020 through, like, July 2020. And then it seems like there’s less people that got infected after that, that went on to get long-haul. Now, that’s not been meticulously teased out statistically and studied. But that’s what we’re seeing as clinicians is there’s something that was a little bit different about that original wild type virus that is not any longer the same after mutations. It’s anyone’s guess, likely. It’s not like you can’t get COVID now and not go on to long-haul. It’s just; it seems to be much less likely than it was then.

Now, what is it about those people who went on to get long-haul then? Because some of them, the majority of them didn’t have, like, massive, really, really, really bad ICU-level, you know, COVID-19. They didn’t have acute lung injury and acute respiratory syndrome, and they weren’t on ventilators. They had various levels of symptoms that the majority of them were not even…they were not hospitalized. In my wife’s case, that was the case. Now, she’s probably not hospitalized because I was doing everything under the sun in my home to keep her out of the hospital, you know, including home oxygen, IV, vitamin C, Myers Cocktail drips, blood ozone, I mean, ivermectin, hey, I mean throw in everything, and I kept her out of the hospital. But she did go on to develop long-haul, and she was an early infectee.

But the archetype, if you will, is they didn’t go, like, to ventilator-level, acute-level disorder. But they were early infections, they went on to long-haul syndrome with a lot of those symptoms that we talked about, and they had pretty persistent symptoms. They tend to be climbing out of it slowly, their trajectory overall. Now, there are differences, individual to individual, but as a cohort, I think most people would agree that they slowly are on an improvement track, but it’s a very slow track.

Treatments

Andrew: Gotcha. So you mentioned a few treatments there. Let’s delve into this. And can we talk about relevant doses? I know there’s gonna be a piece of string topic here with regards to certain nutrients, but can you take us through the nutrients that you found most valuable? And also IV nutrients as well. But also, would you take us through a few of the caveats or through a few of the do not use, what you found, list as well?

Dr Brady: I haven’t found much that was like do not use it, it makes them all worse. There’s been a lot of stuff that people have thrown in that I haven’t seen make it a lot better. But in the sort of natural therapeutics realm, I think glutathione and N-acetylcysteine have probably moved the dial more than I’ve seen anything, and I’ve used them both not only orally, but I’ve used them…I’ve used nebulized glutathione, and particularly in the patients who seem to have lung issues or persistent shortness of breath and things such as that. So those two are very important. We’ve been using a lot of nutrients that go at small vessel integrity and endothelial function and supporting the glycocalyx. So things with a lot of mucopolysaccharides in them like glucosamine sulfate and acetylglucosamine, they’re, you know, things with those kind of constituencies, hyaluronic acid.

But also in combination with polyphenols, resveratrol has had some interesting data out there. But I’ve used also, instead of just an isolated trans-resveratrol, more of a full red grape polyphenol type of compound that I use called Vinia, which has piceid resveratrol, so it’s resveratrol actually from red grapes, not from polygonum or Japanese knotweed, where it’s a glycosyl so it’s way more, way more water-soluble, way more absorbable. And then you get the bouquet effect of the other red grape polyphenols, which is really good for the arteries. But things like quercetin…It’s amazing; all the things that we used for acute COVID and COVID prevention to block viral entry, and viral docking, and replication, and so forth, they all seem to be also appropriate in long-haul COVID. So things like melatonin, things like quercetin, things like vitamin C, and so forth.

Probably the things we’ve added most are things like NMN and NR, nicotinamide riboside, for mitochondrial function. Also, things like Natto-Serrazymes, or nattokinase, lumbrokinase, things that are somewhat anticlotting. And that’s what a lot of people use, baby aspirin as well. And then we do a lot of things to treat the gut per our other conversation. So, you know, I use GI Revive Powder, but things like L-glutamine, again in that GI Revive Powder, there’s N-acetylglucosamine, so it’s an immune block, you know, it blocks a docking of the antigen to the immune cells, so stops viral…it stops immune amplification and kind of runaway gut-mediated immune responses. Probiotics, prebiotics, things like that can all help.

But in the nutrient realm, those are kind of the big ones. We’ve used monolaurin, we’ve used various types of water cluster and other types of silver compounds. We’ve used a lot of things in just our perennial antiviral, particularly anti-influenza, anti-coronavirus bag of tricks that we’ve known for quite a long time. There’s been a lot of literature on it by studying influenza, but also, it’s a lot of…As soon as this started to break with COVID-19, with SARS-CoV-2, everyone immediately went back in mined to all of the SARS-1 data, and they threw a lot of natural compounds at it, and they learned a lot from it. In fact, the first long-haul syndrome related to SARS is not SARS-CoV-2, it’s SARS-1 because there was a lot of SARS long-haulers, and they didn’t call it long-haul then; they just called it SARS post-viral syndrome, if you will. But then, outside the realm of supplements and natural agents in this disorder, unfortunately, we do lean quite a bit on things that would be either in a firm drug class or kind of somewhere in between, like therapeutic peptides.

Andrew: What about antivirals, forgive me, an antiviral drug like the, what is it, remdesivir, things like that? Are they useful in long-haul COVID? Are you utilizing any other medications in long-haul?

Dr Brady: Yeah, remdesivir in long-haul COVID I don’t think has shown any benefit. It’s wildly expensive and would not be reimbursed by insurance and third-party payers here in the U.S. for long-haul applications. It’s been used in acute COVID. The data on it’s pretty weak on its benefits and outcomes. And like I said, it’s super expensive. So, but we have used antivirals. One that’s starting to be used more and more in long-haul COVID is…I don’t know what you would call it in Australia. It’s maraviroc, I think, in the U.S. Sometimes I think the trade names in some countries is Selzestril or Selzestry, Selzentry. They’re basically HIV viral blockers. They were developed for HIV.

Well, I have not used it much personally. It’s just really emerging on the scene in long-haul. So I think it’s yet to be determined. But they are using various drugs in off-label uses that really do seem to be moving the dial, and one of the ones that’s very controversial, and there’s a lot of…Listen, you can go out and find podcasts, and you can look at some of the groups that have been singing this song for a long time. But the very common decades-old, anti-parasitic drug ivermectin, which has gotten a lot of press and controversy in use in long-haul in acute COVID, is used quite effectively in most cases in long-haul COVID.

And then other drugs, I mentioned aspirin before, baby aspirin, 81 milligrams a day or somewhere in that neighbourhood just for a mild anti-clotting, anti-thrombolytic effect, if you will, with ivermectin. And then they’re tending to stack it with some off-label uses of common drugs like pravastatin, a statin, cholesterol-lowering drug. They’re not using it for its HG-CoA reductase cholesterol-lowering mechanism of action. It actually works…it works on, sort of, blocking cytokine and chemokine cascades in the small vessels and with endothelial dysfunction. It works on, like, fractalkine receptors, they call them. So they’re using a relatively low-dose statin, around 10 milligrams or so.

They’re using SSRIs. So classic antidepressant drugs, but not for their serotonin modulating effects, but for other, in many cases, unknown mechanisms of action, but they seem to be changing cytokine patterns and making people clinically improved. So fluvoxamine, or Luvox here in the U.S., is being used. Antihistamines are used. Claritin or loratadine is used, kind of they stack these medications together. Medical cannabis is used a lot, as well as anxiolytics. Even benzos, you know, Lorazepam and things like that mainly to manage the anxiety that a lot of these patients have.

Andrew: Yeah. This is such a complex web that we’ve got to unravel.

Dr Brady: It is.

Andrew: We are running out of time, David, but I would love it if you would join us back. And if we could round off perhaps what we were talking about today, but also then move over to the group of those other chronic fatigue type syndromes, chronic fatigue included, and then maybe talk about stealth infections as well. Could we discuss that in a second podcast? Would you be amenable?

Dr Brady: Yeah, sure. I don’t have all the answers on that stuff. That stuff’s still very fuzzy around the edges. We know what’s involved. We know what we see clinically, but we have not connected all the dots. But I can tell you if people think the chronic fatigue, ME, and the fibromyalgia, and even the chronic Lyme, and co-infections, if they think that those epidemics are big, and they’ve made an impact, they’ve seen nothing yet. I think long-haul COVID is gonna dwarf those like you’ve never seen. Unfortunately, when you run the numbers, when you look at how many people who have clinical COVID-19 go on to experience persistent symptoms six months out, and you run the numbers, it’s millions, and millions, and millions. So I think it’s gonna keep a lot of healthcare providers really busy for a long time, and particularly integrative functional medicine type of docs because they’re gonna be knocking down our doors for years trying to get answers.

Andrew: Yeah. Dr David Brady, I can’t thank you enough for sharing just a little bit of your expertise in this. I mean, you must be stressed because of the weight of this and the responsibility put on you by your patients to try and get them better. So I take my hat off to you for your care of your patients in trying to find a way out of long-haul COVID-19 and for sharing what your experience has shown you today on “Wellness by Designs,” thanks so much for joining us today.

Dr Brady: Thank you, Andrew.

Andrew: So I’m Andrew Whitfield-Cook. Thank you so much for joining us today. And, of course, you can catch up with all of the other podcasts in the show notes for today’s podcast. We’ll also include some of the acronyms that we spoke about today. So watch out for those because in Australia, particularly, we’re not aware, or we don’t get to use a lot of these compounds. So watch out for those on the designsforhealth.com.au website. I’m Andrew Whitfield-Cook, and this is “Wellness by Designs.”