Long COVID Has Evolved—And So Must Our Approach

Janelle: Greetings to all of our ACAM members, friends and visitors. Today we have the pleasure and honor of hosting Dr. Ahvie Herskowitz, presenting his updated state of the art lecture on long COVID.

This webinar is approximately 50 minutes and will be followed by a question-and-answer session. Attendees are encouraged to submit questions throughout tonight’s presentation using the chat box on the right of your screen.

At the end of the presentation, your questions will be read aloud as Dr. Herskowitz answers them. Registrants can expect to receive a recording of this presentation via email within 5 to 7 business days. Our next planned webinar on behalf of ACAM, Dr. Buddy Green will present Environmental Impact and Detox near Palisades. Please watch your email, ACAM Facebook, LinkedIn or ask for that free registration link.

I’d now like to introduce Dr. Ahvie Herskowitz, the president of the American College for Advancement in Medicine. With more than four decades of experience in anatomic medicine, pathology, cardiology, immunology and regenerative medicine. His expertise and experience are extremely welcomed and sought after.

Dr. Herskowitz is a former clinical professor of medicine at UC San Francisco and Associate Professor of Medicine and Immunology and Molecular Microbiology at the Johns Hopkins Medical Centers. In 2010, he founded, Anatara Medicine, a multidisciplinary integrative center in San Francisco. Dr. Herskowitz, welcome.

Dr. Herskowitz: Thank you, Janelle. That was a mouthful. You know, to all my friends online now, we started this around five years or so ago when the pandemic hit in the spring of 2020, and we decided to present maybe twice-a-year, semi-annual updates in terms of where we were as a nation and where we were with the science. And it was confusing and very interesting at the same time. So now I felt it was wise to get an update now, five years into the beginning of the pandemic, in the spring of 2020. So here we go. Let’s go on the ride together.

Well, I’m going to start off my slides with a photo of the Yellow Emperor. He was the emperor who lived 2,700 years ago in China. He may not have even been real, he maybe mythical. At the same time, he’s noted to be responsible for inventing the wheel, the compass, coins, various different musical instruments. His wife invented the way to make clothing and silk.

And he also was a genius integrative doctor. He invented acupuncture and herbalism, and he was the first, basically, system biology doctor that I’m aware of that has written down his thoughts in a book called The Yellow Emperor’s Book. And flash forward 2,700 years, we have the founder of the Johns Hopkins Hospital, Sir William Osler, who also was a system biology-oriented doctor who understood that every cell was connected to the entire being.

And all the systems were one integrated system — that a young physician starts with 20 drugs for each disease and ends his career with one drug for 20 disorders. And we all know what our favorite therapies are for many, many disorders. So now, in August 2022, around one and a half years into the pandemic, this came out in Nature and people were interested in deciding what to do with long COVID treatments, and there were none available.

And there was pressure put on the NIH to start Centers of Excellence. Having had many NIH grants in my career, I sort of understood what would happen — that they would start five or six Centers of Excellence and begin collating and accumulating data on these patients and then deciding, as a group, on certain therapies.

And they were still waiting a year and a half into it, but they only started the NIH Centers of Excellence a year from then, in the summer of 2023. The first showing of this showed that there was confusion in the first year and a half or so — we all remember there was confusion as to whether vaccinated people did worse, or vaccinated people may have done better. Did they have increased susceptibility to long COVID? Did they have fewer susceptibilities to long COVID? It was very, very confusing. What was the effect of protective antibodies and susceptibility to re-infection? And our therapies were, as I’ll go over a little bit later in the talk, very primitive.

And there was also, a year later in 2023, a colleague of mine from Johns Hopkins, Eric Topol, who’s president of the Scripps Center in San Diego, wrote that the medical system was not ready for understanding what was going on with long COVID, especially with its similarities to Lyme disease, to chronic fatigue syndrome and dysautonomia — that we are not prepared in medical school to understand these disorders, which again affect the entire system rather than individual organs.

And there is a blank space in medical training for these types of disorders. And clinicians who are not familiar with these types of things often diagnose psychiatric disorders in their patients — and much like our Lyme patients, chronic fatigue patients, and POTS patients, they get referred to psychiatry. And this was already known a year after the Centers of Excellence were started and began — that this may happen again. And this was to prevent this type of activity from happening again.

On the other hand, what we know as ACAM members and members of the integrative societies that we all join is that every cell in the body is connected to the whole. And this is the systems biology approach, and this is the approach that we all use.

And this is why the FDA has limited understanding of a drug that may have multiple, multiple effects. For example, if you had a drug that increased mitochondrial function, it would be extremely confusing to the regulatory services because it would impact more than one receptor. So, here’s a cartoon of the ACE2 receptor bound by the spike protein. We’ve all seen this over and over again.

We know that the ACE2 receptor is all over the body, and that’s why COVID-19 affected so many different organ systems early on. And the preexisting conditions were mainly on the metabolic syndrome side. And COVID-19 became something that we used to call in the office “something that makes everything worse.” It’s sort of like mold or Lyme disease — if you have it, it makes everything else that you’re susceptible to, whether by epigenetics or by genetics, a little bit worse.

So, we knew right away in the first year that there were increased circulatory disorders as causes of death in the second column, and in the fourth column, dementing illnesses — a little blip in the respiratory diseases — and then flat, and then malignant neoplasms were flat. And this was sort of surprising on the respiratory disease because we know that many, many patients died of respiratory death. But the fact that it interacted with the cohort that had metabolic syndrome and circulatory diseases, and dementia were on the rise, was not surprising.

I had a good friend of mine develop bilateral COVID pneumonia and spent 11 days on his belly in the ICU because he refused intubation, and he developed interstitial fibrosis after as he healed from the acute pneumonia. I asked him to come and fly to San Francisco to treat him — he could hardly walk up the little incline up the hill to the office, came in with nasal oxygen, and the chest X-ray on the left side was his X-ray then. And of all the therapies that we used — and most of you have treated patients with, in this case subacute long COVID, so to speak, because it was about six weeks after his initial event — you know what we used. We used all the different therapies we would use on Lyme patients or chronic fatigue patients or autoimmune patients — we treated it.

But then the real benefits came forward when we used therapeutic apheresis or plasma exchange, or plasmapheresis on him. And then he cleared up and his pulmonary function normalized completely because the fibrosis had not yet taken full effect.

So, we understood that there are viral effects immediately. There are also subacute effects that may be viral, may not be viral, maybe virally induced. I thought I treated him like I would treat, a very aggressively, a person with post-infectious autoimmunity. That was my hypothesis — to get rid of all the inflammatory signaling molecules in his plasma.

We also knew about myocarditis, which is a field of my interest for almost 40 years now. And here you see, from 9 o’clock to 12 o’clock, the small little, microscopic focus of damage — in this case, necrosis to the muscle cells. But, in fact, everything else in the photomicrograph is normal. And you sort of wonder, you ask yourself, well, why does this person die suddenly? I mean, why does it induce a fatal arrhythmia or eventually congestive heart failure?

And the answer is that this is not the only pathology that you see with myocarditis. And, in fact, when you look at In situ hybridization to look at COVID-19 detection, you see it inside the myocardium on the right side, when you notice the three, four large black hybridization stains — and it’s staining the inside of the blood vessels or the endothelial cells either between the muscle cells or in the vein in the upper left corner. And this is the initial pattern that you see when you have a viral infection — you rarely see viruses inside the heart. You see viruses embedded in the vascular bed. And this was no different in the early stages of direct viral injury. We are no longer in the direct viral injury phase anyway — that’s long gone. But, in fact, this is the way it starts.

And then you develop an immune reaction. I apologize for the lack of the color slides, but the panel on the left is the microcirculation of the heart staining. And then the middle is a longitudinal section. And you could see both the blood vessels in between muscle cells, as well as you almost can see the striations in the mitochondrial pattern and then a sarcomeric pattern in the heart. And then, in cross-section, you could see that the staining is surrounding the muscle cells themselves.

So you get an immunological response to where antibodies form, and you also get a response where the virus — or, in this case, the messenger of the virus, the spike protein — with all of the inductions that it has and all the menacing pro-inflammatory state that it produces, going to certain segments of the heart, causing either sudden death early or later on, cardiomyopathy or heart failure.

So ultimately, we came to the conclusion as a society and as a group of integrative doctors that COVID must be having some effect on the mitochondria because we start to see really ill patients that were not directly getting over their — they’re not recovering just from their acute illness. Because we saw people who had relatively benign disorders when they had the acute infection and then developed a more serious condition that we then ultimately called long COVID.

And so, when you look at COVID-19 and mitochondrial disorders, you realize that there’s a very, very fine correlation between the two, whether it’s vascular, whether it’s metabolic, whether it’s overall aging and all the different parameters that we have to monitor aging. And then, in the right corner at the 4 o’clock position, endothelial dysfunction is a very big player in acute disease and long COVID and in post-infectious autoimmune states.

And this all led us to understanding that what we have to also think about as we treat patients with long COVID, is to deal with and try to understand how to treat mitochondrial injury that could lead in the heart, to heart failure and cardiac arrest — or other organs, of course. And the other one that we have probably the most experience with is the brain and the vascular supply and the vascular bed.

So, we understood this. And when you look at the focus on two, three, four, and five, you realize that this mitochondrial dysfunction associated with the very elderly — or associated, in this case, with a post-viral state, post-autoimmune state, or a post-spike protein state — is largely the same. So, Lyme, mold disorder, a serious mold disorder, serious viral disorder, serious autoimmune disorders — all share in the same system biological collapse that’s occurring in the most severe cases.

So, when we had the first phase of COVID, whether it was Omicron, whether it was Delta, we had really ill patients in both of them. We had the MATH+ protocol that was done by a group of sophisticated intensivists that decided to create their own protocol because the CDC did not come up with a single protocol that was nationally understood and nationally followed.

We always knew that convalescent plasma worked, but the FDA shut that down and it suddenly disappeared literally overnight. Thankfully, after it saved my brother’s life in the middle of the night one night, we used hydroxychloroquine and ivermectin, and we all know that that was suppressed. I had a $250,000 fine ready to be committed to my practice because I linked to a study on vitamin D use and COVID, and we took that down immediately, obviously. But we all used Ozone, we used binders, we used so many other things that we wanted to use for acute care and mostly were successful keeping patients out of the hospital, and yet it had little effect on the development of long COVID either in the same people or after they got COVID infection or, as I will sight later, even more so after vaccinations.

And I won’t get into the present case in this particular slide. But we have new therapies that we’re going to speak about later on in the talk, on the right side. We also figured out that there was a great deal of microthrombosis, macrothrombosis, and there was some kind of vascular endothelial injury. It’s the entire inflammasome cascade, that is triggered by the COVID and the spike protein. So, it’s basically an inflammatory paradigm of its own. But, as you’ll see later in the talk, it has some unique characteristics that are unique to COVID and unique to the spike protein.

So, here’s a slide borrowed from Dr. Houston at A4M. This is the glycocalyx. This is basically the lining of the smallest arteriole, and it looks like a hairy beast, right? And this is what it looks like at a tight junction between the two endothelial cells. And this is what it looks like when it’s damaged — it looks like it’s been bombed, so to speak. And the glycocalyx component is lost. And then you develop a leaky endothelial cell with leaky blood vessels, leading to leaks in the brain, leaks in the heart, leaks into the liver, and leaks in the blood vessels and so on.

So, we knew right away that there were increased deaths due to COVID-19. And that’s not surprising — off to the right side, there were excess deaths, and we thought that was simply because the patient, extra patients died in the United States, and we were in the top five industrial countries in the world leading the world in deaths. We were leading the world in metabolic syndrome as well, so that’s not surprising.

And then, in the beginning, it was circulatory disorders and dementing disorders that led the total volume of people that were dying early on — really in the first quarter of the pandemic. This is very early data in my first presentation in March of 2020.

What was surprising then, and still is surprising, is the lower number of malignant neoplasms. We felt that maybe COVID would produce an immunosuppressive state that would make immunosuppression on the side of chemotherapy patients worse. That didn’t really happen. And even more striking is the lack of deaths due to primarily respiratory diseases, because you’d think that that would be targeted in the early parts of the pandemic.

And somehow, whether it’s a coding error or a coding issue, we don’t know. But this was relatively low, and metabolic syndrome came to the top of the list. And we all know these slides here — that metabolic syndrome, hypertension, obesity, cardiovascular disease, and neurovascular disease were at the top of the list. And actually, chronic lung disease, again, was less than 20% of the coded COVID-19 associated hospitalizations that were seen then.

And still today, the data are remarkably solid for lung disease chronically, and asthma and so on. And immunosuppression remains relatively low. And then for a state that produces post-inflammatory or post-infectious autoimmunity, autoimmune disorders — and most of these patients are on biological drugs — were exceptionally low. In fact, you’d almost think that they were somewhat protective. So, we had the early, early events.

And I don’t want to spend a lot of time on this because you all know these things, but you have it on the list now, and it goes on and on. This was a major inflammatory signaling burden on the body for those patients that had symptoms early on. The most common symptoms, of course, were fever and fatigue and cough and pulmonary disorders. But we also had a lot of microvascular injury, a lot of thrombosis and inflammation. And then we ultimately led into long COVID, but we didn’t really know what long COVID really was or how we could even define it. When it was defined early on, it was defined…I have a definition in a few slides from now, but I’ll leave it to then.

But then the subacute clinical effects start getting into our practices. We see thrombosis, we see patients with ITP, idiopathic thrombocytopenia, some level of autoimmunity with positive ANAs, thyroiditis, pericarditis — mainly patients with pericarditis, although I’ve seen many patients with myocarditis as well — inflammation and worsening inflammatory reactions, and really almost a state of immunosuppression relative to viral illnesses.

We’ve seen a lot of breakthrough viral illnesses, a lot of breakthroughs in Lyme disease, a lot of breakthroughs in mold disorders and susceptibility to developing symptoms from these chronic disorders that are hyperinflammatory. Well, then we had this come from the W.H.O. around 15 months after the pandemic started. And it’s a definition that is not really worth remembering, frankly, because it’s arbitrary — so okay, you have symptoms that last more than two months and usually three months after the onset. But most of us don’t really care exactly what month it happened in, or exactly the timing. We really care about the patterning and how the patterning teaches us what we already know about a virus that then produces indirect effects on an autoimmune side — in this case, a viral persistence side — and then on an inflammatory signaling side that is a very deep-seated infectious load, post-infectious, post-inflammatory load placed in the body that makes everything worse.

And we also understood that from the beginning, when we started seeing patients with long COVID, that they had impairments of, let’s say, normal features of accelerated aging — that autophagy either had mitophagy, that exosome releases from different organs that were infected or autoimmune-affected and inflammatory. When you look at the center at 6 o’clock, you realize we saw a lot of patients with vasoconstriction, microthrombosis, fibrosis, inflammation, mitochondrial injury and apoptosis.

And anybody that takes care of our types of chronically ill patients has seen this type of patterning before, although it was more spectacular in many ways with the cohort that started coming into the office with long COVID. And these are the reasons why the spike protein fragments can now be identified in every organ of the body, even from the vaccines themselves. And I suspect that the vaccines have made this much worse over time, even in patients that never received, never obtained the original infection once, twice, or three times, and also is probably responsible for the concept of shedding, which I believe is a real concept that we have to deal with, over what we’re dealing with now, and over the next years to come.

It also has been recently found to have bacterial-like signatures, and I’ll explain how that’s happening — particularly with research work in the gut, with fusion of the spike protein, with bacteria in the gut — toxicological potential. A lot of immune cell interactions producing mainly immunosenescence on the one hand, on the protective side, and immunoactivation on the pro-inflammatory side.

And then it also spins off unique spike protein-like or COVID-19-specific-like toxic inflammatory peptides. It’s sort of like they have packages of inflammasome-oriented pro-inflammatory peptides that they shoot off into their environment and produce more cellular senescence from this and more apoptosis and more mitochondrial injury and damage and ultimately mitophagy.

So the immune senescence thing is — it’s not important to read the text, but just for me to explain why our patients seem to be so susceptible to the second bout of infection, the third bout of infection, an upper respiratory infection that’s viral, allergies, food sensitivities, and so on — because when in contact with the surveillance immune system, it produces a lot of immune senescence, and also on the protective side. It puts the cytotoxic T cells that are normally engaged in the third stage of disrupting and permanently getting rid of a virally infected cell, or an autoimmune-damaged cell, are senescent.

So, what did we do? Two years ago, we had all of our patients trying to — were trying to enhance their mitochondria, any variety of different ways as is listed here. We reduced their oxidative stress, including with ozone. Many of the centers were also using ozone.

The phenols, the flavonoids, the senolytics — all were being used — and we’re optimizing their supplements, we’re doing GI repair, we’re optimizing detox pathways, giving them macro and micronutrients, and most importantly, normalizing to the upper limit of normal vitamin D3 and K2 levels. And yet it wasn’t working for a larger proportion of patients that we were seeing over time — meaning more patients over time were not responding to this optimization type of strategy, as you’d expect that they should if they had a modest defect going on, rather than an entire system that’s basically collapsing.

We used peptides too — they’re listed here, and we can go over them in the question-and-answer period. So then what we were left with was, hey, wait a second — I’ve been seeing you now two or three times a week for three weeks, and you still have these ongoing symptoms, whether it’s cardiac, metabolic, immune, GI, neurological, vascular, kidney, or reproductive. I mean, it was still not solid enough of a treatment concept to deal with real clinical benefit that would put someone into a deeper remission. Sometimes we were successful, but we were unsuccessful more often than I was comfortable with — certainly than many of you were comfortable with. So, you ended up with all these different columns of patients.

But really, the patients ended up having all of these together. They all were immunologically dysregulated with persistent infections on the one hand, persistent autoimmunity in the middle column, all had a very, very dysregulated biome, blood clotting markers and so on were all abnormal, and we were worried about them. Although I did not see an immense amount of clotting in the practice itself because we had everyone on high doses of fibrinolytics.

But then we also saw a lot of neurological signaling issues — whether on the one hand it’s cognitive decline, brain fog, but a lot of different neuropathic illnesses that were difficult to explain, other than the fact that when it was looked at autopsies, we could see that the spike protein was well embedded in the perineural spaces as well. So, any nervous disorder could be elicited by the distribution of the spike protein and, again, the inflammasome that it directed locally.

We also understood the concept of microclots and their connections with mast cells. So, we also saw a rise in mast cell activation and unearthed a lot of patients with mast cell activation disorder, multiple chemical sensitivities, etc. But this sort of opened the kimono up in my practice to mast cell activation where it was relatively subtle and then became not so subtle anymore — and paid a visit to patients as well. Whether they had POTS or no POTS, whether they had nervous disorders or not, they also had events of mast cell activation.

So, what do we have? We have persistent spike protein replication, and this increasing new data coming mainly from Europe and from some colleagues in the United States. I think Dr. Robin Rose gave a talk on this topic at the recent Dr. Shallenberger AAOT ozone meetings, and I reviewed her slides and talked to her a few days ago. And it’s true that this concept of having spike protein-specific toxic signaling — that’s pro-inflammatory — in peptides, and peptides that largely look like exosomes, meaning they’re embedded in a lipid so that they could also perhaps be silent to the immune system that way.

And what do you have? To me, this was from the beginning, a model of the worst post-viral autoimmune state that we’ve ever experienced. We all have seen post-viral autoimmune states before, but in this case, this is the most cardiotropic virus that’s ever been seen. It’s probably the most brain-tropic with both the central nervous system as well as the peripheral nervous system.

It’s a virus that induces — and the spike protein that induces — a great deal of endothelial leaks, whether at the baseline level or under stress conditions. And it has ongoing GI injury. And a point here that I want to make is that even some — not an insignificant number of patients that we have, even before the latest new therapies that I’ll be describing soon, we put them into a deep remission.

So, they had confounding results with Lyme, and they had mold, and they had all of the usual things that we see — heavy metals and whatnot — and they also had long COVID. But we put them into remission, and then we’ll get a call six months later and they’ll say, “Listen, I was feeling good enough, I took a bike ride in the California mountains, and when I came home, I felt a little bit tired and weak, maybe I pushed myself too hard, and now I’m bedridden again.” So, the concept of remission and reactivation is something we have to discuss as well in today’s session.

So how many people have this? It’s unknown, but we think it’s roughly around 15 to 20% of the population that have some form of whatever definition you want to use for long COVID. I like to use it for the patients who actually have something that they don’t think is their normal state. It’s not something that made a symptom worsened over time, but something that is basically new. But in fact, in the original data coming from the sources we had in the hospitals in the United States, we realized that having COVID, having long COVID and having vaccinations didn’t seem to have a patterning that was successful.

It made just more patients worse than it made better. And then when you had your second and third infection or a double or triple vaccination, you were more likely to get the long COVID brain effects — and, I think, all of the long COVID effects together. So right now, the consensus from myself is — of all the data — is that you’re worse off if you’ve had multiple bouts of COVID, in terms of relative risks of developing long COVID, but even more so when you’ve been vaccinated double, triple, single on top of a COVID infection.

And then, developing these symptoms later on, you’re at greater risk, and relative risk is greater for the vaccine group. So roughly 6% — that’s the summation of what we have in the US databases that are difficult to rely on, frankly. And one in five people of those people. So roughly, you know, some three-plus million, three to five million patients out having significant enough impact symptoms that they’re impacting their quality of life.

But interestingly enough, despite having some of the highest death rates that we’ve had in all industrial countries in the world, there seems to be an opposite effect that I cannot explain, frankly. If you look at global prevalence, there’s a third to a half of patients reporting long COVID — that may be simply a reporting nuance because their doctors are writing down the symptoms and saying this may be related to COVID — but it’s even evident in countries that have had very few COVID deaths, like Korea and Japan, but have a larger number of patients complaining of ongoing symptoms, and I’ll get into that in a minute.

But this is a huge financial burden on society and has to be dealt with and is not going to be dealt with effectively by the centers of excellence for COVID infection, as I’ll describe in a minute too. So, the most common things are, as you know, fatigue, dyspnea, memory loss, sleep disturbance. Mood effects are very common. Pain is common. But “I can’t return to work” is the most common thing — or in San Francisco, where most of the tech workers are still working remotely, they say, thank God I don’t have to go to work at the office. But there are increased excess deaths even now, today, and five years after the event. This has been documented in Japan, in Norway, and in the United Kingdom.

I’ll go through these slides quickly because we have to make time at the end for the therapies. But there is a long-term lag drag on causes of death and on actual death rates. So, if you have multiple hits on the target, you’re going to be at increased risk. If you have genetic predispositions, you have increased risks. We just don’t have a long list of genomic risks, and that’s because we just don’t have the datasets to look at. But we do know genetic predisposition, for example, for mold disorders with our testing. But there are immunogenomic risks — predispositions that we will find in the future once we have the data to be tested and once we have the banked laboratory data and the observation that there are unique toxic peptides, the massive induction of the pro-inflammatory inflammasome, senescence and autophagy, and the mitochondrial injury — and then the fact that there are vaccine antigens encoded throughout the body that also produce molecular mimicry.

So, it’s a concept that we all are now more prone to autoimmunity if you’ve been vaccinated, if you’ve had the disease, or if someone in your family is shedding on you. Overall, the risk for autoimmunity is increased, and that is something we will see — not necessarily now, but we may be beginning to see it now — but over the next five or ten years, we’ll see more of.

So aside from the treatments that are on the left side, which are well known and there are so, so many I could run out of room, we’re going to talk about the effects of nicotine, the effect of augmented NAC (N-acetyl cysteine), and two of the filtration concepts — either plasmapheresis or total plasma exchange and EBOO — as many centers already have.

And I also want to make this really clear: Long COVID is an accelerated aging event. Even COVID infection is an accelerated aging event that needs to be treated in a systematic way because it deals with mitochondrial dysfunction and a pro-inflammatory state. But if you understand how to treat a patient with long COVID and you can reverse it and you can put it into remission, then you know a lot more about how to treat patients on the anti-aging side.

On the senescence side, this slide you can look at on your own later on. This produces a lot of degenerative changes throughout the body. And this is what aging does, of course, but this is what the virus does — and the spike protein does — with its inflammatory signaling that brings in the neighborhood, into the pro-inflammatory state, into the senescent state, and probably is the explanation for why turbo cancers are happening at this point.

We also have to deal with the neurological impacts, and we know the astrocytes are one of the main targets of the spike protein.

And when you look at this particular slide later on, it actually is a slide of multiple sclerosis, the effect on glial cells and neurons. But it’s the same concept for a spike protein and the inflammasome that is induced by the spike protein in the brain, leading to neuroinflammation and neurodegeneration. And on the subtle side is brain fog, cognitive decline on a more serious level, and then ultimately dementia. And this is just in the central nervous system.

So how does the brain take out the trash? Obviously, it does so in a weakened state with the post-viral state, post-COVID state, because the cervical chain in the neck is one of the main sites of housing the spike protein over time. And when you do a lot of ultrasound work in the neck, like we do here at the office, you see so many patients now with enlarged lymph nodes in the neck, which are draining the brain, of course, and then the cervical chain and all the chains throughout the brain. So, it’s a bit of a problem for everybody.

Cognitive impairment is off to the right side. These are PCC — a post-COVID event. Cognitive impairment is more prevalent. This is showing that neuroinflammation is most present in patients with Alzheimer’s disease, and COVID versus Alzheimer’s disease or COVID as single disorders. So, there’s an additive effect of more inflammation, more degeneration, more plaque formations, and so on.

And then on the cardiac side — again, this is another photo of myocarditis, and again, it’s a few immune cells with a very broad effect. The question is, what are we looking forward to in the near future? Well, the main location for the virus is in the vascular bed, as you can see in the four slides in the right corner, because that’s where the ACE2 receptors are. That’s where you have endothelial and inflammatory state in the endothelium. That’s where you get a leak. And when you have a patient who has congestive heart failure acutely from a virus, it’s the leak — it’s the fluid that gets into the myocardium — that produces heart failure, which is completely reversible. It’s not permanent injury to the heart.

And here’s a classical example: on the left side, some beats of ventricular tachycardia — just a few of them — all off to the far left. There are three fast beats of VT, then it goes into almost a torsade-like effect on the ventricular, very fast ventricular tachycardia and then fibrillation at the end. So, this is an event that is more likely not a straight arrhythmic event, although you can get this event also with vessel spasm or what we used to call Prinzmetal’s angina. And that’s why I’m showing this particular slide here — not because COVID-19 is associated with accelerated atherosclerosis, but because since it invades the smooth muscle and you may be rupture-prone, you may not be, we’re not seeing clotting disorders and a lot of blockages in the coronaries per se, but we are seeing more vasospastic disorders in the coronaries that are due to vasospasm. And the vasospasm is due to this endothelial glycocalyx that’s involved and is destroyed by the viral proteins and peptides.

So, what did we do? When we first started, we started using EBOO. This is just showing you the difference between the ozonated blood and not — this had beneficial effects. And we did an ACAM session on the use of EBOO about two to three years ago, and we showed that there were remnants of mold, there were heavy metals, different inflammatory signaling molecules in the filters.

But we didn’t look — we didn’t find things that were COVID-19 related. But now, with the work of Dr. Rose, she has demonstrated the finding of spike protein in the filters of EBOO machines, and we’ve not validated that, but I believe the data and more likely than not it is real. The question is whether it’s enough to make a clinically significant effect. And in our hands, we always found a beneficial effect, but it’s not clinically significant all the time. And we now think that we have a better response now to therapeutic apheresis, because here you’re getting back your own blood, whereas here the machine separates red cells, white cells, and platelets and gives them back to you, but the entire plasma is exchanged by albumin, so you’re not getting back any of your plasma.

This is just showing that apheresis is already showning to improve cognitive decline in placebo-controlled clinical trials. So, we look forward to it allowing patients with long COVID to have neurological repair faster. Less clumping, less clumping. We also use the Weber laser because it has similar effects on the coagulation system and similar effects on detoxification, so it overall has some benefits, but not enough to make a very, very deep clinical experience.

So, we also use stellate ganglion blocks to reset the neurological state to upregulate the parasympathetic tone. We don’t have time to talk about it now. So, then the latest things — the two latest treatments I want to talk about and probably take the last five minutes — is nicotine.

And nicotine is actually a very strong nootropic, a very safe nootropic when not inhaled vis-a-vis smoke, and is now being shown to be effective in Alzheimer’s disease, dementing illnesses, and soon will be studied in long COVID as well. But there are colleagues on the line now that are using nicotine patches in particular, or nicotine gum, in long-COVID neurological CNS symptoms.

This is a slide you can look at on your own, but this is the mechanism of action of nicotine on acetylcholine receptors, and this is prior results on nicotine — particularly with the Alpha-7 subtype of acetylcholine receptors — that are also not just dealing with neurotransmitters but also dealing with reducing neuroinflammation. So, it has a dual effect, and that’s why it seems to be working well in certain patients with long COVID who are otherwise unable to resume work because they don’t have enough cognitive support or cognitive depth in order to survive.

This is just a summary slide — it’s both anti-inflammatory and cognitive enhancing — it’s worth a try. Here is the dosing regimen that is given, and you may have a better dosing regimen than this. We have not — we’ve only just begun treating patients with this dosing regimen now.

And then there’s the Zero Spike Project, which is an awesome project done by pharmaceutical scientists and pharmacologists and universities throughout Europe. These are consultants that are taking on the topic of how to negate the effects of the spike protein. So, this is a nonprofit organization run by people who are not being paid, and they now have come up with a solution called augmented N-acetylcysteine. Many of you must have heard this already, but on the bottom, you can see that it denatures the spike protein to a much greater extent than regular NAC does, and it also works well together with other therapies that we normally would be using.

It enhances the effect of vitamin C and vitamin D and homocysteine and other oxidative processes. So it denatures the spike protein to 99%. It dissolves the tissue clots, it denatures — within 24 hours — the spike protein to a great extent. In the blood, it also protects; it allows the glutathione to act longer in the blood and then offer greater protection on the detox, on the antioxidant side.

And it also does the same thing which allows vitamin C to act more as an antioxidant than it normally would with a standard NAC. So, it’s got a lot of good things going for it. There’s a little controversy as to what the dosing should be. The dosing in the packaging that comes from the nonprofit says 200 milligrams or one capsule twice a day.

Anyway, we would start with once a day. We actually start with the regular N-acetylcysteine for one week with binders and other antioxidants to prepare the patient for die-off reactions. Then we go to once a day, twice a day, then three times a day with the augmented NAC. But we feel that the data are just as strong for three times a day as the steady state dose for up to three months, and then people go on to some kind of a maintenance dose. The link at the bottom left is the link to where you can get it, but I think right now there’s a long waiting list.

The confounders — well, we all know that mold — this is the same patients: Lyme, reactivation of Epstein-Barr virus is very, very common in these patients, and they also have Lyme. And then there’s a slide here to show a very severe case of mast cell dysregulation. These cells in the circles are mast cells, and they’re just in a tissue body — that patient has, in his case was the easiest way to find that he had a mast cell activation syndrome.

And what do we expect in the future? We expect a lot of biomic dysregulation — but not exactly for why you think. So, everyone has a biome that needs to be upregulated because of the formation of bacteriophages. This is where a virus infects and replicates a bacteria, and the bacteria becomes the host. The virus bacteriome becomes an obligate intracellular parasite. There are obviously tens of thousands of bacterial species in the gut.

And here’s what it looks like — it’s like little buds off the surface, but also intracellularly; it also goes inside the bacterium. And then what happens is it can produce — on the bottom slide — it can produce a chimera of a combination of a human microbe and the spike protein acting as a chimera. That may, in fact, produce more autoimmune reactions or even new variants.

And the last thing I want to say is my experience in the lab at Hopkins 30 years ago was in myocarditis, and that was produced by viruses. And we noticed a very wide range of genetically modulated effects. So, you can get anywhere from sudden death all the way to no symptoms at all. So, my sum total of all this is a model of post-inflammatory myocarditis leading to heart failure over time, is the following:

We’re already past the acute phase where we had almost all of the myocarditis patients with sudden death — those have already happened, from days to the first four months — this is all based on animal data though. So, this is my extrapolation of what humans will be like. So right now, we’ve passed the subacute phase — still with sudden death and also a few cases of congestive heart failure, which we’ve seen. And then the chronic phase — we’re in the chronic phase, and the peak years, actually, should have been five to ten rather than four to six. So, we haven’t even begun to see the peak years of the development of chronic heart failure due to the initial viral infection in the heart that then led to some kind of autoimmune state and some kind of direct spike protein effect.

So, the future for us is bright — if you take a systems biological approach. Otherwise, you have all these disorders going up in incidence and prevalence. We haven’t talked about mood disorders or fertility disorders — there isn’t enough time — but all this is more likely than not happen. And then we again have the fusion between an important singular event on the virus side as well as aging.

So, it comes down to this saying: “It’s not just about the virus in the person — it is the person with the virus.”In this particular case, you have to understand the personalized terrain of a person to understand how best to treat them — treat them with a systems biology approach. That’s the only approach that will work.

And then you can read these other good books that have been shared with me. The Zero Spike Project book on the right is also a great resource in terms of the website page, but Dr. Ardis’s book is good, and the Pfizer papers are good.

Thank you very much. I apologize for going over — I know I took a lot of time talking very quickly.

Janelle: Thank you very much, Dr. Herskowitz.

We do have a few questions here, if you have time.

The first question: Please explain plasmapheresis.

Dr. Herskowitz: Well, plasmapheresis is — you have two venous accesses. One vein is going out, like it would with an EBOO device. It goes out to the plasmapheresis device under pump pressure, and then the blood is separated into red cells, white cells, and platelets on the one hand, which are given back to the patient — and the plasma — the sort of ocean in which all the cells are swimming in throughout the body, which has all the signaling molecules and has the pro-inflammatory state, has the toxins.

Now there’s a paper coming out that will show that you can get microplastics in the plasma as well — a lot of the forever chemicals, a lot of the heavy metals, mold, etc. — but it hasn’t been proven yet for spike protein. Don’t ever go back to you, so you get back the same equivalent of volume of your plasma that’s lost during the filtration. You get it back with albumin in a 1-to-1 ratio, so you end up with the same amount of blood volume at the end. But you’ve lost probably two, two and a half liters of plasma — that is, again, plasma that you’re not interested in having.

Janelle: The next question is: What can you do for a lymphoma, develop six months after the COVID shot?

Dr. Herskowitz: Well, you have to do everything, right. You have to say that — Well…so that’s not enough information to act on, frankly. But now you have a paradigm in which you could understand that you have to look for all the confounders and treat them, because I think all but one patient of mine in the last 12 years with any form of hematological or solid tumor cancer has had mold intoxication. They also have a pro-inflammatory state, they have a biome that needs to be adjusted, they need more antioxidants, they need other things other than the pure tumor-related specific therapies. So that requires more than an hour to answer, so that’s the best I can do here.

Janelle: More recently, some suggest that enzymes like Nattokinase or Lumbrokinase may break up spike proteins in a detrimental manner, which may then serve as a trigger for more autoimmunity. Do you have any hesitation around the use of these enzyme products today?

Dr: Herskowitz: Well, I’d say the answer to this is yes — I have a hesitation, and I’ve taken some patients off of their fibrinolytics to see what its effect is. I haven’t seen much of a change, and I’m now taking myself off of all my fibrinolytics to see if there’s a difference.

I don’t have a serious case of long COVID, obviously, and I think it’s correct that we don’t know what it’s doing — we don’t know enough yet. We haven’t done a few hundred of these analyses of what you find in the filters of certain patients and others are not. So, it’s really, you know — Nattokinase or Lumbrokinase are very effective and have to be used — they sort of have to be used. The concept has to be used for people with really seriously elevated D-dimer, you know, and the ones that are not moving very much — they’re lying in bed all day. You have to sort of use it as a preventative and as, you know, as a therapy as it was used in the acute setting.

And for the most part, I’d say they’re rather safe. But then there may be individual cases where they’re not helping. And I can’t predict anyone today that has that. I can’t predict who.

Janelle: Is there a lab test to measure the body burden of senescent cells?

Dr. Herskowitz: The body burden of senescent cells? Not that I’m aware of. I think, you know, the best measures of aging are probably still the methylation tests — the TrueAge test, the HOPE, you know, the different clocks — but they’re not exceptionally accurate. They’re good if you want to show that, you know, you’ve just reduced your age by two years and you want to sell a product, or ten years and you want to sell a product, because you can literally find any test out there that’ll show you the results you’re looking for.

It’s really strength and maintaining muscle mass — and growing muscle mass — that’s probably, you know, the greatest measures, the greatest practical measures you can use on yourself on a day-to-day basis. I mean, we can’t do muscle biopsies on most patients to measure mitochondrial function. And while we’re all hoping to have a mitochondrial assay that will be more reliable and more meaningful, we don’t have one today.

Janelle: What portion of your long COVID patients do you believe still have active or persistent COVID virus versus only a portion of spike protein in monocytes, but no active virus?

Dr. Herskowitz: Yeah, I don’t believe that our patients have active virus. But I believe they all have, and I think we all have spike protein activity in our bodies. Every one of us.

Janelle: With research suggesting that COVID could affect our own GI microbiome, how do we remove this without destroying the beneficial microbiome?

Dr. Herskowitz: Good question. So, this is turnover, turnover, turnover — active turnover — because, as you know, the biome turns over every few days. Keeping the biome in the proper proportions — the average patient has bacterial and fungal overgrowth, has poor beneficial microbial, you know, the whole nature of the good microbes it has. But we’ve been living with viruses in our biome for, you know, ever since the beginning of time. In this case, it’s probably, again, the inflammasome that’s produced by these chimeras being produced.

But right now, all we know is that they’re there, and we just have to optimize our systems and, and you know, have the people who are not using their pathway of bowel habits — good bowel movements once or twice a day at minimum — are just not using the most effective detox pathways. So even on that level, optimizing that is probably going to be more effective than worrying about how to maintain the healthy biome and kill off the ones that have chimeras in them.

Janelle: How important is determining the presence of active virus in the treatment plan and outcome in long COVID? What are the most useful markers for finding long COVID?

Dr. Herskowitz: Well, I mean, there are tests that are on the market for long COVID. I don’t find them useful at all. So, you know, to me, what’s useful is: do I have — what’s my inflammatory load? Okay. Do I have enough antioxidants to deal with buffering the inflammatory load? So, the markers that I find the most sensitive for that are: a serum ferritin level — if a serum ferritin above 50 is not normal. If it’s above 100 or 200, 300 — which many of these patients are — you’re wholly deficient in antioxidants, given the burden you currently have. Conceptually, your vitamin D level should be somewhere above 60 — I’d like it to be between 80 and 100 to be most effective, to use the anti-inflammatory qualities of vitamin D — and then having functional mitochondria. So, if you have omega-3 fatty acids, magnesium, the B-complex vitamins, carnitine — if you have these things that feed Complex 1 to 4 and feed the production of ATP — then you’re going to be in better condition.

And yet, it’s not enough just to do that. But at the same time, I don’t treat — we do have most of our patients on ivermectin, high-dose ivermectin up to 50 milligrams, between 25 and 50 milligrams a day for months at a time, just to make sure that they don’t have any residual active infection. But I think that the testing that we use — the PCR testing that we use — is so nonspecific; it just tells you whether there’s a single, you know, PCR COVID-19 organism. It doesn’t tell you anything about infectivity. Without symptoms, I don’t consider it a helpful tool.

Janelle: What’s the latest, in regards to long-term pulmonary fibrosis as a result of COVID pneumonia? Are there any new therapies you can recommend for interstitial lung disease caused by COVID pneumonia?

Dr. Herskowitz: Yeah, well, I think the thing I would try — again, the longer you wait, the more you end up with bronchiectasis, the more you end up with permanent injury to the basic architecture. It’s not just that there’s more fibrous connective tissue; it’s that you’re actually producing cavities within the lung that are just prone to infections. So, timing is important.

I think the EBOO is not effective. The therapeutic apheresis can be effective if used — it’s not a one-shot deal. It’s multiple, multiples — a series of cleaning up the inflammasome burden that people have. And then what I used in that patient was, in those days — when the FDA did not have a rule against using intravenous stem cells — I was using those.

But with people with fixed pulmonary fibrosis and pulmonary hypertension, even the use of regenerative products is actually dangerous, because that has the pulmonary vascular bed — that has hypertension in it — acts in a completely opposite direction than you want it to act. You can hurt somebody with stem cells late in the game with pulmonary fibrosis — end-stage pulmonary fibrosis.

So, then you’re really trying to optimize the release of oxygen from hemoglobin and red cells. So, it’s in a bind, you’re in a bind — and the thing that you can do is increase the inflammatory burden of the body so that it can act more efficiently.

Janelle: Well, a big thank you to Dr. Herskowitz for your time and expertise this evening. If you’d like to reach out to Dr. Herskowitz, you can do so by calling Anatara Medicine Clinic at 415-345-0099. If you’d like to learn more about the American College for Advancement in Medicine, email info@acam.org or call 1-800-532-3688. Any registrants can expect to receive a recording of tonight’s presentation via email within 5 to 7 business days.

On behalf of everyone at ACAM, have a wonderful evening.

Dr. Herskowitz: Thank you. Thank you, Janelle.