Ask Dr. Drew - Help For COVID Long Haulers: Dr. Ram Yogendra & Dr. Bruce Patterson Reveal Research – Ask Dr. Drew – Episode 158
Episode Date: January 1, 2023For most people, a COVID-19 infection lasts about 2 weeks. But others have reported symptoms extending long after the initial illness: fatigue, shortness of breath, brain fog, and difficulty with memo...ry lasting for months. Doctors are calling it "COVID Long Haulers Syndrome" or "Long Covid" but little is known about the condition's cause. Dr. Ram Yogendra & Dr. Bruce Patterson – viral pathogen & infectious disease researchers – reveal what we know about Long COVID and the latest on treatment & recovery options. 「 BROADCAST ON 12/15/2022 」 Dr. Ram Yogendra is a board-certified anesthesiologist with a background in public health. He worked as an Infection Control Practitioner in Florida where he was also a part of the Jail Linkage Project that worked to conduct risk assessments of inmates to determine those at high risk of infection and in need of HIV/STD/TB/Hepatitis testing, treatment, and follow-up services. Follow Dr. Ram Yogendra: https://twitter.com/dryostradamus Dr. Bruce K. Patterson MD is a leading researcher on the effects of viral pathogens on the human immune system. His pioneering technologies and findings have contributed to advances in detection, prognosis and treatment of patients infected with HIV, HPV and cervical cancer, COVID-19 and other diseases. Follow Dr. Bruce Patterson: https://twitter.com/brucep13 Learn more and get help for COVID Long Haulers at https://covidlonghaulers.com/ 「 SPONSORED BY 」 • BIRCH GOLD - Don’t let your savings lose value. You can own physical gold and silver in a tax-sheltered retirement account, and Birch Gold will help you do it. Claim your free, no obligation info kit from Birch Gold at https://birchgold.com/drew • GENUCEL - Using a proprietary base formulated by a pharmacist, Genucel has created skincare that can dramatically improve the appearance of facial redness and under-eye puffiness. Genucel uses clinical levels of botanical extracts in their cruelty-free, natural, made-in-the-USA line of products. Get 10% off with promo code DREW at https://genucel.com/drew 「 MEDICAL NOTE 」 The CDC states that COVID-19 vaccines are safe, effective, and reduce your risk of severe illness. Hundreds of millions of people have received a COVID-19 vaccine, and serious adverse reactions are uncommon. Dr. Drew is a board-certified physician and Dr. Kelly Victory is a board-certified emergency specialist. Portions of this program will examine countervailing views on important medical issues. You should always consult your personal physician before making any decisions about your health. 「 ABOUT the SHOW 」 Ask Dr. Drew is produced by Kaleb Nation (https://kalebnation.com) and Susan Pinsky (https://twitter.com/firstladyoflove). This show is for entertainment and/or informational purposes only, and is not a substitute for medical advice, diagnosis, or treatment. 「 GEAR PROVIDED BY 」 • BLUE MICS - Find your best sound at https://drdrew.com/blue • ELGATO - See how Elgato's lights transformed Dr. Drew's set: https://drdrew.com/sponsors/elgato/ 「 ABOUT DR. DREW 」 For over 30 years, Dr. Drew has answered questions and offered guidance to millions through popular shows like Celebrity Rehab (VH1), Dr. Drew On Call (HLN), Teen Mom OG (MTV), and the iconic radio show Loveline. Now, Dr. Drew is opening his phone lines to the world by streaming LIVE from his home studio. Watch all of Dr. Drew's latest shows at https://drdrew.tv Learn more about your ad choices. Visit megaphone.fm/adchoices
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Here, we're watching you out there on the restream as well as on the Rumble Rants.
We appreciate it all.
And we are having a repeat performance by our friends Dr. Ramya Gendra and Dr. Bruce Patterson.
They have been studying long COVID from way back in the dark days of COVID.
And several different theories have emerged of what's causing it.
And as a result of doing these studies, they have learned a great deal about not just COVID,
but some of the other chronic fatigue, chronic inflammatory-type syndromes that we have perhaps made less of in medicine than we should have over the years.
The old chronic fatigue syndrome or chronic Epstein-Barr.
We always sort of had a passing understanding that something could go on with some of these illnesses, but the very specifics,
one of the things that have come out of COVID is more insight into the biochemistry of these phenomena.
Let's get right to it.
Our laws as it pertained to substances
are draconian and bizarre.
A psychopath started this.
He was an alcoholic because of social media
and pornography, PTSD, love addiction,
fentanyl and heroin.
Ridiculous.
I'm a doctor for f**k's sake.
Where the hell do you think I learned that?
I'm just saying, you go to treatment before you kill people.
I am a clinician.
I observe things about these chemicals.
Let's just deal with what's real.
We used to get these calls on Loveline all the time.
Educate adolescents and to prevent and to treat.
If you have trouble, you can't stop and you want to help stop it, I can help.
I got a lot to say.
I got a lot more to say.
Thank you all for being here, and let's get to it.
Our guest, Dr. Ramya Gendra, an anesthesiologist.
He also has a background in public health, and he got interested in the long COVID syndrome. Well, actually, he got interested in cytokine activation and the Ranti's pathway being interrupted
by some of the medication that was being tossed around as a solution to that.
And of course, Dr. Patterson is a researcher on the effect of viral pathogenesis and the
immune system.
He was very, very active in the pursuit of HIV and HIV treatments.
Guys, welcome.
Thank you.
It's a pleasure to be here.
Thanks, Dr. Drew.
It's great to be back.
Lironlamab, that was the name of that medication.
I was trying to pull it out in the intro, but I couldn't remember.
It was Lironlamab.
And although, I just want to review a little history for a second.
Although that looked very promising, and I remember going to great lengths to getting it for some people that were in desperate circumstance,
it didn't sort of take its place as a routine sort of treatment for cytokine activation, did it?
Well, I think the fact is the CCR5 pathway, which is what's blocked by loranumab, is actually, as we found in long COVID,
now post-treatment lung disease, chronic fatigue, fibromyalgia. So I don't think it's a shortcoming
of the pathway. I think there was, you know, some issues with, you issues with the particular offering, but by no means is that class of drugs or the pathway that CCR5 antagonists block not important. In fact, it's critical in tempering the immune system without being an immunosuppressive. Yeah. No, I remember the whole, uh, when we first
met Rom, he gave us a disquisition on the Ranti system. Yeah, that was, that was back in two years
ago. And I think it was a lot of our friends and colleagues were, were in the hospital and that's
how I got linked up with Dr. Patterson was, uh, so much we didn't know at the time. And but thankfully, a lot of them made it through.
And we're kind of, you know, I don't want to say COVID is over.
I think there's a lot of debate.
Obviously, cases are rising and there's some discussion about that.
But, you know, it's an interesting summer of 2020.
I had friends of mine that were coming down with what we are now calling long COVID or
post COVID complications and linked up
again with Dr. Patterson back in summer of 2020. So we were recognizing it back then.
And quite frankly, I think the medical community was still, and understandably so,
still trying to end up sort of the middle of the worst part of the pandemic. But I think now
we're really shifting from the discussion we have from 2020,
where we're really talking about the after effects of the post-COVID complications. And you're seeing
there's two sides of the argument. There's one group that is talking about, look, COVID is not
really a big thing. I think there was an op-ed article in the Wall Street Journal, Dr. Macrae,
I think brought some valid points. Also a lot of things that we disagree with. And
then there's another group that wants to call everything sort of post-March 2020 long COVID.
So I think part of the debate and the discussion is defining what exactly is long COVID. And I
think that's what one of the things we've done is in the past two years of studying this is
our, like any sort of research in anything in medicine, our understanding has evolved. We have a greater
understanding now than we did, let's say, a year ago when we were last speaking with you. And I
think today's discussion is really going to center on all the new findings and all the etiology and
the pathophysiology that is driving long COVID. And how's your friend doing, the other anesthesiologist that had that terrible, terrible ICU experience?
You okay?
Yeah.
Dr. Purcell is doing well.
Still has some lingering effects from the acute phase of COVID, but he's doing well.
And yeah, I'll send him your regards.
Thank you.
Please.
And you guys actually tested me because I had long collar,
long haul type syndrome. And if you remember, I had elevated VEGF at the time. Bruce is smiling.
Go ahead. Well, I mean, elevated VEGF is one of the most common findings in long COVID. But I think
my take over the last couple of years, as Ron said, we were, you know, in the beginning, if not the beginning of long COVID.
We found this series of symptoms. And of course, now those symptoms are widely publicized,
fatigue, post-exertional malaise, brain fog. And I remember an early interview from a year,
year and a half ago, where we came up with a diagnostic that had a long hauler index and we
could actually, you know, track, you know, response to therapy and if they're getting better. And
the other physician said, well, we don't need diagnostics for long COVID because we know what
the symptoms are. Well, now we know that nothing could be further from the truth. Those symptoms
are indeed found in long COVID, but they're also
found in post-treatment Lyme disease. They're also found in chronic fatigue syndrome. They're
found in fibromyalgia. They're found in some individuals post-vaccination. So they're very
nonspecific. And we've really focused on a new algorithm that's been in our use for the last six months where we can actually determine
with whether this is pure long COVID, Lyme, ME-CFS,
or fibromyalgia so that they could be treated appropriately
because those symptoms are not differentiating
between those groups.
And I think that's why there's a
lot of confusion because people are presenting to their physicians and say, I have these symptoms,
I must have long COVID. And sometimes they've never been infected by COVID. Sometimes when
you talk to them by telemedicine, we find out, oh, I've had these symptoms for five years,
and they happen to get worse during COVID, and that tips our scale over towards
Lyme or chronic fatigue syndrome.
So a lot's been learned over the last few years, but it's been greatly aided by our
efforts with machine learning and artificial intelligence to really distinguish between
these very similar chronic inflammatory conditions.
What do we do with the finding in one of the recent publications that a majority of people
with long COVID have mental health diagnosis? Oh, that's a great point, Dr. Du, because
what we've found is that many of our, you know, 30,000 registered patients have anxiety or
depression. And the fact is, it's very much related to vascular inflammation, because
when these individuals, when we cool off the immune system, a lot of that resolves.
Some doesn't, but a lot of it does.
And, you know, we're starting to treat more of these patients.
We have this interesting combination of an antecedent infection, say with strep or herpes, and OCD or other mental health
um they always thought that pandas was caused by autoantibodies that cross the
blood-brain barrier but not only has auto
antibodies or on a Tory component so that when we treat both
The auto and and the chronic inflammatory
Elevations using some of our approaches they get better and they stop having ticks they stop having
That condition
Inflammation and mental health i think are intimately related um and have
hey i'm gonna interrupt um caleb can we help uh dr patterson with that yeah he has a there's some
connection issues over on his end but everybody else is clear
right now yes can we do something to help improve that do you think no it has to do with this
connection yeah you can talk to dr over yeah so so so and so far as inflammatory goes you know
uh we're people are starting to look at the the uh the clinical mechanism of action of some of the antidepressants might actually be through the sigma-1 receptor and through an anti-inflammatory type mechanism.
I suspect, well, that's why fluvoxamine was one of the original and early sort of treatment attempts.
I had a great response to it personally.
Have you guys continued to use that medicine?
Yeah, it's still in our arsenal. I think it also depends on the patient. I think that's the important thing. I think a lot of times you hear these discussions from patients,
physicians, a lot of things in the media, but finding that one magic drug
for long COVID or post-COVID complications. And I feel like we should probably maybe start
calling it less of long COVID and kind of using post or past or post-COVID complications because
long COVID makes it seem like, you know, I don't think it takes into account some of the other
things that we're seeing, the reactivation of some of the herpes, family viruses, the vector-borne illnesses, the ME-CFS exacerbation that we're picking up. patterns and we'll ask some questions well are they any any time in your in your life that you
had unexplained bouts of fatigue or um exhaustion post-exertional malaise and it's funny sometimes
patients like yeah you know there's like a two three two three month period um where when i was
like in my 20s i i kind of got really bad and then i got better for a couple years and now it's sort
of kicked back in so it's it's the etiology and the pathophys is
quite frankly all over the place. So to go back to your question, Dr. Drew, about
fovoxamine and some of the SSRIs, yes, but it also varies by patient. So I know a lot of times
we talk a lot about CCR5 antagonists and then some of the use of statins, and what we don't
want is people
just automatically assuming, well, this is the magic bullet. I think the very interesting thing
that we're trying to do is sort of, I think it's very important for patients to know that there's
something wrong with them. But the question is, what is causing their symptoms? And I think it
doesn't necessarily mean that they're making it
up. I think for many patients, when you say it's not necessarily sort of long COVID, but I think
it's something else. I think we have to be very clear to them that we are acknowledging that
there is something wrong with them, but we're just trying to find etiology. So a lot of times what
we're doing is actually doing further testing. I think in the past like six to 12 months, we've
really started to, you know, patients come in and say, okay, I want to take X, Y, Z. It was like,
wait, hold on a second. We need to do more, more further testing. And just because all of these,
some of these symptoms manifested after COVID doesn't necessarily mean it's all long COVID.
We still have to use proper, you know, our basis of medicine, but I've got to rule some of the
common things out.
So a lot of times patients will have... So walk me through how you're doing some of that and what the sort of
serological profiles are or whatever other tests you're using to determine
what kind of chronic fatigue...
What's the general category we've been calling this?
Chronic fatigue?
Is there a general category?
I mean, Dr. Truc, can we pull up that there's a PDF I sent you?
It's sort of, if we can sort of pull it out, we can sort of talk through sort of kind of
the overall schematic.
I think that might be helpful.
Yeah, this is sort of what our sort of a rough diagram.
And I think patients that have, and physicians, researchers that have spoken to me over the past six months will be sort of familiar rough diagram. And I think patients that have, and physicians, researchers that have
spoken to me over the past six months, they'll be sort of familiar with this. If we look at
symptoms, the question is what is driving these symptoms, right? I mean, the brain fog, the
fatigue, some of the, something called POTS, you know, a lot of times people incorrectly
attributing it purely just to cardiac when it's more of an autonomic dysfunction
um dysautonomia i mean there's over 200 symptoms that are being described in long covid and i think
that that list gets bigger and bigger um if you look at just in symptoms you're just really just
putting a band-aid on it and what we're trying to do is sort of tease things out um and sort of
understand what is causing it. Uh-oh.
What happened there?
Well, we had a little bit of a technical problem,
so I'm sure Taylor will get right on that.
Dr. Bruce just joined the show
from Dr. Yogendra's link by accident.
That's terrible. So he knocked him looks like he's coming back in.
Yeah, that's what it looks like happened.
That's great.
All right.
So patience, everybody.
So we're about to get to the part where he figures out how to tease out all these symptoms
in different categories.
And I still don't know what we call the syndrome.
You know, syndrome just means a constellation of symptoms, while a diagnosis is a constellation of symptoms with a common pathophysiology
and a common genetic heritage and a common environmental influence.
Go ahead, Bruce.
So there's three things that we look at from our diagnostic report.
We look at the pattern of inflammation.
So we have three markers of vascular inflammation.
And then these other ones will determine whether, you know, for instance, it's Lyme, like interleukin-13. We never see interleukin-13 in long COVID. We only see that in Lyme. So interferon gamma plus interleukin-13,
interferon gamma plus interleukin-8, those make us suspicious for Lyme. And then we reflex to
Lyme testing to see if indeed that is the underlying etiology. But then we'll still go
on and treat the vascular inflammation because that's a new discovery of ours where vascular inflammation
may be the underlying cause of symptoms in chronic Lyme. So can I zero in a little bit on the
inflammation, vascular inflammation? So I've seen now a lot of illness and I've seen now a lot of illness, and I've seen now a number of path specimens that show quite literally an endothelitis.
And it seems that the vaccine can cause this.
It seems like something to do with the spike protein because the vaccine seems to cause something similar as well.
What is the mechanism of that?
Is it a macrophage interaction with the, again, I'm so used to inflammation of the
endothelium and the lining being somehow lipid and macrophage mediated. Is that the case here?
That's absolutely correct. And we identified that a year and a half ago. And we found the S1 protein of SARS-CoV-2
in these pro-inflammatory non-classical monocytes whose sole job is to bind to blood vessels
through the fractal kind-fractal kind receptor pathway. And we think that may also
be at play in Lyme by carrying the cell wall of the bacteria for years, if not decades,
because these reservoirs, when they're presenting antigen, they short circuit their apoptosis or death program.
In other words, they don't die.
Most people respond to me and say, oh, these monocytes have a lifespan of a week.
Well, yes, when they're normal, they're pro-inflammatory.
They bind to blood vessels.
And the strategy of our therapy, and this goes back to the
early 2000s atherosclerosis literature, is solely blocking these cells from binding to
the blood vessels and relieving the vascular inflammation and the platelet activation that's
caused by this endothelitis.
And I think we were one of the first to coin the phrase endotheliitis because the endothelium
makes this protein called fractalkind,
which allows these pro-inflammatory macrophages
and monocytes to bind.
Now, you had seen that in the CNS last time I talked to you.
Are you seeing that more widely distributed? And
again, I want to make sure I get the terms right. It's the non-classical monocytes?
That's right. So there's three subpopulations of monocytes, classical, intermediate, and
non-classical. Intermediate monocytes were the ones that were infectable by HIV. We showed in
2009 that they're infectable by hepatitis C. They've been shown to carry dengue
fever and Zika virus into the brain because they cross the blood-brain barrier. All of this is
fitting in a nice narrative that explains a lot of what's going on in long COVID. And it's based on years of research, some of it by my lab, some by others.
But if you go back and look at the atherosclerosis literature in the 2000 of any knowledge of that literature,
came up with this panel and this set of markers
that was indicative of endothelitis.
So tell us about that.
What is that panel?
So, I mean, that's part of our panel.
We see elevations in this protein called SCD40L,
which is the first protein engaged in the thrombosis pathway.
We see CCL5 or Rantis, which is produced with SCD40L by activated platelets, which
bind to the endothelium. And of course, when you have inflamed endothelium, it's inside the kind.
And you're looking.
By the way, our AI.
I picked out as.
So.
Position.
You.
Told us.
And what was in the literature for something
completely different. And that's what's so fascinating about this
story. You know, we identified it as a major protein that's produced inflammatory protein in long COVID
and others now. VEGF not only promotes new blood vessel growth,
but it also causes neuropathy.
So patients come in, fingers and extremities,
and as soon as you start lowering the VEGF,
that's when they start to see relief
in some of the neurologic symptoms.
Yo, I wonder if you have anything on the slides that will recapitulate some of this.
Want to go back to your slides?
Yeah, if you don't mind, I'll just sort of recap.
Sorry, Bruce, I got cut off.
So as I was just mentioning earlier about the symptoms, And this is sort of the working, kind of our working
hypothesis and some of the work that we've done and continue to do. So if we just focus just on
symptoms, as I mentioned earlier, I think before we cut off, we're not going to understand the
etiology of what is driving symptoms. Okay, fatigue, post-exertional malaise, brain fog,
POTS, all of that. I mean, you can, there's a whole multitude of chronic illnesses that cause the same symptoms.
So by treating that, we, and I think it is important to just treat symptoms too.
Patients want immediate, or at least, you know, telling them to wait for four or six,
you know, eight weeks to get better.
We're starting to see improvement, I think, but many of them, they much rather feel better
within a couple of days or within a week. So I think, you know, we can't just completely rule out
treating just symptoms, but I think it has to go sort of hand in hand in what we suspect is
the etiology. And I think that's sort of the conundrum right now is sort of how do we,
how do we tackle this? So I think our group really looks at, yes, addressing symptoms,
but also try to find the
underlying cause. And as Bruce was talking about, what we use is machine learning and AI to pick up
patterns. Single solitary lab values are, you know, quite frankly, very meaningless in clinical
medicine. We sort of have to look at different markers. We look at, speak to the patient, our
clinical examination history of the patient, and then we have to do
further diagnostic testing. I mean, that's the basis of clinical medicine. So what we do is we
look at patterns. Bruce's team has, and NCLDX has developed the immune subset testing, which allows
us to look to see if the S1 protein is from the virus, is present in those monocytes, as you and Dr. Patterson were just discussing.
Interestingly enough, you'll see on the bottom of that graph, we have the persistent
post-vaccine group, which unfortunately can be controversial. But it is important to talk about
these patients because we have not done any prevalent studies where we can't even comment on
rare or not rare or anything like that. We're just looking at mechanisms. And what was very
interesting because we saw a group of patients probably, I would say spring of 2021, that they
received the vaccines and had some persistent complications. Now, we expect within the first
week or two that most patients, you know, that have the fever chills, sort of an inflammatory response,
but these are patients at least 30 days after.
And we,
one of the patients that we tested that's in our paper was 245 days after
vaccination. We detected the S1 protein, sequenced it.
And we found the S1 protein mutant S1 and S2 proteins in the post-vaccine
patients. So, you know, we can't necessarily
comment on it. I know certain groups want to make grandiose statements and people want to
make grandiose statements and that's their prerogative, but we're just sticking to the
science and we're saying, look, this is what we found. We do need to acknowledge and do more
studies on these patients, but we found the S1 protein in them. And then there's another group
of patients they had long, they had COVID, got symptoms, got vaccinated.
They were told by, you know, there's a lot of media coverage about a year and a half ago
that getting the vaccine was, quote unquote, going to help you with your long COVID symptoms.
And unfortunately, what that ended up doing was people, a lot of people with long sort of post-COVID complications
ended up getting the vaccine and having massive setbacks.
So we have that group of patients.
And then we found another group of patients that they have the S1 protein,
but we're using machine learning and the modeling that we have, our algorithms.
We started to detect reactivation of some of the vector borne illnesses,
picking up possibly EBV, CMV, HSV, the herpes family viruses.
Another group of patients, the ME-CFS exacerbation.
They had undiagnosed ME-CFS.
We can pick this up.
And that research was very interesting because we were using CCR5 antagonists
in the fractal kind, like the statins.
And there was probably about, I would say about 20, 30% of the patients,
they were not having the response like we wanted it to.
And we sort of pulled them out and we looked at them individually.
And it's very interesting.
We also started looking at patients with Lyme.
They never had COVID, but they were post-treatment Lyme disease.
Also looked at ME-CFS patients with known history of ME-CFS.
Started looking at EBV, HSV, all a bunch of different groups of patients,
and then mapping it out.
And then we started to overlap it with our long COVID patients.
And it was very interesting.
We started to see a lot of sort of the overlap with, let's say,
Lyme caused by Borrelia or Bartonella.
We started seeing EBV along with long COVID.
So let me interrupt you. Let me interrupt. To me, it sounds like some major alteration of T cell
function. And I've started to hear that that is beginning to be documented. And so A, is that
true? And what is the specific mechanism there? And B, is the persistence of the S1 spike a necessary component in developing these things?
Or could anybody develop it?
Yeah.
So the answer to both those questions is very interesting.
We published way back in 2020 that acute COVID makes patients highly immunosuppressed.
We may have talked to HIV AIDS and its effects on the CD4 T cells.
In COVID, it's the CD8 T cells.
We showed that the numbers of the CD8 cells in acute COVID,
there was immune exhaustion.
And they also didn't produce
granulocyanzyme A,
they're killing all cancer cells
and virally infected cells.
So yes, there was supreme immunosuppression.
And that's what people don't realize. Acute COVID causes immunosuppression. And that's what people don't realize. Acute COVID causes
immunosuppression. If Lyme is still capable of replicating, that may replicate and exacerbate
Lyme symptoms. You know, frankly, it's a mess. And I think people don't realize
the effects on chronic that may still linger in patients. And I think that's
really important because of COVID. It may be exacerbation of ME-CFS caused by EV.
We spoke of, it may be Lyme is rearing its head in patients who were inadequately treated for acute Lyme. But the one thing that's conditions, Lyme, ME-CFS, fibromyalgia, is this endothelitis.
And I think that's where we've had tremendous success
treating post-treatment Lyme disease. And in many of the cases of ME-CFS, although ME-CFS tends to
be much more multifactorial in terms of the antecedent infection, then of course, Lyme or, you know, long COVID. So, but the bottom
line is they share this endotheliitis. And when we resolve that, that's when they start to feel
better. Because what Ram didn't mention is that in our latest, you know, fingers crossed, it's moving towards finally getting out,
is that we correlated the cytokine or inflammatory marker elevations with symptoms.
Our biostatisticians did an amazing job because that allows us to do precision targeted treatment. Because we know, for instance, interleukin-2 and TNF-alpha are so strongly correlated with fatigue.
The p-values are 10 to the minus fifth, meaning highly statistically. SCD40L and VEGF are highly correlated with the neurosymptoms, the dysautonomia,
et cetera, so that we know when a patient has a certain symptom complex and they have elevated
inflammatory markers of one kind, if we target those with drugs, and what people don't know
is CCR5 antagonists, they've already been shown in the literature to lower VEGF. They've already
been shown in the literature to, and we did, showed it too, they lower interleukin-6. It
lowers TNF-alpha because it changes the phenotype of activated macrophages, which produce IL-6 and TNF-alpha. So CCR5 antagonists shut that down.
It also lowers what we found is SCD40L, as well as statins affecting SCD40L and
VEGF. So we're very targeted approach to first treating the chronic inflammation with the assumption now that we have the correlations that by lowering those inflammatory proteins, we'll see we'll see improvement or resolution of the symptoms.
And it'll be permanent because we're actually addressing the cause of those symptoms
as opposed to just treating the symptoms themselves uh rom you want to go back to your
slides and i do want to hear a bit about treatment and before i do go on uh well actually before you
go back to size me cfs is chronic fatigue essentially um syndrome syndrome, right? And do we have any concern that this CD8 suppression
is contributing to the all-cause mortality increase
we're seeing these days?
Quite possibly it can, because the numbers I see,
the percentage of CD8 should be around 30% of your lymphocytes.
We're seeing things in the teens. In the early days of acute COVID, I was seeing single digits.
And I hadn't seen lymphocyte subset numbers that low, like I said, since I was working on HIV AIDS. And yeah, some people are talking about
whether or not acute COVID causes cancer. And I'm not going to address that because I'm just saying
the CD4 and CD8 T cells are part of the immune response against mostly viral infections and cancer.
So it's something that causes some concern on my part,
although we have absolutely no data in our own hands.
I have a hunch.
I had a hunch about the endothelitis very early on
because I could tell when I experienced it myself.
And there was quick early evidence that the smell problem was a microvascular thing.
And I have a hunch that it's going to turn out that existent cancers are spreading more quickly in the face of the CD8.
It doesn't cause cancer.
It probably maybe doesn't affect cancer surveillance
so much as once a tumor is established,
boom, it can explode with CD8 suppression.
That's my hunch.
Well, I share that concern,
let's put it that way.
Although, like I said,
it's too early
and we certainly don't have data to prove that,
but it's a concern.
So Rob, do you want to go back to your slides?
Sure, we can get that. I think the other ones, you know, Bruce can sort of jump in there,
kind of the ones from our papers. But yeah, Bruce, you want to talk about this one?
One of Bruce's favorite slides over here.
Yeah, I love these slides because this is, you know, from our first paper where we identified the symptoms for long COVID.
At the same time as others were starting to come out with long COVID symptoms.
And of course, there's fatigue, brain fog, post-exertional malaise,
ringing in the ears, et cetera. And then the red blobs are the symptoms of Lyme or post-treatment
Lyme disease. So they're almost identical. And then, of course, when we looked at more and more Lyme patients, we started seeing this endothelitis pattern in Lyme that we're now addressing therapeutically.
What are you guys doing?
What are the therapeutic interventions?
Let's stick with COVID, post-COVID, long COVID. Yeah. It's the same, you know, the basic two, we're actually, you know, really excited because
we're about to launch a randomized clinical trial, you know, in 2023 in long COVID with
this combination, but Moraviroc, which is a CCR5 antagonist, we use because
it really is theization of these inflammatory cells all over the body. Number one,
low L6, all the, and Ranty's for that matter. But interestingly, it also re-adjusts away from
a pro-inflammatory phenotype. So it's a great three-pronged attack on inflammation.
Without, if you were to immunosuppress with steroids or some other drugs, you would be contributing to this vicious cycle, which is the vicious cycle we're trying to break of infection, inflammation, symptoms.
Infection, inflammation, symptoms.
And then the statins are the ones that prevent these cells from binding to the blood vessels and causing endotheliitis.
If these cells can't bind through the fractal kind of receptor, they die apoptosis or death program, and they die. and we have a team assay that we've launched it
because we can look at patients over time on therapy and see the cells go down over time.
And like I said, these non-classical monocytes and intermediate monocytes are really a garbage can for virus and for bacteria and
carrying proteins all over the body and causing inflammation well after you think you've treated
the organism. And like I said, we think that's at play in Lyme. And we think that's certainly in
play in long COVID with the S1.
And now more and more papers are coming out, you know, basically corroborating our early findings of S1 being involved in the pathogenesis of long COVID.
And persistent S1 is a necessary and sufficient, well, necessary ingredient?
I think it's a part of it. I think the other part of it is getting the levels of these pro-inflammatory monocytes back to normal.
And there may be some disconnect between those two, but obviously lowering the number of
pro-inflammatory monocytes that combine to the blood vessels is a key strategy and
even better if they're carrying S1. And can people still come to covidlonghaulers.com
and get access to you guys or are you guys full up? No, we just launched in Australia, you know, so we're scaling, we're, we're live in the, in the EU,
we're live in the UK, um, we're live in Brazil and, uh, we just launched on Monday and, uh,
in Australia, obviously with large, um, lab partners, but in fact, there's a big announcement
with SynLab in, in, uh, the EU and Brazil, um, Helios in Australia. And then Igenix we're partnering with
in the United States. They're one of the global leaders in Lyme testing. That's how closely we
think long COVID and Lyme are related to the point where we've had a great relationship and now a great collaborative
relationship with iGenX. So that, you know, the minute we see a pattern that's suggestive of Lyme,
you know, we can then go right to Lyme screening, which is really exciting.
And so people were asking, how do I, you know, if my primary care person will not listen to me, what do I do?
So go to covidlonghaulers.com.
Guys, I got to wrap up in about five minutes.
I'm going to take some calls after we wrap here.
Dr. Yogendra, any last thoughts you want to push in here?
You guys have done a great job of reviewing and updating because this is fascinating where you are now from where I last spoke to you.
Yeah, I think we, you know, Dr. Patterson just really hit it on the nail right now.
You know, we've mapped everything out. We're continuing to map and sort of get an understanding.
We still believe that a lot of the sort of, if you want to call it the pure PASC or that long COVID, you know,
sort of, I don't want to say classical definition,
because we're still trying to define what long COVID is,
but you get a COVID infection, you develop new onset symptoms, and you don't have sort of any medical history from previous medical history.
We're very confident it's still the S1 protein that's,
that's driving a lot of the endothelialitis and the
vascular inflammation and we're studying the use of ccr5 antagonists and fractal kind but again not
everyone sort of has that um you know it's very interesting you know dr pattison didn't we didn't
have time to mention this but but the kids you know we we're working with pediatricians around
the around the country around the world and the kids are responding really, really, really fast within four to six weeks.
And that's because they have a, you know,
I make a joke that they're kind of pure blooded
because they haven't been exposed to a lot of the pathogens
as many of the adults are.
So I think that's kind of like another interesting
group of patients, population that we do need
to continue studying.
But if anyone is interested, we collaborate. Our
whole model is we're just basically data analysts. We're just collecting data. We work with your
physicians, your researchers, your specialists, and sort of work in tandem with those specialists.
So yeah, covidlonghaulers.com, we've got an amazing team uh amazing collaboration with global partners uh global labs
global um biostatisticians so um yeah i mean the next couple weeks we're going to be putting up
more and academics absolutely we have a couple of institutions in the united states that are
using some of our protocols and the assays um so we're super you know we're really excited
but we still have a lot of work to do and um you know hopefully in our next conversation we'll have more data to share yeah i feel i feel like it's coming into focus you know what i mean i i last
time we spoke i i felt like some of these ideas were there but it was much more of a of a fog
and now there's clarity on so many of these things, we have to be careful about not, I was just going to say,
we just have to be careful
about not politicizing long COVID.
You know, there's one group of,
you know, I see the discussions.
Long COVID is because we want to have
the lockdowns and the masks
and people are scaremongering.
Another group of, you know,
another group out there saying,
well, long COVID doesn't exist.
It's all because of the vaccine.
It's getting so politicized and it's not. Everything in medicine is, there's no conflict lines,
no black and white. We just look at data. We just look at different things and we don't let our
biases come into play here. And I think it's really important just as a medical community,
as the general public, to keep that in mind in these discussions.
Oh, yeah. Just, just,
I,
like I've been saying for quite some time is we used to call outlying opinions that we disagreed with.
Interesting.
That's all we called it.
They were called misinformation.
They were just called interesting.
Thank you.
And made me think about things,
maybe clarify my own position,
but I,
you don't have to agree with everybody.
And Bruce,
last thoughts.
Well, again, I think, I think, I think Ram's right.
Collaborating with the can and sharing the information.
I mean, people shouldn't forget that we are academics ourselves, you know,
coming out of, you know, I came out of Northwestern and Stanford and,
you know, it, those are our peers that, you know, that we're talking to.
And you know what?
The advantage of being in CellDx and being in a corporation is our ability, number one, to scale quickly and disseminate.
You know, we just got CEIVD, which is European approval for a long COVID test.
We're eventually going to take that through with our drugs in the United States to get approval,
not only of the companion diagnostic, but also of the drug regimen.
So we're going through it in all the straight and narrow paths that we go through as an industry through all the regulatory bodies.
But I think it's our ability to disseminate, which I think is exciting for us to reach more patients.
Well, gentlemen, I thank you always for coming by here and for the way for the work you're doing and be for updating us. So again, I suspect you'll have some more people stopping by with COVID long haulers. See you guys soon.
Thanks so much, Dr. Drew. Thank you.
Thanks, guys. And what we will do here is I'm, of course, out on Twitter spaces, and I see some of you already have your hands up. I will take a little break.
When we come back, I will take your calls.
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And welcome everybody. Let's get to the calls over
on the Twitter spaces.
Let's get Andrew up here.
Andrew, go right ahead.
We've got him.
Hello.
There you are.
What's happening?
Hey.
Hi, Dr. Drew.
This is very surprising.
Yeah.
This is maybe a little bit of a, uh, uh, out of the random area, but, um, with all the new
data coming out of a lot of different areas that we've all been affected by the COVID and
the lockdowns, has there been any look at family estrangements and the data that there's just been
a lot of people that have chosen it, just different sides.
Yeah.
Well, but I mean, that was already going on through the whole Trump era, right?
So I don't know how much different that is, but I have seen, I've seen people talking about that.
I can't, I can't quote it off top of my head about essentially domestic violence domestic abuse and strife in a
home system and home setting and it's of course up it's up all over the place right whether or not
it has a political sort of a core to it or the politics is just an excuse i i don't know i suppose
my question then my like question into that is how do people reconcile with something that is seems to just be
moving and just riling people up meaning meaning the information that's coming
through yeah the oddest thing is that medical information has a political tone
which is the oddest thing in the world it is you heard dr. Yogendra just talking about, I mean, that just has no place.
It doesn't even make sense that people who just learned how to pronounce a term have
an opinion about it that day or the next day.
And so I think the important thing is, I'm not sure this is the best advice, but to be
avoidant of this material and
just try to stay in, you know, really what's important in a relationship.
So much of what is going on is projection, right?
And so if, if you can address projection with sort of a calm, uh, query, let's say a calm,
uh, what's called wonderment like you know why do i wonder why
you would think that about me that's nowhere near what i'm thinking or i wonder why you know why
that troubles you so much and don't get into never the of course never get into arguing the points of
view you know the the literature is very clear on that you cannot change people's minds and even if
you change their mind in one narrow area they
sometimes will double down in adjacent areas that uh end up being kind of the same wow wow oh thank
you thank you for taking my call i've been a fan for a very long time all right good luck my goodness
uh this is uh christy who who is our biochemist.
Let's get Christy up here.
Christy, you were talking about low-dose naltrexone on the restream.
Thank you.
How are you?
I'm good.
I feel like we're going to do this Pulp Fiction style, and I'll explain things and then send you the study material.
Okay.
So I'm presenting it backwards.
There's been several people on Twitter that reached out to me after I was posting about low-dose naltrexone. And for those listening, PharmD was my first path in school, even though I didn't complete.
Long story, got in an accident.
But I worked for a compounding pharmacy pharmacy and then was two in the area. And we were seeing some things that are not being addressed from what I'm hearing of people who are
getting treated by some of the FLCC protocol. And I just wanted to chime in on it because people
have been giving up because they've had different kinds of reactions on low-dose naltrexone.
Is this a long-haul treatment or an acute COVID treatment? It's just a reaction to the low-dose naltrexone. Is this a long-haul treatment or an acute COVID treatment?
It's just a reaction
to the low-dose naltrexone itself.
But I mean, are they using,
why are they using it?
What is the...
Yeah, long-haul.
Long-haul, okay, okay.
Or COVID injured.
So it's both.
It's long-haul and COVID injured.
Got it.
Or COVID vaccine injured, rather.
So FLCC states to start at one milligram.
And some people, that's just still too much for them.
And they're stating to take it at night because you've got, you know, it inhibits the microglia cells, inhibits interleukin-6.
But then it also, as you know, it does the endorphin cascade where it blocks endorphins, essentially.
And then your body says, hey, you can't do that.
And then in response, your body makes double of the endorphins.
And then it also impacts the toll-like receptors, right?
But what some people, and it's not a small number, when they take it at night,
they're just too sensitive to the endorphin-type reaction.
So then it makes them feel jittery.
And then in some people, they're stating that it's almost like they're getting muscle rigidity.
It's so weird because we used to use naltrexone all the time before, gosh, before the shot became available. We would use it orally in much higher doses.
Do you want Dr want dr yo to come
back on no this is a totally different topic okay um and i almost the only side effects i ever saw
was some weird interaction with some of the ssris nobody ever had any they had sometimes some
hepatic stuff but nobody ever had any constitutional symptoms weird right yeah right? Yeah. I've had talks, I don't want to name them,
but they are out on Twitter using their real names who speak out about COVID. And like one of them,
she's a doctor who had Lyme's and she had the same complaint. She was a doctor. She was saying,
you know, she had to drop it down in titrates more slowly and not start at one milligram,
but start at 0.5.
And in some cases, people have to start, bless you, sub-therapeutic.
Listen, I'm super sensitive to medication.
I get it.
Some people are just more sensitive.
What did you think of what the long haul team was saying?
Amazing.
Right?
I was actually typing in the chat that I have a recent Lyme diagnosis from jogging out on the trails.
So they were giving some really awesome info. And this CD8 thing is something deep in that. The CD8, and
now you notice how everyone is sort of converging on endotheliitis. You notice how we're hearing
that from multiple different sources, whether people have been ostracized or not, people are
seeing endotheliitis all over the place.
And that does seem to be a major, major mechanism, both of COVID and vaccine injury.
And we have to figure out which is worse and how to, we got to get the relative risk of these things organized.
We just don't know.
It drives me crazy.
Do you think I was thinking about, I wanted to say one more thing about the LDN, but I was thinking about pacemaker cells and the people that had injuries or having myocarditis and they have issues with their heart rhythm.
Yes. impacted because of, like, that was the light bulb going on for me because of the endothelitis, because it's not the signal. It's not the, oh gosh, help with my brain here. It's not the...
I can tell you the two things that are being observed. I've seen three things. Somebody told
me that there is something about the AV node blood supply, which is not the sinus node,
which is where it's all starting, but the AV node that feeds into the ventricle. There's something about that node that may make it more vulnerable to
endotheliitis. I've not been able to confirm that. I can tell you some of the supraventricular
arrhythmias I have seen have all been generated in the high AV node, not in the atria as they
normally would be. So it's a weird nodal tachycardia, and the rate is much higher
than sort of the run-of-the-mill
supraventricular tachycardia.
And I'm hearing from cardiologists
that they're seeing scarring,
and then, of course, the scar can be a source
of irritation and irregular rhythms.
Now, is that scarring ventricular?
What's the difference?
All this stuff needs to be sorted out.
It's terrible.
Well, it's terrible
that we're not all rowing in the same direction
to just figure this all out. Just
figure it out. Let's just figure it out, everybody.
Let's just get to it and figure out the
relative risk. Let's figure out
what the best choices are.
Let's go. Let's do it. Look, COVID
is terrible.
No disagreement. The question is,
are there things we might be doing to prevent it
that might be making things worse? That's all. Can I chime in on one thing really quick about
the LDN back to that? I've heard that several pharmacists are not telling their patients,
if they can't take it at night, to try it in the morning. It's not going to be as impactful.
I think there's not as much impact on the toll-like receptors.
That makes sense.
But that you'll still get the interleukin benefit and the microglia inhibition.
That makes sense.
You won't have the added energy from the endorphin blockade.
But then also there's one other side effect that I was reading about that somebody I knew said they had, and they were being told that they were just stressed out and that wasn't true.
The kappa receptor on that opioid, some people get euphoria.
Yeah, kappa opioid system is a very special system.
And I don't think, well, I mean, who knows?
Naltrexone is particularly a mu blocker, right? And the, and the Kappa system may be getting some effect in the crossfire.
Maybe it's the upregulation of the endorphins. Maybe it's some blocking of Kappa somehow, but
Kappa, Kappa is very strange. It has sort of dissociative qualities. It's, it's, it's different.
But interesting nonetheless.
Christine, thank you so much.
I appreciate you always when you're listening and paying attention and sending me good information.
Nadine's up next here.
Let's see what Nadine has to say.
Nadine.
Oh, hey.
Hey there.
I have some questions or one question that you might know.
Is there a team of doctors that is kind of studying and working with vaccine injured?
It seems like here a lot of the doctors are kind of in denial and pushing them around.
I've had about 100 in Saskatchewan come forward to me.
And I'm wondering, is there a team we can send them to to get evaluated?
Is anyone doing that anywhere in the world?
There's a German team that just published a whole pathology series.
Let me see if I can find that very quickly for you.
And then the Long Hauler Group.
I think this Long Hauler Group is where a lot of this should go
because I feel like at least a significant percentage of the vaccine injury is
going to be this endothelitis and some of the stuff they are studying uh hold on here let me
see if i can find the study it's almost coming up this is a from heidelberg university of heidelberg
the let me see if i can figure out who the lead authors are maybe rom knows
i'm looking at it susan um dr campbell gets into it a little bit rom said to email their nursing
team okay how do we do that okay what we should have kept him on he's like he has good wi-fi okay
you want to bring him back in here yeah okay if he can hear us i don't
know yes tell him he can use the same link as before i'll bring him back in same link peer
reviewed study they are not giving the names on here let me just god darn it it's nursing at
immunotrack.org okay nursing at immunotrack t-r-a-c-k he'll be back in a sec immunotrack, T-R-A-C-K. With a K. K. He'll be back in a sec.
Immunotrack.
It's T-R-A-K, yeah.
I-M-M-U-N-O-T-R-A-K.org.
Nursing at immunotrack.org.
I can't get the name of this thing.
The lead authors, but it is out of Heidelberg, Germany.
I will tell you that.
And then Dr. Yogendra will be just on here in a second to talk to you.
You can bring him on the Twitter spaces.
He's actually on there.
He can raise his hand and do that too.
What's that?
He can come on at the same time.
He's on Twitter.
Bring him in on the camera.
Don't bring him through spaces, please.
Okay, V-Mix.
Yeah, yeah.
He was in on the Twitter spaces.
So hang on there, Nadine.
Let's see what we get.
Nadine, I'll tell you what.
I'm going to put you on hold and I'm going to get
somebody else up here while we get
oh goodness
here's a long hauler
I tried to get him to come
back before the question came out
meant Jew
hi there
I hear you
can you hear me now? I do. All right, cool. Yeah, sorry. That's my music's
name. My name is Kevin. We've actually spoken before on Adam Carolla's show. How's it going?
I have a question. It seems to me that everyone has their hypothesis of what this chronic fatigue
or post Lyme post COVID is. And it looks like
doctors kind of come to it from whatever background they're looking at prior to it
is kind of what they bring into the fray. So for example, Dr. John Chia works with enteroviruses.
I saw him and he was dead certain that all of my symptoms were caused by enteroviruses and then hearing the
other team of talking about microclots and uh yo gender uh yo gender and patterson have their
thing going on so one of the things i just want to voice is my frustration that it seems that
nobody nobody is really coordinating right and uh right looking at each other's studies and what you're talking about is this phenomenon in medicine is that when you're a hammer, the whole world's a nail.
Exactly.
That is a very common phenomenon in medicine.
Yeah, and I don't know if there's any way to fix that, if that's just human nature of how we look at, how we discover things.
People have occasionally tried to find ways to get integrated
science better as you get science better integrated it just does not seem possible
and my guess is as more and more of this information comes i mean this is just the
process as more comes out more will start to get shared they'll see overlaps and we'll start to
again come into focus which of these things are are you know sort of common features of everything yeah what could be discarded and what can be
included yeah you were talking i i have a question and then i'll i'll take my answer off the air
are there any teams looking for biomarkers that would indicate a endothelial fibrosis so a bunch of scar tissue and kind of a more uh not to scare
everybody in here more of a permanent yeah what are you experiencing what are you experiencing
so i i had covid in presumably i never tested positive for anything antibodies or pcr but i got
the the i lost my taste of uh or sense of taste and smell in March 2020.
And I just didn't get better for a couple months.
It was really bizarre.
I tried to exercise through it like I would with any normal cold or flu.
And that just walloped me.
And then a couple months later, I started getting all these neuropathies, POTS.
I remember people complaining about that.
Did you, have you had any nerve biopsies or anything?
Any pathology specimens done?
Dude, my neurologist won't do it.
Oh, we talked about this last time, didn't we?
Small fiber neuropathy.
Yeah, it's been two or three years.
My head goes there immediately, you know, a serial nerve biopsy or something,
just because you put it under the microscope,
it answers questions.
That's what you find. Yeah, they did MRIs and CT scans
and all that stuff
and blood tests, common blood tests.
I did the Patterson panel.
Everything looks pretty normal
except for kind of a low CD4 count,
which isn't fun.
I mean, I could talk about this for hours, but
my question is, is the endothelial... Yeah, let me get, I'm going to, I'm going to, good, I'm going
to have you again to come right in. There you are. So two questions. A, once there is endothelial
inflammation, are we seeing shutdown of arterioles? Are we seeing scarring of any type?
It's a good question, doctor. And I just heard
your listener just now in the comments. So it's very interesting. One of the things we always
talk about is up doesn't necessarily mean bad, down doesn't necessarily mean good. One of the
things we're seeing with some of the patients that are having, maybe I am always very cautious
about using the term cured, but actually having
improvement in symptoms and quality of life. As we start to see some of these inflammatory,
pro-inflammatory macrophage markers go down with the Rantese, interferon gamma. But very
interestingly, we'll see elevations in some of the vascular markers, the VEGF and SCD40L.
They actually start to go up, but the patients will say, hey VEGF and SCD40L.
They actually start to go up, but the patients will say,
hey, we're feeling better.
And that's because we're suspecting we've, you know,
I almost look at it like you're putting out the fire,
but you have to regrow the forest, right?
And I think a lot of these patients,
especially that first wave of patients back in March and April of 2020,
by the time they even got tested with us or other groups or even started any therapeutics, you're talking
about 18 to 24 months of them being chronically inflamed.
The question is, okay, we put out the fire, how much damage has already been done?
And I think that is a sort of a conversation, a difficult conversation to have with these
patients.
Is there a limitation in terms of the therapeutics that we have?
Well, look, if this is happening in the brain, which it is,
there is damage, right?
I just liken it to CTE.
It's like a head injury.
It felt like a head injury when I had it.
It felt like somebody hit me in the head.
And the brain, particularly
under the age of 80, let's say, and particularly when you're younger, extremely resilient.
Even all that early research on shrinkage, right, it's shrinking. No, that's all glial cells for
the most part. They regrow, things get better, the brain heals, even when it's smaller, it adjusts.
This idea of brain injury necessitating neurological symptoms
or progression, just not so. It's not so. You worry about it, and it's certainly a risk factor
for those things, but we don't have to be in a total panic about it. Just think about it as a
head injury. People live nice, long, healthy lives after a head injury. It's very, very similar to that. The other question was, why can't we share info better? Why all these different camps?
I think beta-hemlock strap or something came up a minute ago as the cause of, or what was it?
What did he say? Some other bacterial organism was the cause. How do we get everybody together
and get the overlapping data together?
It's a good question, Dr. Drew.
It's something we've talked about amongst our group.
There's more of a competition than collaboration in this not only long COVID space, but just COVID in general.
You know, I think everyone has whatever motives or they want prominence.
I'm not going to sit there and comment.
We can speculate but you know the interesting thing about our group i think a lot of times people see bruce and i kind of on on podcasts
and kind of being on the forefront of this talking about our program is we're actually our collaboration
is huge um it's you know we don't treat we're not writing prescriptions we're really just looking at
data and looking at patterns and suggesting i think think this looks like this. I think we need to do a diagnostic testing to further confirm it.
Because you can't look at one cytokine or a couple of them and say, oh yeah, you have long COVID,
or you have this. It's saying suggestive, let's do some confirmatory tests, whether it's getting
immune subsets, looking at S1, whether it's doing further testing. So I think, yes, I think maybe
in the social media space, there does seem to be some sort of competition, which our group has
talked to everyone. We read the research. One of the interesting things coming out there is
the whole theory about, is there a replicating virus? There's another group that's, they're
looking at some of the anticoagulants. We might disagree.
We might professionally and respectfully disagree. And I think that's mutual across the board,
but I think something, so a lot of this is sort of pushed out on social media when in essence,
we are kind of all in really working together. And I think a lot of people do have the best
interest of patients and the general public. But I just, again, as I mentioned earlier,
just not letting biases and not just, you know, well, one of the concerns I have is everyone,
you know, we lose our principles of medicine and just that's not automatically suggest that it is
all due to long COVID. There could be other things taking place. We don't want to miss
cancer screening, patient doing full cardiac respiratory
workup. Once we rule everything out, then we can start looking at some of this inflammatory
persistent issues that are taking place. So I think it's very, very important that patients
get proper care and not just jump to the conclusion that this is all S1 driven or Lyme or anything
like that. We have to be very cautious and still keep our principles of medicine and how
we practice.
All right. Let's get a caller up here. This is a Kaysville.
Get her up here.
Kaysville. Hey, I think it said, Hey, Hey there.
How's it going? Good. What's happening?
Oh, a long time in the well not long time recently more recently now but a long time back in the old days i remember in the 80s
listening to you maybe early 90s way back a little i'm a dentist so i've i've kind of seen this from an interesting
um aspect in that so i'm i'm in salt lake city and my office is right below the
the major medical center in this in the state of utah and I see a lot of other healthcare professionals from the center
in my practice. And one thing that I saw right off the bat or that people would come, other doctors
or nurses would come and talk to me about was things they were concerned about but that they didn't dare to their fellow
um professionals about things that they did not agree with and it was it was this
really just massive fear to speak out this is still still going on. This still goes on.
And that was from very early on.
Yeah.
Very early on.
Listen,
that's why we got into such a mess.
And with masking.
And I,
I can remember sitting in class and in second year dental school talking about
masking and why we're wearing a mask and never was it ever said to stop respiratory viruses
right that was never the point right um blood-borne pathogens are focused and then also
keeping the surgical site clean yeah nothing to do with respiratory viruses in in any way shape
or form correct so i it's just very very early I started, I've heard you say the same thing.
Like what is going on here?
And I'm a, and I'm a dentist, right?
So I'm not, I'm not an internist, but I see that where I see that the different is I see
these people every six months and even through the pandemic, I did not close my practice i we canceled unnecessary work but we went to work
and waited for people to to call with problems with pain you know these people couldn't go to
the emergency room for dental issues all they're going to get is an antibiotic and sent out the
door well then if they even get in the door during all that.
Exactly.
And then they have to deal with days of intense pain until an antibiotic might help.
But that's besides the point.
There's so much I could talk about.
The main thing I wanted to ask you about or kind of discuss is, very, as we're going through, um, our normal exams,
I'll have patients want to ask me about certain things that they won't ask
their healthcare provider because of the same environment that,
that I talked about earlier, that's amongst the professionals,
patients feel the same thing. And, and, um,
I remember one in particular, she had the vaccine and shortly after
she broke out in hives that they could not figure out. And they couldn't, the only way they could
control was on steroids, like constant steroids. And then they tried to transition her to, um, like Benadryl, uh,
Benadryl would help, but it wouldn't quite manage it like it needed to. And she was looking all over
and nobody could ever give her an answer of what was going on. They couldn't find any allergy or
any reaction. And she would ask them and say, well, could this be the vaccine? And immediately it was always absolutely 100% no.
And when I saw her, I said, you know, I'm a dentist.
Take that for what it is.
But my understanding is there's no way to give informed consent in this circumstance.
And there's no way for them to be able to tell
her for sure no that's not it you know we're we're just undermining and alienating so many people
and it's it's really frustrating well i am with you it's why i've been doing these these uh
interviews particularly on wednesday we're bringing people in and trying to get at the
material that has been suppressed so I just quickly pulled up uh cytokine production and CD8 T cells
and the peripheral blood mononuclear cells in idiopathic urticaria so hives from CD8 suppression
so there you go so COVID I I've seen hives from COVID, so it makes sense to me that it would also be something from the vaccine.
So there is a possible mechanism.
Yeah.
One other one.
This is just last week.
Patient that I've had for several years, young, healthy patient, female.
She was pregnant during the pandemic.
Now her child is one year old.
She was showing me pictures of her and we were talking. I noticed immediately her left eye was, you know, not to the left, not centered. And she could tell I was looking. She said her eye,
she's had a problem with her eye and
I said well what do they know what's going on they said well actually we're just finding out
that they they think that she had an in utero stroke um and this is a one-year-old child
and um they had no idea at first as she, as she's gotten older, they started, her eyes started to deviate. And then as she started to crawl her whole left side, it doesn't work. I mean, she basically belly crawled and has to try and get her left leg and left arm to work goodness so she told me this and she said an in uterine
stroke and i said oh my goodness that has to be rare and she said yes and i don't know if this
is right i think i could have misunderstood her she said um it could be as rare as one in a million
or one case in the country a year is could that be correct that seemed crazy to me i'm gonna look it up in so she was
vaccinated when she was pregnant okay so yes i'm getting susan jumping right to it i'm on this
and this individual she's a medical researcher and has done cancer research in the past. And now she, now she's not currently in the field. She's
at home with her daughter. But so I wanted to approach this subject. So I said, huh, I'm
curious. Are you vaccinated? And she said, oh yes. And she immediately, her next sentence was,
I don't want to blame the vaccine. And I said, oh no, no, no, no. I said, I'm not saying that. I said, I just talked to a lot
of people every day. Uh, and I see, I've heard a lot of different things and I'm just curious. I'm
just trying to understand. And she said, yes, I'm vaccinated. I was vaccinated in the third trimester.
Interesting. Uh, one in three, one in 3000 to one in 4,000 is the incidence.
So not nearly.
Not one in a million.
But we'll see if it changes, you know, with everybody being vaccinated.
We'll see.
And then the really crazy thing is there are no rush seemingly to differentiate COVID, post-COVID injury versus vaccine injuries.
This is not being actively worked on.
So that's what bothers me.
But she told me she had not had COVID at the time.
Again, in utero strokes happen.
Whether it's vaccine-related or not,
we'll see if it goes up after a while.
All right, my friend.
Thank you for calling in.
Appreciate it very much.
Somebody asked earlier if you had the vaccine
and you felt injured, Ram,
you were going to answer where to contact the nurses?
Yeah, we've been looking at this for the past 18 months, patients having some post-vaccine complications.
It's interesting.
There's a lot of discussion.
There we go.
So I was just saying before I just lost you for a second, Drew.
There's been a lot of interesting discussion lately about the myocarditis and the pericarditis,
some of the cardiac inflammation and the vascular inflammation after the vaccine.
You know, interesting, what we're seeing is really,
we're not seeing those patients in our program, because I think a lot of those patients,
they're more acute, they're ending up in the emergency room or immediately with their primary
care doctor. We're seeing patients that three to six months after the vaccination, that they're
experiencing more neurological. So they're coming to us with the fatigue the tinnitus uh the neuropathy peripheral
neuropathy um some of them with with pots which you know i think it's it's got it's really an
autonomic dysfunction in my opinion but what pots is more less than the cardiac stuff so we're
really approaching sort of months maybe even a year down down um after vaccination and we're
seeing that after the first second the booster, that's what we've
been seeing, some of these issues. So what's interestingly, we're detecting the S1 protein.
We can't tell. I know someone, the dentist just on said, well, that one patient said,
I absolutely know I didn't have COVID. There's really no way that we can say 100% definitively you did not have COVID. You could
have a subclinical course of it. You may not have made antibodies. It might have worn off.
We've done what we've done in our vaccine paper, which we're resubmitting it. We went through a
little bit. We got some feedback from the peer review process. So probably in the next week or
so, I'll have that paper out. We screened the patient using negative nucleocapsid and the T-detect, which still is not
100%. That is limitations of the studies. But basically, what we are seeing is we are detecting
the S1 protein. We did sequence it in the papers. Bruce and our team did that. So that's what we
are addressing. Now, interestingly, again, we get this question quite
a bit. Are you guys using C-serum 5 antagonists of statins? Hey, for some patients, all it was,
was I just did a consultation, a pilot from Europe, major airlines. I'm not going to say
which airlines. He's been flying. He got the booster a few months ago, maybe about eight
months ago, and had severe neuropathy, tinnitus, headaches, fatigue, we just put him on a statin.
We recommended a statin and I believe a, I think it was either Plavix or an aspirin.
I can't remember exactly.
And he said in six to eight weeks, he felt better.
And this is someone that had vaccine complications.
So, you know, again, it all depends on the patient.
It depends on the history. It depends on the comfort level of their physician. It also depends on the country that they're in and what medications and things are available. So again, there's no like this one thing to go and let's go get these, you know, this one magic drug. that have been through our program that have maybe gotten tested that have not responded to
the medication. There's no one in clinical medicine that has a hundred percent success
rate. I always tell patients this, if anyone says they have a hundred percent success rate,
they should be selling used cars. So again, you know that we don't have that. And we do have some
patients that got, had issues after the vaccine that have not responded to steroids or CCR5
antagonists. And we're like, okay, okay ivig there is uh happy bag treatment i
mean there's so many different things all right we don't really have quite an understanding and
what we've been doing and bang your head against the wall is saying we need more help we need more
focus on these patients um and rather than saying it's weird to me there's not an urgent
you know this is the part that I'm confused about, again,
why our system isn't gearing up to manage this as opposed to pretending it's not happening
and focusing on more vaccinated people.
It just seems, it seems, let's keep vaccinating the risk population.
I'm all about it.
But let's understand what's going on everywhere else first, maybe.
Yeah, I think we just need more focus and
research into it. And just saying, look, it's not an anti-vax, pro-vax. We've never had medicine
like this. We always ask questions. People always have side effects. Now, risks of those vaccines.
I mean, I don't know what the percentage is. I say rare or not rare.
I mean, we can have the debate.
I don't have any data to support that.
And I think that's where now you have
one group of patient people out there saying
everything's caused, everything is the vaccine,
everything is all sorts of problems.
And another group saying it has nothing to do with it.
These patients, it's all in your head, go away.
That's a little bit, it's somewhere in between.
Let's come together.
Let's try to understand and help these people let's worry about helping people how about that
not worry about who's right who's wrong but uh all right my friend uh as always as i said great
to see you and can you give them the email address again for if they have for the nurses
they want to reach out our nursing team is is nursing at immuno i m m u-M-U-N-O-T-R-A-K.org.
Or you can just go to covidlonghallows.com.
You'll just see our research, the work that we're doing.
And if it's something that you feel like you might want to explore, get more information,
you can just reach out to us and get the testing done.
Caleb, did you catch that?
Can you put it up there on the screen?
Yes, I'll actually also put it up on the website too.
The nursing one?
The long one? the long one.
I didn't type it down, so I don't want to type it incorrectly,
but if they go to the COVID long haulers.
Can you find the link on COVID long haulers?
Yeah, the email is on the website.
The email is on the website.
And patients, their physicians,
I think it's also very important that their physicians are also included in
those emails too.
We're happy to talk about the research and things that we're doing with
them.
Okay. Well, very impressive. And as always, I, I learned something every time I talk
to you guys. So, uh, as always, thank you and stay in touch. Okay. Sounds good. Thanks. Thanks
for coming back on. Good to see you. Thanks guys. Uh, all right. I got to wrap everything up here.
We appreciate the calls. We appreciate the participation. I appreciate the long hauler
guys coming in and giving us an update.
Yeah.
If, you know, I would recommend people, I've learned a ton talking to all these different people.
We're going to get repeats.
We're going to get Paul Alexander back and Ryan Cole back and see if there's much the
way we bring the Long Hauler guys back.
I mean, more information.
There's more things to learn.
I learned a little more about the physiological observation today.
I knew some of this stuff was in the making last time I talked to them. Now it's more clearly the case.
Well, I appreciate that YouTube is letting us keep it up and we have Rumble and we have platforms
that allow people to watch you. But there was a really significant piece of data here today,
which was about the CD8 cells is a that is a very concerning piece
of information and uh i i have no doubt that it's contributing to the all-cause mortality problem
my concern is though that's not the only part of the story obviously the lockdown
the lack of screening and then i'm worried about the vaccine
uh hanging with all that stuff was way over my head so well good you like that yeah i do hanging
with us and we'll try to keep uh the data coming and i appreciate our fans and for listening and
lieutenant colonel theresa long coming in on december 21st we have a simulhatra you've seen
him in great britain making a lot of noise in the parliament there january 3rd megan kelly you
forgot steve kirsch steve kirsch coming in next week, right after Teresa Long. Byron Brindle and then Ryan Cole returns. And Paul Alexander got him on
the schedule again today too. And December 22nd is my birthday. So buy my favorite package at
GenuCell.com. Okay. Or get me some gold. How about that? And mixed into that calendar will
be some caller shows as well that just aren't on the schedule yet. Yes,
of course. Of course. In fact, the next
show will be a strict caller show, which
is next Tuesday, the 20th. Correct?
I believe so.
Everybody? Okay. We will see you then
on Tuesday, 3 o'clock Pacific.
Ask Dr. Drew is produced by Caleb Nation
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