We know that vitamin A, vitamin D is zinc. Those are really important nutrients for immune support. People that are low in vitamin D are more susceptible to getting other types of infections. We have zero evidence right now that they work for Covid-19.
Welcome to the Biore Reset Podcast. This is my friend Dr. Helen Messier. It's Friday, thank God. And uh, we are both, uh, drinking tea. We are drinking tea. We're comparing what our cups say. Compare What is your cup? I think, I think dot, dot, dot. Oh, that's a good one. In 1837, mine says, life is sometimes not to risk more dangerous than adventure.
It's like some kind of English interpretation of a Chinese proverb. I love it. But, um, so that's maybe a great place to start because we're trying to figure out what to do and we're trying to, we're we're talking about risks and how to manage this chaotic situation. How to, how to understand research. And I think Helen is a great voice in, in helping to talk us.
Talk us through that. Um, do, just from the research perspective, we were talking about that and peer reviewed research and, and how as physicians we. We contextualize and interpret research. Do you have any thoughts you'd like to share about that? Yeah, so I think that's a really good question and um, you know, in light of all of the papers that are being published right now around covid, I think we really have to look at how research is done, what it means.
You know, like I said, we could talk for hours just on research and how it's done, uh, alone. But in general, if we look at before the pandemic, how was research done before the pandemic? It was done where, you know, scientists, physicians, they would either do, uh, research in the lab or. Clinical research, uh, we would cap, they would capture the results.
They would write it up into a paper, and then that paper is submitted to a journal. Now, when the journal gets it, they take the paper and they disseminate it out to other experts in the field. So that's what we call peer review. So that peer review process, these other experts look at, they read the paper, they, you know, punch holes in any lo logic flaws, in any methodology flaws, um, and ask for clarifications, potentially ask for more, uh, data to be supplied.
That's really the sound robust peer review process. Once that paper has passed the peer review process, then it's published in, in the journal, whatever journal that is. So usually when we see papers published, we can, you know, count on, you know, at least it's, it's gone through a, at least a. Some due diligence, right?
To show that, you know, the findings are fairly sound and other experts in the field think that this is suitable for publication. What's happening now, because we're in the midst of this pandemic, we have this crazy amount of need for information and this need for research, and a lot of those rules have been, uh, kind of lightened up on, uh, you know, we're doing a lot of research very fast and we're putting them in what we call pre-publication.
So these are pre preprints. They actually are being published online before, um, they've gone through that peer review process. And what's happening is that, you know, the press, other people are seeing these, they're picking them up and they're reporting on them. So it could be a study with very, you know, poor methodology, a terrible study.
Yet that gets taken as, oh, this study said this. And so I think that's happened a number of times already in, in different medications that are being used to, you know, possibly treat, uh, covid. And, and then, you know, I wanna also, I. Kind of fill in and step back from that and say, you know, what's the type of studies, you know, there was a really beautiful study that, again, put in pre-print on online, uh, looking at, um, what we call in silico data.
So it's, it's kind of in silico is just kind of in the computer, right? Let's look at what we know about the human interact and the virus interact, and how do they connect to each other. Are there any, uh, places or drugs or supplements that we see could fit and interfere between the virus and the human?
And, you know, some, and that's like using AI right? To Yeah, exactly. It's, it's using ai and so we call it kind of silico, uh, evidence. Now that's, Awesome and it needs to be done, but it's really all about generating hypotheses that then need to be looked at in more in depth. You can't just use that kind of data and say, yes, everybody should be on this particular drug if it's found in that kind of study.
Another kind of study that we see a lot of are in vitro studies. So studies that are done in, in vitro essentially means outside the body in the test tube. So, you know, you're looking at, uh, models of, you know, lung epithelium. In, you know, you grow models of like the tissue culture and you grow it in a Petri dish and then you add different things and see what happens to that.
Or you add a virus and then see what might inhibit that virus in vitro. Okay? So that's very different once again than actually using that substance in the body. So it's another step in the process of discovering if that is a good substance to use. Um, and, but you can't take it at face value. You know, taking something, adding it to a, a Petri dish is, has a very different effect than if you swallow it and it, you know, gets, uh, used in your body with all of the other things that happen in a human body.
Another type of testing and that's done is in animals, right? So we are, we're familiar with rats and mice. Again, another important step in understanding things. But rats and mice are not humans. And so even though we get a lot of insight in animal studies, oftentimes, and it's happened time and time again, where we find something in an animal, get very excited about it, and we try it in a human and it just doesn't work the same.
So, you know, we're very different, uh, from mice. And so, and then we get to the human clinical trials and there's a lot of things you have to look at in terms of how the methodology was done. Was it observational? Was it a randomized trial? Was it a blinded trial? How many people were in it? Did they appropriately track the endpoints?
So there's a lot of, um, you know, definitely a lot of different ways of doing human research and not, again, not all human research is the same. So it's very complex. And, and now when I think the world is looking on anything that's published on covid, I think a lot of people don't understand or all of the differences between the different types of research.
Okay. That's a good one. So then that's our framework today, that we are gonna start to then have some conversations about some of the mm-hmm. Issues that are going on and know we've got all of these different levels of evidence. Mm-hmm. And so then we have to try to, and, and so what we're basically faced with is trying to make judgment calls about what to do.
Right from very different levels of evidence and then trying to put that together and interpret it. Exactly. And that that's exactly what we're facing. And you know, we are in a very high need. We need to use something. And so sometimes in these cases we use information from say, lower levels of evidence because it's worth a try.
So that brings up the other concept that we use in medicine a lot is what's the risk and what's the benefit of trying something. Now if it's uh, a very potentially high benefit, meaning someone's in the I C U and they're going to die unless we try something, then we're going to be a lot more lax in terms of what kind of things we'll try.
They might not have sound evidence around them, but we're gonna try it anyway cuz we wanna save that person's life. Right? And now then the same idea is what are the risks of that? Uh, so now you have a healthy person. And they might have a few symptoms, but they don't have any underlying health conditions.
And, um, you want, you know, they get, they get the symptoms, but you wanna prevent them from going on to get a further, you know, end up in the ICU u you don't want them to die. Are you going to use that same drug that you might have used in the ICU to save someone's life with someone that's healthy, that could potentially cause a lot of harm.
Okay. And, and I think everything we do has to be a balance of what's the potential risk and the potential benefit. Okay. I got, I have a good one. You're gonna love this. So, so then what? So it's so great because today I did a podcast with my good friend Matt Dawson Uhhuh. And so he, he has a practice that's kind of similar to ours and, um, Uh, we all kind of have to some extent, a little bit of a concierge practice that is wellness based and probably we've all seen some of the same people, uh, for sure, a hundred percent.
We've all seen same, same people. And so we have, he's, he like you, is also interested in genomics. And I can say that Helen's one of the smartest genomics people probably out there. And, and tell, tell people a little bit about your experience with, uh, with Craig Benner and what you did there. Yeah. I, um, worked at, uh, human Longevity, uh, Inc.
Which is a company that was founded by, uh, Craig Benter was one of the founders. He is, uh, for those of you who don't know, Craig is well known in the scientific world as the person who first sequenced the human genome. And so I had a, a very privileged, I had the opportunity to work at h l I, you know, under the leadership of Craig.
And, um, and not just Craig, but I worked with, I think, some of the brightest minds in the biological genetics world. I was very, very privileged to be able to collaborate and work with, with all the people. And obviously, you know, when we all get together, there's a lot to be learned from each other. Okay, great.
So then my friend Matt, uh, is an ER doc Uhhuh, and so he is in a small town in Kentucky. And so basically all the er docs that work and pick up the ER shifts are older guys and a bunch of 'em are immunocompromised. And so basically nobody's agreeing to work. And so he has 20 shifts next month that he has to work.
Wow. Just because in his community. Yeah. And so then we, it's worth a listen for people, but then what, and I, I, we had this real procedural podcast because he told me a story about a woman who was coding and he ran in and he couldn't mask ventilate her because if he did the mask ventilation will spread viral particles to everybody in the room.
And so he ran in and did a video laryngoscopy and intubated this woman. And saved her life. Wow. And so then what I'm gonna do is I'm gonna compare and contrast cuz that we, we, it was really a procedural, how do you manage the logistics? Yeah. And so then it's gonna be interesting because, so every day, for the next month and at least for 20 days, and some of these are 24 hour shifts, he's gonna be continuously exposed to people who are positive Right.
And then intubating 'em and there's probably no higher risk Right. Exposure than intubating somebody who's got mass amounts of virus. Absolutely. And so then we, um, and so then what I'm gonna compare, and, and so I said there's kind of two conversations. There's this, what do you do at the moment? Like he was making a judgment call, do I mask, ventilator or not?
Based on who's in the room. And then were, he also had to make a judgment call. Do I take some kind of form of prophylaxis? Like a supplement or like hydroxychloroquine or do I not? And so then we kind of talked about that. And so then what I'm gonna do is I'm gonna launch, well just go, let's go ahead and launch into the hydroxychloroquine conversation because this is a drug, uh, a pre-publication came out suggesting that it was good.
And ta tell us about that research because I think it's interesting to hear kind of the peer reviewed academic kind of take on it. And then we're gonna compare and contrast that to a guy running around the hospital intubating people that are Yeah. Loaded with virus in their lungs and trying to decide what to do.
Yeah. And if we, uh, can we do screen sharing on here? I would love to, um, show sort of some of the critiques of that paper. So I think the paper that you're referring to, um, and I may not get it up in time, uh, but the paper you're referring to is one where they, uh, took, uh, patients coming in, uh, to an ice, to a, to a hospital.
And they either gave them, you know, hydroxychloroquine, hydroxychloroquine and azithromycin or, um, a control group that didn't get that. Mm-hmm. And um, the outcome of that was looking at viral load in a throat swab. And, and so, you know, how did the treatment actually reduce the viral load in the throat swab?
So, you know, you could right off the bat, um, argue is that the right outcome to be looking at the amount of viral load in a throat swab. You know, it does. And cuz we don't necessarily know whether that viral load actually has anything to do with overall outcome, you know? So that I think in and of itself is something that we, we can argue with.
But if you give the, sort of called the secondary endpoint, right? So we're looking at viral load rather than, you know, did they die? Did they get better? That's sort of the more relevant outcome. And, um, they ended up, uh, basically the paper published saying that it, the, the treatment of hydroxychloroquine and azithromycin reduced overall viral load at a certain day and I can't remember the exact day six or day seven after treatment.
And, um, that was, you know, a big, uh, A lot of social media picked up on that. A lot of, uh, people said, let's use hydroxychloroquine azithromycin based on that study. Now some of the problems with it are, you know, sure. They used low numbers of people. I think 26 were registered in the treatment arm. Um, the control arm was actually recruited from some people in a different hospital.
So some in the same, some in a different, so right then, and there was treatment different in that other hospital. So now you can't compare apples to apples anymore. We're now comparing, in a way, apples to oranges. And um, and then what happened is a number of people. Uh, they couldn't follow up for those people.
They couldn't get the final, um, swab for the viral load because they were taken out of the study. And if you read why a couple were transferred to the I C U, one of them died and, and they ended up not including those people that were in the treatment arm in the results of the study. Now, clearly if they did, it would make the treatment not look not nearly as good If, you know, three people, you know, people ended up in the ICU because they, you know, they were on that treatment arm.
So that's just some of the sort of controversy around that particular study and, you know, It's currently kind of going through peer review now, because a lot of people are commenting on it, which is the process that's supposed to happen, right? This is the idea that allow other scientists, other researchers, other physicians to comment on it, punch holes in it and, and cease.
But what's happened is it ended up getting spread to the world before that could happen. Right? So then, but then even now it's kind of interesting because here, here we are and, and so we may be punching holes, but there may be still some benefit to it, right? Yes. I'm not saying So we're punching holes in the study.
That's correct. We're not saying just because there was problems with the study, uh, also doesn't mean that there may not be benefit. That's exactly right. Exactly. And so it's uh, it's like the most interesting moment. To me of our career because mm-hmm. Now we're at this. Interesting, it's like peer review real time.
Yes. It's like it goes out and then obviously cost to run on the hydroxychloroquine market. So you can't even, you can't even get a prescription for it if you wanted to. Right. That's right. Um, and which is a problem even, and you might be on lupus, have lupus or rheumatoid arthritis, and you might be taking that medication, you can't get it.
So that's a, it'd be interesting kind of comment. Mm-hmm. Um, which is unfortunate. Um, and, uh, and so it's, it's, and so, and, and we are gonna, we are gonna play this forward, but it was interesting because my friend, you know, India, I was telling you on the phone before we talked, India is actually giving hydroxychloroquine to every healthcare worker who's, uh, dealing with this.
And so my friend Matt, today, we talked on the phone. One of his best friends is the ER doctor in New York who's pregnant. Yeah. And she tested positive. So then, and I think that probably most of the ER docs and most of the anesthesiologists in the country are gonna end up testing positive for this probably.
And so it's interesting then to, to take that back. Now you have these people out on the front lines that are in between a rock and a hard place. The science isn't perfect. Mm-hmm. We're punching holes, but we're trying to also understand, we're trying to help them, right. Make their judgment calls. And then it was interesting because, you know, this is a, because this jumped from animals, our immunity is not as good as a normal flu.
Right. And so it was his conversation and I just, I loved the attitude, but it was almost a little overwhelming to hear because. The attitude of the ER doctors is kind of like, well, if you get sick, just hope that you'll get better in a week or two. And then that you can go back to the front lines and then release all the people who are getting sick.
Right. And then hope that you have a month or two of immunity. Mm-hmm. Which is kind of like a crazy thing to say. It was just, it was just like, I've been kind of overwhelmed by that idea all day. And then he said, and, and this was, and it's just interesting to think of different specialties. Mm-hmm. Because then he's like, but then what's gonna happen is everyone in the ER is gonna be positive.
And so then we're gonna go to, just go to, we're just, it doesn't ma cuz right now the idea is don't go if you're positive. Mm-hmm. Cuz you're gonna infect everybody there. Right. Then pretty soon what's gonna happen is everybody's gonna be positive. Right. And so then all the doctors are gonna be positive and they're gonna be, they're just gonna go to work anyways because there's people coding in hospitals and there's not gonna be, I read a post of an anesthesiologist that had said that he had worked 5 24 hour shifts in a row.
Wow. And that's just so, yeah. That's crazy. That's crazy. And, you know, that's, I, I can un totally understand that attitude. And part of it is, you know, other countries, for example, have created dedicated C hospitals. That everybody in that hospital is positive so that you don't have to do that same, oh, I'm going to, you know, we have to protect the other patients from getting it, you know, everybody in that hospital and, and you keep non covid patients for all of the other things in different places.
So that's, you know, one way to address that. We're not currently doing that in most of our hospitals right now. Um, but, you know, doing 5 24 hour shifts, there's no better way to make yourself more susceptible, as we talked about earlier. I know, I know. I don't know this person. Barb. Barb just showed it to me.
Yeah. You know, lack of sleep makes you much more susceptible to, um, sick. I know. Sick. And it's, uh, yeah, unfortunate that our healthcare workers are being put in that situation in the first place. Now, now I proposed, I gave you a little case study and it was just a made up case, but I said, okay, I have a 50 year old woman in.
In Santa Clara County, that's where we are. Right? Mm-hmm. Which is, and let's say she got a sore throat and a fever, and she is worried that she's got covid. So then what does she do to get tested? And then how do we manage her? Like if I gave you that case and we can spin it around. So, uh, uh, yeah. Yeah. What would, what would you, and, and you told me a great anecdote about a friend of yours.
That's right. Yeah. The, so, you know, the testing is still not very readily available for, you know, to test anyone who wants to get tested. We're still at a point where you have to meet certain criteria in order to get tested. So healthcare workers clearly are on the higher on the list in order to get tested, cuz we wanna know if they're at risk and gonna spread it.
Um, uh, if you have an underlying condition, uh, you know, like we talked about last time, high blood pressure, cardiovascular disease, diabetes, the high risk people, um, are more likely to get tested or they should be tested. And then, and then there's everybody else. Like, you know, so my question is this case, this 50 year old woman, would, you know, does she have any underlying conditions?
Right? Does she have high blood pressure? Does she have diabetes? That, so the answer always, as we talked about before, is it depends, right? Yeah. I gotta get the context. It depends. I have one, I'll wear it next time. I, okay. Yeah. So we have to, you know, understand the context and, you know, my feeling is if there was enough tests, everybody should be tested because that's the best way that we can trace what's going on and actually be able to control, um, the virus and the spread of the virus is by, is by testing everyone and seeing what it's doing.
Mm-hmm. Unfortunately not at that. We don't have the ability to do that right now. So tests are being rationed to the higher risk people, the healthcare workers, the higher risk patients. Mm-hmm. Um, And so, uh, yeah. So what would we do with this lady? You know, I would love to be able to test her. Um, but most times people are told, being told to just quarantine yourself.
Stay home, don't spread it and, you know, monitor your symptoms and if your symptoms got worse, then call someone and, you know, go in the hospital if you have to. It's not a perfect answer, and nothing about what we're going through is good or perfect or easy. Uh, you know, on the other hand, yeah. So that's, that's kind of the testing question.
So to get back to my friend, that's exactly what happened. My friend, um, young, healthy male, uh, he. Came down with very classic covid symptoms of fever, a cough fatigue, but he doesn't have any underlying conditions. He actually reached out to his physician and was kind of sent an email back, said, you know, are you, if, are you in one of these categories, healthcare worker, do you have a chronic condition?
If not, you know, just quarantine yourself and here's how to wash your hands. Here's how to separate from family members. It was really, wasn't overly helpful, at least what I saw. And you know, I think this is the response a lot of people are getting when they, when they get sick right now and they're reaching out and there's nothing, no help for them.
Yeah. Isn't that crazy? It is crazy. Um, okay. You can critique my answer. I'll, you can critique my answer. So now I know of some cases. Mm-hmm. I know some cases of people who were in. Either in hospital or in ICU and deteriorating. Mm-hmm. And someone brought them hydroxychloroquine and azithromycin and I know I, I know of a couple cases where they turned somebody around mm-hmm.
That was circling the drain. That's a kind of a, kind of a house of God type of comment that, that sometimes doctors use that I probably shouldn't use. Um, but, um, so I would like to prescribe hydroxychloroquine, uh, for your friend or for, uh, for our hypothetical 50 year old woman, assuming that they didn't have any risk for QT pro prolongation.
Right. And stuff like that. Right. Uh, that being said, I don't think we have access. So we don't, so we don't have access, so we can't do that. Um, even, yeah. Even if we wanted to, um, I just got messages from pharmacies that I use saying that they will not, they've been told by the fda, uh, that they will not fulfill any, uh, hydroxychloroquine prescriptions unless very specific criteria are met.
You know, are they on lupus? Have they been, you know, do they have lupus? Have they had prescribed before, et cetera. Yeah. So then number two, if either of those people proceeded to develop a pneumonia mm-hmm. I would be interested in giving them azithromycin. Mm-hmm. Um, because I think that that has the potential.
It's interesting and we don't know whether that's an antiviral mech mechanism or whether that's just treating a super infection. Mm-hmm. But I would like to treat them with that. Not to prophylax the pneumonia, but if the pneumonia started to come on mm-hmm. And I don't have, and then it's really good for me to be talking to you, cuz I think my attitude is more procedural.
I come from kind of like my friend Matt, I come from a procedural and you come from a more of a data driven right. Worldview. And so I like, I like that interaction and that, so, so just on that, what, what do you think about my, what I said what, yeah. Do you think, is that totally unreasonable or do you think I don't think it's unreasonable at all.
Um, you know, I think, again, here's the, it depends T-shirt. Yeah. Yeah. You know, it, it's, um, you know, if someone, I would, maybe I would challenge and say if someone's getting pneumonia, which would be associated with shortness of breath and other things, I would really want them monitored in a hospital. You know, um, I think, and that at that point it's very reasonable to use Azithromycin or something like that.
Mm-hmm. Mm-hmm. Or, and or in addition to hydroxychloroquine. Um, so, you know, I think that brings something else we were talking about. Uh, and even a bigger point is that, you know, not only do we need to care for that one individual, which is really what we as doctors have been trained to do, right? Care for that patient in front of us, be that patient's advocate.
And we have to do that very strongly right now. But we're also in the middle of a pandemic where. The rest of the world is going through the same thing and we have to look at scarce resources right now. You know, to the point there's no hydroxychloroquine available because a lot of people have been stashing it.
They've been saving it for just in case it happens, I wanna have someone hand or using it maybe inappropriately. So now there's none left. So we have to look at the risk benefit on the broader kind of community level. Mm-hmm. In addition to the risk benefit for that individual in front of us. And it's not something, I mean obviously in the public health world, that's how they think all the time.
But as physicians sort of looking after individual patients, it's not something we're used to kind of thinking about. Right. We're like, if I decide that this is gonna be the best thing for my patient, I want them to have it. Whereas now we have to go. Which one of my patients do I need to give it to? You know, we have one dose of this or one course of this, who's the best person to get it?
And it's an awful situation to be in, but this is where we are right now. Yeah, I know. It's crazy to to think about like, you know, when you, when you intubate someone, if you ventilate them before your, the probability that it goes better goes up by like an order of magnitude. Right? Right. Cause you're pre oxygenating the lungs.
But my friend had to make a judgment call and not do that cuz he didn't wanna expose everyone else. So it's uh, it's analogous to the public health conversation Exactly. Of trying to take care of like ever think of everybody in the hospital, everybody in the room, everybody in the world. And I think that's kind of cool because.
Most of us never think that way. Most of us are just sitting looking at the person in front of us thinking of that person. Yeah. And I hope this leads to a little bit more connection. Yeah. And a, a more thoughtful, um, experience. Now then let me ask you, here's, here's the next thing that I would do for your friend.
So I'd give oral vitamin C every day. Mm-hmm. Um, I'd give zinc, I'd give some low dose vitamin A, I'd give oral quercetin. Mm-hmm. I'd give some olive leaf extract. I'd give some herbs. Yeah. Uh, and I would try to try to do all of those things to, and, and, and both. And I would give zinc lozenges. Mm-hmm. And then I would, and, and my herbs.
And I would, I would give, um, I would give SBI protect, which is a immunoglobulins or, or colostrum. To try to bind onto any virus that was in the gut because, uh, my sense is, is that a lot of patients are presenting like what we're talking about with these upper respiratory things. Mm-hmm. But it's also in their intestines.
And if we can kind of mop up some of that virus with colostrum or something that was gonna be somewhat protective, that might change the time course of the. Of the illness. Right. Even though I don't have data, that's just how me and you would normally manage a case like that. Right. Right. Yeah. And I think that's a really, really good example of the risk benefit that we were talking about.
You know, we, we know that vitamin A, vitamin D is zinc. Um, those are really kind of important nutrients for immune support. Right. We've seen it. We know that people that are low in vitamin D are more susceptible to getting other types of infections. Those things are, you know, clearly important. We have zero evidence right now that they work for, for Coronavirus or for Covid 19.
Mm-hmm. But, you know, based on, based on our understanding of what happens in other infections, You know, the same thing with the, with the colostrum or using immunoglobulins, uh, in your, you know, orally in your gut. Um, we don't have any evidence that this will work, but, you know, it makes, it makes sense, it makes theoretical sense that it could work.
And what's the risk of taking it pretty low? Right? We, it's, you're probably gonna benefit in some way or another by taking it because these, um, these things have very few side effects if you take them in the right dose. Like if you're not taking mega doses of vitamin A or mega doses of d, you know, in appropriate amounts.
So I, I a hundred percent agree that it's absolutely worth trying because there's very potential for very high benefit and very low risk. Ok. And yet, you know, we don't have the solid evidence supporting them. There's enough evidence out there in other, other situations where they make perfect sense. And, you know, one of the things, and maybe we can get in today or, or later, but trying to track some of that real world outcome data, kind of real world research.
If we can track someone, you know, this my friend, this theoretical, uh, hypothetical 50 year old lady, uh, and have track the course of their disease over time. Uh, and this is one of the things I'm working on. You know, send them a daily questionnaire to, to see how they do. And at the same time we learn, are they taking vitamin D and vitamin A and zinc?
Uh, and now we have thousands of people where we have that information on. We're going to start to see, wow, we know that everybody that's taking vitamin D. They're not ending up in the icu. Right. And maybe there's something that could be really beneficial. So this is also an amazing opportunity to really learn, and we should be doing this real world outcome research, you know, on, on everybody that we can.
Okay. I've got two real world questions for you. And, uh, we know that the, the receptor that this virus attaches to is a receptor called ACE two. Mm-hmm. And, um, it, it turns out that it's related to two very large categories of blood pressure medications. Mm-hmm. And, and so then this is a real world question because we know that, um, people with high blood pressure and some other problems are at higher risk of the infection.
So I've got that on one hand. And then we know that those drugs can affect this receptor. And so there have been some voices who've said, right, you gotta get off those blood pressure medicines because it may make you at a higher risk. And then we've got some other voices that are coming out strongly and saying, yeah, oh no, you've gotta stay on those drugs because they're protective.
Yeah. And so then now this, and, and I'm, I'm mentioning this in the context of everything that you said about data and how we, we interpret at all of these different levels of research that is happening. Yeah. Um, given that a real world question, let's say our 50 year old woman has high blood pressure and she's on a, uh, arb.
Mm-hmm. Uh, or a pill. Mm-hmm. Should she stay on that? Yeah. Um, so I think, again, very good question. Now, the, the, the idea is that, and I, we touched on it a little bit last time, but the ACE two, which is angiotensin converting enzyme two, is found on the surface of, of lung cells. You know, the lining of our lung, the lining of our gut, the pneumocytes, the enterocytes, um, and that's how the virus gains entry into the cell.
So the concept is that if you have, again, theoretical concept, if you have more ace on the ace two on the surface of your cell, there's more places for the virus to attach and to gain entry. So making you more susceptible, we know that, um, Some of these medications can increase ACE two on the cell. Now that's one part of the process.
Right? Um, the, so, so that's the, that's the reason why people would say you would take her off mm-hmm. Or take her off the arb. Uh, the other, the, the other side of that argument is that, um, the ACE two acts differently. It has a different effect depending on whether you're on one of these drugs or not.
Mm-hmm. And it looks like the effect that it has is more beneficial when you're on one of those drugs and it acts because those drugs actually inhibit angiotensin two, and that al that affects how ACE two acts. Mm-hmm. Uh, and so, you know, there's, um, I think there's, again, it's all theoretical cuz we don't have the data to say, you know, we haven't done a, a controlled trial where we say, if you ha you're on an ace, you go down this arm, you're on a, you know, an arb, you go down this arm, you're, you're the control arm and see what happens to these people.
We don't know that that would be the ultimate study to do. I don't think it'll have ever have that actually. Uh, so we have to kind of act on hypothetically what makes the most sense. What's the risk, what's the benefit? Personally, you know, from all, and I've been delving into this quite a bit, uh, what would, what would I suggest she do?
I would say don't go off it. Okay. I would say she would stay on it, you know, um, that the benefit, the potential benefit of being on that outweighs that theoretical risk that it might cause it. And in this case, especially since, you know, this hypothetical case, she's already infected, so it's not gonna change the infection.
It's like I changed the infection. So then, um, that just, that, that, that's an interesting point that is, is related to a bunch of these where we're trying to make a decision, should I do it or should I not? Right. And then it is, um, the, there is a theoretical reason mm-hmm. That might lead to a higher risk, but then there's also a real world how things work.
That seems to be, that is probably gonna be a lower risk. And so we're, we're trying to mitigate and manage between that, which is, I think is right. Exactly. Interesting. Ok. Uh, I know we talked about this and you don't have an answer, but I think it's a real world question. Somebody has pain this weekend.
Yes. Somebody's in pain. There's a lot of people out there in pain. And what they normally do is they take two Aleve. Mm-hmm. And they're gonna call me in the morning. So then, and uh, th these are, uh, what are called non-steroidal anti-inflammatory medications, NSAIDs, what is your feeling? What is your feeling about, uh, that are you gonna recommend that they take that medication or not?
Yeah. And, um, that's, again, one exactly the same kind of thing. We don't have a final answer. Mm-hmm. So I am actually, one of the things I'm doing this weekend is delving more into the literature to see what the, um, what we can find, uh, as to whether you should or should not take it. So, uh, I'm coaching my answer with, I haven't done that final delve into the literature, but, you know, not other, not everybody is going to have that ability.
Right. We, we have to make these decisions world, world time. Mm-hmm. Don't we, um, in, so some of the idea that. Uh, NSAIDs, things like ibuprofen, things like the, you know, the Aleve, they, um, there's been some observations that there may be worse outcomes when people take these medications. So that's kind of where it started from, and then people started going, uh, maybe it's because ibuprofen increases ACE two on the surface of the cell.
Maybe that's why they're having worse outcomes. I don't think we know the answer to that, if that's the reason, you know, is it inhibiting the, uh, resolution of the inflammatory response, right? We know that it inhibit these, these, um, medications inhibit the COX enzyme. We know that that's important for both making inflammatory mediators, but also, uh, what we call resolvins, right?
The resolution of the inflammatory response, and is that what it's being inhibited? Then I could come up with a bunch of other mechanisms as well as to why that might be. Again, all very theoretical. What I would have to go on is the very limited number of observations to say that, Hmm, there's some evidence that, uh, taking it can cause a worse disease or worse, you know, prognosis, worse outcome.
And I would probably err on the side of not taking it. Okay. And also knowing that, um, the gut, you know, it affects leaky gut. It can, you know, be associated with a lot of those things as well. Now what's the alternative? That's the other problem is that then a lot of people say, take acetaminophen. Right?
Take Tylenol, uh, instead of, uh, the ibuprofen or the nsaid. Well, I, we know, you know, you and I know very well how Tylenol can decrease people's glutathione levels and, and, you know, hurt their liver. So, um, is that a better alternative when we know that glutathione is so important in overall lung health? As an example, right?
I would say that's not a great alternative either. So what, you know, what do you have left for the pain? You know, that it becomes very problematic. Uh, if you are to take Tylenol, you would definitely wanna take glutathione with it, um, to, to mitigate that issue. Okay, that's a good one. And so then for all of those people out there who were taking, for example, I had a call with a friend of mine who's in a lot of pain and he's taking, um, uh, a medication that has a narcotic, but almost all of those, they include a little, uh, acetaminophen with it.
I'm all acetaminophen goes with it. Yeah. Yeah. And so then, so for all of those people taking pain medications, like Vicodin is maybe a one you may have heard of. Adding in some glutathione may be a real good thing to do to protect your liver. Yes. And as we, as you think, as you think about ibuprofen, I generally try to get everybody off of ibuprofen.
Absolutely. Um, because it affects your stomach lining. Mm-hmm. And then it can affect your esophagus lining and that can affect your kidneys. Yeah. And these are all places that this virus that we're talking about can go. Exactly. And so then we, we don't wanna stack the deck against ourselves. Right. Um, with some something.
And so then maybe, you know, we've had some, we've had success with C B D. Mm-hmm. We've had success with manual therapies. Yeah. We've had, we're, you know, we're, I, I think there's a lot that can be done from the, in the integrative space. Yes. Yes. From a pain perspective. I agree with that. You know, you would wanna try all of those other modalities, um, and then, you know, you don't wanna be in pain either, right?
Crazy. So it's always, again, we're, we're getting back to that risk benefit. You know, if you're in pain and the stress that that causes, that's going to suppress your immune system too, right? And they put you at higher risk, uh, because of that. So how does, so let me, I'm gonna take that, how. How does stress make your immune system work?
Not, not as well. How would you define that? Yeah. You know, so I think people have probably heard of prednisone and some of these steroid drugs. They, they, we take them to suppress the inflammation, right? To suppress globally really suppresses our immune response, our inflammatory response. Well, we're, when we're under stress, one of the things that we make, we make adrenaline or epinephrine, those type of things, but we make cortisol.
Cortisol is released when we're under stress and cortisol is a steroid, um, is very similar to the prednisone we take as a drug. Cortisol suppresses our immune system, our whole inflammatory response. And so, you know, now you're under a lot of stress and you're releasing all this cortisol, um, and now you get exposed to the virus, then, uh, you're, you're at higher risk, you're less likely to fight it off.
Teleologically. Does that make sense? Do, why do you think it is that our body is designed so that in a high stress time we turn down the immune response? Do you think it's because the concept is, is we're trying, we're trying to get away from that tiger, so we don't need to focus on immunity. And then once we get back to base camp, And sit down around the campfire and reset, then we can kind of deal with whatever bacteria we picked up while we were running away from the tiger.
Exactly. I think that's very much the case. You know, our stress response is really designed to be acute, you know? Mm-hmm. So when we're running from that saver tooth tiger. Exactly. We need the adrenaline, we need all of those things to, for survival mode. Uh, and what's happened is, you know, probably people have probably read the book or heard Robert supposed be wrote, it is why zebras don't get ulcers.
You know, the idea behind. Uh, zebra, as they see something, they run from it. They either escape or they're killed. Once they escape, they go back down and start eating the grass. Right? And, and that whole stress response is dissipated in humans, especially modern humans where, you know, and especially with pandemics going on, we have constant stress and we produce cortisol all the, you know, constantly.
And, and so we have this base, uh, level of cortisol that suppresses our immune system. And, um, I don't think humans, you know, evolutionarily were designed for having constant cortisol release, right. You, you know what I lo I, I, I take care of a lot of people with PTSD and dramas almost like probably 20 or 30% of my practice.
And I totally like, love it. It's interesting, like people told me, don't go into PTSD cuz they never get better. And to me, like everybody gets better. Yeah. That's like my favorite thing to do. But, um, what I say is like, if, normally what happens is when you're a little kid and something stressful happens, like real, like somebody super scared you, right?
Mm-hmm. Then in about three minutes, like the epinephrine is fun, and then if somebody said, Hey, Helen, go lie down and take a nap, you'd be like, oh, ok. You're just like, you, you, you can shake it off like you were a zebra. Yeah. You know what I mean? Exactly. But, but when, when you're sitting here and there's no end in sight for this thing, it is, so it's gonna be here tomorrow.
Mm-hmm. So, and then it's gonna probably gonna be here on Sunday and it's probably gonna be here Monday. So then we get stuck in the fight or flight pathway. Yeah. And so then next thing you know is two or three months, and I think that that's a, um, import. I did like a consult with this lady. Today. That was like my favorite thing I've done in about a year because I started, I'm back to doing telephone consults, right?
And we basically just reframed the whole thing that everything's gonna be fine and we just kind of reset everything. And I did this kinda cool conversation about the hero's journey, which is kind of how I interpret everything. And so I, and so then in we, basically, what I did is I gave her a bunch of homework to do about how this is a, a pivotal moment in how the rest of her life is gonna turn on this and that she is gonna transcend everything and become who she was really meant, who she was meant to be.
Right? And, and then it was interesting cuz I said that, and I. I kind of, I thought ended pretty good and then all of a sudden she screamed in the microphone. Yes. You know, and, and, and so I think interestingly, if you can do that, and at least for our hour, we totally, completely reset it. I was having so much fun, I went 20 minutes over.
But what, um, we all kind of need to do that for ourselves so that we don't have too much cortisol. So what, so that just like, we don't wanna be like that anesthesiologist doing five, five days in a row. Exactly. Because he's gonna get it. Right. And so we need to, we, we, the, the mental and the mind frame I think is super important as we, as we kinda, because we have to hunker down for.
I don't know. I think Do you think two months or three months? Yeah, I think at least three. Mm-hmm. Yeah. Crazy. We're looking end of May now. Um, you brought up a, a very big word when, when our pre-conversation the inflammasome. So, so tell people what's an inflammasome? So it's, it's, think of it as a way that the immune system uses to signal, um, okay.
So it's, it's a protein complex essentially, you know, that, um, transmits a signal that turns on a, uh, capsized enzyme. So it's, it's really we, our body has nu a lot of different, um, Inflammasome complexes, we name them all different kinds of things. Uh, the one that seems to be most relevant in, uh, covid and in the lung diseases, it's NLRP three inflammasome.
Uh, and, you know, we can get into show pictures of it and show that, but it's really, when that inflammasome gets activated, now different signals will activate it. Um, you know, the, uh, bacteria will, um, when they bind to receptors, we call them, you know, uh, pumps, right? Um, pathogen associated molecular patterns or damps damage associated molecular patterns.
They will, when the immune system essentially sees them, they'll transmit the signal through one of these inflammasome to turn on the whole inflammatory process. And i l one beta or cytokines will be produced from that. Okay, good. So then where would, where exactly is this inflammasome in the lung? So in the, um, it's in the, the macrophages we'll have it, the mm-hmm.
So it's in the different, um, immune cells. So, um, you know, it's the, yeah, it's just, think of it as a signal molecule for the whole, so when you trigger these, you're triggering this release of cytokines and inflammation. And that's kind of one of the things that leads to the cytokine storm that we were talking about, which, you know, it recruits more immune cells and creates this, the leakiness, um, that leads to the lung, that filling up with fluid, the a r D s that we, we ended up talking about.
Right. So, you know, we have to start looking at, uh, some of the things we, we can, you know, start looking at is what inhibits those inflammasome. Oh, so what does, yeah. So, so things like, um, well we, we we're, we're learning more, but, um, sirtuins, um, so. Things like resveratrol, um, you know, that, those type of things.
And we can, why don't we do like a whole episode on looking at those, because I think they're really interesting. Yeah, that'd be perfect. Yeah. Yeah. I think, you know, that there's, that's a, a whole area that I think can be really valuable to, for therapeutic targets, right. Again, we're still being in the theoretical world, right?
So we're in molecular biology, hypothe, that's useful. Mm-hmm. That's useful for people to think of. So we've got therapeutic targets. So some of our targets are just upleveling the immune system mm-hmm. With vitamin D, right? Some of the, some, sometimes there's a, a, a message or a signal, uh, intermediary that may be responsible for, for example, a cytokine storm.
Right. So that could be a target where we could try to damp that down. Mm-hmm. Or we could try to affect how the virus is getting into the cell, or once it's into the cell, try to try to have an effect there. Okay. And so then, uh, or we might try to mop that virus up in certain parts of the body. So these are very diverse and very different mechanisms.
Yeah. So it's interesting. So then maybe next week what we'll do is, we'll each, each time I talk to you, we'll dive into one or two of those. Yeah. One of those mechanisms, you know, that would, coming back to the hydroxychloroquine thing, you know, some of the idea of why it works is it inhibits the virus from binding to the ACE two, right?
Mm-hmm. So it changes the changes the ACE two, so that the virus doesn't bind as efficiently. So that's one of the, the, you know, Molecular mechanisms that it might be working. Uh, it changes the pH of the, the inside of the lysosomes in the cell. Uh, so yeah, there's lots of reasons why, and again, this is part of the, the discovery process and part of kind of tying it into what we started talking about, um, it's hypothetical.
We're looking at, you know, data that we know how the immune system works. We don't know exactly how it works in this situation, but we can use that knowledge of our molecular biology, of these molecular targets to say, is there something that we can use that might address those molecular targets, that it's still low risk.
So even though we don't have the, the full, um, understanding of whether it's going to work in this situation, we can say, yeah, you know, taking this supplement is not going. It's quite low risk and this is how it could work. So I think it's worth a try. Now you're doing very well and you've almost passed your functional medicine boards.
But I've got one final question for you. I didn't realize we were in a board exam. Okay. No, but you know, it's, it's interesting cuz it's like I, you know, I, I love oral exams. It's like my favorite thing. Yeah. And so it was interesting cuz when in anesthesia, when, when I did my oral boards mm-hmm. Everyone knew that I was doing them.
And so then if I failed, it would've been like, humili. Right, right, right. And so I actually spent like a year and studied every day and then I was livid because I was like, I, I didn't, I didn't feel like they asked me hard enough questions. So it's like, it's kinda, it was kinda hilarious. That's great. I was like, you guys gotta be, you gotta ask me harder questions than this.
Like, it's funny. Um, but, so, um, I think we're, we've painted the picture of this early thing that happens in the upper respiratory stuff, the early thing that happens in the gut. We're trying to, we have some strategies. Yeah. People know that people can get pneumonia and sometimes that pneumonia can lead to a cytokine storm or a cytokine tsunami, that, that can lead to some more severe lung problems.
And one of them is a R d s. Yeah. And then, and then that is the moment when after people get that, that's when all the other bad things happen. Mm-hmm. And so can you tell me a little bit about a R D s, why it happens and how you think about that from kind of a scientific or mechanistic perspective?
Mm-hmm. And, and, and then how that relates to, uh, the immune system. Yeah, that's a big question. And it was funny, I was just delving into some of the, the literature we know it's a r d s is one of those things. Now, I'm not a pulmonologist. I'm, you know, this isn't my specialty, but I can tell you what I've read, um, and it, acute respiratory distress syndrome, and it's one of the, a lot of things can cause it trauma infections.
Uh, so it's something that we've known about for a long, long time, well before, you know, covid and, and this coronavirus. But, um, it seems to be the final common pathway that, you know, we, everyone talks about the. The CT scans and the chest x-ray findings of this ground glass appearance, right? Where our lungs look all white, essentially they're filled with fluid.
That's kind of this, this a R Ds, uh, the start of the, the A R D S. So, um, there's sort of the three phases. The, what we call the exudative phase, the leakiness. So our immune system, um, causes the, the, the cells, the blood vessels to kind of leak fluid into the little air sacs in the lung. Um, and then there's this proliferative phase.
The cells start growing trying to, uh, deal with it. And then the third phase is a fibrosis phase where, you know, it starts layering down some of the fibrolasts start laying down, um, tissue again, it's all in a. A kind of attempt for our body to heal from this, but that trying to heal tends to, cause you know, our lungs don't work anymore, right?
They fill up with fluid, they're not going to do the air exchange. Um, so that's really, and the immune system is very much a part of that because the cytokines, so tho those cytokines are just molecules that our immune system uses to communicate with each other. Um, and when there's a whole bunch of them, it recruits a lot of, um, immune cells and they release all kinds of different chemicals that end up causing that leakiness the fluid.
And then that whole process, that basically when your lungs go up with fluid, you can't breathe anymore, right? It's like drowning almost. You, um, you can't exchange any oxygen. One of the reasons we use, uh, ecmo, right? You probably, uh mm-hmm. You know, more, a lot more about it than I do. But, uh, you know, using how can we get oxygen into someone's blood, if not through their lungs.
Mm-hmm. Support them and keep them alive until this results. Um, and again, we just don't have enough ECMO machines Right. To do that. The extraoral membrane oxygenation. So, um, you know, can we, and if things like the infl, inflammasome are that inflammatory trigger, you know, targeting those, makes a lot of sense.
Um, some of the experimental drugs that they're using in the i c right? Well, they're not experimental, but some of the drugs they're using to try to, you know, help with this process are I L six, um, inhibitors. So there's different, uh, drugs that will. Uh, keep i L six is one of those cytokines. It's, it's an inflammatory molecule really, you know, increases the whole inflammatory response and they're giving a monoclonal antibody that, that inhibits i l six and that's being used in the I C U right now.
So we're trying to, you know, where can we target those, um, that whole immuno immune process. Right. Yeah. How, uh, I'm concerned that a lot of people that end up with this, there's some, there's some evidence that some of these people have that even the, you get pneumonia, have some long-term fibrosis. Yeah.
From a pulmonary, pulmonary perspective. Yep. That seems to be what's happening. Unfortunately, you know, even when people go through this and, and they, they survive. They're ending up with long-term. Um, and again, we still have to see how long-term, but, uh, damage, damage to their lungs. And that's, you know, we talked about that fibrotic phase of a R D s, you know, now you get fibrosis of the lung and your lung, you know, our lung's supposed to be very pliable.
It's supposed to be able to expand and contract and, and when it gets much stiffer, it, it doesn't work as well to exchange oxygen. And, um, yeah, we still have to see what the consequence of that's gonna be. It, it was interesting and to tie it back to where we started and wrap a bow on it, my friend, he said, interestingly with when you intubate people with covid, A lot of times you would think that because they get this fibrosis and stuff like that mm-hmm.
That it would be real hard to ventilate them. Mm-hmm. But he said it's actually very easy to ventilate. The lungs are actually surprisingly very compliant. Interesting. So they'll expand and contract very easy. Yeah. But he goes, don't be fooled by that because they're actually very sensitive to trauma and, and bar pressure to the pressure.
Mm-hmm. So he goes, you have to, you have to use low title volumes and all of these Right. Kind of strategies that are anesthesia and ICU approaches mm-hmm. To, to minimizing any trauma because it's like, it's very vulnerable and then it's crazy to think that somebody might be on a ventilator for it. A while, you know what I mean?
Weeks and weeks. Yeah. They don't on a ventilator and they, they're subject to every ti as long, you know, the longer you're on a ventilator, the more trauma your lungs can, uh, are exposed to. Right. And, you know, and now we're talking about hooking up four different people to one ventilator, you know, in terms of, because we just don't have enough ventilators.
And so there's all of these things, if you look on YouTube, how do you, how do you ventilate two people from one vent, one ventilator, four people from one ventilator? And, and if you think about the how fine tuned you have to be for each person, how do you do that when you have multiple people from one ventilator?
It gets, uh, not ideal. Um, now then, uh, this is, and it's interesting to talk about evidence. Um, there's some actually some very good ozone practitioners in Italy. And apparently I just got a text as I was walking into record with you. That Italy is, uh, authorizing ozone for people with a r d s. And so ozone I think is an interesting one.
And then I think vitamin C uh, is interesting because I, my hypothesis is that when this is all done in a year from now, we get on the podcast, I predict that what we're gonna find out, that all of the techniques that we generally use that we've, we have found are relatively safe mm-hmm. Uh, for complex illness mm-hmm.
Are gonna be, they are all gonna be either of, of benefit and, and very little harm or benefit and no harm. And, and, and they're gonna be, they're gonna be valuable. I think ozone and vitamin c I, if I was to guess, and so this is the opposite. Of what we were talking about with science and data at the beginning of the conversation.
Right. If I was to guess, I, I'm gonna guess that if you treated people with ozone and vitamin C, that you could cut the, the intubation rate by 20%. Yeah, that's, that's my guess. You know, and, and so then the question is, will, can we talk somebody into doing that study? And then you say, well, what is the cost of those modalities?
Right. Low. What is the risk of those modalities? Vitamin C, very low, low. Mm-hmm. Um, and so then it, it's, and so then it's kind of interesting. It's like we're in, and then how do we ethically create a, a, a way to actually study that so that we could have a peer reviewed conversation around that. Yeah.
Because that's, that's what we really need. And yet we're trying to, we're we're trying to accelerate, um, and do 10 years of research in, in, in a day, essentially. That's true. You know, and, um, I don't doubt that that's what we're going to find. I know that they are doing some clinical trials on IV vitamin C and China right now.
Right. We're talking about that. Yeah. So, you know, I think there is, you know, if we can start to collect, um, things from around the world, you know, and in China they're also using a lot of different traditional Chinese medicine modalities that look really, really promising that we just don't even, haven't even heard of in the States.
And so, so what, what's your, what's your thoughts on the intravenous vitamin C? What do you, what have, what's your, your perspective on that? Well, I, I think it's, I completely think it's worth a try to your point, it's low risk, high potential yield. Um, so I, you know, I can't see any reason other than, you know, the getting it, which is, is the challenge.
But, um, to me it seems like we have to look at that. We have to try it cuz it's a modality that could have amazing results with very low risk. So, so to anyone that, if, if there's any hospital anywhere, there's a, a company called Archway Apothecary, it's a compounding pharmacy and they've told me that, uh, if, if a hospital wants to get intravenous vitamin C, they can call them and they will ship it to 'em.
And I will teach that hospital how to put it in bags and I'll tell them everything that need they need to do. And they can just find firstname.lastname@example.org. So, uh, and that, uh, that offer goes to any hospital in the world. So, uh, because I think it's, it's provocative. I think so too. That's awesome. So, uh, for as we sign off for the week, we thank God it's Friday.
Do you have any, uh, any tidbits of that you wanna share, uh, for people as they, as they launch into the weekend, launch into the weekend, do all the things that maybe you didn't have a chance to do this week? Sleep. Sleep in, take some deep breaths, go outside, uh, for a walk, you know, work on that cortisol response.
Try to lower that. Try to, you know, get your immune system working by sleeping and cook a gourmet meal. You know, spend time with the family and maybe just turn off the news for a day, uh, to try to, You know, ignore that, um, that massive, um, cortisol producing, you know, media that we see all the time. That would be my, that would be my recommendation.
I'm cooking a gourmet meal every night. I'm gonna be nice singing at the top of my lungs even better. And, uh, it's gonna be amazing. So, uh, thank you so much for being with us. And then, um, uh, on next week we're gonna dive into some science. We'll do some screen shares and we'll go through some pictures. We should be great.
And until then, stay healthy and happy and have a wonderful day. Have a great weekend. Thank you.