Part 1: Dr. Cook Podcast Series with Dr. Helen Messier

 You know, the medical community are all pulling together and trying their best to actually cooperate at, cuz we have a common goal right now. That's the most promising thing that's happening. You know, that should help us all, uh, try to cut through some of the fear that we're feeling.

Hello and welcome to the Bio Reset Podcast. My name is Dr. Matt Cook and I'm here today with Dr. Helen Messier. Uh, and the, the negative thing about her is she's not a very good self promoter, but, uh, she is amazing. She's a friend. Uh, she knows an enormous amount about immunology, biology, and medicine. Uh, she has a, a PhD in MD and she's on the faculty of the Institute of Functional Medicine.

And what I like about her is that she seems to be able to pull wisdom and knowledge together from disparate fields and, and pull it into a coherent. Voice, uh, that is helpful in, in good times. And I think, uh, we need her now more than ever as we try to tackle, um, a pandemic that is sweeping over the world.

So, welcome, uh, Dr. Helen. It's delightful to have you here. Thank you, Matt. I am very happy to be here with you. So we're gonna try to do, uh, a regular, maybe even daily, uh, just update of, uh, what we're, uh, learning, uh, looking at studies and, and talking about things. And maybe, maybe just to kind of get going, give me, give me your, your highlights of, of, uh, what's your status update of where we are right now.

Uh, and, uh, what's happening. Yeah, you know, this is something that obviously the world is watching. You know, this is something that I think most of us alive today have never lived through a pandemic. You know, the last one we had was back in 1918, and, um, so this is something that's new for all of us.

Clearly there's a lot of fear around it and a lot of unknown. And, uh, you know, we've been talking daily, Matt, you know, trying to just keep up with everything that's going on. You know, daily, there are multiple papers published, uh, on, uh, very, all kinds of different aspects of the virus and treatment and, um, you know, uh, Prevention.

So, so it's really difficult to stay up to date, but really, I think in general, uh, what. Is striking me the most is how we're humans, you know, the medical community are all pulling together and really, uh, trying their best to actually cooperate at. Cuz we have a common goal right now. And, um, so I think that, uh, that's the most promising thing that's happening.

You know, that should help us all. Um, try of cut through some of the fear that we're feeling. You know, we can get into, and I, you know, hopefully we will, uh, with, as we go on with this podcast in future ones in terms of, you know, the details of what we should look at. But I think, I think clearly, um, you know, there's no, we're still in the midst of it.

I think clearly in the States and California, the Bay Area. Going to continue to get worse for a while. Uh, and so, uh, we need to kind of look at everything we can do both from prevention and treatment if you do get exposed. Mm-hmm. Yeah, that's a good one. Um, y you know, we have, we're having a great conversation yesterday and you were telling me.

Some of the approaches that China has taken in terms of taking care of their healthcare workers. I thought that would be a good story for you to kind of start with. Mm mm-hmm. Because it, it shows you how good an authoritarian nation is. It, it, it, it, it making what would probably be good decisions that would be hard for us to do, but I don't know.

Tell me that story. Yeah. Yeah. You know, there's a lot of, um, talk now about how the infection rate has, China has been able to contain it. You know, they, they've been able to stop new infections. I think yesterday was the first time where, uh, news came out that they didn't have, uh, any new infections in China.

And so one of the things that, you know, they have been very proactive, uh, in terms of really quarantine. People, uh, putting them in quarantine. So healthcare workers, for example, anyone, um, that works with covid patients, they were kind of kept in separate housing. So I'm not quite sure the extent what the housing was, but hotels and other things.

So healthcare workers were kept. Separate from their families and they were, uh, you know, all housed together. So they would go to work, they would go back together, so they wouldn't get out there into the community, even their own families to spread it. Uh, China then took, you know, anyone who was, uh, te who had tested positive, they also were quarantined in a separate place.

Again, separate from. Um, from their, you know, homes and, and family just till, um, they were over the disease. And you know, that they seem pretty drastic, but obviously we're very effective at containing the spread of it. Yeah, that's a good one. So now we're gonna dive into some questions, but maybe I like the way, I love listening to you talk.

Give us, can you give, give us what is Coronavirus 1 0 1? Kind of give us at a, at a high level, like what's a virus? How does it work? How are, what's going on with this virus? Yeah. That makes it different. Do you have any, how would you, what would, what would you tell somebody? Yeah, I mean, I think that's a really good question.

I mean, we all have heard the term virus. We all know that, you know, we get viral infections and colds and the flu is a virus. But what really, what is a virus? Well, a virus, um, you know, we're talking even right now about live viruses. I would even argue that. That's not really a good term. Viruses aren't really live, so a virus is, you can think of it as a particle with some type of genetic material inside.

So either D n a or rna. So there's different D n A or RNA viruses. Um, and that's the genetic. Code in, in this case, coronavirus or the, the official name of this virus is called SARS Cov two. Um, that's the name of the virus. And then Covid 19 is actually the name of the disease, sort of when you're infected with, with.

SARS COV two. So it is a, um, RNA virus. It has RNA inside. And the outside of viruses are either a protein and a fat type of coating. And what viruses do, so when they're on their own. They can't, um, replicate, they can't make any more copies of themselves. They need a host in order to do that. In this case, humans, we're the host of this particular coronavirus.

It needs to attach to the host cell. Um, in this coronavirus case, it's uh, often attaches to, um, receptors on our lung and, uh, sometimes in our gut, and I know we'll get into that a little bit more, but then it gets inside the human. Cell and it starts to leverage the machinery of the cell. So, you know, the way that we make copies of our own dna a, you know, our DNA polymerase, it hijacks all of that molecular machinery, all of our molecular machinery, and makes a whole bunch more copies of itself, and then it ends up breaking open the cell and killing the cell and releasing a whole bunch more viral particles.

And so a virus by definition cannot replicate on its own. It needs to use a host. And now viruses can be very specific and we've probably heard it talk, you know, people talking about, well, this virus came from a bat, or it came from, you know, different animals. So viruses because of the way that they attach to their host cell, it can be very specific, you know, so, um, human viruses, you know, we often don't get the same viruses as our dog does, but they'll get a cold and, and, and we don't cross them.

But once in a while we can get viruses that are found in animals that can mutate a little bit. The other thing with virus is that they, because they can replicate so quickly, they. Can develop new mutations. And in this case, it's felt that, um, an animal, likely a bat had this coronavirus and it mutated enough to be able to, uh, infect a human.

And, uh, that's kind of how this whole thing started. There was human number one who got this, um, infection with this coronavirus and then ended up spreading it, um, you know, to, to the world essentially. It is really crazy. And, and so the, you know, the, we, this coronavirus is similar. It belongs to the same family as other coronaviruses that do com.

Cause you know, a lot of times the coronavirus can cause the common cold. This is a different, um, the sequence is a little bit different, but it belongs to the same family. Of, of these coronaviruses, uh, what makes this one so severe and also a bit paradoxical, right, is that it can spread very readily because it can spread in people without symptoms.

Now, typically you, if we think of back of the Ebola epidemic, um, that happened a number of years ago, we were able to contain it pretty rapidly because when you get Ebola, you know, your. Sick. Uh, the symptoms are very profound and they happen very quickly so that we were able to contain anyone that was infected with that Ebola virus and quarantine them so that they didn't spread it and pass it on.

And, and that's really the key to containing and presenting pandemics that we're in now. But with this particular virus, a lot of people can spread the virus before they even know they have it. And in a lot of cases, you know, they have such mild symptoms that they don't even. They don't even think about it and people don't even get symptoms at all.

So that spreads it very rapidly. And you know, and that was also one of the reasons why we didn't pay a lot of attention to it initially. You know, we thought, oh, it's mild, right? Very few. You know, it's kind of like the flu. It, you know, a lot, only certain susceptible people get it. We're not really worried about it.

If you're young and healthy, we're not gonna come down sick. And so we really didn't pay enough attention to it, but, There are people who, when this virus infects them, obviously, as we all know, it can be very serious and it can kill them. And so, uh, it's, it's a bit paradoxical in that we have two sets of population.

One where very mild symptoms, if at all, but they spread the virus and then those that get very severe symptoms, it's kind of the, the worst of both worlds, which is clearly what the kind of virus that can result in a pandemic that we're in now. Okay. That's a good one. Now I have my own ideas, so I'm gonna ask you, but I'm gonna ask you.

Mm-hmm. What, what do you think is the typical avatar of the person who doesn't have any symptoms and just seems to be a spreader? What, what do we know about them? Yeah. Um, that we're still really looking into that, but it seems that, you know, children for example, um, tend to be, you know, young people though there was the first, you know, announcement of a child death I think today.

But in general, uh, kids seem to be quite resistant to, um, the effects of this virus, but they're very good spreaders of it. We call them very good vectors. And so, um, I think that kind of, that young, healthy, um, Sort of person, teenagers and children, uh, in their twenties tend to be the ones, at least that it seems to be, that are spreading it a lot without all the symptoms.

What, what's your thought, um, Matt, on, on who that avatar is? Well, I would to, I would totally agree with that. So then our question, then our next question, and I also I'll ask you is who do you think the people who are susceptible are? Yeah, and, and so you know, from the, what we know now and if we look at the demographics of the people that have died and that have more severe illness, you know, the ones that are admitted to the icu, they tend to be older, you know, so clearly over.

You know, 80 is, you know, the, the mortality rate rises quite significantly in people over 80, but even it seems to be above 60, yeah, you have an increased risk. And then combine that with, uh, sort of co comorbid illnesses. So, high, high blood pressure, hypertension seems to be a big one. Diabetes, cardiovascular disease.

And then anyone who's immunocompromised, you know, either because of a disease. That they have or because of medications that they're taking, uh, could be more susceptible to it. But the big ones seem to be high blood pressure, cardiovascular and, uh, disease and diabetes right now. Now interestingly, and I don't want to geek out too much, but I kind of do the, the, there's this receptor called ACE two that we've spent about.

25 hours talking about, um, that is the receptor that this virus, uh, attacks and that, do you think that that's related to why people with hypertension and cardiovascular disease are, are potentially more susceptible? I. Yeah, you know, it's a really good one. And, um, we are, you know, there's a lot of debate going on right now as to the significance.

But yes, we do know that ACE two, which is uh, stands for angiotensin Converting Enzyme two, which is found on the. Surface of cells. You know, in our lung, the pneumocytes in our lung, it sound and the surface of cells, uh, the enterocytes in our gut. Um, that's how the, the spike. So the little, I'm sure everybody's seen pictures of the coronavirus.

It looks like, uh, a little ball with these spikes sticking out. Um, that's, it looks like a crown, right? That's why we call it corona, which means crown coronavirus. Nothing to do with the beer, even though their sales went down significantly because of this. But, but it binds, those spikes bind to the ACE two, uh, on the surface of the cells.

And that's how in conjunction with a, a protease another enzyme, it, it g gains entry to the cell that way. And so there's a lot of speculation as to, you know, is, um, certain things like when you're taking certain drugs, when you have certain conditions like diabetes, they tend to have more of these a. Two, uh, enzymes on the surface of their cell.

And so there's thought that when you have more of them, you actually make yourself self more susceptible or you're more susceptible to the virus gaining entry and infecting you. So does that, I think, you know, I think clearly that's a piece of the puzzle as to why some people are more susceptible than others.

I don't think it's the full piece, uh, it's not the full puzzle, but it is definitely a significant piece. And then this one, we're gonna dive into a little bit over that, maybe now or later. But you know, it's, it's. I, I, I, I described, uh, uh, dealing with this outbreak as trying to feel your way through a dark room with your eyes closed.

Yeah. Um, exactly. And so, you know, it was interesting because we both have a lot of patients who are on drugs that act on the angiotensin converting enzyme enzymes, and so they're an. There's ACE inhibitors and then there's angiotensin. There's these other drugs that are receptor blockers, but they're kind of working on those and, and initially some information came out saying, oh, everybody's gotta get off of those drugs.

And then, Another day or so people came back and said, well, maybe not so fast. Um, and so then obviously mm-hmm. That's a, a whole bunch of people are at home sitting trying to figure out, should I take my blood pressure medicine, should I not? And I know mm-hmm. You've done some deep thinking about that from, at a high level, what is your sense about what people should do about.

Uh, the two categories of drugs mm-hmm. That, uh, that the, some of our probably more vulnerable patients who are, who have high blood pressure and who are trying to figure out how to manage themselves in this kind of crazy situation. What, what are, what are, what are your, your, your thoughts about that? Yeah, I mean, it's a really good question and you know, as you said, we've had many discussions on this already and, and really delving in and I think clearly we just don't know the final answer yet.

So that's number one is there's a lot of. Speculation happening, a lot of hypotheses, and we just don't know what we, um, so from a high level, my recommendation currently, I always leave it open as we find more information. But right now, if you're currently on an ACE inhibitor or an angiotensin receptor blocker, so the, as you know, the ACE inhibitor usually end that in pri, right?

Like, Cil, um, the, the ARBs or the angiotensin receptor blockers and in artan, so losartan as an example, um, if you're currently on them for heart disease or blood pressure control. Um, I would stay on them. I would not change that medication because of what's going on right now. At the same time, because we don't know if you're starting a brand new medication for blood pressure, maybe you would choose.

Not to start one of these until we have more information on it, because there is to, to your, what you said earlier, we know that these medications, um, can increase the ace, uh, two on the surface of cells, but we also know that they can. Potentially make that ACE two less susceptible to the virus attaching to them.

So they kind of do both. They increase the number and they may make it less susceptible. So they, you know, they were actually being looked at as treatment for coronavirus for this, uh, SARS COV two virus. Um, so. I think that we're, we're sort of playing the middle road here. You know, don't go off of them if you're on them.

Um, and, you know, maybe just hold off and start a different one if you're not currently on one. I think that's really, really, I love the way that you said that. And then, um, Th that, you know, we, we've, we've, we're making a lot of about turns on, on big, big topics where all of a sudden, and so it, it, it, it, I think it highlights the concept of slow slowing down, taking a breath, and, um mm-hmm.

And, um, and, and fortunately we've got new science coming in every day. Um, so then here, let, let's tell me, let, let me lay this one on you, because I've been, you know, reading these articles about how people present and mm-hmm. You know, initially, This was what was coming out was this is gonna affect the epithelium in your nose and your nasopharynx.

And your oropharynx, which is basically your throat in the area behind your nose. And so everybody was looking for a sore throat and this, a little upper respiratory prodrome before people started to get, mm-hmm. Sometimes it would go down into the lungs and it can cause a pneumonia, and then they, they can keep going and we will go there.

Um, yeah. Now we're hearing about people who are presenting with abdominal pain. And nausea and some abdominal symptoms. Some people have those and they don't have the upper respiratory. And then some people have the upper respiratory and they also have abdominal symptoms, and that's because this receptor that we're talking about called the ACE two receptor, happens to be on cells in your intestine called in Enterocytes.

Huh? That's exactly right. Mm-hmm. And, and, and, oh, go ahead. Mm-hmm. Go ahead. No, that's fine. Keep going. Well, so then my, um, so then one thing that I think both you and I have found over the years is that if somebody has. Inflammation in the gut. I e leaky gut, i e parasites. They may, the small intestines supposed to be sterile, but let's say some bacteria went on a road trip and went up there, that's called small intestinal bacterial overgrowth.

Or maybe they just have an imbalance between the good and bacteria, which is called dysbiosis. There's a whole bunch of other things. Then, uh, We know that those people are more susceptible to getting another thing happen to them. And so, for example, uh, and uh, if somebody already has four infections in their gut, it's real easy for them to pick up a fifth.

Um, and so it, it makes me wonder if having some of those problems might predispose someone. To getting a gastrointestinal version of, of this, of this coronavirus, and I was wondering what your thoughts was on that. Yeah, nicely, nicely said. And I, it's a really good question. Um, you know, to reiterate what you said is that, um, sometimes people will present with only gastrointestinal symptoms and not respiratory symptoms, right.

Uh, diarrhea, vomiting, abdominal pain seem to be the big ones that they present on. And sometimes that starts and then they develop respiratory, um, symptoms as well. The good news, and again, this is very preliminary data, so we don't know the whole story on this, but it, the good news is that it seems to be that people that do have the digestive symptom component of it tend to be, uh, have less severe, uh, respiratory illnesses.

Not always, but in general, there seems to be a link between that in, in gastrointestinal symptoms and less. Um, Less chance that they might die from the respiratory, uh, symptoms or, uh, infection. But the other thing is that, uh, just on this vein, we clearly know that, um, the, this virus coronavirus can infect.

The gut, um, just like you said through the ACE two on the surface of the enterocytes, um, we know that people sh also shed the virus in the gut, so that's another thing. You know, we're always very, very careful about, uh, not touching our face and not putting it in through our mucus membranes and our eyes and nose and mouth.

But, um, people. Seem to be shedding that virus in their stool as well. And even when people have gone through a respiratory infection and then they test negative, if you do a swab, they actually are able to, you know, shed the virus in their stool for another up to two weeks. Um, or more. The virus is still showing up in, there's stools.

So, you know, the whole idea of. Good hand washing after using the bathroom and really being careful from that perspective as well. Just kind of wanted to throw that out there. And so, coming back to sort of your original question is, you know Yeah. The immune system, uh, we sort of in, in the functional medicine world, look at the gut first, right?

I, in terms of when there's any type of inflammation or autoimmune disease, we always wanna see, um, what's going on in the gut. Do they have the. You gut, and we can get into that in a lot more, um, later map. But, uh, and part of the reason is because the immune system, you know, 70 to 80% of our immune system actually lives in the lining of our gut.

So just on the other side of the, the lumen of where our microbiome is, all the bacteria, so clearly, um, our gut is. Central in how our immune system is really working and functioning. And so I think that's going to be very relevant in terms of, um, how we can, you know, potentially deal with this virus, um, by approaching the gut, uh, in terms of treatment.

Okay. So we've come this far, so I think we deserve to just keep going just a little bit more. So then Okay. Let's, so then let's say, That we've got somebody they, they may have picked up a gastrointestinal version of it. They may have picked up a respiratory version of it, but let's say they had a sore throat and it went down to their lungs and then they started coughing and they got a pneumonia, and that pneumonia was going along.

And then let's say that it turned into, they became, they got this thing called the cytokine storm. And became mm-hmm. Septic. Mm-hmm. Tell us in your words, how, how, how do you like to explain that to people? What's your, how would you define that sequence of going, of how, and in particularly how this virus can lead to the cytokine storm, and then what, what that means.

Yeah. So, you know, cytokine storm and, and yeah, that's a, a great term. I'm glad you brought that up. Um, it, it's referring to our immune system. So the way that our immune cells signal to each other, uh, is by producing cytokines. So cytokines are just molecules that act as signals and they can attract other types of immune cells.

They can. Make them change what they do and how they act. They can make them attack and kill. And, um, when the sort of, you have this massive release of cytokines, we call that a cytokine storm. So you can imagine that, um, your lung cells get infected with this virus, uh, and your immune system is trying really hard to, you know, recognize our immune system's.

Very good at recognizing. Cells are infected with, um, viruses and trying to, you know, either kill those cells that have the virus inside them in order to clear that virus and protect us. And now in some people what happens is their immune system just gets kind of over rambunctious. And it acts too strongly and you get this cascade effect and all of these cytokines released with this massive inflammatory reaction in our lungs that ends up causing kind of our lungs become really leaky and all of this fluid because of that.

Because when our immune system attacks that can, uh, kind of cause leakiness, we all know, um, sort of the hallmarks of inflammation, you know, redness. Swelling. Right? That swelling when something's inflamed, that's part of the immune system just making blood vessels leaky. It happens in our lungs as well. It makes them leaky.

And when you have this fluid accumulating, it's something we call a R D F. Right. Acute respiratory distress syndrome. It's a well known phenomenon that happens for other reasons, other viruses, other things can do it. But that seems to be, uh, one of the things that this virus is good at in certain people, and.

Is is causing that cytokine storm cuz their immune system just goes overboard and, and getting that their lungs filled up. And then of course, you know those people need oxygen. They need to be intubated, they'll need to be on a ventilator so that we can help them breathe. Right. And sometimes we even use ecmo, which is this extraoral, um, membrane oxygenation.

So we, we give oxygen into their blood when their lungs aren't working really well. And, and when we support people through that, a lot of people can survive. Uh, when they get that appropriate ventilation and care, some people don't, you know, we're not perfect at it. And, and it does have quite a high mortality rate still, but it's that overwhelming of those ventilators that is really the problem right now with our, you know, the whole.

Uh, too many people getting it all at the same time. So that's kind of the, the sequence of events. It also seems to be kind of this, um, multi-organ failure. So there are these receptors. It looks like this virus can also get into, you know, the heart, uh, the liver, uh, kidneys. And so, you know, when you're not getting enough oxygen in your blood, when your other, uh, organs are affected, then clearly everything kind of just shuts down.

Yeah, it's interesting cuz I read some, some literature that, um, if you look even people who are positive of having the virus in their throat, the probability that it's in their blood is super, super low. But mm-hmm. If they get a pneumonia and then they become septic and then all of a sudden all the blood vessels in the lung get leaky, that's when some of that virus gets into the bloodstream, and it's only then when it's able to go to the internal organs like the liver and the heart and the kidney.

Exactly. That's right. That's right. Now, you know, it's that leakiness of the, that causes a problem. You know, leaky gut, leaky, leaky blood vessels, leaky lungs. Um, that seems to be, you know, one of the things that causes the more severe cases. So we need a plumber for the body to fix all of the leaks. Yeah, exactly.

We need to fix the leaks, essentially. Do, do you have a sense in your mind of. If, if we go back to that term of an avatar or an archetype of the person who's most likely to go from having a pneumonia to, all of a sudden the cats are the dogs and the cats and the horses are out of the barn and everybody's running.

Mm-hmm. I mean, I think that, I think that's the, sort of similar to the one, the high risk people, right? And the reason they're high risk is because they're more likely to have that severe cytokine storm. So the, the elderly, um, the, uh, people with high blood pressure, you know, um, diabetes, cardiovascular disease, those are the ones that.

Tend to have that severe reaction. And, you know, so our immune system isn't, um, you know, and, and again, this is a great topic to get into. Our immune system isn't one thing. It's not on or off. You know, we talk about immune boosting our immune system. That's not really an accurate way to think about it. You know, we can support our immune system, but our immune system consists of, you know, cells that cause inflammation.

Inflammation is a, a really critical part of being alive, you know, um, inflammation. Helps us, um, you know, Attack different bacteria and viruses and other things that we're exposed to. Inflammation helps heal damage and heal wounds. Uh, so without inflammation, none of us would be alive. So we need inflammation, but we also need to turn off the inflammation once we're done with it.

So once you've cleared that infection, once you've healed that wound, then we need to turn off the inflammation. And so that's another, you know, aspect of the immune system. We have sort of the, we can think of the immune system as the innate immune system. So that's the part that causes inflammation that.

Kind of the first responder, if you think of it that way. Then you have the adaptive immune system, which will be the, the second responders, and then you've got the regulatory part, which kind of now, okay, we're done. Now we can dampen it and shut off the, that the inflammation we don't have to do anymore, we're done.

And when you can't turn it, Off. That's when you get a lot of issues that leads to the chronic inflammation that's associated with many, many diseases. And when that's really, in this case, when you can't turn it off and it just keeps going, um, that leads to the issues we were just talking about with the pneumonia and the a r d.

Right. And you know, it's interesting, I used to. We used to, I used to see a lot of patients with a r ds back in my anesthesia days. I bet. Mm-hmm. And you know, I thought, uh, that I was 100% past that. But surprise, surprise. Exactly what goes, comes around again, doesn't it? What goes around comes around. Isn't that true?

Mm-hmm. Um, and then also just so, so people know you have a, a deep. Um, and a biting interest in immunology. But, uh, uh, you have a, a real medical background too, cuz you have a, you have a, you teach functional medicine, but then mm-hmm. You, you, you went to a residency and your, your residency was in. Family medicine.

So I did, yeah, I did family medicine residency. Mm-hmm. So I did, uh, a PhD in molecular immunology, you know, kind of the genetics of the immune system, really. That was what I worked on. And then, uh, went into medicine, uh, did med school and did family medicine mostly. Because I wanted to really bring some of this amazing stuff that we were learning in the scientific world into, you know, helping people in real time, kind of into the clinical world.

And that's really sort of been what I try to focus on is, is trying to really bring that science and the clinical together. Well guess what? This is maybe the greatest opportunity of your entire life to help people in real time. It is. I know. And it's, uh, I mean, it's just an amazing, and you know, I obviously, I feel so much for the people who are suffering and, and going through this, you know, dying from this, um, and the people who are out of jobs and, I mean, it's a terrible disaster for the world.

It's also a, a time where we're learning so much, you know, kind of what I started out at the beginning where, uh, just studying the, the medicine, the biology, the physiology, the sociology, psychology of what's going on it, it is an amazing opportunity. And it's an opportunity to really bring people together.

Mm-hmm. You know, where, I know we're talking about social distancing, it's really physical distancing that we're talking about, not social dis