Q&A #10: COVID-19 Immunity—Vitamin D, Vitamin C, Cytokine Storms, & Sauna

Hello, everyone. Glad to be back. Welcome back to round 10 of our FoundMyFitness Crowdcast series. I have no doubt that everyone's lives have changed pretty, pretty dramatically since the last time we had this hangout. There's a lot going on in the world. with the COVID-19 illness. We are going to discuss a lot of that today. There were a lot of questions related to COVID-19. Before we, we dive into everything, I just want to make sure everyone has access to this Crowdcast and previous Crowdcast videos, as well as the audio only. You can find access to those on your members dashboard at foundmyfitness.com/ dashboard.

That'll take you to links to the YouTube videos where they're recorded if you'd like to watch them, as well as there's a SuperCast private feed which all subscribers should have access to. And if you haven't downloaded it, you'll, you'll get a link to download that as well so you can listen to this in your podcast feed player. I also just want to say that because we're going to be talking a lot about COVID-19 and other immune-related issues as well as, you know, potential supplements involved in boosting immune system. I just want to remind everyone that this is not medical advice.

This in no way, you know, I am not a medical doctor, so there is no patient-doctor relationship here and that you should always Always talk to your physician when you change anything in your routine, any supplements, any medications, anything like that. You need to speak with your primary care physician. Um, and, and so this is definitely not medical advice. So please just take this information and, um, use it for information purposes only, or use it to share with your physician. So with that, we are going to be— we're gonna get started. And I see that Jessica is asking in the chat, is it true that I will only be discussing coronavirus?

There is definitely a— This Crowdcast is heavily focused on COVID-19 or things that are related, immune factors that seem to be sort of related to COVID-19. There's a few other questions as well. I'm also going— I'm also releasing another COVID-19 Q&A next week. It's an hour-long podcast where I go deep dive into a few really important questions as well. So I'm trying not to have too much overlap there. All right, so I'm going to get started, and I kind of rearranged these questions a little bit so that they, they make sense, starting with explaining things.

There were some questions wanting to explain what, what a cytokine storm is, how people infected with COVID-19 have a cytokine storm, explain Possibly how to prevent that and how to, you know, potentially boost immune system to handle that. So we'll start with that. Alright. Sorry, just one minute. I feel like that was not the question I wanted to begin with. Sorry. Yeah, I'm gonna start with another question. The first question, and I'll go back to the cytokine one, the first question has to do with, can you explain the mechanisms of SARS-CoV-2 infection and pathology? So SARS-CoV-2 is the virus that causes the COVID-19 illness. So let's talk a little bit about the mechanism of infection.

So coronaviruses have spike proteins, and these spike proteins stick out from the viral particle to anchor themselves onto cells. It's sort of analogous to a tennis ball getting stuck onto Velcro. And the features of these viruses, there's kind of like a These spikes kind of look like a crown. So that's why they got their name coronavirus. And one of the receptors that these spike proteins can bind to is the human ACE2 receptor. This receptor is an enzyme— binds to— it's basically an enzyme that normally helps regulate blood pressure. And that happens through the effects of sodium and potassium. So this virus binds to ACE2 and actually inactivates it, leading to the excretion of potassium.

This explanation is supported by the finding that excess potassium is found in urine in patients with basically hypokalemia and indicates that potassium loss is mainly through the kidneys. And this is also common in COVID-19. So the cells then engulf the virus and the virus uses our own cells to make new viral proteins. And basically these viral particles then are released and the cycle repeats. So unlike bacteria, which can replicate on their own, viruses are not technically alive. They need the host cell to replicate. do everything. So it's really the spike protein on the envelope of the virus that actually determines what kind of cells the virus can infect. In terms of the pathology, we know that coronaviruses in general are responsible for like 15 to 30% of the common colds.

There are certain strains that have different pathologic properties. For example, there's coronaviruses that are responsible for SARS-1, which was in an outbreak in China in either 2002 or 2003, and then MERS, the Middle Eastern coronavirus that also happened a little bit later than that. So there's a variety of different features of these coronaviruses. The specific SARS-2 coronavirus, in addition to affecting or infecting lung cells, it can also infect immune cells such as macrophages, dendritic cells, And while it does not necessarily reproduce in these immune cells, it can overstimulate the immune cells to produce pro-inflammatory cytokines and produce a cytokine storm, which we'll talk about in just a minute. There's also parts of these viruses that are non-structured.

They promote cellular mRNA degradation. They block— basically, they block the host cell's innate immune response. So it's a kind of a tricky way that it's able to inhibit important cytokines that are released early on in infection, like interferon, which signal to the immune system there is a threat and we need to basically fight this threat off. So the SARS-CoV-2 virus is very good at basically blunting the body's innate immune response. Particularly does that better in some people compared to others. And so that initial interferons response, which is really important for activating the innate immune system, seems to be not occurring in some people. Some other features also have to do with these non-structured regions are basically Shielding viral RNA from being recognized from the host.

That's another way they're basically able to stop the host immune cells from fighting it off because they're able to shield their recognition sites from the immune system. So there's lots of things like that going on. A lot of different clinical presentations. I'm sure many people have already read in detail a lot about that, so I'm not gonna go into too much detail about that. There are a lot of similarities to other viral respiratory infections with COVID-19. In a study in 138 hospitalized patients from Wuhan, initial symptoms were fever in 99%, but in another study, fever was only present in 44%, and another study was only 89%. So it seems to be a huge variation in some of these clinical presentations like fever, Fatigue. Fatigue. 70% of people seem to have fatigue.

Dry cough in about 60%. There's also loss of appetite in about 40%, shortness of breath in 30%, and a variety of other little potential clinical presentations as well. Some people have sore throat. So other people have digestive symptoms. Diarrhea is another one. In terms of clinical outcomes in pediatric populations, I'm gonna go into this in more detail in another podcast, but about 55% of children are asymptomatic or mild symptoms. 39% can have moderate symptoms including pneumonia or a dry cough, fever, possibly even lesions on the lung. 5% of children can have a severe— and this is according to the most recent data as of March 31st. 5% can have more severe symptoms: fever, cough, GI symptoms, shortness of breath, and also decreased oxygen saturation.

And only about 0.66% of the pediatric population experiences respiratory failure and heart failure, as well as multi-organ dysfunction. Infants less than 1 are more likely to have a severe infection, and children were mostly infected by household members and child-to-child transmission, and also fecal-to-oral transmission may be possible based on studies in children. So that's sort of a brief overview of some of the mechanisms and pathology. I want to go in a little bit detail on the cytokine storm. This was another question. That was submitted, which I initially read first, and it has to do with explaining what a cytokine storm is and if there's any ways to prevent it.

So cytokines are, as I mentioned, they're initially released by the immune cells to help communicate with each other and to signal to the immune system that there is a threat and we need to ward off this threat. Cytokine storms are a part of the sepsis process where basically there's an overstimulation of the immune system and that can impose a lot of damage and risk to the body. So the best way to prevent the cytokine storm is to have the initial innate immune response happening so that your body initially deals with the threat and doesn't try to overcompensate later on by producing tons and tons of different cytokines, which can lead to a cytokine storm.

So really the important factor in trying to prevent a cytokine storm, and we'll get into genetics in a minute, but genetics aside, the important thing is having that innate immune system well-functioning and optimal and primed to respond initially when there is an infection. Uh-huh. When there actually is a cytokine storm already present, that's obviously not the time you wanna boost your immune system even more because your immune system's already sort of over-responding, and there's a lot of— there's a lot of conflict and nuance in medical practice in terms of how to treat cytokine storms. You know, some treatments involve giving things that can dampen the immune system, such as steroids.

In this particular case, I know that the World Health Organization has recommended against steroids for the treatment of COVID-19. I don't know if that's in all cases or it depends on where in the illness. I think that's obviously something that's outside of the scope of this discussion, but— Typically, again, the important thing is trying to prevent the cytokine storm, and that typically occurs by having a normal innate immune response early in the infection. There are some genetic links to overactive immune systems and cytokine storms. This is a really fast and growing research area. Lots of stuff that's still unknown, but I'll just give you a couple of examples.

So those people that have a hyperfunctioning— so there's a single nucleotide polymorphism, a SNP as they're referred to, in the toll-like receptor 1, TLR1. And people that have this certain SNP have a more hyperfunctioning toll-like receptor 1. And studies have shown that people with that specific SNP are more likely to die from sepsis. when they're infected with certain types of infections than people without that SNP. There's another SNP in another toll-like receptor, toll-like receptor 4, and the same thing where it's— they're more likely to die from sepsis when they're infected with a certain type of bacterial infection.

I don't know about— I think right now with SARS-CoV-2, there are researchers looking into potential SNPs, and there have been some possible hypotheses that certain SNPs may play a role. We're not going to discuss that right now, but that is a topic that I am reading about and also my team is looking into as well. So the next question is, it's a really big one, and this question has come up several times in a lot of different formats on Crowdcast. It's come up on the Q&A form that I sent out on the newsletter where I'll be answering these COVID-related Q&A questions this coming week. It's come up on social media posts, and it has to do with vitamin D and COVID-19 illness and risk for COVID-19. And the question specifically has to do with, does vitamin D increase ACE2 receptor expression?

And if so, would taking vitamin D increase the risk for infection with SARS-CoV-2 in the lungs? And I want to start off just by saying that it is, after doing lots and lots and lots of literature reviews, myself, my team, other scientists, other collaborators I'm working with, It is our conclusion that vitamin D is very important for preventing respiratory illness and possibly extremely important in COVID-19 illness. I personally think that vitamin— having sufficient vitamin D levels is extremely important. Some interesting data coming out of the United States as well as Sweden. What we know is that— so let's take a step back. Most people know this, but we'll do just a brief overview.

Vitamin D is a steroid hormone, and vitamin D3 is predominantly made in the skin, and it's made in the skin upon UVB radiation exposure from the sun. So you have to be out in the sun. There has to be UVB rays hitting the atmosphere in order for you to make vitamin D in the skin. A lot of things can regulate that process. One of the main things is melanin. It's responsible for the pigmentation that helps prevent the burning of UV rays. So it's people that have— that are genetically from regions that are more equatorial regions, that are closer to the equator, tend to have more melanin in their skin, and they tend to be darker skin. And the reason for that is that it protects them from the burning rays of the sun.

On the flip side, because it filters out UVB radiation, it also filters out the ability of the body to produce vitamin D3 from the sun. However, most of the time people in these equatorial regions are out in the sun quite often, and so they are still getting a lot of vitamin D. When you take a person with with a lot of melanin, with darker skin, and you move them to a region that is not equatorial, you move 'em to, for example, Sweden, or parts of the United States that are more northern latitudes where UVB radiation isn't as prevalent as places in the southern parts of the United States, like Southern California, for example, you end up having people that are at very high risk, and data has shown— are the most vitamin D deficient populations.

And these people are African Americans in the United States. In other countries like, for example, Sweden, a lot of Somali immigrants have immigrated to Sweden. And right now we know that the Somalis in Sweden are, right now they're getting, they're becoming infected with the SARS-CoV-2 virus and coming down with COVID-19 illness much more readily than people from Sweden with lighter skin that make more vitamin D from sun exposure. Similarly, in the United States, not everyone is breaking down the data according to ethnicity, but there have been some preliminary datasets coming out of different states that there seems to be a very high prevalence infection rate with African American populations who are, again, that they have been shown in many different NHANES studies that have been done over the years.

African Americans are the most deficient in vitamin D in terms of different ethnicities from people that live in the United States. So other things that also regulate vitamin D synthesis in the sun also your age. So as people age, their body is less efficient at doing that. And of course, older people are much more vitamin D deficient than younger people. So that was kind of a just really brief over— you know, view of how to make vitamin D and also just some interesting epidemiology data coming out showing that it seems as though people that are that we know are the most vitamin D deficient are also the most susceptible to COVID-19 illness. So to get back to the question specifically about vitamin D and ACE2 receptors.

So if you remember correctly, ACE2 receptor is how this specific coronavirus binds to the surface of cells and gets in. So the spike protein extends from the membrane envelope on the virus, and it's able to bind to cells that have an ACE2 receptor. Many organs have cells with ACE2 receptors, such as lungs, heart, kidney. And I mentioned the ACE2 receptor is responsible for— it regulates the renin-angiotensin system, which we'll talk about in a minute. But once the virus binds that ACE2 receptor, The cell engulfs the virus, and basically the virus then uses the cell's machinery to replicate. SARS-CoV-2 enters the human cells, and basically then, you know, you can start to— as the virus starts to replicate, you can start to have more infection.

as more viral particles bind to more of these ACE2 receptors. Here's the thing. We know from SARS-CoV-1, the first SARS, we know that actually that infection downregulates or decreases ACE2 expression levels. And actually this may be involved in disease severity. And other studies have shown that when ACE2 levels go down, there is all sorts of problems with the renin-angiotensin system. ACE2 acts alongside ACE, the angiotensin-converting enzyme, to regulate blood pressure and inflammation and also body fluid homeostasis. So this renin-angiotensin system has to be balanced. It has to be balanced to perform its functions. And we know that ACE2, that receptor, plays a critical role in balancing the renin-angiotensin system.

So in disease models, we know that imbalance of this renin-angiotensin system with lower ACE2 expression can result in hypertension, heart failure, kidney disease, serious lung injury, including acute lung injury, also known as acute respiratory distress syndrome, ARDS, which is a complication of COVID-19. So we know that having more ACE2 protects against that from happening. So this balance is really critical and it requires ACE2 expression to be higher in order to have that balance. If renin-angiotensin system activity, it's also referred to RAS, if that activity becomes imbalanced, then a lot more of these severe events can occur. This can be the case when SARS-CoV-2 also binds to ACE2 and starts to downregulate ACE2.

We know that basically the loss of ACE2 function results in neutrophil infiltration and inflammation into the lungs and causes acute lung injury. This was found in a mouse model. Loss of ACE2 function released pro-inflammatory pro-inflammatory cytokines, all sorts of problems in the airways. It increased neutrophil infiltration and caused lung inflammation and injury. It's like a vicious cycle. So people that are actually at increased risk for a decreased ACE2 expression is people with chronic diseases like type 2 diabetes, heart failure, Basically all the diseases that put people at an increased risk for COVID-19 illness, their chronic diseases lead to an imbalance of the renin-angiotensin system and lead to ACE2 receptor decreases.

We know that it also decreases with age, and males actually have ACE2 levels that also seem to decrease with age. So the ACE2 gene's on the X chromosome, so women have higher levels of ACE2. And from data coming out, multiple countries, it seems as though males are at a— they're at a 2 times higher risk of dying at a younger age from the COVID-19 illness. So it's very interesting that All the same factors that put people at risk for COVID-19 illness happen to be not factors that increase ACE2 expression, but factors that are associated with decreased ACE2 expression, which again leads to decreased renin-angiotensin system regulation. We know that, let's talk about vitamin D. Vitamin D and how vitamin D comes into this ACE2-renin-angiotensin system.

But before we get to that, I just wanna mention that vitamin D really is one of the most— it has been so well studied in terms of its very important role in decreasing the risk of respiratory tract infections. Multiple meta-analysis studies have found of randomized controlled trials which is the gold standard for testing whether or not something has an effect on a disease, shows that basically it's protective. And people that have low levels of vitamin D, it's protective by more than 50%. Supplementing with vitamin D in people that have low levels of vitamin D at baseline, for example, African Americans, which we know have the lowest, some of the lowest vitamin D levels of anyone in the country in the United States, supplementing with vitamin D cuts their risk of respiratory tract infections by more than 50%.

People that already have normal levels of vitamin D, which oftentimes normal levels are considered around 30 nanograms per mL, those people still had a protective effect of cutting their risk of upper respiratory tract infection by 10%. So again, vitamin D is playing a big role. And these are randomized controlled trials. This is hard empirical data. This is not theoretical hypothesis. This is facts. We know that the severity during a cytokine storm, the renin-aldosterone-angiotensin system, R-A-S. It's severely disturbed. And this whole purpose of this system is to regulate blood pressure. And it does through a variety of different enzymes including ACE2. It's involved in the kidneys, adrenal glands, the lungs, heart, and brain.

Vitamin D normalizes the renin-aldosterone-angiotensin system, this RAAS system. Uh-huh. To, to, to, to be in a variety of different diseases. It's been shown to do this in so many different, different types of diseases. And this one of the studies that people refer to and are worried about taking vitamin D because it was shown to increase an ACE2 receptor. Again, everything I've been talking about has been talking about why you actually want increased ACE2 receptors. To regulate the renin-angiotensin system and the renin-aldosterone-angiotensin system. Very important. And how infection with SARS-1 and SARS-2 seems to downregulate that system. Even though the SARS-2 virus is binding to that receptor to dock, it's downregulating that system.

And it's having— that's having a major effect on disease severity. The There was one study in mice, mice that actually had acute lung injury. They had acute respiratory distress syndrome, ARDS. These are interchangeable terms to express acute lung injury, which again is a very severe complication of COVID-19. Those mice that were given vitamin D did increase their ACE2 receptor expression. Yeah. Not— I mean, we're talking actually it was just mRNA that was looked at. We didn't even see the actual protein, but it protected against the acute lung injury because it did that. And it did that because it regulated the renin-aldosterone-angiotensin system. So yes, it did lead to an increase in mRNA of these ACE2, you know, mRNA that makes the ACE2 receptor protein.

But it also protected from the lung injury. And I also want to mention that, first of all, this is an animal study. We don't even know how much it's increasing the ACE2 receptor protein function. It may just be a very tiny increase. It may just be enough to help regulate this whole renin-angiotensin, renin-aldosterone-angiotensin system and protect against the acute lung injury, protect against ARDS, the acute respiratory distress syndrome. And we know from clinical human data that it does that. It protects against respiratory infections.

And so if you're looking, you gotta look at the data and go, okay, if there's even a 5% increase in mRNA in this ACE2 receptor, these mRNAs that makes the ACE2 receptor protein, and yet there's a 50% protective effect in protecting against lung injury, yeah, there's a net benefit effect. I mean, you can't take something in biology and just pull it out of context. When you're talking about vitamin D increasing ACE2 mRNA and you go, oh my goodness, well, that makes the ACE2 receptor. That's how the virus gets into the cell. I better not take vitamin D. It's gonna increase my risk of infection. That's complete absurdity. That is not how biology works. You have to look at the whole picture. You have to look at all the interacting systems. Context is so important, so, so important.

And everything in this, in this, in the biological systems here indicates that vitamin D is protective against acute lung injury. It's protective against acute respiratory distress syndrome. It's protective against upper respiratory tract infections. And basically, any sort of worry that vitamin D is going to potentially put you at a higher risk for infection, to me, is very— it's unsubstantiated. There's just unsubstantiated evidence of that. We also know that another study in rats showed that vitamin D also did increase ACE2 levels But this was not in cells. This was actually soluble in the blood. So basically, it could be protective because having more ACE2 could potentially even in the blood bind up these viral particles and prevent them from infecting cells.

You see, there's so many moving parts here. There's so much nuance. There's so many things you have to consider. And someone— Yeah. Finding a study and saying, oh, vitamin D leads to increased ACE2 expression in these couple of animal studies can really be misleading to people. And it's— I am extremely concerned that people are concerned about supplementing with vitamin D when that's like the one thing that's very, very, very possibly gonna protect people from COVID-19 illness. I think there is very much evidence, very strong evidence to suggest that it will be. So to kind of just to wrap this part up, there was a study published titled Using AT1R Receptor Antagonists, which are basically, they're used to increase ACE2 expression. which increase ACE2 expression to treat COVID-19 patients.

And while this seems a little counterintuitive, several observations from studies from SARS-CoV-1 seem to suggest otherwise, that when the coronavirus spike protein binds to the ACE2 receptor, it leads to ACE2 downregulation, and that results in excessive production of angiotensin. And while less ACE2 is available to convert it into the vasodilator, it contributes to lung injury and pulmonary vascular permeability and actually can lead to increased lung pathology. So higher ACE2 expression following, you know, following the SARS-2 infected— people with SARS-2 infection may actually have a protective effect on acute lung injury. So really, I think, again, it's just a matter of understanding that the whole biological processes and interacting systems are important to keep in mind here.

It's not just a simple thing like, oh, ACE2 receptor increased, bad. No, that's not the case. It's not just as simple as that. In fact, you want more of the ACE2 receptors expressed to protect from the lung injury, to regulate the renin-aldosterone-angiotensin system. So I think I've gone into way too much detail on that. And as you can tell, I'm very passionate about this because— and I'm actually gonna go into this again in my COVID-19 Q&A, which this podcast is a private one, so please do not post this on public forums. I will be repeating this information in even a little bit more detail, and I will be posting it on my YouTube, FoundMyFitness YouTube channel, and also on— Awesome. ITunes. So this information is going to get out there next week. I will move on.

Bobby's asking, what about taking ACE2 inhibitors for lowering blood pressure? That is another question that my team and I are looking into in great detail. So it's not going to be answered in the first round of the COVID-19 Q&A. That I'm going to be releasing next week, but it probably will be in the second one that I'm going to be releasing. So another question, and this question was also asked quite a few times in some form or another, has to do with vitamin C. And the question is, what role does vitamin C play in interferon, and would taking vitamin C increase risk for COVID-19? Would love to hear your rationale as to why you believe the benefits of vitamin C outweigh the potential risks.

And this was kind of a multi-question that I broke down into Several parts because it's just a very big question. So let's just first start off quickly by talking about the role interferon plays in COVID-19. So interferon is the alarm system for the immune system. When a human cell recognizes virus or any signs of virus in the cell, it releases interferon. It really heightens the cell's antiviral response. It informs nearby cells to also heighten their antiviral response. It calls the immune cells to the location where the virus is to fight it off. Without interferon, the immune system is not properly activated, and subsequently, the host is not able to fight off the infection.

So again, we talked about this earlier, the SARS-CoV-2 virus seems to be particularly good at blunting that initial interferon response, particularly in some people, people that seem to be more prone to severe illness, severe COVID-19 illness. Later in the game, After you've been infected with a virus, the virus has been replicating, it's been spreading in other cells, too much interferon at that point can be a problem. It can lead to a cytokine storm. And so I think people hear about cytokine storms and the role of interferon in cytokine storms, and they think, oh my goodness, I need to do everything I can to not make my interferon. They want to dampen their interferon, and that's just not the case.

You want to keep your immune system primed to have that good interferon response initially. So the way that SARS-CoV-2 has some really nasty tricks that can basically make the interferon response blunted at first and then slingshot it into making an overactive— having an overactive interferon response and cytokine storm. So initially it hides from the immune system and, you know, so there's no interferon being released. And one way it does this is by infecting the immune cells that are macrophages and dendritic cells. And this kinda buys them time to replicate, and then it overstimulates the immune system with the excess interferon, and this is where the cytokine storm comes in and the respiratory distress syndrome or shock happens. So what about vitamin C?

Well, vitamin C, it's an essential nutrient. Most of you guys know we need to get it from our diet. We don't make it. Humans don't make it. Uh-huh. It plays a very important role in the immune system, and people that are actually deficient in vitamin C have increased risk of complications from viral respiratory infections. We know if you look at one animal study in mice that were— so mice actually make vitamin C, so you have to do some genetic tricks to kind of help to make them vitamin C deficient and then supplement them with vitamin C to kind of give them more of a human-like scenario there.

So when you make mice deficient in vitamin C, they have lower interferon levels because vitamin C is important in that initial interferon response, and they're much more likely to die from influenza virus, for example. So when you then give them vitamin C, their vitamin C levels raise and they have a normal response to the influenza virus and they don't end up dying. So my team and I have been working over the last several weeks on a vitamin C topic page. Right now it's about 27 pages long in a Google Doc. We've been all collaborating together. Massive, massive article we're going to be releasing Also next week, and I'll be doing a podcast on that as well—a very, very in-depth podcast.

But I do want to speak a little bit about vitamin C, and it's something that I am currently supplementing with. And I told you guys that last time. I've been convinced. I went into this a little skeptical, just because of some conflicting data. For example, if you look at randomized controlled trials. people that were given vitamin C prophylactically or on the onset, for example, of the common cold, you'll find mixed results. You'll find data that shows it protects, it delays the onset of symptoms, or it shortens the duration of a cold, or you'll find studies where there seems to be not much of an effect at all.

And, it wasn't until really diving into all the studies and looking at the oral bioavailability and plasma levels of different doses and frequency of doses that I was able to convince myself that difference in protocols make a huge difference in what the end effect is going to be. And, that all comes down to plasma levels of vitamin C, which orally— so we're talking about oral consumption right now— most people, their plasma levels range from anywhere between 50 micromolar to 70 micromolar baseline. And that's depending on what your diet is, depending on— some people eat more foods that are higher in vitamin C, and so they have higher plasma levels. You can't get plasma levels higher than around 220 micromoles from oral consumption. It saturates at that.

You can do intravenous vitamin C and get up to 70 times higher than that, but that's a different story. So what I found is that dose and frequency of dose are really important determining Yeah. If you can get higher levels of vitamin C in your plasma and if you can maintain them. And the only way you can maintain that is by frequency, so more frequent doses. Higher doses had a much— have a much, much more robust effect. Higher doses of at least 1 gram per dose and 3 grams per dose will get you saturated levels. So studies have shown, for example, people taking 3 grams 6 times a day literally can keep their plasma levels at 220 micromole throughout the entire day period, 24-hour period.

People taking, for example, 2.5 grams 4 times a day can maintain pretty close levels around 200 micromoles per day. If you just take 1 gram once a day, you will get higher plasma levels than what your baseline is. So you can get a little bit higher Perhaps to around 100 micromole, around 100 or so, but there's a short half-life and that starts to taper down and you will be back to baseline after 24 hours. So a lot of the studies that had beneficial effects were higher dose studies and they were higher dose studies with frequency, not just one dose a day.

I'm not going to focus all on those studies right now, but I just wanted you guys to hear that because It really, you have to, you know, it takes a lot of time to look through all the data, look through all the randomized controlled trials, look at the methods, look at the patient populations, people, their age ranges, all these things. They all play a role in what the outcome is. Aside from that, there are also studies that show vitamin C even orally can play a very important role in in the lungs. So we know that the innate immune system is important for, you know, basically for protecting the lungs from pathogens and respiratory diseases like pneumonia, asthma, COPD. These things are, you know, pathogens also lead to these similar types of illnesses that can be found.

And vitamin C has been shown to play a role in basically negating a lot of the damage from some of these respiratory illnesses. For example, multiple studies have shown that vitamin C plays— part of the role that vitamin C plays in protecting the lungs There's a twofold role, you know, so one, if we're talking about a viral illness, it is very important for— immune cells play a very important role in lymphocytes and neutrophils, and they're 50 to 100 times higher concentrations in your neutrophils and in your white blood cells compared to the plasma levels that I just mentioned. So I just mentioned your plasma levels are saturated around can't get above 220 micromolar, or that baseline levels are around between 50 or 70 micromolar.

Well, your white blood cells and your neutrophils have 50 to 100 times higher levels than your plasma. And the reason for that is because they play a very important role in, um, in, in helping your, your innate immune system to eliminate pathogens, to eliminate viruses. And the other thing that it does, and the reason why the immune cells have such high concentrations of vitamin C is because these immune cells are producing damaging products. They are producing hydrogen peroxide. It's something that your neutrophils are making. The hydrogen peroxide is killing viruses or killing— I mean, since viruses aren't technically alive, I mean, I guess that you could make an argument inactivating the viruses. Uh-huh. But they are not damaging the neutrophils themselves.

And the reason for that is because vitamin C is negating the damage from the hydrogen peroxide. And that damage is also protective against other cells where, you know, a lot of— so this cytokine storm, the hydrogen peroxide, the hypochlorite release from immune cells, these things can damage other nearby cells. But when there's enough vitamin C there, the damage doesn't occur. And that's been shown in randomized controlled trials as well in humans where given even very high doses of vitamin C, normal cells are protected from oxidative damage. So that's one of the reasons— that's one of the mechanisms by which vitamin C protects from Uh-huh.

From the damage from a cytokine storm even though vitamin C also plays an important role in activating the innate immune system and also helping with interferon production. In the end, you know, while you don't want too much interferon later on during a cytokine storm, it's really beneficial to have that vitamin C there because it is protecting against the collateral damage That is being produced from a potential cytokine storm. And vitamin C is used to treat sepsis. I mean, it's commonly used, intravenous vitamin C, and we'll talk about that in just a minute, but it's commonly used in hospitals to treat sepsis in multiple, multiple studies. And part of the reason for that is that it plays a major role in reducing that collateral oxidative damage.

So I see people asking in the chat about vitamin C levels and measuring— I'm sorry, vitamin D levels and measuring vitamin D levels and being worried about taking too much. Most of you that have heard me talk about vitamin D, I've also published academic papers on vitamin D. I always, always mention that a vitamin D blood test is the best way to know how much to supplement with because you need to know what your vitamin D levels are. And then so doing a test at baseline, then doing one after supplementation to see how much you've raised your levels is very important. In this particular case where society is much different than it was a month ago where you could easily go into a Quest lab and get a vitamin D blood test or to your doctor and get a test.

Now it's probably, I would say, puts you at a higher risk to go anywhere where in any sort of healthcare setting. So, you know, there are some tests offered at home, but even A lot of labs are not running right now, so I'm not sure that's possible to do. But there's a couple of things. There's been the upper tolerable intake of vitamin D per day has been 10,000 IUs. So at 10,000 IUs, the Institute of Medicine has determined that that is safe for people to do There is not toxicity associated with taking 10,000 IUs per day. A good rule of thumb is that multiple studies have shown that 1,000 IUs a day generally raises blood levels by around 5 nanograms per mL.

And, I say generally because there's a lot of single nucleotide polymorphisms SNPs in enzymes that are responsible for converting vitamin D3 into the active steroid hormone, which is 1,25-hydroxy vitamin D. And some people do it better and some people do it less efficiently. And so most of the time you can say, okay, 5,000— sorry, 1,000 IU will increase my blood levels by about 5 nanograms. Okay. So that's a good rule of thumb. I am currently right now taking 5,000 IUs of vitamin D. I just had my levels tested and got the data back about a week and a half ago. I got the data back while I was actually in shelter-in-place. And my levels pretty much are pretty much always around 50. Somewhere around 50 nanograms per mL.

So yes, you don't want to go and overdose on vitamin D. Thank you for bringing that up in the chat. But also, you don't want to not— you don't want to still be in the insufficient range. And the insufficient range according to the Endocrine Society is less than 30 nanograms per milliliter. So, again, you know, 10,000 IUs a day has shown to be safe. And I'm currently taking 5,000 IUs a day. And I think most people now are spending more time indoors. They're actually spending even less time outdoors than they were previously. And people were already not getting enough vitamin D from the sun. So I think there's going to be an even bigger issue in terms of vitamin D insufficiency and deficiency while people are now spending even more time at home and less time outside.

Heather in the chat is asking, does it matter what kind of vitamin C, liposomal vitamin C versus ascorbic acid, etc.? These, these, you're going to get so many details on these questions. I mentioned I have a 27-page topic page going to be posted soon, covers everything with references. I will just tell you, there, there is evidence that you can raise plasma levels of vitamin C slightly higher with liposomal. But liposomal vitamin C, there's a lot of brands out there that are really not really great. And I think right now it's just sold out and hard to find. And really the important thing is that ascorbic acid, as long as you're getting the high enough dose and frequency, can raise your levels just as high as liposomal.

You may have to take a little bit more of it, but that's the bottom line. So let's move on to the next related question. I'm going to be going into this question in much more detail in the next COVID-19 Q&A that I release next week. So I'm just gonna kind of keep this one a little short. And it also has to do with vitamin C, but in this respect, the question has to do with intravenous vitamin C. And the question says that this person had heard that this is an effective way to both resist and treat COVID-19. And if this is true, why is it not widely known? Why are pharmaceuticals being sought as the only real way out of this crisis. So first of all, I will say there is no evidence that megadosing orally with vitamin C or intravenous vitamin C is going to prevent or treat COVID-19 illness.

We don't have those randomized controlled studies We don't have data from those randomized controlled studies right now. So we can't— you just can't make a statement that it is an effective way to treat COVID-19 without that data. It's just a big unknown. And what we do know is that there is a randomized controlled trial that began on February 14th in Wuhan, China. The study is looking at the effects of intravenous vitamin C on severe COVID-19 pneumonia. And so that study is scheduled to be completed by September 30th. So hopefully data will be emerging in the next few months on that randomized controlled trial.

There has been a correspondence that is not peer-reviewed that has been posted, and I've seen this on several, in several different places, social media posts, emails, things like that. A correspondence from doctors in China that have treated about 50 cases of, or claimed they have treated about 50 cases of moderate to severe COVID-19 infection with high-dose intravenous vitamin C. They were using around 10,000 milligrams, so about 10 to 20 grams a day for 7 to 10 days. And basically, they claim that patients that receive the intravenous vitamin C improved and that there was no mortality.

So they claim that the average 30-day hospital stay for all COVID-19 patients was about 3 to 5 days shorter for the patients getting the intravenous vitamin C. So there's also some anecdotes coming out of New York. Physicians are treating some COVID-19 patients with intravenous vitamin C. I believe their dosing is a little different. They're doing lower doses more frequently, so I think they're doing multiple doses throughout a day, maybe 10 grams total, and they're also claiming to have some success. This is again anecdotal, just like the anecdotal correspondence I just mentioned.

So I'm gonna be talking a lot about actual published data on intravenous vitamin C and mechanisms and how they differ from oral vitamin C in great detail coming up next week in the COVID-19 Q&A illness— COVID-19 Q&A podcast that I release. So I'm gonna leave it at that, but just to kind of touch on the, you know, the the part of the question that says, why is this not being pursued? You know, why are pharmaceuticals seem to be the only thing that's being pursued? And I'll say, personally, I think from, from doing a lot of reading and from my knowledge of immunology and micronutrients and how important it is to have adequate levels, a lot of these micronutrients, which are cofactors Which are regulating the immune system in multiple ways.

To have them to prevent illness is so much— it's so much easier to prevent than to treat. And unfortunately, there are people, there are lots of people with poor diets. There are lots of people that don't have— aren't getting enough of important micronutrients like zinc, vitamin C, vitamin D, and others from their diet. And I think this can have an effect on, and it's been shown in studies to have an effect on, the innate immune response, initial innate immune response. And that may play a role in, it may play a more important role in a person's ability to fight off the infection and a person's ability to even prevent themselves from becoming severely infected.

I think it may play a major role in, in fact, You know why 20% of the population has a much more severe case of COVID-19 versus you know the other 80% in in addition to many other factors. There are many other factors that are also playing a role in that. It's not just your your micronutrient status, but I do think that plays a very important role. But pharmaceuticals, I mean the reality is is that people have this disease. They have severe— they're getting severe cases of it. And, you know, for whatever reason that is, right now, you know, we need pharmaceuticals to help treat that disease as well. And, you know, like, just look at what antibiotics have done for infections, you know, in terms of mortality rate.

I mean, it just— you're talking serious, serious drops in mortality rate from just you know, therapeutics like— and pharmaceuticals like antibiotics. So I think it's very important to pursue, you know, pharmaceutical therapeutic intervention— interventions as well. So George is asking about the role of zinc in COVID-19 prevention and treatment. I will be getting into that into much, much more detail in the next Q&A I release next week. So I don't want to be too repetitive, but you guys will be getting another podcast very soon on that. I'm going to move on. To the next question, which is kind of, kind of related to everything that we've been talking about.

Someone asked, based on since the last Q&A, Crowdcast Q&A last month, I told, I told you guys a little bit about my supplement routine and what I had changed and what I was kind of doing for immune boosting, what I was, what I was, you know, what I changed to kind of focus more on what I thought solid evidence existed for boosting my immune system. And so, I will say that not much has changed in the sense where I have stopped taking anything that I mentioned last time. And the things that I mentioned last time were I think I was only taking 4,000 IUs of vitamin D. Now, I'm taking 5,000 IUs of vitamin D daily. I'm taking my multivitamin.

Very important because it has other, you know, important micronutrients in there, including many of the B vitamins and some zinc, magnesium, some vitamin A, and just, just, just the sort of— it's like insurance, particularly more important now than ever. I have noticed that it is harder for me to get all the same fresh vegetables and fruits and foods that I was able to shop for before this global crisis. And I'm sure many of you have found the same hurdles and issues and are facing those. And so, you know, my diet has changed a little bit. And so this, the multivitamin has become even more important to me now than ever. I've also continued to take zinc. And, right now, I have some in my multi and then I'm taking another extra 15 milligrams. I also have some with the 30 milligrams.

And, I'm taking quercetin. I'm taking about 250 milligrams of quercetin, which is a zinc ionophore. I'll be talking about that in detail soon. Which helps get zinc into the cells. Zinc does inhibit RNA, the RNA replication of viruses, but zinc is hard to get into the cells, so you need what's called a zinc ionophore, and quercetin has been shown in some studies to be a zinc ionophore. So I'm taking quercetin. Quercetin is found in foods like onions, apples. It's found in green tea. It's found in another type of tea called Buckwheat tea. So I'm also taking N-acetylcysteine and liposomal glutathione. I mentioned those last time. They've been shown to improve oxidative stress factors in the lung, and also glutathione has been shown to boost immune cells.

I'm taking sulforaphane in the form of moringa powder, and I also take prostaphane. Okay. So, what else have I added? The other thing I've added is benfotiamine, which is a fat-soluble vitamin B1, form of vitamin B1 or thiamine. Vitamin B1 is called thiamine. The reason I've added that, it's a Very complicated and sort of hard to explain, but I'll kind of just generally speak on it. So for one, there's multiple studies, the treatment of sepsis and also acute respiratory distress syndrome in hospitalized or critically ill patients, often vitamins, intravenous vitamin C is used in combination with thiamine.

And there's a lot of overlap between thiamine and intravenous vitamin C in terms of pathways they are affecting, reducing lactic acid levels and LDH, which are also things that are elevated with COVID severe COVID-19, or complications with severe COVID-19 illness. But in addition to that, um, uh, acquaintance of mine reached out to me and, um, has given me a hypothesis that they— um, so thiamine is, um, for one, thiamine is actually, um, 20 to 30% of older populations are, are deficient, or deficient, I guess they have insufficient levels of thiamine. People with type 2 diabetes have insufficient levels of thiamine. Um, And so it's definitely consistent with, you see populations that are more at risk with severe COVID-19 illness.

Thiamine is also a— it regulates— it's a regulator of RNA, which then regulates protein expression, and it's This is kind of hard to explain and it can be very, very confusing. So I'm gonna try not to be super confusing, but there are things, there's something called riboswitches. And riboswitches are, they evolved from bacteria and they're found, they're also found in RNA viruses. And they also have been found in human. In humans as well, which is kind of interesting. But basically, there's a certain riboswitch that needs thiamine. And thiamine will basically can— so the riboswitches turn on or turn off thiamine synthesis proteins.

And so someone found that— so this was an acquaintance of mine, found that this thymine-dependent riboswitch was present in the— it was present in SARS-1 virus, the MERS virus, and also SARS-CoV-2 virus. And it was very weird and strange that it was in these viruses, and it seems to be a pretty, pretty close match. And so the hypothesis that he has is that Basically, when thymine levels are low, that the— and where these riboswitches are located are in regions that make the spike protein, which, you know, is important for the virus docking, and also in another glycoprotein region. And so the hypothesis is that when thymine levels are low, the virus can replicate more, particularly those regions that make more spike proteins and other regions that are important.

for the virus to basically be able to infect other cells, and that when thymine levels are high, it kind of switches off that riboswitch, and so the virus stops making those things, and basically it leads to the immune system's able to handle whatever virus that is there and can basically, you know, you basically have a less severe case of potentially COVID-19. So I have reached out to other physicians and scientists and some collaborations and IRB protocols are now being, you know, they're underway to try to look and investigate this hypothesis both in the clinical setting as well as a scientist who was doing research in cells that has, you know, clearance to do research on SARS-CoV-2 in cells to kind of test this hypothesis. And so that's underway right now.

In the meantime, I don't think it is harmful at all to increase the thiamine uptake. And the reason I'm doing the fat-soluble form is because it bypasses saturation. It bypasses transport of thiamine into cells and saturation, you know, things that can happen. So I'm taking the fat-soluble form, which is benfotiamine, and I'm taking About, I believe it's 250 milligrams a day. So that's pretty much my supplement protocol. It hasn't changed much with the exception of the addition of a few things. I haven't taken anything out. Oh, and I am still doing— I'm doing the vitamin C and I'm doing it frequently.

And when I release this vitamin C podcast coming very soon, I'll talk about Any potential risks for mega dosing with vitamin C. The major concern has been kidney stone risk, and I will talk about those studies and how the risk is very, very, very, very low. In fact, what's interesting is that there's a couple of meta analyses out there that say vitamin mega dosing with vitamin C can can cause kidney stones, and the reason for that is because. vitamin C metabolism, an end product of it is actually oxalates. And so people that are at higher risk for kidney stones, it's thought if they have— if they're taking in a lot of vitamin C, potentially could have an increased risk for kidney stones.

What's interesting is that when you look at this meta-analysis and you actually look at the data that they analyzed in the meta-analysis, What's really weird is that they did their what's called a univariate analysis. So they adjusted for age and they found no risk. In fact, they found vitamin C was protective against kidney stones, particularly in females. And then when they did— so there was no risk found. So then they did a multivariate risk, which is very weird. Because typically when you don't find a risk, the first— with the first association, doing the multivariate analysis is very strange. That's when they found a very, very, very slight increased risk, very slight. And I'll get into those numbers later, but I'll give you an example of why this is weird.

So meat consumption and type 2 diabetes risk. It's known that meat consumption increases type 2 diabetes risk. That's a positive association that's been found in multiple studies. But then when you adjust for all these potential confounding factors, you see that it's only in most cases, 90% of the time, that risk is only when you have a high BMI. So the risk goes away if you don't have a high BMI. If you were to start off and say meat consumption does not increase type 2 diabetes risk, which is like I said with the case of vitamin C, high-dosing vitamin C does not increase kidney stone risk. That's the initial risk, the initial association they found.

So if you found that meat consumption does not increase type 2 diabetes risk, then you went on to say to do another analysis and you say, oh, it increases it when there's these other confounding factors. You see what I mean? It's really confusing when there's not this initial risk, but then, you know, But only when you find the BMI is there. So the bottom line is that there potentially is some weird interacting confounding factor that may increase the risk slightly, very slightly of kidney stones in some people. But I have found that data to be extremely weak. And now this is people that have not had a kidney stone. If someone's already had a kidney stone, that's a different story.

But in someone that's never had a kidney stone, I am not finding a really compelling argument that taking vitamin C is going to increase kidney stone risk, particularly in the short term. This isn't something that I'm going to be doing forever, but right now, while the threat's kind of high, I'm actually trying to keep my plasma levels pretty high. And, the way to do that right now, I'm taking 1 to 2 grams probably 4 times a day. That's pretty much what I'm doing right now. Heather is asking about supplements for toddlers. Of course, I can't give you any sort of medical advice. I can tell you, so what I'm doing for my son who's a toddler, I give him a multivitamin that is a gummy that mostly has xylitol in it.

There's a little bit of some juice, so there's a little bit of sugar, but it's like 2 grams in the whole serving size, which is not bad. So you do definitely have to brush their teeth. It's, you know, it's hard to find a toddler gummy with zero sugar. It's just extremely hard to find. So I was happy with the one I found. And, it's from Pure Encapsulations. And, it's their toddler multivitamin. I also give him their EPA/DHA formula as well. It's a little gummy which has zero sugar at all. It's lemon-flavored and has xylitol which is good for the teeth. And, I'm also giving him— I've got some chewable vitamin Cs. I give them vitamin D, so there's vitamin D drops that I give them. There's also— I've also gotten some vitamin D gummies which have no sugar.

There's xylitol, and they're from Nordic Naturals. Nordic Naturals, they're kind of hit or miss. Most of their stuff I'm not a huge fan of. A lot of their toddler vitamins are full of sugar. The only non-sugar one I found was the vitamin D, and it's 1,000 IUs per gummy. And then, I'm giving my— I'm giving my son some vitamin C, extra vitamin C. I got these chewables that are from Swanson and I break them up because they're hard. So I have to break them up into fourths and I give them to him. Interestingly, the literature on vitamin C supplementation and preventing common colds or even shortening the duration of common colds The evidence is much more robust in children, much more robust in younger children.

There are much more— it's much more robust data and consistent data in children that are given vitamin C supplements. It really plays a big role in helping prevent at least common colds in younger children. So I've got some more COVID-19 related questions here. I'll skip to a non-COVID-19 one since I have to get going soon. So this question has to do with Studies on non-caloric artificial sweeteners showing that it can disrupt microbial metabolic pathways, particularly in the gut microbiome, and potentially lead to insulin resistance. Do we know why this is? If so, can we use this information to basically infer long-term outcomes from these non-caloric plant-derived sweeteners?

So there are there are some some studies that have linked the effect of non-caloric artificial sweeteners on microbiome in animals, including humans. It does it does modify the micro microbiome, but not in a way that's super predictable. So there are several studies. Yeah. There are several studies showing that artificial sweeteners, non-caloric artificial sweeteners, can lead to insulin resistance. And this is partly because artificial sweeteners can stimulate sweet receptors in the mouth, and that actually initiates the release of insulin. It's very interesting. And that sort of in the long run can possibly cause insulin resistance.

The other studies have shown, and these have been some animal studies as well as some pilot studies in humans, have shown that it can change the composition of the gut microbiome, which can basically lead to gut bacteria that can cause increase— basically lead to increased blood sugar levels by changing the composition of the gut microbiome. There's also a lot of mixed data on artificial sweeteners or non-caloric artificial sweeteners in terms of health outcomes. You know, so it's hard to really make any really definitive statements.

What I can say is that certain sweeteners, particularly the sucralose, Splenda, That's one that's really been shown to have an effect on changing the composition of the gut microbiome in such a way that it can possibly lead to increased blood sugar levels after a meal, postprandially. But, you know, the data on that's still emerging, and it's something that I'm definitely— I've been following that literature for a while, but there's just no really definitive conclusions that can be made from that. So Evan is asking in the chat, what about monk fruit or stevia? I haven't seen any evidence of— in fact, I've seen evidence, animal evidence of stevia actually improving insulin sensitivity.

But, you know, I did mention the whole sweet stimulating the sweet receptors and possibly that being a mechanism, you know, that's— there's always sort— there's always compensating things happening in biology. So that necessarily isn't going to always be the case or isn't going to necessarily, you know, it may happen, let's say, once the first time you're given the sweetener, but maybe it's not happening in subsequent times, you know. So, so even that itself, I would say we can't say definitively that You know, every time you eat something not that's non-calorically sweet, like monk fruit, for example, or stevia, that it's going to stimulate an insulin response because your body learns that oh this there is no sugar happening. There's no sugar in my in my you know bloodstream.

I don't need to have an insulin response here. So that's not it's not always the case. But I haven't seen any any evidence so far that monk fruit does this or stevia either. But it's something to keep an eye on because, you know, as more data comes in, we might see that change. And that goes for pretty much all these non-caloric artificial sweeteners. So, someone, someone was asking about the quality of sleep. Dr. Matthew Walker has convinced many of us of the importance of the quality of sleep. And now many of us use or wear devices for sleep monitoring, such as the Oura Ring, Fitbit, Can you outline the Oura Ring measures and how to use the measures to identify the onset of illness?

So I believe this person is referring to the COVID-19 detection trial where Oura is basically using body temperature changes to potentially detect whether or not a person may have COVID-19 or any other illness that may lead to changes in body temperature. So first of all, I think that sleep is hugely important for immune function. And, you know, there's just been so many studies that have shown that as sleep quality and quantity decrease, that immune function is depressed. And it's just pretty robust data on that. So it's really, really important to optimize for sleep, particularly during this time for that reason. And some people like wearing their trackables to track how their sleep has been. Each night. Um, you know, these wearables are only so accurate.

They're, they're using heart rate and body temperature changes and movement to sort of have this algorithm to determine, um, whether you're asleep. And, and the sleep cycles certainly, um, are not, are not very accurate, you know. In order to really accurately determine, uh, sleep stages like REM or non-REM deep sleep. You really, you know, polysomnography is really the gold standard. And I think anything else is sort of just a guesstimate at best. But sleep duration, total sleep duration, you know, you might be able to get some good data from that. And so that may help you figure out certain things that may have a negative impact on your sleep or Have a positive impact on your sleep.

If you want, I mean, so in terms of figuring out how to use the the actual data, looking at the aura ring for your body temperature changes, you're it's going to be hard for you to look at that data. But if you if you do have, for example, an aura ring and you Click on Trends and then Readiness. So once you're in Trends, you click on Readiness, and then you'll see a list there where it has Body Temperature. And if you click on Body Temperature, it kind of shows you some graphs, and they're arbitrary. They have an arbitrary assigning system, which makes it really difficult to interpret what's going on there. for the user. But that's how you get to the body temperature data. Again, you go to Home. So you click on Trends and then Readiness and then Body Temperature.

And that's how you can look at your body temperature data. So that's about it for this, this Crowdcast. I will mention there's some people mentioning the sauna. I am, I am going into great, great detail on the sauna in this upcoming COVID-19 Q&A. I'm fortunate right now to have a home sauna, and I realize many people don't have that luxury. And with gyms closed right now, it's really impossible for people that don't have a sauna at home to use a sauna. And the good news is, is that hot baths have been shown to increase heat shock proteins, heat shock protein 70, for example, which heat shock proteins play a major role in boosting immune immunity, innate immune system, and also in increasing immune cells.

So I'm going to be talking about several studies where using the sauna not only protects against pneumonia, it protects against COPD, it actually even can help treat COPD, and also some older studies showing that it can protect against common cold. Although those studies, it seemed as though frequency was very important and the protection wasn't shown until 3 months after 3 months of frequently using the sauna. So there it wasn't like an overnight thing. And I'm going to be talking about some studies showing that that sauna use increases certain white blood cell and neutrophil numbers as well as as well as the mechanisms like heat shock proteins. So I guess I guess Costco may still be selling sauna, so maybe you can still somehow get a get get a sauna.

Although I would I would be very cautious going into any sort of store at all. Certainly wearing some kind of mask, any kind of mask that you make at home or if you have any other types of masks is best. I personally am staying out of stores 100% right now and I think that Yeah. The best thing that we can all do right now is stay home as much as we can. But my point was is that I do think there's pretty convincing evidence that the sauna boosts the immune system and the sauna is really important for lung function. I've been writing a review article on the sauna and I had a whole section on immunity and lung function and I— so I sort of refined that section a little bit more.

And also added in some other modalities of heat stress like the hot baths, which have been shown to increase heat shock proteins. And I think that so in this one study, people that sat in a hot bath, and I will cite the exact temperature numbers when I when I record this podcast next week. I believe it was 100 and something degrees Fahrenheit, but they were sitting in it for from the waist down for an hour. Now, that's a long time to have to sit in the hot water to have the 50% increase in heat shock proteins and also elevations in core body temperature, which by the way happens during a fever response. Part of the fever response is to activate the immune system. And part of the way it does that is by activating heat shock proteins, which become active when you have a fever.

So those things also get activated when you are going into a sauna or in a hot bath. So I mentioned that people are sitting in the hot bath from the waist down. The question is, what if they are submerged from the shoulders down? What if you lay down in the bath and more of the surface— of your surface area is being exposed to the heat? Well, anyone that's sat in a jacuzzi from their shoulders down versus just sitting in, you know, when you sit on the stairs and you sit from your waist down, know You get much more hot much more quickly when you are more submerged in the hot water. So do I think that you can cut that time in half, possibly more, by submerging from the shoulders down?

I think that is very, very likely for someone that does not have access to a sauna and can— most people do have bathtubs at their house. So I think that most people can at least do hot baths. Personally, right now I've been doing the sauna 5 days a week. It's been critical for, for my mental health. Also, I'm not getting as much aerobic activity as I usually do. I usually do a lot of outdoor running, and I'm even— I've even been having to kind of cut that down a little bit just because I don't want to my encounters with people. Even outside, I'm trying to kind of minimize all that. So, the sauna, because the sauna mimics aerobic exercise, has been just really key for my overall health. And, hot baths. Hot baths do a similar thing. Physiological mechanisms kick in.

You can elevate your core body temperature. You get increased blood flow. Heart rate increases. Many of the same things happen That happened with the sauna, that happened during aerobic exercise. Afterwards, you know, similar endpoints also happen where you have, you know, improved heart rate variability, you have improved lower blood pressure, lower resting heart rate. This has been shown in randomized studies that have compared moderate aerobic activity to a 20-minute sauna session. And again, I think that there is a place for hot baths in this. Steam showers as well if you have one of those. You know, any modality that you have at home and have access to, safe access to, to get that heat stress, I think is something that is important to do now if you can.

And as David is mentioning here in the chat, if you are using hot baths, You may have to, to sort of, you know, refill the water and make it, make it warmer every, you know, you know, 10 or so minutes or 15 minutes depending on— I mean, when you're, when you're sitting in a really, really hot bath, I mean, you get really hot and you get uncomfortable. And so, so basically it's pretty, it's pretty obvious. Huskers is asking if I'm still doing 30 minutes. So The sauna I'm using now actually is much hotter than the sauna I was previously using at my gym. So, right now, the sauna that I'm using technically can get up to 194 degrees Fahrenheit. When I get in it, it's around 186. Okay. It's really hot Fahrenheit, and I also have water that I pour over the hot rocks, which increases the humidity.

So according to my hygrometer, my humidity detector, it's about 40% humidity. I get I can get it up tonight, and when I when I keep doing that repeatedly, I mean it is just so hot. And so I'm in there for like. Yeah. Between 15 to 20 minutes depending on the temperature and the humidity. Sometimes I've got a lot going on and so I'm just making it really humid and it's really hot and I'm in there for 15 minutes. And I'm telling you, I'm wiped. I mean, I feel like I had just gone on a 3-mile run doing 80% max heart rate. So that's what I'm doing right now. Someone's asking, Ismail is asking, shared sauna in my apartment building, yay or nay? I would say right now you want to avoid anything shared, any type of shared gym or sauna. You do not want to be in a closed place with other people.

So I would say that That isn't a— it's unfortunate. It's an unfortunate thing that I would bypass. People are asking the brand of sauna I use. I got my sauna through Nordic Sauna, and they're— the actual maker of the sauna that I'm— so they distribute it, but the actual maker of it is Finleo. And I got a 2-person sauna, and it's, um, it's really cool because it can plug into a regular old outlet, um, so you don't need— it really makes it, um, very, you know, very easy to use, um, for, you know, a home. Yeah, London is asking in the, in the comments infrared recommendations on temperature and time, and so that's one of the things I will be covering. There's something called Waon therapy, very commonly used in Japan.

They use infrared saunas, and they've used it to even help treat chronic pulmonary obstructive problems, so disorders, so COPD. And typically, their sauna temperatures are around 145 degrees Fahrenheit, and the heating protocol is around 45 minutes. And it's daily. So it's a longer time. It's a lower temperature but a longer duration spent in the infrared sauna and also frequent as well. I'm doing these 5 days a week right now because as I mentioned, I'm not getting all my exercise routine is pretty drastically changed. And I find that I just feel better and I certainly would be doing hot baths if I didn't have a sauna. I absolutely have done them in the past and they do help.

It's more difficult, at least for me, hot baths are more challenging because I have the tendency when I get uncomfortable to want to stick my legs out or stick my arms out. And it's so easy to do. When you're in the sauna and you get uncomfortable, you can't— the only way out of it is to get out of the sauna. And I'm not willing to do that until I'm really at that point where I know I've at least gotten gotten, you know, depending on the temperature, at least 15 to 20 minutes. So, so, so the challenge for the hot bath people I have, I have for you people that are going to be doing hot baths is when you start to get really hot, because you will, you got to stay in and not cheat. Because, because when you start to take one limb out or two limbs out, you cool off.

So I think Costco saunas are great, by the way. Huskers is asking, uh, is talking and comparing about saunas. Costco, Costco's got a really affordable price. I know I have, I have, I have friends that have them and they're great. Um, so, um, you know, if you can, you can get a Costco, I mean, it's so hard to get anything these days delivered and all that. So You know, but, but eventually things will, things will get a little bit better and it'll be easier to get, to get things like that. Thank you everyone for the great questions. And I always love doing these, these Q&As. Again, you can find, you will be able to find the, this Crowdcast replay as well as the other 9 Crowdcast replays. You can find them on your dashboard at foundmyfitness.com/dashboard.

You will find links to the YouTube videos and also you will find, you will find the, the link to your SuperCast podcast feed, which you will, which is the private podcast feed, which this goes on. If you already have that downloaded, then that, that should be uploaded early next week onto the SuperCast feed as well. So thank you so much. Be sure, I will send out a reminder of the next Crowdcast, which will be happening next month. And as soon as I get that posted, you guys can start submitting questions. Please, please, the sooner you submit your questions, the, the, the better, because my team and I, we go through these questions earlier because they oftentimes take a lot of background research.

So I hope everyone stays safe and stays healthy, and I hope your family and friends are healthy and safe, and that you're maintaining good mental health and trying to maintain— you know, I have also found that having virtual hangouts with my family and friends has been really nice. We've been doing dinners. You know, there's Google Hangouts, there's Zoom, there's Facebook Portal. I've used all 3 of these, and I found that they've been really nice to help stay in touch with my family and friends, and I hope you guys are able to do the same. I look forward to talking with you guys again next month, and again, you'll be getting a lot of really good information and a COVID-19 Q&A coming out this week, another Yeah. Vitamin C-related topic page and podcast coming out shortly after that. And then another Crowdcast as well. So with that, I will talk to you guys very soon. Again, stay healthy and safe. Goodbye.