Dr. Rhonda Patrick debunks viral myths, stressing CMV’s immune training over supplements like vitamin C or zinc, while highlighting vitamin D’s critical role—70% of U.S. adults deficient, linked to 8–98% lower COVID-19 risks in studies from the Philippines, Indonesia, and England/Wales. She advocates for IV vitamin C (10g) to neutralize spike proteins via hydrogen peroxide, citing llama antibody research and sepsis trials, but warns of antibody-dependent enhancement risks. Blood type O’s lower susceptibility and sauna’s 40–50% heat shock protein boost (Finnish studies) emerge as key tools for resilience, alongside zinc, quercetin, and microbiome health. Rogan’s sleep apnea relief via a mouthpiece contrasts with Patrick’s circadian light therapy, both underscoring how sleep fragmentation spikes glucose—her fasting levels rose to 109 despite no diet changes. Their discussion critiques lockdowns as misguided and champions personalized, evidence-backed interventions over blanket restrictions. [Automatically generated summary]
Well, we've been talking and we've been talking about immune systems and this is one of the main things that I wanted to talk to you about.
All we're hearing is shelter in place, wear a mask, don't touch anybody, don't go outside.
But we're not hearing, what can you do to strengthen your immune system?
And I think that as a public health, a public service, you know, health thing, this is one of the most important things that I think you can really focus and concentrate on and an actual thing that you could be proactive about during this weird time.
Well, definitely, I think focusing on lifestyle factors that you can possibly modulate your immune system and strengthen it is important.
What's interesting is that the immune system You know, after doing just so much, of course, the past, like, couple of months, I've been nothing but, like, reading about the immune system and trying to understand, of course, this new virus, SARS-CoV-2.
But I've just learned so much, you know, over the past couple of months.
I'm not an immunologist.
I'm not an infectious disease expert.
So, you know, while I've had some training in immunology, I definitely, you know, didn't know – don't know everything there is to know.
But what – just, you know, doing some reading about, like – Why are people's immune systems so different?
That's the big thing.
When you take a young population, as you get older, your immune system does decline.
I mean, there's lots of changes that occur.
But in general, people have different immune systems.
And what's interesting is that there's been tons of genetic studies done on identical twins, and they're followed over time.
And what's found is that genetics is not the major regulator of immune function.
It's something in the environment.
This is what surprised me, and it's not totally going to answer your question, but we can totally get to that.
But one of the main things besides age that regulates the immune system is previous exposure to viruses.
So I thought that was really interesting.
And in particular, one virus, the cytomegalovirus, CMV. Did you know like between 50 to 80% of the U.S. population has it, like at least by the time they're like an adult?
But here's the interesting thing about this virus is that...
So this is one of the major things.
Multiple studies have been looking at, like, you know, just immune variability.
And it's like CMV has been identified in multiple studies.
And the reason it got me interested, because I was like, almost 80%, I mean, I could have it, right?
I could totally have it.
It changes the immune function.
It's totally different between young and old.
So when you're younger, and if you have it, it actually enhances immune function.
So they've done studies where, like, they have given people influenza vaccine.
And oftentimes these vaccine studies are used to kind of test the immune response and, like, how robust your immune response is because you're given a vaccine and there's all different types of vaccines, you know, pieces of an antigen or all different types of, you know, ways that you can expose someone to.
to Bacteria or virus, but you have a response to it and the response is, you know, involves your adaptive immunity.
You make what's called neutralizing antibodies that, you know, basically eventually bind to the virus and neutralize it, prevent it from entering the cell.
So people that have CMV that are young have a really robust response to the vaccine, much better.
But older people have the complete opposite where it's like, you know, deleterious.
And the reason for that, scientists think, is because basically this virus, it's stuck with you lifelong and it kind of reactivates every few years.
And like every time it reactivates, it kind of trains your T cells, which are part of your immune system, to become focused on that CMV. And so as you get older, your T cell population becomes more focused on fighting that virus and less so on other viruses that you're exposed to.
Most healthy people don't have any symptoms with it.
I know.
It's really weird.
So what I'm wondering, and the reason I'm even going here, it has nothing to do with taking vitamin C or zinc, and we can talk about that stuff, and vitamin D, but I just thought it was so damn interesting because we hear all these Stories in the news where, you know, some people are asymptomatic.
Some people are, you know, then some people are just really getting, you know, hard hit.
And these people, let's say they're more age matched, right?
We know that elderly people are more prone to severe form.
But it just made me think, what if this, you know, previous viral exposure to something like CMV is also kind of shaping people's immune responses in some way.
Surely people are going to be looking at that, but I just thought that was a really interesting thing to come across.
And then the other sort of along the same lines as previous virus exposure is something that really seems to be something that is a main regulator of what your immune response is.
Yeah, I mean, like, if you cut the flu, is it like a three-day kind of thing, or is it going to knock you out for two weeks kind of thing?
That's what I mean, right?
So...
I mean, if you get a sample, like, there's been these zero surveys where they basically...
That just means they'll get a sample of plasma and look for different antibodies, viral antibodies, and they'll find at any given point a person has, like, antibodies against 10 different viruses, just randomly.
You know, so you're constantly being exposed to viruses.
You're not always getting sick, and so, you know, like...
Another really interesting kind of thing is like, you know, there's...
So the SARS-CoV-2 virus is part of a family of coronaviruses called the beta coronaviruses.
So SARS-CoV-1, the virus that was responsible for the original SARS outbreak in 2002 or something.
The MERS-1 in the Middle East.
And then there's two different ones that are responsible for the common cold.
between like 15 to 30% of common cold cases.
So it's not like the common cold is the illness you get, but there's lots of different viruses that can cause it.
But what's interesting is that there's been studies showing that these two beta coronaviruses that are responsible for some of the common cold cross-react with, so there's one that cross-reacts with the SARS-CoV-1, which has a very, it's very, the sequence is very homologous to SARS-CoV-2 which has a very, it's very, the sequence is very homologous And it's also been showed that the SARS-CoV-1, the antibodies against the SARS-CoV-1 can neutralize the common cold one.
So there's like cross-immunity happening between these other viruses, right?
Right.
And so there's been some studies by the CDC on SARS-CoV-2 where they found basically that people that are infected with SARS-CoV-2 also boost their antibodies against the common cold one.
So, you know, there's certainly, I think, a good hypothesis to be made that potentially, you know, one or two of these common cold viruses could – the antibodies you make against them could also somehow – Maybe, you know, interact with the SARS-CoV-2 virus, potentially neutralize it.
I mean, that's a big open question that seems possible.
We don't have an answer to that.
I think we will.
Like, there's large-scale serial surveys being done.
I know at least three that...
I think his name is Dr. Michael Bush.
He's at UCSF. He's doing really large surveys where they're going to be analyzing CRF and people from blood donors and stuff and following them over the course of several years to see – just basically understand more.
Now, what is the speculation, if there's any sort of uniform speculation as to why, when you hear about prisons, where a lot of these prisoners...
I don't know if you've seen that there's a video going around where one prisoner had SARS-CoV-2, COVID-19, whatever, and spitting into a cup and then passing it around to all these other inmates so they could all get it so that they get released.
Because they're releasing people, especially California, which is so wacky.
They're releasing sex offenders.
And there's been some really high-profile releases of these horrible people that should be in jail probably forever, and they're releasing them.
It's really disturbing.
What would cause, other than something like that, what would cause all these prisoners to not just be positive, that makes sense, but to all be asymptomatic?
Is there any speculation as to why these large groups, there was another one that was a meatpacking plant where most of the people were asymptomatic as well?
So this is like, there's one thing that it's important to keep in mind when we say asymptomatic.
Like, you know, there's asymptomatic in like a person that never actually gets symptoms, right?
And then there's asymptomatic.
So there was a study done at the CDC, I don't know, a month ago, maybe a little more, where they measured like, they did this nasal pharyngeal swab test in a nursing home.
70-something people.
And 13 of them tested asymptomatic, like they had no symptoms, but they tested positive.
But then they went back a week later and 10 of those people had symptoms and three were asymptomatic.
So unless, like, there's another, like, if you test someone and they're asymptomatic at that time of testing, they could be pre-symptomatic, right?
In other words, like, you have to go back a week later and see if they have symptoms.
Because that's really important.
So let's say even...
You know, 60% were asymptomatic.
I don't know if they went back and tested a week later, if it was just like a single time.
But this is what got me thinking about this whole thing was, you know, in the prisons and jails, I mean, they're in close quarters, and you got one virus that someone's exposed to, and they all get it, right?
So, like, what if there's, I don't know the CMV, you know, percentage there, but what if the coronaviruses are going around there?
What if Some common cold coronavirus has gone around and those antibodies that they've made to neutralize that beta coronavirus are somehow helping with the SARS-CoV-2.
I was trying to figure that out as well because the tuberculosis, one of the types of vaccines they do for TB... I think they do it in Japan and some other countries where they've got a really low death rate.
That's a clinical trial that's now going on where they're trying to test.
But I was trying to figure out, is there a vaccination?
But the whole, the thing that I just think that I would like to see more research and I'm just hoping, you know, that CDC and other people are investigating these other, the cross immunity, right?
Like, if there's antibodies that you're making against another coronavirus, beta coronavirus, that's in the same family as this SARS-1.
No one's had SARS-1 in the United States, right?
So that's not as relevant as...
But the common cold, that's very common, right?
So if 15% to 30% of the common cold is composed of coronaviruses, we know at least two of those coronaviruses are in the same family that have been identified to make...
At least in one case, there's been neutralizing antibodies, so there has been cross-immunity.
Then you'd think...
Why not test that?
Let's get some animal studies started on that, you know?
Speaking of animal studies, there was an article that I was reading yesterday that was saying that they're hoping that they've found some antibodies in llamas that they're hoping they're going to be able to...see if you can find this...
Because of these antibodies in llamas, they're hoping they can either transfer them to people or learn something about how these antibodies are created.
But llamas seem to be...
Here it is.
Llamas could be the key to fighting new coronaviruses, research says.
We'll make that larger.
It says, it may sound bizarre to most, but llamas could be the key to fighting a new coronavirus.
Researchers from Belgium...
Oh, remember?
That's the big lady that I was showing you earlier.
She's the health lady.
And the United States published an article this week in the journal Cell that highlights the potential use of llama antibodies to prevent COVID-19 infections.
Antibodies from a four-year-old Belgian llama named Winter show promise in blocking coronavirus from infecting cells, according to research from the University of Texas, Austin.
The National Institutes of Health and the Ghent, how do you say that?
Ghent?
G-H-E-N-T University.
Studying earlier forms of the coronavirus, researchers have found an antibody in winter that effectively attached itself and neutralized spike protein in SARS-CoV-1 and MERS-CoV.
Researchers believe the particular antibody, which has been found in other llamas as well, can be injected into an uninfected individual to protect them from getting infected with the new coronavirus.
Yeah, so I think there's lots of avenues for therapeutics, in addition to repurposing drugs.
So monoclonal antibodies, you know, being able to basically identify antibodies that do neutralize SARS-CoV-2 virus, whether they come from llamas or humans, you know, and basically identify the specific antibody that can bind to that spike protein that you just mentioned, which is that region.
It's known that the antibodies bind there and neutralize it.
It's also the region that is used to get inside of the cell.
So monoclonal antibodies, I think, are a really big possibility for a promising therapeutic because you can then...
I mean, the problem is growing, like, large-scale manufacturing them, right?
So if you can identify these antibodies and then manufacture them, you can inject them in people and then potentially get some protection.
The problem is that it's just going to be a short-lived protection.
It's not like a vaccine where your body is making its own antibodies and they're more longer-lived.
It's probably enough to, like, if you're a healthcare worker, your first-line, you know, first responder, people that are definitely, like, being exposed to large doses of the virus, that could be a promising area.
But also, I think, even just treating patients, like, that have already been infected.
So that's also another – so like in combination with some of this other stuff like remdesivir, which is – it's not like a silver bullet, but it seems like it's also promising probably with a combination of other factors as well.
But yeah, the monoclonal antibodies is a really...
I know there's like...
Regeneron's a big company.
They're growing some large-scale ones.
I think they isolated from humanized mice or something.
But there's other companies that have isolated them from humans that have been infected.
So, you know, that's definitely...
A promising area, for sure.
And a good thing about that is that, have you heard of antibody-dependent enhancement?
So basically, when your body is exposed to a pathogen, like a virus, your innate immune system, the first line of defense, like neutrophils, things like that, are making hydrogen peroxide, trying to kill the virus.
But then in the background, your adaptive immune system, and I'm just totally generalizing, is also working in the background.
And part of that adaptive immune response is to produce antibodies.
So you have memory B cells that are making antibodies that are specific to bind different regions, epitopes on the virus, and neutralize them, prevent them from getting inside of the cell.
And so that adaptive immune system usually takes about seven days after you're exposed to the virus, right?
The problem is antibody-dependent enhancement.
So sometimes a neutralizing antibody is an antibody that can bind to the virus and neutralize it, stop it from entering your cell, right?
So it's doing its job.
But you sometimes make antibodies that are non-neutralizing or don't do as good of a job.
They don't bind as tight or something.
And Then you can have what's called antibody-dependent enhancement.
And this was a big problem for the RSV vaccine.
Most kids get RSV. It's a respiratory tract infection.
Most kids get it by the time they're two.
There's no vaccine that's given.
Back in the 60s, there was this antibody-dependent enhancement happening in some clinical studies with toddlers.
And some toddlers got really, really sick and a couple died.
But what happens is basically...
The antibody binds to that.
There's a couple of things.
The antibody binds to the virus and can basically change its conformation and allow the virus to get into the cell better.
So then you become like, you know, you get like a higher viral load and then you don't have antibodies to neutralize it.
And it just, you know, it could be more, it could be, it could lead to death.
The other thing that happens is the antibody binds to the virus, doesn't neutralize it, but it like makes this crazy immune complex that like, It activates your immune system to just go haywire, and it causes all sorts of pathology, and that's what happened with the RSV toddlers.
So there's a few viruses that this happens with, and unfortunately, coronavirus is one.
Like, this has been identified with the SARS-CoV-1 virus, and I think marriage as well.
So this is also a problem with vaccines.
So giving the vaccine people's immune response, some people can have that antibody-dependent enhancement.
And that's what was shown to happen with the SARS-CoV-1.
There were some non-human primate studies that did that.
And also animal studies as well.
So, you know, the thing with monoclonal antibodies is they're a little more specific because you know they neutralize and you're like growing them up like you've done all that test as opposed to just letting your immune system do its thing.
And then potentially, you know, you may have this like non-neutralizing antibody that could cause problems.
But that's kind of the concern.
I know that the vaccine people that are working on vaccines are working on them.
It's like they're concerned about that and completely trying to figure that all out.
And it's funny because it's kind of connected to this antibody-dependent enhancement.
There's been quite a few different, like, forms, like, mutations that have been identified.
But two particular in that spike protein region, that's, like, an important region because antibodies bind there and because that's the region, like, that, you know, the virus uses to get into the cell.
And so there's been two major, like...
Strains that have been identified and one of them, so it's in the spike region and it's an aspartate to glycine mutation.
And basically in Asia, in China, the predominant form is the aspartate, the original quote unquote form.
And then in Europe and also in North America, this other form, the glycine mutant, is predominant.
And there's been studies that have shown...
Looking at like, okay, looking in parts of Europe, different countries in Europe that have this predominant form, that basically there's a higher mortality rate.
But they didn't actually measure infected patients.
So, you know, it's kind of like correlation.
But what's interesting is that there's actually been a genetic link to this mutant.
So there's studies, there's been some large-scale genetic studies that have found that Asians...
About 20% of Asians have basically a nucleotide change in a gene that encodes for a protease that's involved in this, you know, basically in allowing this virus to get into the cell.
But that basically prevents them from having this mutant that's predominant in Europe and also in New York and North America in general.
I know that I was mentioning that TB vaccine, that's one thing that they're investigating.
I mean, there's all sorts of differences in handling the whole, you know, from the beginning, just how you handle the virus.
There's too many factors to say one thing, but there's lots of...
There's lots of possibilities.
And I think that eventually there's going to be therapeutics that are identified, you know, multiple ones maybe.
And I think vitamin D is going to potentially play a role there.
But I mean, just like things like remdesivir and the monoclonal antibodies, and then you eventually like, you know, a vaccine will, you know, eventually, you know, be available.
But I think until that point, I do think that things will be identified that just kind of help us like deal with this like better, you know.
There's been some data, and this was also identified with SARS-CoV-1, that people with type O blood, they make antibodies, they make type A antibodies, whereas people with type A blood, they make antibodies against...
Like they make against the B antigen.
And so the type A antibodies were identified.
So there's been studies looking at people with type O blood or type A blood and also type B. In type O blood, there's like less frequency of getting COVID-19.
So as opposed to having a severe form, it's just like you're less likely to contract it even.
And it's thought because the type A antibodies that people with type O blood make We neutralize the—they basically bind to that region, that spike region, and neutralize the antibody and prevent the virus from entering the cell.
So that's—at least that was the mechanism that was shown with SARS-CoV-1.
So it's thought, oh, well, the same—we're seeing the same— You know, pattern where people with type O are protected from SARS-CoV-2.
Possibly that's also why.
But another really interesting thing is that people with type O blood...
We were also talking about these, like, blood clots and, like...
I mean, there's all kinds of crazy things you read.
I mean, I'm reading all these publications.
And then the other thing is all these publications are being uploaded on, you know, before they're peer-reviewed.
And, I mean, some of them are just a mess.
And it's just...
You kind of just take it with a grain of salt.
Where these clots are like, you know, there's clots in people that are healthy and young, certainly people that have severe cases, people like older people, people that are pre-existing conditions and stuff.
And the type O blood, people have lower levels of this von Willebrand factor, which basically is involved in clotting.
And it's been shown that that von Willebrand factor also is higher in people with SARS-CoV-2.
It was shown to also be that with SARS-CoV-1.
And it's involved with clotting.
So having lower levels may somehow even help protect against...
A theory.
It hasn't been shown.
But what is known is that people with type O blood are less susceptible to contracting COVID-19.
It just seems like in the beginning, at least, they're trying to figure out what the correct treatment was for these people as they were just showing up in mass in the emergency rooms.
And they didn't really know.
And doctors, they varied in how they approached it.
My friend Michael, his doctor, didn't put him on a ventilator.
And he said, if I put him on a ventilator, he's probably going to die.
Because he said his body's going to stop working because it's going to let the ventilator do the breathing for him and it's going to give up.
And what he was talking about after the fact, what Michael was talking about was how that is proven to be correct in New York and that some people A monstrous number.
Like, 80% of the people that put on ventilators wind up dying.
I've had friends that are physicians that have, like, you know, in New Orleans, I mean, same thing, where it's like, you know, there was someone on my team, we were doing some research on this, and I didn't sort of dive into the whole thing, but he was telling me that ventilators do actually,
like, cause more damage to the lungs, and, like, he'd been reading some studies to, like, confirm that, and he was pretty certain that That ventilators actually cause damage and actually could induce damage, where it's making it worse.
Right, but it's hard to say is that the cause of it or is it just that they're so fucked up by the time they get on a ventilator they just wind up dying?
There's been some really interesting data looking at like in the Philippines and Indonesia.
Where else?
I think New Orleans as well.
They've looked at patients that have died and their vitamin D levels.
And basically like in the Philippines, people that for like every standard deviation increase in vitamin D levels, serum vitamin D levels, the people had like an 8% or were eight times less likely to have a severe form of COVID-19.
And if they had – and they were 20 times less likely to have critical form of COVID-19.
Whoa.
So that was the Philippines.
And Indonesia was a really interesting study where like they measured vitamin D and this was measured in the patients.
There's been some vitamin D studies also where they're like looking at countries that have been affected the worst and they all like have low vitamin D.
And it's like, OK, well, anyways, that's a correlation.
But, well, so is this.
But it's a little stronger data.
In Indonesia, patients that died, almost 100%, it was like 98 point something percent of patients that died with COVID-19 were vitamin D deficient.
4% of patients that died from COVID-19 were vitamin D sufficient.
So basically, they were all vitamin D deficient, all the ones that are dying.
Vitamin D deficiency is what makes it worse, and then you're staying inside, so you're not getting any vitamin D. Yeah, you're becoming even more deficient, you know, like somewhere like 28% of the US population is actually deficient, like less than 20 nanograms per mil, you know, like that's defined deficiency.
So there's a lot of people in the United States, as you mentioned, you make it from the sun.
So particularly UVB radiation, there's a reason why I want to talk about this.
You make it from UVB radiation exposure, you know, basically, it's made in the skin.
And but you know, there's certain times of the year, depending on where you live in a more northern latitude, where That UVB isn't even hitting the atmosphere.
You're not making vitamin D. Also, if you have darker skin, melanin protects you.
People with darker skin, people from maybe Africa or India or South Asia, They're more equatorial regions.
They're closer to the equator and there's more UVB radiation throughout the year.
And so as a protective mechanism to not get burned, you have melanin, which protects you, right?
The problem is that melanin also blocks your ability to produce vitamin D.
But if you're out in the sun all the time in a place where you're getting UVB radiation, it's not a problem.
So what happens when you take a person from South Asia, from India, from Africa, and you put them in Sweden or in Minnesota or in the U.K., a place where UVB radiation doesn't hit most of the year, and you don't give them a supplement?
What happens is they become severely vitamin D deficient, severely.
And what happens when you take – I mean you can flip this over and say, okay, what happens when you take the guy from the UK, the Brit, and put him in Australia?
And they're not getting enough They're not getting enough sun because people stay inside more.
People stay inside.
It's not like the old days when we were out hunter-gatherer and out in the sun all the time.
We're inside all the time.
We're in school.
We're at work, in our office, in our cubicle.
So the CDC, you know, obviously there's been studies showing that African Americans are more hit, but they didn't really correct for tons of like other factors because socioeconomic status is important, other health factors, you know.
But there was a big study just released not long ago from like the National Office of Statistics in Britain or something like that.
I don't know what their official name was, but they released some statistics from England and Wales.
And the, I don't know what the correct name to say, I mean, the blacks there basically living in England and in Wales are four times more likely to die of COVID-19 than whites.
When they adjusted all that data for socioeconomic status and for other health factors, they were two times more likely to die.
So clearly socioeconomic status and other health factors are playing a role, but there's something else unidentified.
And I think it's vitamin D. I think that, you know, so...
The vitamin D, I'm not saying that vitamin D is going to prevent you from getting COVID-19 or it's a treatment, although I am involved in a clinical study where we're going to be testing a very small open-arm study we can talk about.
But I'm not a physician.
I'm a medical doctor.
I've never intubated anyone.
So don't think I'm saying that.
I don't want people to think I'm saying it's a treatment.
It's a hypothesis that needs to be tested.
And thankfully, there are Clinical trials, randomized controlled trials that are now ongoing and there are some that are recruiting.
And also in Sweden, there's a huge population of Somalis that have migrated to Sweden.
And they have been identified as being severely vitamin D deficient because a lot of the Somalis have also – like autism rates are really high there.
And there's this link between – I published a link also between vitamin D and autism.
So there's been studies looking at vitamin D levels in the Somali population.
I mean they are so deficient because you're taking – again, you're taking someone who's supposed to be – who's evolved to be getting a lot of sun – But not burn from it.
And then putting them in a place where they can't get any vitamin D from the sun.
And if they don't get a supplement, they're going to be deficient.
And they're so much more likely.
It's wreaking havoc in Sweden on the Somali population.
What is happening to people when they are vitamin D? Like, what's happening in vitamin D deficient?
What is happening in the body that's causing their immune system this hormone deficiency, not having this vitamin D? Whether it's through sun exposure or diet?
I mean, there's vitamin D receptors on, like, your immune cells.
And the reason for that is because when the hormone, vitamin D hormone, binds to the receptor, it activates all these genes and the genes do stuff that regulate immune function.
You know, there are studies that have shown people, and I love these studies because...
Because they basically take away people's complaints about, you know, there's lots of epidemiological studies showing that low vitamin D is associated with disease X, Y, or Z. And everyone's like, well, you know, they're not in the sun as much, so they're not as healthy, they're not as physically active, they're not whatever, even though those confounding factors are usually corrected for.
At the end of the day, it's an association, right?
And everyone's like, correlation's not causation, which is true.
But sometimes you've got to look at the full body of data, you know?
There are genetic polymorphisms.
So there are people that have variations in genes that cause them to genetically have lower vitamin D. And so this is called Mendelian randomization, where you can take a person that's That has a genetically – like they're genetically low vitamin D. So you're not categorizing them based on their vitamin D levels.
You're categorizing them based on their gene.
And those people are more likely to die from respiratory infections just based on that gene alone.
So yeah, that gene that it's known to lower – it lowers vitamin – it leads to lower vitamin D levels.
And so like those people are more likely to die from respiratory infections than people that don't have that, which – It's a great way of kind of randomizing people by their genes as opposed to doing a randomized control trial.
Those have been done as well.
There was a study that was over 25 randomized control trials.
People that were given a vitamin D supplement varying doses either weekly or daily.
Monthly didn't work.
The people with low baseline vitamin D levels, so people that were deficient, they were 50% less likely to have a respiratory tract infection if they were taking the vitamin D supplement.
Over 50%, actually.
And people that had already normal levels still had a protective effect.
They were still 10% less likely.
So even people that were already considered normal taking a vitamin D supplement helped prevent the respiratory tract infection.
So the tolerable upper intake has been set by the Nutrition Board and the Institute of Medicine to be 4,000 IUs a day.
But there's been studies that have shown that people that have taken 10,000 IUs a day for multiple years haven't had any hypercalcemia or had problems.
Too much vitamin D can be toxic.
It's not good to take that.
It's best to like get a vitamin D blood test.
And I think that personally, there has been a trend.
So people that have blood levels higher than 60 may have just a little bit higher calcium levels, but not much, not like it's not like Anything to be hugely concerned about.
But there are studies also showing that either vitamin K1... So there's been a meta-analysis looking at 12 different studies, I think, where vitamin K1 or vitamin K2 were given.
And both of those improved bone mineral density and prevented any hypercalcemia.
Because when you take vitamin D, you absorb calcium better.
Like something crazy, like 40% more dietary calcium is being absorbed.
So the problem is that...
Calcium can easily form a precipitate in general, and particularly when phosphorus is around.
And phosphorus is another thing vitamin D does increase the absorption of.
But again, like I said, it's really hard to find any studies where vitamin D is causing...
You know, hypercalcemia unless it's like really, really high dose for a while.
I personally think taking the vitamin K... And what's interesting about the vitamin K1 versus vitamin K2 without going into too much of a tangent is basically the vitamin K1... Normally, it goes to your liver and it's involved in blood coagulation.
But when there's enough vitamin K1 around, it stays in the periphery and it moves calcium, periphery being the bloodstream.
It moves calcium out of the bloodstream and takes it to places where it's supposed to go, like the bones and the muscle.
Vitamin K2 usually stays around in the periphery.
It doesn't really go to the liver.
So that's usually what it's just doing is moving calcium out and bringing it to the bones and So I take a...
I actually have K1 in my multi that I take, but I also take a K2 supplement, MK4. I take it like a couple times a week.
And what dose are you taking for K1? Well, the K1's in my multi, so I don't...
Vitamin K1 is really...
It's found in dark, leafy greens.
So I get a lot of those as well.
I get a lot.
So I'm getting a lot of K1. Vitamin K2 is not as, it's not as readily found in like the western, I mean it's like the food that's highest in it is that fermented soybean natto.
There's a big reason I think that vitamin D is so important.
It's for the lung function and the respiratory function.
But what's really interesting is that, you know, the very receptor that this SARS-CoV-2 virus binds to to gain entry into the cell, it's called ACE2, that very receptor plays a really important role in preventing lung Lung damage and basically preventing acute lung injury,
preventing acute respiratory distress syndrome ARDS. And what's been shown with SARS-CoV-1 is that, because SARS-CoV-1 also binds to that receptor, ACE2 it's called, and that's how it gets into the cell, just like the SARS-CoV-2.
When it binds to the receptor, it, like, it attaches in, like, through this, like, weird endocytosis mechanism.
It takes the receptor in and decreases the receptor, what's called down-regulates.
Down-regulates the receptor, so you end up having less ACE2, which causes, like, can cause severe lung injury.
Not having the ACE2, it plays a big role in protecting.
That's been shown in multiple studies.
Like, so the SARS-CoV-1 virus does that.
It's thought the SARS-CoV-2 also does it because it goes through the same, enters through the same receptor.
And it's been shown that like if you, for example, if you give mice lipopolysaccharide or something that's going to cause lung injury, and then you give them vitamin D. So the lung injury itself also causes the ACE2 receptor to decrease.
And so it's like this vicious cycle of like making the damage worse.
But if you give mice vitamin D before that happens...
The ACE2 receptor increases and it protects them from the lung injury.
But you give the vitamin D to control mice that don't have the lung injury, it doesn't do anything to the ACE2 receptor levels.
So it's not like full stop.
It's not like, you know, drugs, the way drugs are designed is they like, they target a certain molecule and they boom, they like do their thing.
They either increase it or decrease it.
A lot of times with hormones, vitamins, things like that, they maintain homeostasis.
You know what I mean?
So when shit goes wrong, they fix it.
They're not just like, boom, full stop, going to increase something when everything's normal.
And that's important because there have been some concern about taking vitamin D, increasing the ACE2 receptor.
And there's another study that was with hypertensive rats.
Where the hypertension caused ACE2 to go down and that like makes lung...
It makes all sorts of problems.
It also causes like kidney problems and all sorts of things, right?
But the vitamin D increased the ACE2, but only in the hypertensive rats, not in the normal control rats, again.
So, you know, and then there was another study that was like some other messed up diabetic animal model where the vitamin D actually didn't increase the ACE2 receptor, but it increased what's called soluble ACE2, which is in like...
It's in the periphery, and that actually potentially could bind SARS-CoV-2 virus and prevent it from – it's like sequestering it, preventing it from entering the cell.
That's actually being explored as a potential therapeutic.
So the bottom line here is that sometimes you'll hear this ACE2 receptor, and that's how the virus gets in, and it's like, I don't want that.
I want less of that because that's how the virus gets in.
But, like, biology is always way more complicated than just a simple – Taking it out of a big picture, right?
You know, so like the ACE2 receptor, the ACE2 is part of the renin-angiotensin system.
It plays a huge role in inflammation.
It's also like when you decrease ACE2, all these signaling cascades happen and it's like ACE2 is important for producing pro-inflammatory cytokines at the end of the day without getting into all the stuff, you know, specifics.
So it causes massive inflammation to have a decrease.
It basically causes acute lung injury.
It exacerbates it.
I mean, it's crazy.
So I really...
I just...
I really...
Can you imagine if vitamin D really did help?
Like, if there was something that could be given along with the other stuff from Desivere, whatever, whatever it's going to be the stuff that we identify.
But like, vitamin D is so cheap.
It's so easy.
And so many people are...
Deficient and insufficient.
So yes, as you mentioned, you don't want to take too much vitamin D. You don't want to overdose on it.
But I think in the short term, particularly in the short term, and particularly in people that have already been infected, it may be wise to try giving your patient, like if you're a physician dealing with this, it may be wise to try and see their vitamin D levels and perhaps give them some.
So there are clinical studies, unfortunately not a ton of them in the United States, that are looking...
Randomized control trials looking at vitamin D, the effects of vitamin D on already, you know, patients with COVID-19.
Which what would be great is like giving them to like...
First responders or healthcare workers and seeing, like, how does it – what role does it play in prevention?
Because that's really the easiest thing, right?
I'm involved – a friend of mine, Dr. Eric Gordon, he's put together, so I kind of – with his help, I've – Helped him design an open-arm trial, very small, 40 patients, where he is going to be giving them 50,000 IUs every five days of vitamin D. So it's like a weekly dose because a lot of times these people are severely deficient and so you want to give them a higher dose.
And doing 50,000 IUs weekly isn't something that's necessarily going to be toxic or anything like that.
And then we're doing some other things, vitamin C, I think it really should be explored.
I think it has huge potential.
It has to be shown.
Like, this isn't something that people can just, you know, take it home and think I'm protected.
Like, a month before all this lockdown happened, so I got my data back pretty recent.
And I still hover around 50 nanograms per mil, even though before I was taking 4,000.
Generally speaking, 1,000 IUs will raise your blood levels by about 5 nanograms per mil.
And there are people with different variations in genes that are related to vitamin D metabolism where they have lower levels and they need a higher dose.
The only way you're going to know that is by, of course, measuring your vitamin D levels multiple times.
And then potentially even doing, like, a genetic analysis, you know, as well.
But you have to measure your levels.
Like, that's the only way to know.
Of course, right now, it's, like, you can't go to a lab.
I've studied vitamin D so much, I've got two publications on it.
I certainly take that with a grain of salt as well.
But I just think the data is strong.
I really think the data is...
I think it's mounting data and I think that eventually something will come out and it's going to, just like the randomized controlled trials, showing that it protects against respiratory tract infections.
Everyone wants randomized controlled trials.
No one wants to believe anything until it's a randomized controlled trial.
I want to believe it because it's easy, it's safe, and I think people need vitamin D anyways.
I mean, you know, so of course I want to believe it, you know.
But, like, there was this interesting study where African Americans who are very deficient in vitamin D, they were given a vitamin D supplement for like a month and It decreased their epigenetic age by like two years.
So if you have the Dr. Rhonda Patrick pyramid of supplementation for preventative symptoms of COVID-19 or preventative measures dealing with COVID-19, that's your base?
I mean, my mom, I've got my mama, I've got my dad, I've got my whole family.
Everyone's on the routine.
You know, vitamin D is like the most important.
So that's the foundation is vitamin D. Right now, yeah.
I mean, I'm always trying to get them to have that.
But it's easier to convince when people are scared.
People are more likely to make change.
They have to be motivated to make the change themselves.
Otherwise, it doesn't work.
So I think that in this case, people are motivated, especially people in my parents' generation that are older because they're more scared.
They're more scared that...
They could be affected by a severe case of this, right?
So I think that's certainly the issue.
Yeah, I mentioned I'm drinking my vitamin C water.
It's funny because I probably got like a thousand questions about vitamin C in the past.
Month, month and a half or whatever.
My team and I just dove in and put together an article, released a podcast on it, a video where it just kind of covered everything.
I mean, I can't believe how many studies I read on vitamin C. 190 references in our article, the 28-page article on our website.
But vitamin C is interesting, too.
I mean, I don't...
I certainly...
The interesting thing about vitamin C is there's oral and then there's intravenous vitamin C. And the intravenous vitamin C is what seems to be really relevant right now.
But I think the most interesting thing that I learned really had to do with the pharmacokinetics, which is basically like...
How much vitamin C raises your plasma levels and is there a saturation point where you can eat 20 grams of vitamin C but still only get to this certain point versus what you do if you inject it into your veins intravenously?
So what's interesting is that most people that are just like eating, let's say that people are just eating like five, somewhere between five to nine servings of vegetables or fruits a day.
Those people have anywhere between like 70 to 80 micromoles of vitamin C like per liter.
So it's micromoles per liter in their blood.
If you take like a 200 milligram supplement, you only raise your levels to like 90. So it's not much over that like baseline.
Most people that aren't eating that many servings probably have around 50, which is still considered normal, 50 micromoles or micromolar.
And then what's interesting is that like, but those levels you take, if you take 200 milligrams, it doesn't do much.
If you take a gram, it can raise you up to like 130 or something.
If you take three grams, it can raise you to 220. And that's like the maximum level you can get from oral supplementation.
220 micromoles.
That's a big difference.
220 versus like 50. So three grams.
Three grams.
But here's the other interesting thing is that if you don't take it multiple times throughout the day, if you only take it once, You'll peak at around five hours after.
I think there's like a really nice graph on my website on the topic page.
It shows it's like you'll peak like five hours after, but then you go down steadily and over 24 hours, you're back to normal, your baseline.
But if you take it like, you know, four times a day, you can stay at 220, like the whole time.
And the reason that's important is because a lot of studies looking at oral Vitamin C consumption and like, for instance, the common cold, incidence of the common cold, really depends.
Like there's huge variations in the results and it all really seems to come down to dose.
Like it really does.
And when you know the dose and how that's changing your blood levels, like if you're only taking 200 milligrams, which some studies are doing, It's barely doing anything over your baseline.
So I found that really interesting.
And then the intravenous vitamin C, so far the maximum I've seen measured is like 70 times that.
Your blood can get 70 times 200. So it's like 18,000 or 17,000 or something like that.
Oh, it totally overcomes all those saturatable mechanisms.
And it's not only more effective, it's a completely different What dose do you recommend for intravenous vitamin C? Jamie, can you pull up foundmyfitness.com and there's a vitamin C topic page so that way I can answer that question better?
The intravenous vitamin C is a completely different game because It literally generates hydrogen peroxide.
When you get doses above, when you start to max out over that plasma level, 220 micromole, the vitamin C itself, so vitamin C kind of cycles between being oxidized and reduced.
It's called dehydroascorbic acid, dehydroascorbate, and then ascorbic acid or ascorbate.
Dehydroascorbic acid is the oxidized form and hydrogen peroxide is generated.
Which is really interesting because it's one of the mechanisms by which at least it's thought that intravenous vitamin C kills cancer cells.
It also has been shown to like kill viruses and stuff in a variety of different studies.
But that's interesting because your neutrophils generate hydrogen peroxide.
So the intravenous vitamin C is like generating hydrogen peroxide.
At the same time, it's also acting as an antioxidant for your own neutrophils.
And that's been shown.
So people...
You know, in clinical studies, but also it's been shown that the hydrogen peroxide does not damage the normal cells.
Like normal healthy people, given intravenous vitamin C, it's generating hydrogen peroxide, but there's no oxidative damage happening in people's like lymphocytes and stuff.
If you just had access to it every day, how often would you take intravenous vitamin C? You know, it's something because if you if you look at the graph, it's kind of a trans intravenous vitamin C is transient.
So it's like it's having it's not something that like necessarily needs to be done all the time.
It's something like I was I was interested in doing it like my mom was my mom had just gotten sick and like common cold, you know, she had like a runny nose and stuff.
And so I took her we went to get the IBC and they did it was 10 10 grams that we did.
And I took it because I was like, well, she's sick and I've been around her and like, I don't want to get sick.
So, you know, I thought, why not try it?
And, you know, so, you know, the intravenous vitamin C, maybe there's like a reason to do it, but it's not something that I'm certain that people need to do on a daily basis.
It's different than like vitamin C, you know, normal vitamin C you do need.
You need to get it from your diet.
It's important.
Like it's important for normal immune cells, normal immune function, and that's been shown.
Well, the IV is totally – the IV is totally different. - Right.
The IV is really being used as a therapeutic treatment.
Like it's a therapeutic treatment more, you know, the IBC, where it's been shown to help with like, for example, at least in the hospitals in San Diego, it's routinely used for sepsis.
Like friends of mine, you know, use that for treating sepsis and there's been...
Large randomized controlled trials showing that it dramatically reduces mortality with sepsis.
So, like, that's, especially in combination with thymine as well, like, huge differences in people dying from sepsis, which is obviously very relevant now, but hasn't been shown.
I mean, there are clinical studies that are ongoing right now, some in China and some in the United States looking at IVC potentially to help treat sepsis.
COVID-19 associated pneumonia.
You know, it'll be interesting to see the data from those trials, whether or not there's going to be an effect, it's not known.
But the fact that it has been shown to improve sepsis outcomes in multiple studies.
It's also been shown, obviously, cancer is a big one.
Linus Pauling was deemed a nut, the Nobel Prize-winning chemist who basically is the vitamin C guy.
He, back in the 70s, was championing intravenous vitamin C for cancer patients because he was claiming it was curing them, quote-unquote, curing them.
I wasn't quite doing that, but it was improving the outcomes of cancer patients.
And there's all these studies from the Mayo Clinic came out and they were like, nope, doesn't do that.
Turned out they were using oral vitamin C, which is like comparing apples to oranges.
There's another meta-analysis that looked at 200 milligrams up to, like, 200 milligrams up to two grams.
And that study kind of just lumped everything together rather than the other study, like, okay, what happens is two grams in one, and they did all these sub-analysis, and that was great because they, like, got to the bottom of it.
Dose matters.
The other study, it was like, oh, it reduces the duration by, like, 4%, you know, basically nothing.
So there was all these conclusions.
It doesn't do anything.
Well, yeah.
200 milligrams, look at that graph.
It doesn't do shit to your plasma levels.
Like, you're still at baseline.
So I think that people designing clinical studies, like, that needs to be in their mind before they design their trial.
Okay, what am I trying to measure here?
Like, I want to get, I need to, like, I need a measurable, like, I need something to measure.
I need that to change, right, to get an outcome.
Like, if you want, you're trying to, like, see what effect vitamin C has on whatever outcome, you're going to want to raise someone's plasma levels, right?
I guess it's good at the end of the day to know that 200 milligrams doesn't do anything because then you go, okay, well, 200 milligrams doesn't do anything.
But it's also good to know that, oh, wait, if I take a higher dose, there is an effect.
So, you know, making this general statement that, oh, vitamin C supplementation doesn't do anything is accurate in some respects.
Yeah, 200 milligrams, it doesn't do much for the common cold.
But when you take two grams...
It can help.
And also other studies have shown that prophylactically is slightly better than like therapeutic.
So like after the onset of symptoms.
So if you do it like before symptoms, like there's a better, you know, outcome as well.
I don't even know if it's necessary, honestly, to be honest, because again, it's a therapeutic treatment.
I will say this, like one of my friends, she's an MD, and she has reactive airways.
There's interesting studies that have shown that intravenous vitamin C is dramatically reducing inflammation as well.
It's doing all kinds of crazy things.
But her cough, and it was very transient.
It only happened while the vitamin C was high in her plasma.
She's got this crazy cough.
I mean, you'd think she'd had COVID. It's just like a constant nagging cough, you know, that it completely 100% went away.
I noticed it.
And she like my friend is a little bit, you know, she's a little bit of a skeptic when it comes to like vitamins or anything like that.
You know, so I wasn't going to say anything because her and I have gone in so many debates about it.
So but she said something and I was just like, you know, I'm so glad.
And so she now she's wanting to do it like she's wanting to do it like, you know, once a month at least.
So I thought that was, you know, interesting.
Again, I don't know that the intravenous vitamin C is necessary.
There's also interesting effects on, like, fat oxidation.
Like, it affects fat oxidation because it's important for carnitine, which isn't necessary for oxidizing fat.
Like, there's been clinical studies where people are, like, burning more fat when they're exercising if they have vitamin C and if they have low vitamin C levels or not, like, burning as much fat.
And elderly people are more, zinc deficiency is not really common in the U.S. Most, you know, zinc is found in, it's really high in oysters, but not a lot of people with oysters.
Red meat, poultry, you know, if you eat enough of that, you should be getting enough zinc.
What about vegetarians?
Vegetarians, they are more prone to zinc deficiency.
In fact, because the zinc is bound to phytate, it's less bioavailable and they need to eat up to three times more.
The RDA needs to be almost three times as high for them.
which I know a lot of vegetarians do.
But yeah, zinc, zinc's really important for immune function.
Like there's been studies where they've like depleted healthy people of their zinc just transiently.
And like T cell function like is all messed up.
So it like totally messes the immune system up.
Randomized controlled trial showing that zinc, zinc acetate or zinc gluconate, like lozenges, they can dramatically lower the duration of common cold.
It's got senolytic properties, which means it's been shown...
It's been identified as a possible compound that can clear out senescent cells, which are those cells that are...
They accumulate with age and they're basically like...
They're not dead, but they're just like...
Not really functioning and they're secreting cytokines and things that age in your bicells.
I always like to think of like, I was mentioning to Jamie that I'm going to be 42 next month.
And so yeah, I have some gray hairs.
Hey, gray hairs.
And it's funny how like you'll get one gray hair And the other gray hairs, like, cluster around that one.
Like, they're clustering.
And I always think of, like, because cellular senescence happens in the melanocytes that, you know, are responsible for pigment.
So I always think about, oh, the senescent melanocyte is, like, secreting all this pro-inflammatory stuff that's now accelerating the age of my other nearby hair follicle melanocytes and it's causing them to...
Anyways, quercetin's been identified to clear away senescent cells, so that's kind of cool.
No, that's just my analogy for people to understand why senescent cells are bad because they age other nearby cells by secreting all this stuff, pro-inflammatory cytokines.
Once I started doing it during the lockdown, one of the things I noticed, the runs that I do, the last hill is fucking brutal.
And I always finish on this last hill.
But now I've been able to run that last hill, the last hill.
It's like a marked difference.
When I hit the hill, I'm like, wow, this is crazy.
Either I'm getting in better shape, and I know I am for sure, but it's also...
I gotta think the sauna has a big impact, because it feels like I'm on a drug.
It feels like I'm on, I don't know what EPO feels like, but I would imagine it would feel something like this, where the increased cardiovascular benefit is very noticeable.
I would love to have something to measure it without having to take my watch in there because I don't like sitting like it's like you know well the whoop strap measures it really well and it'll give you like you could actually mark it down as an activity and it'll show you what your heart rate so it's you had a mountain of data it's really good that's cool yeah let me It's also great for sleep.
It just makes sense that if you have more leg strength, that means you're doing more activity.
That means you get more blood flow.
That means everything's probably functioning better because it's such an enormous part of your body.
When you look at your musculature, the large percentage of it is from the waist down.
And when I'm doing legwork, most of what I'm doing is kettlebells, but I'm doing lunges and presses and squats and all these different things with heavy kettlebells.
So it's a lot of weight that your muscles are pushing.
Dan is always trying to get me to do squats like I don't know what back when I was in grad school I was doing squats and I was using the stuff and then I was doing I guess what are they called leg presses yeah and I like injured myself and in this I want to call it sciatica what's the other one that's like sciatica there's another sciatica is is a nerve that comes from your discs like right here yes well you know what that's from though I don't know what it is, and I'm calling it sciatica.
But the reverse hyper, the reason why it's so special is...
Forget about this for a second.
Yeah, there's a girl.
There's a girl using that.
That is a more primitive version of the one that we have out there, the new one that Westside Barbell sent us.
It's just a cable that comes through the floor and the weights are actually behind you.
You're carrying all the weight on your hips, so it strengthens the legs without putting a load on the back, which is fantastic.
I like that for that.
So you can get all the leg work that you get from squats, but you don't get the pressure on the discs.
And then the Reverse Hyper is a machine that he actually invented.
Louis Simmons invented it because he had a herniated disc and the doctors are telling him, hey, we have to operate on you because you have this compressed disc.
And so he's a very smart guy and he knows so much about physical fitness and weight training.
That's Louie right there.
He came up with this machine.
So he said, well, listen, if something compressed it, something can decompress it.
So he came up with this machine.
And with this machine, the reverse hyper does on the lift, it's strengthening the lower back muscles.
But then as you drop it down, it swings low and it actively decompresses all of your discs.
It has those inversion tables, which are great for the same thing.
You're hanging by your ankles and it's decompressing your spine.
But I actually prefer this product from them because this completely isolates the back.
And you're not pulling on your knees and your ankles when you're decompressing.
It's all just decompressing the back.
And also you can do leg extensions and a bunch of other things.
You see people doing dips and other exercises from the...
The Teeter.
But it's a great machine and it's just really specifically good for back health, lower back health, decompressing it, and even strengthening it because you can do those back extensions.
So you hook yourself into it and then you just lift your back up and down.
Lifting weights increases bone density, tendon strength, so many different variables that are so huge because as your body gets older, those are the things that go south.
So I think it was 2014. But, like, the sauna, you know, it's just been, like, something...
I came on your podcast the first time when we talked about it and then, of course, continued to...
You know, publish videos and articles and stuff.
And I'm writing a review article for peer review publication right now.
But there's a woman who reached out to me.
She had done her, I think her PhD, either her PhD, I don't know.
I'd say psychology, but she had done it with a guy I interviewed on the podcast, Dr. Charles Rezon.
He's the guy who showed that like a single hyperthermic treatment, which was with a device that raised the core body temperature like almost three degrees, could have an antidepressant effect.
Well, she reached out to me and like the FDA shut that whole machine down.
Like, no, you can't use that for research anymore, which kind of shut down the whole sauna depression, you know, research area.
So she basically, she has gotten some funding and she's doing a pilot study with a new device, which is something you can like buy off Amazon where it's like a sauna, like your head's out, but like it's like a tent, like a sauna tent.
Yeah, so it's different, but it's something that she's got to prove that it's safe before the FDA will allow her to even continue on to study how it affects depression.
And so I've been able to help with connections I've had, help fund new studies she's going to be doing where she's going to get depressed patients.
To basically be exposed to this sauna and it's like an intense like she's like this intense protocol where like she's like it's like an hour long and they get really hot and people are giving them wet towels because like it's like it's like imagine being it's like 140 degrees Fahrenheit so it's an infrared but they're in there for like an hour you know and they're getting they raise their core body temperature they're measuring that rectally so um But she's going to measure the effects on, you know, on depressed patients.
So it's really exciting because, and they're going to do like a dose response where they're going to see how many, the Charles Rezon, Dr. Charles Rezon showed one, just one single session could result in an antidepressant effect six weeks later.
She's going to try to do eight sessions where she's going to see if these people can handle...
So infrared saunas, the main difference between infrared saunas and like the regular dry saunas that you and I use is that the regular dry saunas are heating the ambient air, right?
And that's then raising our core body temperature through that mechanism.
The infrared saunas are, like, they're, like, changing electrons.
They're, like, directly heating your body, basically, without having to heat the outside air as much.
There have been some studies that have compared...
I mean, there's benefits with these infrared saunas.
In Japan, it's called Weyon therapy.
It's far infrared.
And they use it...
It's been used to, like, help even treat different cardiovascular diseases.
Like it's been shown to improve like chronic heart failure or something like that, I think.
So there's benefits with these – with the infrared.
Personally, there's – I think there's a lot stronger.
There's much more research on not only dry saunas, but in Finland, they take the sauna – A dry sauna that has like these hot rocks and they pour water on top of the hot rock and so it creates humidity, right?
Steam.
And so that's really a common sauna.
Like I went to Finland a few years ago, visited Finland, some other saunas there.
I mean, like I said, ours is really small, and so like, I mean, you're breathing like it's like burning you there's a direct formula too between the percentage of humidity and then the increased temperature the way it feels like if it's at 180 but you have 10% humidity it's like feels like yeah there is i don't know what that formula is absolutely there's a formula and In a lot of the studies coming out of Finland, many of the people there are doing the humid saunas as well.
So, I mean, I guess they're called Finnish saunas, which means they're using the hot water and steam.
So what we did, I visited the Sauna Society, and it was in November, so it was cold, and it's right on a lake.
And so they have, like, the day I went, it was not co-ed day.
So, you know, it's only women saunas that I went in.
It was, like, sectioned off.
But so you go and you do these different, they have all these different types and I don't remember and they're like whipping each other with like birch wood, you know, which it's interesting.
Anyways, they jump in the lake and then they go back and they're doing this.
Did I ever tell you my crazy story?
Which crazy story?
There's a friend.
Some of your friends are a little eccentric, right?
Well, this guy, he's got a huge property in the country, in the woods, in Finland.
And this was the first time I ever went camping.
And it was snow camping.
It was crazy.
It was the worst thing ever.
He had a...
He had us do this like – there was like two tents and it was a conference that I gave a talk at and so some people paid extra to like go to this event that was after it.
So there was like 30 or so people there and they were – from all around the world.
There was only like three Americans, me, Dan and some other guy.
No, four Americans I think.
But anyways – It was my first time camping outside.
I've been to Yosemite, but I stay in a cabin.
I don't like to sleep in a tent.
So it wasn't a great experience because, one, there was this guy who snored all night.
Two, because it was snow camping, there was some weird fire thing.
This guy was in the military, and so he had us do this thing where everyone had to wake up at, I forgot what it was, every hour.
So anyways, I'm in the sauna, everyone's naked, and the guy who's my friend, he's still my friend, he's an interesting guy, but he had people come and started doing yoga, and they're naked too.
Then he had some whipping technique with the birch wood, and he wanted, like, to demonstrate it, so he had, like, one of the Britain girls, like, and she was laying...
And I've had those conversations in public saunas before, too, where people start getting into the toxins and the whole sauna, and I'm just sitting there quiet, and I'm just like...
Okay, let me start to tell you some benefits, like some real benefits, cardiovascular.
Did you know that it actually mimics exercise?
Like, literally, like, that's been shown.
It's been, like, compared, like, 25 minutes in the sauna, 25 minutes on a stationary bike.
And same things are happening, you know, like...
Blood pressure goes down afterwards.
Heart rate variability improves.
Same things are happening.
You're increasing plasma volume.
Heart rate increases.
Core temperature increases, right?
Exercise is doing the same thing.
The antidepressant effect that I feel from the sauna that Charles Rezon published and that Dr. Mason will hopefully carry on the torch I think it's real, and I think that there's potentially multiple mechanisms, immune modulations, but also just the fact that BDNF. There's a study showing that hot baths do increase BDNF. BDNF? Brain-derived neurotrophic factor.
What's so amazing about this neurotropic factor is that it's always thought about in the context of like...
Brain aging because it helps you grow new neurons.
It's neurogenesis.
It helps already existing neurons survive.
But there's studies now showing that it regulates what's called neuroplasticity, which is like the ability, like your brain, your brain changes, you know, with the changing environment.
But you have to be able to adapt to that, right?
Like children are really good at that.
Like they have a lot of neuroplasticity.
But neuroplasticity is associated with depression.
Like, not being able, like, stressful conditions and stuff like that.
Like, not being able to, like, adapt.
I'm not using, like, the best of terms, but neuroplasticity is something along those lines.
And so...
And BDNF plays a role in that.
And BDNF has been shown to increase with exercise and also with heat stress.
There is like a huge link now between the immune system and chronic inflammation...
And depression, brain function in general, brain aging, but inflammation.
So, I mean, there is a push for a looking...
But not all depressed patients have it.
It's like there's a subset of C-reactive protein.
But yeah, depression is measured...
It's a very much like, you know, have someone...
So a subjective measurement would be a clinical person like measuring a whole battery of things they do.
I forgot the name of the test.
But yeah, that's the test.
So it's like basically a battery of feeling things.
So it's not like a hardcore quantitative biomarker, which so badly is needed.
But the hot baths have also been shown.
So heat shock proteins...
There's so many amazing things that heat shock proteins do.
They've been shown to prevent muscle atrophy.
And that's, you know, in the brain, they're so important, like preventing proteins from aggregating in the brain.
That's how I first got in, like, one of my first biological experiments ever, because I was a chemistry major in college.
So I was doing all chemistry stuff, organic chemistry and, like...
Chemistry.
But after I graduated, I went to work at the Salk Institute for Biological Sciences in La Jolla.
I was working in an aging lab.
And one of the first experiments that I was doing, like one of my first projects, was we were taking the human amyloid beta gene And injecting them in these worms, these nematode worms that only live, like, 14 or 15 days.
And we're making them form amyloid plaques in their muscle.
So, like, basically, you look at these little worms under a microscope.
So they're only, like, half a millimeter.
You know, they move around.
And as, like, they get older and they're aging, they don't move as quickly.
You know, they're kind of slower, a little more decrepit.
But anyways, you give them this amyloid beta.
And after, like, a couple of days, they become paralyzed, where they're, like, laying in their little Petri dish plate on the E. coli food you're giving them.
And they kind of just move around just to feed, like their nose is just moving around.
And so when we would give them tons of heat shock proteins in addition to the amyloid, totally reversed it, like completely.
They would move around and be young.
So anyways, heat shock proteins play a role in neurodegenerative disease, also some links to improving depression in animal studies.
So the sauna, I know of one study where people that Sat in a 163 degree Fahrenheit sauna for 30 minutes, had heat shock proteins, their levels were 50% higher over baseline, which is great.
And that usually, like, animal studies show that they can stay elevated for like 48 hours after that.
There's a hot bath study where they also elevated, it wasn't quite as high, but it was like, you know, 40 or so percent higher than baseline levels, and it was 104 degrees.
But this study, instead of doing it from the shoulders down, where I told you about the depression, it was like only 20, 30 minutes, it was like from the waist down, so they had to stay in there for an hour.
It's like a jacuzzi, you know, where you're sitting there from the waist down and like, that's hot.
Like staying in 104, that's pretty hot.
But heat shock proteins did increase.
So I think...
For people that don't have access to a sauna, that hot baths absolutely are a good modality for heat stress.
And I used it for a long time.
Like I said, I just got a sauna.
I've made a career about talking about saunas, and I just got one last month.
So I understand what it's like to not have a sauna and to have to use hot baths.
But I was also using the gym saunas, but right now it's like...
There's no gyms that are open.
Hot baths are the only choice if you don't have a home sauna.
So, I mean, there's differences in, I mean, so it depends on how long you're staying in a cold, you know, water, like cold shower, like actually being submerged, like from like, if you're like in the ocean or something or a lake and you're like from your shoulders down, like that's...
Probably much more powerful than just having the shower on.
But by the way, the shower, like some days I'm like, what does the matter?
But the cold shock, you were asking me cold shock proteins.
That hasn't really been measured in humans.
What is measured most of the time with cold shock is norepinephrine release.
And norepinephrine in plasma, and there has been studies correlating norepinephrine in plasma upon cold exposure, norepinephrine release in plasma in the brain, where it's involved with mood and focus and attention.
So there's been studies where you could do a two-minute cryo Whatever the average temperature, it's really cold.
But I also just I think it might be a little too much before like I'm always trying to regulate how much activity I do with whether or not I'm be exhausted when I do a podcast.
Because I used to do yoga, and then I would come out, I would get out of yoga at 11, or at 10.30, and I would do a podcast at 12, and I was like, oof, I think I better wait till 1. Because I'd just be so, because 90 minute yoga classes into 105 degrees is fucking rough.
Well, I would wonder, and I know there's supposedly some sort of Harvard study that's ongoing right now measuring all sorts of markers in people that have done hot yoga.
And whether or not it mimics heat shock proteins that are created in the sauna.
Because the thing is, you are getting this incredible cardiovascular exercise because your heart's beating like crazy.
And you're not doing cardio per se, but your heart rate gets jacked because of the heat and the stress.
Totally.
And then on top of that, even though it's only 105 degrees, your body is heating up.
You're really sweating up a storm in there.
I've taken some friends there that have never experienced it before, and they're like, fucking yoga.
Come on, bro.
Yoga.
And then they get in there, and then I look over at them 15 minutes in, and they're like, fucking A. And I'm like, yeah.
Like yoga, even uncoupled from the heat, like the hot part, yoga is also like...
It's pretty intense, like holding those positions and stuff.
And like your heart rate does start to elevate.
I mean, it's like just from that alone.
Adding on the sauna, which mimics moderate physical activity that's been shown, absolutely mimics it.
And then all the, you know, studies that have shown that.
On top of that, I mean, that's like...
It's super intense.
It's super intense.
The really cool thing about...
And I want to get my mom...
I think once we move the sauna to our home where it's not like the office, people that are sedentary and people that are sedentary for whatever reason, maybe they're sedentary because they're disabled or maybe they're sedentary because they've had a lifetime of being sedentary.
It is just hard to get them motivated to go exercise.
The sauna to me is like...
So important because it's giving these people a potential cardiovascular workout.
No, it is.
That's been shown.
It's giving them a cardiovascular workout without having to force them to go for a run or get on a bike.
You know, people think, like when you tell them to go sit in the sauna, they think of like a spa.
Like, yeah, I want to go do that.
You get someone who's like my mom.
She's sedentary.
She's not like a physically active person.
And she needs to be.
But like the sauna, that's kind of my goal is to get her doing...
And we'll have to start slowly because you have to adapt.
The heat shock proteins help with that.
The more times you're exposed to heat stress and the more adapted you are, the heat shock proteins increase quicker.
And so it's part of the adaptation process as well of being able to handle the heat stress.
But I want to get her to do that because any cardiovascular...
Improvement is going to help her mood.
It's going to help her, you know, all-cause mortality.
That's been shown, you know, four to seven times a week, 40% lower all-cause mortality.
Cardiovascular-related mortality is 50% lower.
You know, so, like, I think that's a really cool thing about the sauna is that you can get people that are disabled, people that can't go for a run, you know?
I mean, I still think exercise, I mean, it's just the best thing ever.
But there have been studies, at least were localized heat on people that had a limb immobilized.
I don't remember what limb it was, but after a week, people that had the heat treatment, local heat treatment, had almost 40% less muscle atrophy.
That's huge.
That's huge.
In animal studies, and I remember I shared this animal study in an article I wrote years ago before the human study came out, and there were critics, well, it's animals, and blah, blah, blah, you can't say it does this, and I would get on the mechanism, and they showed it was heat shock proteins, and I was so happy when that human study came out, because I was like, told you!
That's what I wanted to say.
There's just a few of those guys that you're just like, maybe I just do a big comprehensive search of the literature and understand things and don't have that exact study just yet, but I know that it's going to help with muscle atrophy.
I think that happens a lot too with social media because, for example, if I share one study, I'll share an epidemiological study.
And it's like, it's Twitter.
You know, I'm doing 140 characters, whatever the chain, I don't know what the characters are now, but I'm doing a small number of characters.
And I'm just sharing one study.
And if it happens to be a non-randomized controlled trial, then, you know, it's just correlation doesn't, you know, doesn't equal causation.
It's like, sometimes I just share a story because one, I think it's interesting, or two, because I I've read a bunch of, you know, evidence surrounding this topic, you know, about all the other clinical evidence, all the genetic evidence, all the animal.
And so I have a knowledge base here.
And so I share a study that may be isolated in and of itself.
This is what I tried to explain to a friend of mine who was on the podcast, who read the comments, and I go, you just have to stop and think.
Okay, even if just 1% of all of my people that go from Instagram, like if you're reading the Instagram comments, 1% Just one, which is probably really conservative, right?
If you get a room full of people, there's a hundred people in the room, what are the odds that one of them is going to be an asshole?
Well, if you had rational people who are kind folks who have interesting viewpoints and they looked at something and they found something to be wrong with that and they handled it with, you know, grace and some sort of modicum of dignity and kindness, that would be great.
Like if you were having a discussion with a good friend and the good friend was looking at something that you said and said, I disagree because of this.
Look, I have conversations with good friends all the time and even on the podcast where I disagree with them.
But that's the problem with Twitter is that you don't see that person.
You don't know them.
You don't want to please them.
You just want to be mean.
Right.
You know, and that's what a lot of people are doing, and they're just getting their rocks off.
And I feel like now, for a while, during the pandemic, when it started and the lockdown started, people were nicer.
There was less social justice outrage, there was less this.
But now, it seems like as time's gone on and people are getting more frustrated and more desperate and more depressed because they're locked up, it seems like it's ramped up.
Yeah, I thought I should, but I've decided to just accept where this is, and then when comedy clubs are about to open up, Then I'll start writing again.
But I'm just accepting where this is, and I want to have an honest take on it.
I don't want to be manufacturing a take or trying to come up with some sort of a hot take on how I feel.
But I want to know how I really feel about this.
And how I really feel about this is very different now versus the way it was in March.
Because in March, I was concerned.
And I was like, Jesus Christ, this could be terrible.
We really have to stockpile food.
We really have to make sure that we have water purification.
We really have to be careful here.
Now I'm like, we gotta be careful these fucking politicians.
Now I'm in the place where you guys have to understand these people, people are starving.
People don't have any money.
You're telling people they can't go to work, but you're telling people they can go to work in some places.
Like, why is it okay to work at Target, but it's not okay to work in a family business?
Why is it okay?
Let's figure out testing.
Let's quarantine the people who are sick.
This strategy that you guys have, you're not adjusting and adapting.
You're not adjusting and adapting to the mortality numbers, too, because they're way lower than they were before.
Plus, now we have this understanding of the asymptomatic people and how many people have tested positive that are asymptomatic.
It's off the charts.
It's somewhere in the range.
In many studies, 70-plus percent of people that get in contact with this Are asymptomatic but test positive for the disease?
There's your diet that's included in it, your vitamin D status.
The other interesting thing, and there's been no studies with SARS-CoV-2, but there have been influenza studies showing that viral dose, it's really interesting studies that have been done where, I don't know who volunteers for these studies, but like, sign me up to get influenza.
And there's been these studies where people are like intranasal, like they'll give them various titers of influenza virus.
And they try the point of the studies to figure out what viral dose.
And they have like some measurement like in tissue culture number or whatever.
And they found like to make people have symptoms.
Right.
And they found with influenza.
I forgot which A or something.
I think one of the strains was like they could do a certain dose like 10 to the 7 in tissue culture or whatever units where it's 70% of the people would get like symptoms ranging from fever, you know, cough and all the influenza, you know, flu symptoms.
But then when they went down to from 10 to the 7, let's say they went down to 10 to the 5, only like 10% of people were getting symptoms.
So like it's kind of interesting that viral dose At least with influenza.
And there's actually been some other studies, I think measles also.
It is a thing, not something that you want to like go and experiment with yourself.
Yeah, I think with the masks, you know, for people, I mean, reopening the economy and, you know, some places have been more successful, you know, like, you know, even like Japan and stuff where, you know, the wearing the mask, like the cloth mask doesn't do much to prevent you from breathing in maybe a respiratory droplet or something or aerosol.
Right.
But it will prevent you from spreading it.
To a certain degree, I get that people don't want to wear masks.
It sucks.
Who wants to wear a mask?
But maybe to open up the economy again now, maybe everyone could wear a mask if they're going to be inside around a bunch of people, grocery stores, theaters.
Oh, I think that, I think things are gonna, I mean, I think that these therapeutics can start, the monocle, so like remdesivir has already been identified and there may start to identify other ones like the pancreatitis drug, pancreatitis drug in Japan.
I mean, there's a lot of different repurposing drugs that are being investigated.
And I think over the next couple of months, and then Regeneron's already doing one of these monoclonal antibodies, I think in the next couple of months, we'll have more therapeutics than we have right now.
That'll make things less scary.
People will be less scared of getting sick because They'll have, you know, they'll have a better idea of, oh, we have some more, you know, things that can therapeutically treat this, you know, successively.
Hopefully, people are going to start looking at the vitamin D. I really like that.
I really hope that.
If not, just I hope people are going to, you know, take their vitamin D or ask their doctor to take it, you know.
But yeah, I think that in a couple of months.
So like, can you wear a mask for a couple of months?
And like, here's why it's not going to work to just have the people that are vulnerable wear the mask.
Because the cloth mask isn't going to prevent them from getting...
The aerosolized droplets, if you're spreading it and asymptomatic, which it's been shown, if you are asymptomatic.
That CDC study I mentioned a while ago about how pre-symptomatic versus asymptomatic, after a week when they came back to measure the people again, they found that out of the 13, 10 of them actually did get symptoms.
The other three that were asymptomatic were shedding as much virus that could make them basically...
Contagious and, you know, basically able to transmit to others.
So there have been quite a few studies looking at children that are asymptomatic, children that have mild symptoms, and children that are symptomatic.
And so far, the studies have shown, for the most part, that children even that are asymptomatic are shedding as much virus as both children that are symptomatic and adults that are symptomatic, meaning they're able to transmit it.
They're like notoriously like, I used to never get sick.
And then I became a mom.
And I mean, I think first of all, the first year it hit me hard because I wasn't sleeping, you know, because you have to like, every three hours, you got to feed, you know, feed the baby.
I would like to see, in New York City, particularly when they were getting hit, you've got to think, this is New York City in January, which is January.
It's wintertime.
People are not going outdoors.
I wonder how much the vitamin D deficiency varies, depending upon winter.
Yeah, that's why it's so rough with all these people stuck inside and stressed out, you know, all this the financial pressures that people are experiencing right now because of the lockdown.
I hope, I just hope, I hope that, you know, we can reopen the economy in a very safe manner where we don't have, like, flare-ups that, you know, we don't want to be set back to, like, shelter in place again, like, full on, you know?
What factor do you think play, like when we're talking about saunas before, one of the things, this is a respiratory disease, and this is something where you're breathing in these particles.
And from what I understand, this is a vulnerable virus in terms of the temperature that it can survive in.
But if it's in your nostrils or if it's in your respiratory tract and you're breathing in that heated sauna air, does that have any effect at all on viruses?
If the virus is, like, right in your nostrils, I don't know, maybe, but I think it's already, like, getting...
If it's already getting inside, you know, the respiratory, you know, area, like, your body's kind of maintaining homeostasis, so, like, the heat that you're breathing in...
And I think that doing the sauna is making you more resilient against infection.
That's been shown.
There's been small trials showing that people doing a sauna...
I forgot the duration, but they were much less likely to come down with a common cold.
But they had to be doing it for at least three months.
It wasn't just something that you're mentioning at the time of getting it.
Also...
The respiratory illness connection, there have been correlation studies out of Finland showing that people, actually I think this study was men, only men, that use the sauna two to three times a week, they're 27% less likely to have pneumonia after correcting for,
and if they use the sauna 47 times a week, they're 41% less likely to come down with pneumonia after correcting for socioeconomic status, physical activity, cholesterol, Lung, you know, smoking, COPD, like asthma, all those like, you know, lung disorders.
So, you know, the sauna does seem to be associated with lower incidence of pneumonia, but it's thought to be because of immune, you know, perturbations and also like the, there's the heat shock proteins and all those things like help, there's like an antioxidant effect in the lungs, like things like that.
So heat shock proteins also do have antiviral activity against at least influenza A. So the heat shock proteins directly can activate your innate immune system, but they also have antiviral activity against influenza virus.
So, you know, I think that the heat stress in the sauna does help.
Now, there's another study that did look at humidity and the effect of humidity on basically like the ability of your epithelial cells and your airway and nostrils and stuff to filter out.
Particles and particulate matter and viruses and stuff.
When the whole thing started, when the lockdown started, I was getting the sauna really hot, and then I was pouring a bunch of water on it, nose breathing.
Big, long, deep nose breathing, and it was burning.
And I would take these long, deep nose, and the whole inside of my nose would be like stinging and everything, but I was like, it's got to be killing these things.
It's the other thing that happens is, and then we'd go into this ice bath and there's like this bath right outside and we like did all this ice.
And like I said, I was like trying to impress Rick.
So I was like staying in the ice bath as long as I could, you know.
So then I get back into the sauna and like getting back into this like 210 or 20 degree sauna and you feel like it's like room temperature because you were just in this ice bath.
I get addicted sometimes to things that are really hard to do.
In my mind, I'm like, because it's so hard to stay in there for 20 minutes at 210 degrees.
I mean, it hurts.
Everything hurts.
Your skin hurts.
Your toes hurt.
Like it hurts and then so then the next day I would like look forward to doing it to see if I could do it easier again And then I'm like in this weird loop that my own brain creates which is really bad that I'm very addicted to Trying to conquer things.
It's from the birch plant we were just talking about.
It's the natural, it's naturally found in plants.
So it's that birch, you know what they're whipping?
It's from that plant.
Yes, it is used as a, like if you're eating it, you know, I think it could cause like...
Like the erythritol kind of thing effect where it's like too much GI distress.
But when you're chewing gum or using toothpaste, many studies have shown that it kills anaerobic bacteria like streptococcus mutants that cause cavities and dental decay.
We were doing a cleaning, you know, mental hygiene thing.
And he comes back and he's like, you've got two cavities.
And I was like, how the hell do I have cavities?
I don't even need sugar.
Like, you know, I've just – I've got like a bad oral microbiome or something that I've just – for years, I don't know.
I shouldn't have cavities because I don't need sugar.
But anyways, I had – so he goes, you have two cavities.
They're at the point of no return where, you know, like you – they're – I guess they penetrate the enamel a certain amount and they're like, you have to like – Get them out.
And so the way I am is I always like to look into everything before I do anything.
It's like, okay, this is not my field.
I understand.
I told him, I'm like, I'm going to do some reading research and see if I can find, you know, if there's any possibility that I don't have to get a filling, right?
And he's like, okay, well, if you find anything, please send it my way.
So then I found out I was pregnant.
And so I was like, okay, well, I can't go back to the dentist.
And at that point, I was like...
Looking through everything, all my toiletries and everything.
I'm like, what do I have to get rid of?
What's in there that could be harmful?
So I was like, fluoride, like in my toothpaste.
So I was like, I don't want to use fluoride toothpaste anymore.
And these stories are going to connect.
So fluoride has been shown.
A lot of people are worried about the effects on the brain.
The only solid evidence I could find on negative effects of fluoride on the brain are in utero, meaning...
Pregnant women, you know, and the effects on babies.
And I don't know if toothpaste has enough to even do anything, but in my mind, I was like, nope, getting rid of the fluoride, you know?
I got a water filter that got rid of the fluoride in the water, and I was, like, doing all that.
So I came across this xylitol toothpaste.
And I was like, what is this xylitol toothpaste?
So I started doing research on xylitol while I was looking for alternatives.
Anyway, so I was like, I've got to find something other than Thompson, Maine.
So I came across this xylitol stuff, and I started doing research, and then I found all these studies.
And not only did I find studies that basically kills these bacteria that cause cavities, the S-mutans, pregnant women that chew xylitol gum By the way, the studies were with gum, not the toothpaste.
People were chewing this gum.
And pregnant women, if they were like six months pregnant, the study started at six months, and they chewed this xylitol gum all the way up until anywhere between the baby being six months, and there were some studies that went out like a year.
And then they met, the researchers measured the oral bacteria of the toddlers, and then they measured them multiple years out as they became children.
And the mothers chewing it, chewing the gum, it lowered the incidence of the S-mutans in the children.
Because, you know, mothers kiss their kids and you transfer oral bacteria.
And so their, like, their chewing the xylitol gum had a positive effect on the child's oral microbiome.
Fuck yeah, I'm gonna do this!
I gave myself TMJ. I chewed so much xylitol gum while I was pregnant.
Different people have different results when it comes to CBD. And some people find that CBD with THC benefits them more.
And some people find that it's just the CBD itself.
But the CBD MD the company that I use what I really like is they have a bunch of Muscle creams and like stuff that you rub on the outside of sore muscles.
That stuff's fantastic It's really good penetrates into the skin and just really good at alleviating soreness and I had a so like one of my old colleagues science colleagues was telling me that like they were measuring some samples from like different CBD products and like The majority of them didn't actually even have much CBD in them at all.
Really?
I mean, this has been shown with vitamin supplements as well.
There's been so many studies showing, even vitamin D supplements, it'll say it has 10,000 IU, but it only has 6,000.
There's been sampling where you go to...
Walgreens or CVS or just whatever random place and grab the vitamin.
The concentration isn't high.
Also, those echinacea things, a lot of it's just clover leaf.
But what I really wanted to talk to you, the reason why I wanted to bring you in here is this conversation that we just had to talk about what are the methods you can use to help boost your immune system, keep your body healthy.
I think we kind of got it dialed in.
So...
Vitamin D seems to be very critical.
Sauna if you have it.
If you don't, bath.
Vitamin C. Orally, you need a big dose and it's still not going to have the same effect.
If you can do, IV. You don't need to do it but once a week.
Well, it's like when I'm stressed out, particularly it flares up, and it happens like when I'm shifting from one sleep stage to the next where I am asleep, but somehow I wake up, but I'm not awake, but I'm moving my body, and I think that someone's in the room and that they're going to come get me, and I freak out and I scream.
And it's happened where I scare Dan, of course.
He's like in the middle of the sleep.
And it happens earlier in my sleep cycle.
So it's like...
So I started doing, I started reading about this stuff and it's like, I don't want to, like, the treatments were like benzos.
And I'm like, hell no, I'm not going to take benzos.
That's, you know, been shown to, like, cause dementia, right?
But there was some studies showing that high-dose melatonin...
You know, more in the, like, 10 milligram range.
Sorry, I'm taking 9 milligrams a night.
And I totally stopped having them, for the most part.
Dan says, yeah.
Like, I went through one episode where what happens when someone has a night tear is, like, if someone else sharing the bed with you, like, tries to stop you or help, like, because I'm still asleep, I'm not aware that that's my husband doing that.
And I really think someone's trying to get me.
me and so I just go into like crazy mode and I like I like somehow like crawled from our bedroom all the way out to the living room and by the time I woke up I mean I had bruised myself I was like how would I get out here you know like this was like the worst this was the worst that's ever happened to me so usually I just kind of scream and wake up and like I'm like like I think someone's gonna get me you know Melick Melatonin totally, totally stopped it.
Totally stops it.
I measure, I track my sleep as well, and I think that, you know, I don't know the sleep stage stuff, how accurate that is.
I think it's not very accurate, but duration is pretty accurate.
Because I've had multiple incidents when I was nursing my son, back when I was nursing my son, where he was on a nursing pill, and I'm very relaxed, of course.
I'm nursing him, right?
I'm making oxytocin, and I'm scrolling on my phone reading, and it calculated me as being in REM sleep.
And it happened more than once.
There's other times.
So Dan and I don't, we don't have a TV in our room, bedroom.
But when we go travel, we're in a hotel, we're in bed.
So we're laying in bed watching a show and I'm like totally relaxed in bed.
And it's totally putting me as, calculating me as asleep.
So I'm like, you know, it calculates heart rate and movement and body temperature.
So, you know, I like it.
I do.
I just, I don't think that it's, Totally accurate in measuring my...
The idea is a lot of people have a problem with CPAPs.
It's uncomfortable.
You're wearing a mask over your face.
That's how I felt.
And so this mouthpiece, the Sleep Appium mouthpiece, it sits in my mouth and the tongue depressor keeps my tongue from sliding back and closing my airway.
I thought I had that at first because I was like, am I just like freaking out because I'm like not getting enough oxygen or something, you know, but they had me do a pulse oxymor thing and...
It's one of the ways that there's operations that they do to try to alleviate it and they just cut out some of the tissue inside your mouth and then they also cut out your tonsils.
I can't breathe because my body's forcing to adjust.
I remember I was on a plane once.
and there was this guy behind me and he was a kind of a heavy fellow and he was uh he was really snoring loud he was laying on his back and really snoring loud and then he would go without breathing for multiple seconds and i filmed him and i uh i i told him when he woke up i go hey man i go do you know you have sleep apnea and he's like no i go listen i go i have it too i go but you got to do something about it i go you hold your breath For long periods of time.
He goes, really?
I'm going to show you.
Yeah.
So I showed him.
He's like, fuck.
And I go, yeah, dude, this is really bad.
It's associated with so many different things.
It's associated with high blood pressure, heart attacks, the risk of all sorts of ailments.
Plus, you're just not sleeping enough.
You're not getting real sleep because you're constantly being woken up and shocked into this state of like...
So I do the Philips Hue, where at like 5 o'clock, all the lights in our house go red.
That makes a huge impact on my son and his sleep cycle because children are really sensitive to light because they don't have cataracts and stuff.
And so the melatonin is not being produced.
So if we go travel or go to my in-laws or somebody and they have the lights on, I'm like going around the house turning them all off because I want my son to go to bed at a normal hour.
So I have, like, all the apps and stuff, and most of the time, like, and I turn my iPhone screen is, like, down, and I have the black background and all that.
I might have to because when I actually get a chance to watch TV, like, it doesn't happen much because right now my son falls asleep at, like, nine, and he wakes up at six.
And so, like...
I have to go to bed immediately after he does.
It's a race.
So I'm wondering, when can I cut the nap out?
I'm Googling everything, just trying to figure it all out.
It's like, you have to keep napping until they're three.
But I most of the time constantly wear it sometimes because it's like the sensor lasts for 10 days and I have to change it and sometimes I like...
Forget.
And a couple days go by.
And then I start eating the pomegranate because my son loves it.
And I'm like, I wonder what this is doing to my glucose.
But the lack of sleep, because he would wake up...
I would be getting interrupted multiple times at night, where it was like, I don't know, he was going through some developmental stage and he would stand in his crib.
So I was getting woken up multiple times at night for prolonged periods, very, very fragmented sleep.
And nothing had changed with my diet and my blood glucose, my fasting blood glucose levels, if my exercise routine is dialed in, I'm not shelter in place.
It's about mid-80s.
And so I was up to like when fasting blood glucose would get up sometimes to like if I wouldn't exercise, like wake up in the morning and I'm like 106, 107, 109. Wow, that's a big difference.