Q&A #9: Viral Defense—Sulforaphane, NAC, Glutathione, & Vitamin D

Hello everyone, it's nice to be back. Welcome to round 9 of the Crowdcast Q&A series that I do once a month. We have a lot of great questions. I also went back to some previous questions that were submitted in previous months that were not answered for various reasons. For example, sometimes the question is a pretty— requires a pretty in-depth research, literature research review. And so sometimes I make note of questions and it's sort of a work in progress and then I get back to them later. So this time around, I've got a couple of those and I guess we'll get started with that. So one of the questions that was submitted Last time, last month, uh, was from Lindsay, and Lindsay asks, how strong is the evidence on the carcinogenic effects of EMF exposure?

In particular, should we be concerned about cell phones, Bluetooth earbuds, and wearable health trackers leading to brain tumors and other types of cancer? So this was sort of a big question, and it's certainly been a question that's been repeated. I've had people asking me that question on multiple platforms. So I'm happy that I was finally able to kind of dive into some of that evidence and see what the literature really is showing. So let's start with, okay, the main concern or the main type of cancer that many studies are looking at are brain tumors, for example, gliomas. And the problem with— so there's mixed evidence in the literature.

You'll find studies that show an association between, for example, using cell phones and gliomas, but you'll also find evidence that show no association between those. And We're going to talk a little bit about actually like what types of studies these are and what kind of problems there are with these studies. So 100% of these studies are prospective studies, meaning they're looking at people, a population of people, and within those population of people, a certain percent of them have various types of brain tumors. Like many of the times they're looking at gliomas, but other types of cancers have been looked at as well, like eye tumors or looking neuromas.

So those people are then asked, like they're asked as a recall, like how often, you know, they used a cell phone within a certain time period. So as you can probably tell, there's— it's not a very, you know, ideal study for establishing causation, right? And the problem is, is that the majority Yeah. A lot of the studies that did find a link between cellphone use and brain cancers or other types of cancers, for instance, were very, very subject to what's called recall bias. And what recall bias is, is if you have a person, if you ask a person that has some sort of disease, in this case, a glioma, a brain tumor, You ask them, well, how often did you use the cell phone?

They're going to be subject to what's called recall bias, meaning they have a strong emotional response because they have a disease. So they are going to think that they use the cell phone more often than they did, versus if you ask someone who is disease-free, how often have you used the cell phone in the past week? You know, they're, they're not going to have a really strong emotional response. It's kind of casual, like, yeah, I use the cell phone, you know, X amount of times. So that's a really big problem with these types of studies, recall bias, because people with disease are much, much more subject to emotional responses. And so they sort of in their minds think they're doing something more often than they should be because they think, oh, that must be what's causing my brain tumor.

So I'm really, really hesitant to say there is strong evidence to you know, linking cell phone use to brain tumors and EMFs in general. I would say that the strongest studies found no evidence or no association between tumor risk and cell phone. They were done a little bit differently. So for example, you know, there was one study that was a really, really large sample size. It was over 400,000 people. Wow. And it was not subject to recall bias because they used records and stuff to figure out how many people had cancer. And then they also used records to figure out like cell phone use. So I find that study a lot stronger because it's not subject to recall bias versus a couple of other studies that did show an association. Again, not all studies are showing that.

So I would say that personally, I am not super convinced that using a cell phone is going to give you a brain tumor. That's, that's just my opinion, looking at the evidence. The only studies that show that there is a link, it's a weak link. And again, those studies are totally subject to the recall bias. It's just, it's really, you know, it's just not strong data at all, particularly in the in light of the fact that other studies that aren't having a recall— that aren't subject to recall bias show no association. So really sort of, in my mind, it seems very likely that the studies showing weak association are possibly due to recall bias. Okay.

So, the next question that was asked was a question that was referring to a fairly recent study that was— the title of the study was Reversal of Epigenetic Aging and Immunosenescent Trends in Humans. which suggests that a very— it was a very, very small pilot study where people were given a combination of human growth hormone, they were given DHEA, and they were given metformin. And their epigenetic age was measured. So epigenetic age is basically a measure of your biological clock, but using these methylation patterns as a biomarker. I've got a topic page on website, which I'm actually gonna be announcing on Monday on epigenetic aging clocks. And I have a podcast coming out with the leading expert, Dr. Steve Horvath. It's in post-production right now.

We're kind of plowing forward with that. That will go into more detail on epigenetic aging. But essentially, Yeah. There's patterns of what are called methyl groups. They're a carbon atom with 3 hydrogen atoms. They sit on top of various regions of your DNA, and they follow a certain pattern with age. And it's a very distinct pattern, and so distinct that chronological age can be accurately measured by just looking at this methylation pattern in someone's blood. And it can— the person's age, chronological age, can be measured, can be guessed plus or minus 4 years with 96% accuracy. So it's pretty, pretty good measure of chronological age.

Well, it turns out some of these clocks, there have been little tweaks and things that have been done to them, and biological age is actually also able to be measured. So as we've talked about many times in the past, people age at different rates depending on a variety of factors, including genetic factors and lifestyle. environmental factors. So, for example, you have someone that, you know, is a smoker. They're doing constant damage to their cells, and that can accelerate, you know, biological age, even though their chronological age could be the same as someone else who is a nonsmoker. And there's other things that also contribute to that, other dietary factors and lifestyle factors like exercise, for example.

So, so what this study found was that taking that combination of growth hormone, DHEA, and metformin was able to reduce epigenetic age. And it reduced it by about 1.5 years. And this was actually— these were in normal, like healthy humans. These weren't like people with metabolic disease or anything like that. And It also was able to sort of regenerate their thymus. The thymus gets smaller with age, and you know the thymus is a big. It's a it's a it's a it's a place where immune cells you know are first you know generated. It's like a reservoir there for immune cells, and so it's very interesting that that the the thymus was regenerated, and the the authors of this study think that the the. Reversal in epigenetic aging was solely due to the growth hormone and not the other compounds.

The reason they gave the other compounds is because growth hormone itself, while it's sort of a double-edged sword, and we've also talked quite a bit in detail about growth hormone in the past, while it's a very good, you know, in the brain, it can be, you know, activate IGF-1, it can be involved in growing new neurons and facilitating the Yeah. The survival of already existing neurons. It can help with really important survival factors in the brain and also just helping with cognition. In muscle tissue, it's important for repairing damaged muscle tissue. But there's also negative effects ranging from allowing unhealthy damaged cells to keep growing when they otherwise would would, you know, die.

And also there's an association with causing insulin insensitivity and metabolic syndrome, which is why metformin was given along with it, and same with DHEA. So it appears that as the growth hormone affected the thymus, so it was important for regrowing thymic tissue, which is what the authors think may be linked to the reduced or the reversal of epigenetic aging. There's another study that showed metformin itself did not reverse epigenetic aging, although it's possible the study was underpowered. Perhaps if there was a larger sample size, they would see, because there was sort of a trend in possibly having a, you know, reversing epigenetic aging, but it wasn't statistically significant.

So, you know, either it's possible there was a larger sample size is required, or metformin just isn't affecting epigenetic aging. So that's sort of the findings of that study. I thought it was a very interesting study. The other thing to note is that after— so this was a year-long study. People were given growth hormone and DHEA and metformin for a year. After the growth, after these compounds were, you know, stopped, people weren't given them these compounds anymore. The epigenetic age reversal completely reversed back, meaning the the effects on epigenetic aging were only apparent while taking the compounds. Once the compounds were stopped, their epigenetic age went back to baseline.

Kind of kind of disappointing in my in my mind because you don't want to be constantly having to take growth hormone and metformin and DHEA. Okay. Nonetheless, still very interesting. And we will be getting a lot more in depth about epigenetic aging. Like I said, a podcast is coming out very soon. I have a topic page on my website, fitmyfitness.com. Hit topics on the navigation bar and you'll see the epigenetic aging clocks and you can read all about that. Jeremy is asking in the chat, what biomarkers do they test to check biological age? It seems it would be more extensive than just neurological and mitochondrial health. There's a variety of biomarkers that are usually tested when measuring biological age.

I mean, there's like 18 different ones ranging from looking at insulin sensitivity, your, your glycated hemoglobin, your HbA1c, LDL, looking at liver function, immunosenescence, telomere length. They're trying to now add epigenetic aging to that panel. It's another sort of biomarker as well. Your blood cell count. I mean, there's a ton of different markers that are all looked at in combination with each other to figure out Biological age, inflammatory status, and things like that as well. So let's move on to the next question, which was from Yuri. Yuri asks, what is your opinion regarding low-dose or baby aspirin as a supplement between 80 to 100 milligrams per day for healthy people above— over the age of 50?

Does it have any value with regards to prevention of cardiovascular disease and cancer? Can you refer especially— can you refer especially to those who don't keep a very healthy routine? So, um, before I get into what the science, you know, says about this. I just want to say that I am not a medical doctor, so I do not have an MD. I am not giving medical advice. This is not a doctor-patient relationship here that I, you know, this is, this is completely just me reviewing the literature. Anything, any type of health change supplement, you know, anything that you're gonna do, you should, you know, basically contact your primary care provider and run it by them and discuss it with your primary care provider, 'cause I am not your primary care provider. I'm not a medical doctor.

So with that said, I will talk a little bit about what some of the science says about aspirin. So baby aspirin in particular, low-dose aspirin. With respect to cardiovascular events, It appears as though, so if you look at the data, taking a low-dose aspirin can reduce the annual risk of cardiovascular events from 2% to 1.74%. So that's really an absolute risk of 0.26%, which means out of 385, healthy people with no history of heart disease, those 385 people that would need to be treated with low-dose aspirin, you would then have only one person would have— you'd only prevent— you'd only expect to prevent one person from having a cardiovascular event out of those 385. So it's really a very minor reduction in reducing a risk of cardiovascular events.

And those with the highest risk of a cardiovascular event, so for example, let's say you're obese or you're obese plus having a prior history of having a cardiovascular event like a heart attack or a stroke, then the annual risk of reducing a cardiovascular event goes from 5% to 4.35%, which is a absolute risk reduction of 0.65%. So it's a little bit higher. So that means that you'd have to have out of 153 people that are obese and have had a history of a heart attack, giving them low-dose aspirin, only one of those people would have protection. So, you know, it's a pretty minor effect on reducing cardiovascular events both in healthy people and in in people that have had a prior history of having a cardiovascular event.

With respect to cancer, the only type of cancer in the literature that I could find that low-dose aspirin seems to have an effect on is colon cancer, and it seems to help prevent the return of advanced polyps. And so there was a study showing that it reduced the risk by 40%. Um, of basically preventing and, you know, and returning of these advanced polyps. So, Dr. John Highsmith is asking about all-cause mortality in the aspirin studies that I did not look into. to all-cause mortality. But that could be a question you could submit for next month if you would like me to look into it. So the next question was from James, um, and James was asking about NAD boosters like nicotinamide riboside and nicotinamide mononucleotide.

and how, you know, there's been some association with boosting cancer growth. And the reason for that being because NAD+ is also used for the growth of cancer. So, so James was wanting to know, is there any way you can, you know, split or like not affect the cancer pathways but, but have the positive benefits with NAD+? And I would say that no. You know, the thing is, is that NAD is a coenzyme. It's involved in, you know, a lot of metabolic pathways. And these metabolic pathways including, you know, including enzymes important for making energy through glycolysis, which is essentially what cancer cells used predominantly, so not using mitochondria. NAD is also used from enzymes in the mitochondria to make energy. Uh, it's used for, um, you know, by PARP to repair damage.

It's used by a variety of other enzymes as well. And so, um, these, these enzymes, you know, you can't differentiate between their, you know, they're in cancer cells or normal cells. So it's really not possible if you're taking an NAD booster to kind of like separate that out. I mean, if a person has cancer, then that becomes more of a risk. The problem is not everyone knows if they have cancer. And, you know, the studies that were done were in animals. And the one study with nicotinamide mononucleotide was— it was an injection, a very high-dose injection. I believe it was in the peritoneum injection. So, you know, Translating this is always— you have to be very cautious, right?

And— but the same goes for the positive effects on, you know, looking at nicotinamide mononucleotide because there's no human studies with nicotinamide mononucleotide yet that have been published at least. So, you know, you got to be cautious with trying to translate what you find in animals to humans whether or not it's, you know, good data or scary data, right? Yeah. It kind of goes both ways. And for more information on that, I've got— we've got topic pages on the foundmyfitness.com website on NAD, on nicotinamide mononucleotide, and on nicotinamide riboside. I really— I highly suggest you check those out. They're great resources. They have references, you know, so it's really A good resource to use.

See a few people here talking about viral coronavirus and viral preparedness and stuff, and we did have some questions about general, you know, viral defense, and I will be getting to that soon. So we'll be getting into some of that. So briefly, the next question was submitted by Joss. And Joss was asking, what do you think of hormone replacement therapy for women who recently entered menopause? Any specifics on protocols or dosage, et cetera? So I would say, looking through the literature, that there seems to be a lot of negative long-term possible long-term side effects of hormone replacement therapy. The benefits that I could find seem to be really short-term and sort of just helping facilitate the transition to menopause.

So helping facilitate the transition would be a very short-term treatment with it. And the long-term effects that I was finding in the literature ranged from causing— basically causing the lining of the uterus to grow and increasing the risk of uterine cancer. It's associated with a small increased risk of heart attack. Combined hormone therapy and estrogen therapy alone are also associated with a small increased risk of stroke. and deep vein thrombosis. Um, forms of therapy not taken by the mouth, so patches, sprays, rings, and others may have less of a risk of causing deep vein thrombosis than those taken by mouth. Combined hormone therapy is also associated with a small risk for breast cancer.

Um, there's also a small risk for gallbladder disease, um, with and without estrogen therapy, with and without progesterone. So honestly, there seems to be a lot of small but, you know, risks nonetheless that are associated with, particularly with combined hormone therapy. So, you know, that's something that you can talk about with your primary care physician. It seems as though the benefit really seems to be short-term use and really only help with transition to menopause with things like hot flashes and night sweats and relieving vaginal dryness, then helping protect against bone loss which occurs early in menopause is another thing, preventing hip and spine fractures. So, um, so that's about it. So James asks, what types of antibiotics are there?

It is often said medicine overuses them and we aren't coming up with new ones fast enough. Are there antibiotics or things that can act like antibiotics, however weaker, that bacteria cannot adapt to? I think even honey and oregano are antibiotics? So there's a lot of different types of antibiotics. There's bacterial cell wall inhibitors. There's penicillins. There's cephalosporins, monobactams, vancomycin, and daptomycin. There's bacterial protein synthesis inhibitors, tetracyclines, macrolides, clindamycin. There's— oh, I mean, fluoroquinolones, all sorts of metronidazole. This always gives me a problem. Yeah, it's known as Flagyl. Lots and lots of different types of antibiotics out there. And it's true that new antibiotics have been decreasing since the '80s.

And in addition to new antibiotics decreasing, there's also, in addition, an amount of bacteria that now have become resistant to our already existing antibiotics. So it's sort of a twofold combined problem. So let's look at the good news. The good news is that there are infectious disease specialists that are almost in all hospitals that are looking and overseeing these trends in antibiotic resistance. They are changing changing recommendations to try to make sure treatments remain effective and resistance is minimized. And they do this by a couple of ways. So first, there's a hierarchy of antibiotics where the antibiotic with the least amount of resistance is used last in order to preserve that low resistance profile.

There's also some antibiotics that are used as a last resort when everything else has failed. The other thing is doctors are also making sure people try to take their full antibiotic course to make sure that the antibiotics don't mutate, and also giving antibiotics a holiday. So when certain antibiotic is not used for a while, the prevalence of bacteria that it's resistant to, it decreases. And sort of there's a theory behind that. The theory is that antibiotic resistance comes at the cost to bacteria. Uh-huh. And in an environment without the antibiotic, those without resistance have a competitive advantage. So those are some of the things that are being done in hospitals to try and minimize the problem with antibiotic resistance.

There are a variety of other compounds that also have what are called antimicrobial activity. They're not necessarily referred to as antibiotics, but, you know, some of these compounds do include, you know, for example, the person mentioned honey and oregano, but there's also things like colloidal silver, you know, tea tree oil, green tea, so EGCG, grapefruit seed extract, garlic, you know, these things all have been shown to have antimicrobial activity, and some of them also have antiviral activity like the garlic and EGCG. So, um, you know, these are, these are things that are also used, um, sometimes in combination with each other and things like that for, um, you know, killing, killing bacteria as well.

Okay, um, I'm, I'm starting off— I'm do— I started off this Crowdcast with some of the, the questions that I've never, um, that have, that have been asked before but I haven't answered. Um, so I will continue that and then we'll get into some of the, the viral defense stuff, um, and some of the, the, the bigger questions like meat consumption and type 2 diabetes. So Andrew asks about Extra virgin olive oil as the best oil to cook with, even compared to oils with higher smoke points. He's wondering—he links to an article and says the article explains that unsaturated fat fats oxidative stability and UV coefficients are important predictors of oil stability. What do you think about different practices with oils like salad dressing, sautéing, and high heat cooking?

And the question really is with respect to using extra virgin olive oil. It's really interesting because literally last week, a study came out on— the study was basically extra virgin olive oil maintains its health-promoting properties when used for cooking. So it couldn't have been more timely. Olive oil is, is, it's one of the primary sources of fat used in like the Mediterranean diet. And there's been a variety of studies that have suggested that it has antioxidant, anti-inflammatory, anti-carcinogenic properties, likely due to its high polyphenolic content. There's been studies showing that it helps reduce LDL and increase HDL. So the concern has been heating olive oil, especially the high temperatures.

And whether or not you know it's it's safe to cook or good to cook with that oil, so it can cause the the phenolic compounds to deteriorate. And the findings from this recent study suggest that actually the cooking techniques used typically in in home kitchen kitchens don't negate the beneficial effects associated with olive oil consumption. So the study mimicked like home. Cooking processes. So they did sautéing, they did pan frying, and they did this with either meat or potatoes. And so the 2 different foods were pan fried in olive oil, either heated at a moderate— so 120 degrees Celsius, which is 248 Fahrenheit— or high heat, which was 170 degrees Celsius and 338 degrees Fahrenheit temperatures. They heated them for 15 minutes and for 30 minutes, so 2 different durations as well.

Chemical analysis of the oil after the cooking process showed that both the time and temperature did affect the polyphenols. So the higher the heat and the longer it was cooked, the lower the polyphenol content. So, but temperature was actually the main driver. So cooking for a longer duration at the lower temperature wasn't as bad as cooking at a higher temperature for a shorter duration. So temperature was really the key. with degrading the polyphenol content. Um, so cooking it at around moderate, so 120 degrees Celsius, degraded the polyphenol content by about 40%. Cooking it at 170 degrees Celsius decreased it by about 75%.

So I think that for most people that are doing some sautéing, they're sautéing their spinach, for example, uh, you know, you're gonna have about a 40% decrease in your polyphenol content, which is not so bad. And olive oil is hot— is low in polyunsaturated fat. So it's, you know, the oxidation issue isn't the concern that it would be, for example, in using canola oil, which is, you know, high in— or canola oil or soy oil, other vegetable oils, which are higher in polyunsaturated fatty acids. So Daniel is asking in the chat, are there any supplements you would recommend for a 15-month-old child? Again, I'm not a medical doctor, so I can't recommend any supplements.

I can tell you what I give my son, who is now 2 and a half, and when he was 15 months, I don't I didn't start it until he was able to really chew things very, very well. So I give him Pure Encapsulations essential fatty acids. It's a little— it's kind of like a gummy, but it's really, really softer than normal gummies. And it's Uh, each one has 250 milligrams of DHA, and I forgot the EPA content. I give him those— those, um, he gets them 4 times a day. But I also just use my fish oil, which is like the best fish oil. It's, um, uh, N-Pure 3, and I use that. I, I just put that in his food. Um, if he doesn't— if he doesn't want it, like if he, you know, in his oats or, or whatever, if he decides that he doesn't want the fish oil, then I, I give him the, the Pure Encapsulations gummies.

I also do their Uh-huh. Their, um, their multivitamin chew, which, um, the, the chews have xylitol and a little bit of erythritol in them. Um, the multivitamin chews are a little bit harder, so I would say if, you know, 15-month-old, probably not ready for these ones yet. But, um, they also have a liquid nutrient version that, um, is a multivitamin that you can, that you can, uh, give a couple of teaspoons to. I've also done that as well. I think that the easiest thing for— that I did when my son was younger was I did the N-Pure 3, and I just opened the capsules and put it in his food. And I still do that continually. Like, sometimes though, sometimes it's a little fishy and he's kind of like, no, I don't want it.

But most the time I'm able to slip slip him the fish oil that way, which is my favorite way to do it. Janet's asking, do you know when N-Pure 3 will have fish oil again? I know they're working very, very hard to get the N-Pure 3 fish oil shipped in the United States, and that's hopefully gonna be happening in the next couple of months. So they're really working hard on that. In the meantime, I really like third-party testing sites. Labdoor, you can look at Labdoor. They've tested a variety of fish oils. You can look at the International Fish Oil Organization. They also do some third-party testing as well. Okay, so a couple of other bigger questions that were asked that probably will take a little bit longer to go into.

So there's been a couple of questions, and this is kind of related to the EMF in a way, but not necessarily, have been about what's called photobiomodulation. Which is basically the history of photobiomodulation is that it was discovered by a doctor back in Hungary in the '60s. He was using a ruby laser to treat cancer in mice, and he noticed there was rapid hair regrowth in these light-treated animals. And so, that kind of sparked him to look into the other benefits of what's known as photobiomodulation. And photobiomodulation basically uses wavelengths in the 400 to 1,000 nanometer range, which is non-ionizing, so it doesn't damage your DNA. It's— so for example, things like gamma rays and X-rays, those are really short, so that's 0 to 10 nanometer range.

So red light— so you'll often hear a variety of names Unfortunately, in published in the scientific literature, you'll hear red light therapy, you'll hear laser therapy, you'll hear infrared therapy. There are scientists that are trying to standardize the nomenclature so that it's called photobiomodulation because it really confuses scientists and it confuses readers in general, the general public, as to like. what this is and, you know, what the differences are between red light therapy versus laser therapy versus— and so we'll talk a little bit about all these things. But generally speaking, photobiomodulation uses the wavelengths for 4,000— sorry, 400 to 1,000 nanometers. And red light is between 630 and 700 nanometers. And near-infrared is is light is between 700 and 1,000 nanometers.

And photobiomodulation is not using heat at all. It's completely independent of heat. It's light only. There are some really important factors with photobiomodulation. And those— the most important factors are the wavelength and the power. Wavelength and nothing else, wavelength determines The penetration, the depth of penetration. So whether or not you're wanting to affect, let's say, an organ, muscle tissue, you want to affect the thyroid gland, it's it's the wavelength that determines that versus just you know cutaneous skin or your hair follicles. The power, the output power, which is a different variable, also matters. But That variable is the amount of light that reaches whatever tissue the wavelength, which determines the depth of penetration, is going to get to.

So another way to think about it is, you know, power is just the amount of photons are increased that are actually getting to whatever point, endpoint, that has been determined by the wavelength. There are also other factors that can affect the amount of photons that are getting to a certain tissue. So, for example, 30 to 40% of the light that's passing across the dermis is basically lost by just passing through the dermis. So, it doesn't actually get to where it's supposed to get to, 30 to 40% of it. Wow. The higher the output power, the better. So the more power you're going to have, the more light will get to that tissue, of course. And melanin also absorbs, particularly absorbs red light.

So melanin, which is the pigment, it gives people pigment to protect against UV, you know, UV radiation. It also absorbs red light 4 times more than it absorbs infrared light. So it suggests that people with darker skin wanting to use particularly red light wavelengths may require more power to get the same amount of light there as someone with lighter skin. There's also different devices that are used. There are LEDs. LEDs can produce a broad range of light, so it's less concentrated. And there's lasers. Lasers can have light that is much more concentrated. So in the literature, you'll see a variety of studies using different things.

You'll see them using LEDs, you'll see them doing lasers, you'll see them doing different wavelengths, and sometimes it'll be referred to as red light therapy or laser therapy or, you know, so, or sometimes it is referred to as photobiomodulation, but it's sort of just kind of all a mess and all over the place. Proposed mechanisms, photobiomodulation is thought to mostly act by chromophores absorbing light, and the chromophores are then able to like induce a biological change. So chromophore is basically a molecule that has atoms that can absorb specific wavelengths. For example, copper is a big chromophore.

And the primary chromophore inside human cells is thought to be located inside the mitochondria, and it's a protein called cytochrome c oxidase, which has— cytochrome c oxidase is really an essential enzyme for producing energy, but it has a copper molecule at the center of it. Copper acts as a cofactor. So light is thought to be absorbed by the copper molecule in in the cytochrome c oxidase inside the mitochondria inside of cells. And once that happens, the thought is that mitochondrial activity increases, ATP production increases. So it can address problems with mitochondrial dysfunction. It doesn't seem to address if there's a healthy cell with normal mitochondria, there seems to be no effect. So it really seems to be specific to damaged mitochondria, aged mitochondria.

And there's all sorts of genetic pathways that have been proposed to be involved or, you know, showed to some degree to be involved. But really, when you look at what is important, I think the clinical evidence, it sort of depends on what outcome or what endpoint is being looked at. I would say there's mixed evidence. And really, there's a big— there's a lot of heterogeneity in the literature with respect to protocols, what wavelengths are used, how much power is used, if it's a laser or an LED, how frequent they're given, how long with respect to, like, for example, muscle performance and recovery, which I would say is the most inconclusive area because there's so many different protocols used, particularly with respect to when the exercise is done. Is it before? Is it after?

You know, is it— how long is it done before or after and what the wavelengths are? It's really just kind of a mess. And some of the meta-analyses that I've looked at are really kind of fishy in respect to the authors that are doing meta-analyses. Meta-analyses are when you analyze a lot of different studies, individual studies and kind of pull them together and say, look, does— is there a significant effect with whatever treatment we're looking at? And I would say with, um, with the muscle performance and recovery, um, there's an author there who for whatever reason gives 50% greater weight to all of his studies versus the other studies, um, and doesn't ever explain why his studies are weighed more.

So it's really sort of a red flag in my mind why, you know, that's kind of a biased thing to do. Additionally, if you look, for every 1 study you find a positive effect, you can find 3 studies with no effect in terms of muscle performance and recovery. So there's really sort of, you know, you can cherry-pick and find the studies you want to show, yes, there's an effect. But again, you'll find many more studies showing there's no effect. Again, it could be due to the fact that protocols haven't been established, the right protocol hasn't been established, and once that is established, then we might start to see more consistent findings. But the other thing is that even looking at meta-analyses, which are usually the best thing to do, even those seem to be very flawed.

Again, I mentioned that one of the authors who authors a lot of these meta-analyses, weighs his studies more. And also, he seems to select certain studies and doesn't expect and doesn't really explain why he's disregarded all these other studies in his meta-analysis. When you look at the individual studies, you'll see no effect, but when they pull them together, then you get statistical significance. So the question then becomes, well, is it because there wasn't a large enough sample size in the individual studies, or is it because, you know, They had some manipulation of choosing which studies they wanted and then found an effect.

So, I would say that muscle performance and recovery with respect to any type of both red light therapy, so 630 to 660 nanometers, and near-infrared therapy have been used, 800 to about 950. I would say that it's really inconclusive. Um, other studies, some of the, some of the promising studies I would say that I've seen, typically, um, they're, they're involved in things that are more surface. So, uh, androgenic alopecia, for example, there's been, um, the studies that have looked at that have been mostly showing positive effects. And, um, most of the times these are people wearing a helmet device or using a comb. So it's like the, the They use either LEDs or lasers, and it seems as though lasers are more powerful.

They have a stronger effect, at least in the studies that have been done, in terms of regrowing hair. Skin aging is another promising area that's been shown, and near-infrared laser seems to be more powerful, although red light, the red light spectrum seems to work as well. So again, that that's a more cutaneous effect. I would say those are the 2 most promising areas I've seen. Rheumatoid arthritis and osteoarthritis are also claims that are also made. I would say that's very, very weak data. And in fact, this is sort of an example of why it's so important when you're looking at a meta-analysis, you know, you have to come at this with an unbiased, you know, approach. And you have to be a science— you have to be very scientific.

A scientific approach is an unbiased approach where you come into this, like myself, where I really had no— I don't really care whether or not photobiomodulation works or not. I mean, I want— I would love to know, like, it seems very interesting. So I didn't have, you know, any sort of conflict of interest as to why I would, would want it to work or not want it to work. Whereas other— there are people that may have more of a conflict of interest. And so you can just kind of try to cherry-pick studies that you find supports your hypothesis. And that's always a problem with any field.

And the reason it's so important to read the studies and look at the data presented, okay, not just read a conclusion, not just read an abstract, is because you will find, you will find the quality of data really is important. And I'll give you an example. There was a meta-analysis that looked at many different studies done on rheumatoid arthritis and also osteoarthritis. And it found that people with rheumatoid arthritis, about 70% had 70% less pain if they were given the laser treatment versus people that were given a placebo laser. Now, if you were to just read the conclusions of the meta-analysis, you would go, oh, okay, well, this has looked at multiple studies and they found that the treatment was better than the placebo treatment. So yeah, it must work.

But then when you look at the data, you start to see that they— there was multiple different types of placebo studies that were used in this meta-analysis. There was a group of placebo studies that had People with rheumatoid arthritis that were given a placebo laser. So that was, that was one type of placebo that was used in some studies. Other studies used a placebo on the same person. So this one person with rheumatoid arthritis had a— had the real treatment on one hand, and on the other hand, they had a placebo laser treatment, and they didn't know which one was the real laser. Okay.

Within the studies that use the placebo on the same person, the person felt an improvement in both of their hands, even though one of the hands had a placebo treatment, which sounds a lot like a placebo effect because we're getting a treatment and both of their hands felt better, even though only one of their hands actually had the treatment. So it was the studies that the placebo, the people given the placebo laser, didn't have as much of an improvement as the people that were given the real laser. So I would say that it's really inconclusive with respect to rheumatoid arthritis because the placebo given on one hand and they felt improvements in that hand even though the laser wasn't, you know, didn't have any effect on that hand, I would say it's really inconclusive.

So whereas you'll find people making strong statements with rheumatoid arthritis, I would say looking at the data, I would disagree. Osteoarthritis, no effect as well. So I know this was a long— I've had this, I've had so many people ask me this question. And so I really wanted to kind of take some time to finally dive into it so that people, I could cover a lot so people kind of really understood. There's a company out there, Joovv. They make a, and this is what a lot of people have asked me about this company. And I, you know, I looked into their stuff a little bit. And they make LED lasers, and they're not doing— I'm sorry, LEDs, not lasers. So the LED, again, is the broad, you know, it's kind of a broad spectrum versus the very focused.

And they do red and near-infrared wavelengths between mid-600 to mid-800 nanometer range. I would say that they make a lot of strong claims on their website based on cherry-picking studies. So, so there's a lot of claims on their website, I would say, that are unsubstantiated. To their, to their credit, they've also, they've had some third-party testing of their lasers and they seem to be very powerful, meaning their, their output power seems to be pretty substantial, particularly with the very, very expensive big, big LEDs. I would say that in the scientific literature, most of the studies are doing a very targeted treatment. Most of the time it's actually in contact with the skin.

And it's a very focused treatment on a tissue, whereas the Joovv is like some kind of device where you stand in front and it's supposed to like do some kind of full-body thing, which there's no evidence of that in literature yet. So, you know— No. I think Joovv has some potential for sure. I'm, you know, I'm certainly interested, particularly with skin aging and possibly wound healing and things on the surface. You know, I would say that, you know, there's big potential there, I think, but I also think there's also a lot of marketing and unsubstantiated claims as well. So kind of take it with a grain of salt. Okay, so the next question, which also covers a lot, a lot of ground, is I've had many questions about viral defense. particularly respiratory viruses.

And so I'm gonna speak a little in general terms. You know, again, I am not a medical doctor, so this is not a doctor-client relationship. I am not giving medical advice here. And I'm not speaking specifically to the COVID-19 illness since that's a very new illness that's being caused by the CoV-SARS-2 virus. I would say that I'm not speaking to that in general. I'm talking about general studies that have shown viral defense, particularly with respect to respiratory viruses. Some of the things that I've been looking into, some of the precautions I'm taking, I am 100% listening to what the CDC recommends in terms of washing your hands and not touching your face. Staying away from people that are sick and, you know, that sort of thing. But I'm not going to talk about that.

I'm going to talk a little bit about some of the science behind other things that have been shown in randomized placebo-controlled trials to affect immune function, particularly against viruses. So probably one of the So really, one of the most easy and important things that, you know, people should do is ask their doctor to measure their vitamin D blood levels. And it's important because, you know, there are a lot of people that aren't getting enough vitamin D. Vitamin D is made in the skin from exposure to UVB radiation, but that depends on a lot of factors. It depends on location where you live, UVB radiation during certain times of the year and certain more northerly areas doesn't even make it to the atmosphere.

And so people living in more northern, northern regions during, you know, fall, winter times of the year don't, don't really make vitamin D from the sun. Additionally, sunscreen can block UVB radiation. Melanin, the pigment that protects you from burning, also blocks it. And then age— people as they get older become less efficient at making vitamin D in their skin from exposure to the sun. Of course, elderly people go out in the sun less. In addition, people in general are going out less in the sun. You know, people working in their offices, technology's really sort of made people, you know, people stay in more and they're, they're on their, their computers or laptops playing video games. They're researching things and they're going outside less. There's a, there's a variety of factors.

Um, body fat also affects how much vitamin D is bioavailable to be released, because vitamin D is a fat-soluble vitamin and stored in fat. And so it needs to be released into the bloodstream to be converted into the active steroid hormone. The reason I think it's important to get tested is because there was a study published a couple of years ago, and it was a study that was It was a big meta-analysis of 25 different randomized controlled trials that were across global, across the world. So they were from UK, they were from USA, Japan, Afghanistan, Belgium, Italy, Australia, Canada, just all over. And what the study found, again, this was randomized controlled trials, people that were given vitamin D supplements Uh-huh.

That at baseline were deficient, so they were pretty heavily deficient in vitamin D, they cut their infection influenza risk by 50% if they were given a vitamin D supplement that raised their vitamin D levels. And people that already had normal levels of vitamin D that were still given a vitamin D supplement cut their infection risk by 10%. So pretty significant findings and pretty easy to get a vitamin D blood test. Personally, I like my my blood levels somewhere between 40 and 60. I usually am around 55 nanograms per mil, and right now I'm taking 4,000 IUs a day vitamin D. Lots of mechanisms.

Vitamin D affects immune function in many, many, many different ways, and I could just go on and on for hours about how vitamin D affects immune function, but it's really been shown in multiple studies to help cut the risk particularly of respiratory tract infections. Another vitamin that also plays an important role in immune function, and it's really kind of been— it's been sort of controversial in many respects, is vitamin C. There have been meta-analyses of 9 randomized controlled trials that have shown that vitamin C supplementation can shorten the duration of a common cold. There have been randomized controlled trials showing that vitamin C, high doses, so 1,000 milligrams for the first 6 hours of the study and then 3 times a day after, was able to dramatically cut the risk of flu.

And this was like an 85% decrease in risk. And this is a mega dose of vitamin C, you know, 1,000 milligrams. 6 times for the first day and then 3 times a day thereafter. And this, this study was in students. It was in about 463 students, and they were between the ages of 18 to 30. Um, the, the control group got sort of your standard of care over-the-counter decongestants and pain relievers and stuff, whereas those in the treated group were the ones that got the, the hourly doses of vitamin C for the first 6 hours on the first day and then 3 times 3 times a day after that. And the megadoses of vitamin C really did cut the appearance of cold and flu symptoms compared to the control group.

And if you look at oral supplementation studies and you look at— there is a plateau of how high you can get your vitamin C levels in plasma. it doesn't go above 200 micromolar. No matter what dose, it doesn't matter if you take 10 grams orally, you're not ever gonna get it above 200 micromolar. That's the highest dose that you can get your blood levels of vitamin D. If you look at a variety of studies and you look at the bioavailability orally in terms of giving various doses of vitamin C and giving them either once a day or giving them for example, 4 times a day or 6 times a day.

What you'll find is that, for example, 200 milligrams of vitamins— most people— so first of all, most people have around in their plasma, most people from their diet, they're just getting from their food they're eating, their levels are somewhere between 60 to 75 micromolar. So that's kind of like a Uh-huh. A standard baseline for everyone. You're not— you're not at zero, obviously. You're maintaining levels about 75, around, roughly. So the goal is to get yourself up to 200 or close to. That's like the highest you can get. And a dose that'll do that— so if you give one, like a 1-gram dose, people's blood levels go up to about 175 micromolar. 2 grams. 2 grams will get you pretty close to about 200 micromolar. So 2 grams will get you there.

If you take 2 grams just once a day, once, one time, let's say you take it out, you know, in the morning, you can get your 200 micromolar plasma levels and they'll gradually decline over the course of the day. And 24 hours later, they'll be back at your regular baseline of around 75 or so micromolar. If you continue to take repeated, like 4 times during the day, if you're taking your 2 grams or 3 grams in some cases they were showing here, then you can maintain 200 micromolar plasma levels. So if you're taking, for example, 2 grams 4 times a day, then you will, over a 24-hour period, your levels will stay at 200 micromolar. They will not go below that. They will stay high, really high. Wow. So 1 gram a day, 1 gram 3 times a day is what I was talking about in that study.

But I just kind of wanted to mention the plasma levels because we are going to talk a little bit about intravenous vitamin C in a minute. So the risk, so taking, I'm personally actually, I'm taking about 1 gram I would say 4 times a day. And I usually don't do this. I usually don't take really high-dose vitamin C, but I am doing it sort of just as a precaution during this kind of scary, you know, this time where we don't really know. I just, I kind of would like to have my plasma levels around 200 micromolar is the bottom line. And the risk with taking high-dose megadoses of vitamin C orally frequently on a daily basis is for people that are prone to kidney stones, which I am not.

So the concern is that for people that are prone to kidney stones, there could be a potential accumulation of oxalates. And so that's a concern for people specifically that are prone to kidney stones with taking high oral doses. Again, I am not prone to kidney stones, and I am personally just based off the evidence I have read and based off of looking at plasma levels of various doses of vitamin C, personally trying to maintain around 200 micromolar levels for the time being. Um, with respect to other types of oral types of vitamin C, uh, really many of them are the same. There's been like one study showing liposomal vitamin C is slightly more bioavailability, but it really doesn't matter. Like honestly, a lot of the liposomal vitamin Cs out there are complete and utter crap.

And, you know, um, you can, you can just get a regular old ascorbic acid. Um, I also get the ascorbic acid powders and mix them in the water. Um, my husband Dan really likes doing that because he, he just likes to drink the water. He, you know, he likes the taste of it, and, um, it's, it's a way for him to easily get throughout the day the vitamin C. So that's what he gets. Um, so I would say I wouldn't worry so much about getting liposomal vitamin C because it's really— it's sort of not, not really that different in terms of bioavailability. And I see, I see Dr. John Highsmith was asking that very question, so I'm glad I answered that. Mike Da Silva is asking, do you spread your vitamin D intake throughout the day or take 4,000 IU at once? I take the, I take the 4,000 IU at once.

It's the vitamin C that that I spread throughout the day. So vitamin C is a water soluble vitamin. Vitamin D is fat soluble. It's stored in fat, so it's a little different. And in fact, there have been studies showing that the bioavailability of vitamin D is is increased with higher doses. So so for example, people were given 1,000 IUs, they were given 4,000 IUs, or they were given 10,000 IUs, and more vitamin D was bioavailable and more was absorbed, more was released into the bloodstream, more precursor, which is 25-hydroxy vitamin D, was measured with higher doses. So that's also another reason why I take the 4,000 IUs daily. Okay. Janet Cole is asking in the chat, is ascorbic acid the complete vitamin C? Yeah, ascorbic acid is vitamin C. That's— it's ascorbic acid is its actual name.

Emma is asking, do you take vitamin D with vitamin K3, which I think she means vitamin K2? I do take vitamin K2. I take it a couple of times a week. So, I take— I believe my dose, it's either 50 micrograms or 100 micrograms, but I take it a couple times a week. Okay. So, I'm going to move on to the next viral defense topic. Topic that I'm covering. And as you guys know, I love broccoli sprouts. I love sulforaphane in any way, shape, or form I can get it. So there was a randomized double-blinded study that showed broccoli sprouts— when— so basically, when broccoli sprouts was given with live attenuated influenza virus, it was able to to basically— pulling up the study— it was basically able to kill some of the virus and activate natural killer cells.

So basically the nasal influenza infection It was— that was given, it was an attenuated influenza virus that was given to them. It induced changes in the peripheral blood natural killer T-cell activation. And the broccoli sprout extract, what it did was it increases the natural killer cells to make a certain compound that kills the virus. So I'm eating broccoli sprouts. I'm also taking— I've also put moringa powder in my smoothie. Moringa powder, it has moringa, which is very— as Dr. Jed Fahey, the sulforaphane expert, has told me, he thinks it's very similar to sulforaphane. And I really— he's done some research on that, and I really trust what he says. And so while there is not as much research being done on moringa, there is some, and a lot of it's been done by Dr. Jed Fahey.

I do think that taking the moringa powder may be pretty equivalent to the broccoli sprout extract. The moringa powder I buy is Kulikuli, and I get it from Whole Foods. I don't believe I found it anywhere else, but Whole Foods does sell it. And it's pretty cheap, particularly in contrast to some of the the sulforaphane supplements, which I also do take. I still take prostafane. I'm taking 20 mgs a day of prostafane. But in addition to that, I'm also taking moringa powder. Another another sort of interesting some interesting studies that I've that I've been looking into are the effects of N-acetylcysteine. on, um, on the lungs.

There's, there's a growing body of evidence that N-acetylcysteine has a positive effect on reducing the oxidative stress and inflammatory response in people with community-acquired pneumonia. And so this was 1,200 mgs a day. And other studies have also shown that N-acetylcysteine breaks down mucus in lung function in patients with asthma that have a mucus profile. So I am taking around 1,200 milligrams a day of N-acetylcysteine, and which is a— it also, there's other benefits of it as well, but it is not something I usually take, but I do, I am taking it right now just based on some of the evidence. Along the same lines, I'm taking some liposomal glutathione.

And, uh, there's some evidence that— now, now this evidence is weaker in the sense that it was a dose, um, they did different doses in this, in this pilot study, but they didn't have a placebo control. So what the, what the study, um, looked at was liposomal, liposomal glutathione at 500 milligrams or 1,000 milligrams. Uh-huh. After 2 weeks. So this was 2 weeks, a 2-week-long trial, and the glutathione levels increased in both plasma and they increased in various types of blood cells after, after, I think even after 1 week. Yeah. There was a maximum increase in 40% in whole blood, 25% in erythrocytes, and 28% in plasma. And 100% increase in PBMCs after 2 weeks.

So in glutathione levels, so obviously glutathione was getting into the plasma, it was getting into other cell types, it was getting into blood cells, right? Which is important because glutathione, if it's not liposomal, is like 100% destroyed, you know, in the stomach. It doesn't, you know, doesn't make its way into your bloodstream. It's essentially just a placebo in my opinion. There are no transporters for glutathione to get into cells, which is another reason why liposomal is important because to some degree liposomes can under— can overcome some of that because they can sort of fuse with cell membranes and sort of deliver their contents within that sort of— sort of— I'm totally doing a very simplified explanation, but it's part of the way that liposomal glutathione can help overcome the fact that there's no actual transporter to make glutathione.

Glutathione is something that is made inside cells by enzymes. You have glutathione synthase, and you have— once, you know, once you make the glutathione, you have glutathione transferase enzymes, which are, you know, transferring them to wherever is needed. Which, by the way, sulforaphane is one of the major, major Uh-huh. Compounds that I've seen to increase plasma levels of glutathione. I haven't seen it. I've read studies in— it increases plasma glutathione levels in people. It increases it in their brain in people. And this happens through activation of the NRF2 pathway. Sulforaphane is one of the most powerful naturally occurring compounds that is able to activate NRF2.

Um, so, so there have been, there have been studies looking at broccoli sprout extract, um, and sulforaphane, stabilized sulforaphane, how it increases glutathione in plasma, how it increases in the brain. There's been studies showing that, um, eating foods that are rich in sulforaphane, like, like Brussels sprouts, for example, um, lower DNA damage in cells by almost 30%. And this is in humans, you know, where it matters. So, um, Just another sort of, you know, the— it's interesting that the glutathione— I haven't gotten to why I'm taking the liposomal glutathione yet, but the sulforaphane is another way to increase glutathione within cells because it increases enzymes. It— NRF2 pathway increases the enzymes activity that actually make glutathione inside of your cells.

Um, so, so this, this— the glutathione, um, it is one of the major, major antioxidant systems in the body. And it was shown to reduce oxidative stress biomarkers by like 35% in the blood cells. And it also— and this is what was very interesting to me— that natural killer cell cytotoxicity was elevated by 400% after 2 weeks. Lymphocyte proliferation was elevated by 60% after 2 weeks. And there were no differences between the 2 doses of 500 milligrams or 1,000 milligrams. So really, it seemed as though 500 milligrams was sort of the minimal effective dose in terms of, you know, having that effect on the immune system. So preliminary study, still very, very profound increases. You know, 400% increase is a really a big difference even though it was a small sample size.

And definitely larger studies need to be done. And this is something that I'm sharing with you guys. It's something that I'm doing. So I'm really just kind of giving you the background as to why I'm doing it and the science, you know, the limited science that I'm basing that on. Some of the other things I'm trying to do is the sauna, 4 to 7 times a week, 20 minutes at at least 174 degrees Fahrenheit. Wow. So I've shared the study on social media about the sauna reducing the risk for, you know, chronic acute respiratory illnesses including pneumonia. So men who use the sauna 3 times a week were 27% less likely to develop pneumonia than those who did the sauna once a week. And those that used it 4 times, 4 to 7 times a week were 41% less likely to develop pneumonia.

And this was after adjusting for like a million other potential confounding factors, including asthma, physical activity, socioeconomic status, LDL levels, hypertension, smoking, just a lot of other things that were, that were, um, could possibly influence the, the data. Um, there's other studies that have shown that, um, the sauna, sauna bathing has been shown to reduce the incidence of common colds. Now this was a— I'm writing a review article on the sauna which I'm hoping to submit in the next month or two. So I wrote a section on, on the lungs and respiratory function. Um, so I was kind of diving back in the literature, you know, sometimes back into the '80s or even sometimes further.

But there's some interesting studies out there showing that intervention trials with the sauna was able to reduce the incidence of common colds in people that did the sauna once a week. And this was a trial that was done, it was a 6-month-long trial, so it was quite long. And it actually, it actually took, um, 3 months of doing the sauna 1 to 2 times a week before there was an effect on reducing the incidence of common cold. So it wasn't a sort of immediate thing. It took some time. Other studies have shown, and these again are older studies, they've shown that frequent sauna use may decrease pulmonary congestion and lead to other improvements in lung function, including vital capacity, tidal volume, minute ventilation, and force expiratory volume.

Another study using not typical Finnish sauna but Weyon therapy, which is infrared sauna, was also shown to improve lung function in people with chronic obstructive pulmonary disease or COPD. So, a sort of interesting thing is that many but not all of those studies were out of Finland or were using a Finnish sauna. Which typically is a humid sauna. So they, you know, in Finland, they're often throwing water over these hot rocks and they're creating steam and they're increasing the humidity. And the reason I find this interesting is because there have been some studies. So there have been quite a few studies showing that viruses in general, influenza particularly, is a virus that's studied quite often, that influenza viruses transmit less effectively in humid conditions.

In other words, in dry conditions, they're able to better— they have a better transmission rate, the R-naught. But that's not what I found most interesting. That's sort of been known, and it's thought that's one contributing factor among many other contributing factors as to why Viruses like influenza virus and respiratory viruses seem to circulate more during dry or winter months, right? As opposed to the summer months when it's more humid. The other interesting factor comes from an animal study. And the animal study basically took 2 groups of animals and they changed the humidity Within the animals' cages, and they exposed them to influenza. And what they found was that the animals that were in the low humidity cages, there was pretty profound effects on the immune system.

So lower humidity prevented cilia from removing viral particles and also mucus. Low humidity reduced the ability of airway cells to repair damage caused by the virus in the lungs. And low humidity prevented signaling proteins like interferons that are released by cells that are infected by viruses to basically alert nearby cells that viruses are here and to kind of, you know, up their immune response. So there was a variety of ways in which low humidity seemed to give viruses an advantage, not by, you know, allowing viruses to transmit better, but by literally affecting the host immune function. Right?

So I found that very interesting, particularly with the sauna data where, you know, there seems to be a pretty robust effect on preventing ammonia pneumonia and other respiratory illnesses and effects on lungs. And a lot of the times the saunas used do have a humid— in those studies, they were Finnish saunas, oftentimes are humid. Um, David P is asking in the chat, would mold accumulate more in a steam sauna than a dry sauna? Um, yeah, probably. Steam rooms have to be really cleaned quite frequently. Um, I mean, obviously, that's pretty— the problem with humidity, having a humid house or a humid anything, is mold, right? Uh, so David is also asking about the temperature of the sauna. Most, most gyms don't— he says most gyms don't go up to 170 degrees Fahrenheit. Um, Yeah.

Some of them go up to 140. So 140 sounds like infrared. That's— if it's only going up to 140, that sounds like an infrared, not a dry sauna. But regardless, typically longer durations are required if the temperature is lower. So there have been— so if let's say, for example, we're trying to look at the cardiovascular benefits of sauna use, of which there are many. There have been studies in using a more Finnish type of sauna or even dry saunas where the temperature is 170, about 174 degrees Fahrenheit, and staying in there for 20 minutes seems to be the key. Whereas there are also studies that have been done with infrared saunas that get up to about 140, but those studies, people are staying in there, are staying under the heat stress for about 45 minutes.

So more than twice as long as people that were in a hot— hotter sauna. So typically, you can make up for lack of heat with longer duration. And some other things that I've also added for me is, for my use, is supplementation with garlic extract. There's been a few double-blind placebo-controlled trials showing that supplementation with garlic can improve natural killer T-cell function and can reduce severity of cold and flu symptoms. Another group showed something similar, similar, another randomized placebo-controlled trial. Where this was, you know, resulted in fewer sick days. And, and so that there's another study that showed it helps prevent and treat viral upper respiratory tract infections in adults.

So, so I'm doing the garlic and I'm also taking one VisBiome sachet a day because there's also some studies looking at the effects of probiotics on immune function. You know, gut bacteria generate what are called short-chain fatty acids, and these short-chain fatty acids are major, major signaling molecules for immune system and immune function. So, so that's another thing. Um, we're putting together— my team and I are putting together a topic page on intravenous vitamin C, and also we're going to be doing one on vitamin C But the intravenous vitamin C is interesting.

I've talked about it before when I was guest on other podcasts and probably I've talked about it in Crowdcast before and I've certainly talked about it in my monthly hangout I have the first Sunday of every month with a select group of supporters. We've talked quite a bit about vitamin C and— IV vitamin C and cancer. Intravenous vitamin C is completely different than taking oral vitamin C in a couple of ways. One, it— you— I told you, you can't, you can't get plasma levels above 200 micromolar with oral supplementation. With an IV vitamin C, you can get doses in the millimolar range. You can get, depending on the, the IV dose, anywhere between 25 to 70 times higher plasma levels than you would get with oral. So it's a really, really kind of big difference.

And there's been quite a few studies that have come out over the years looking at IV vitamin C as an adjunct therapy for cancer treatment. And Yeah. You know, there's been a variety of mechanisms for this, and one of the mechanisms is thought to be the production of hydrogen peroxide, which basically kills cancer cells because they can't increase their antioxidant response because they're— they have tons of mutations and they're completely screwed up cells, whereas the hydrogen peroxide doesn't actually damage normal cells because Uh-huh. Normal cells are increasing their antioxidant response, and, and so it's sort of this selectively killing of these cancer cells. Well, it turns out, you know, hydrogen peroxide is also used to kill viruses.

So there's also some literature out there on IV vitamin C and its use for treating a variety of viral infections, including herpes virus, Epstein-Barr virus, and a variety of other viruses. There's also one on influenza. So, so it's really interesting, you know, it's a— it's been an interest of mine for some years now, starting— I first became interested in it because of the effects on cancer. And so, so we're putting together a topic page, we're kind of doing a deep deep literature dive, and, and that, that should be coming hopefully very, very soon. Um, Deb is asking which glutathione liposomal glutathione supplement I take. Uh, so I'm taking the liposomal glutathione from Pure Encapsulations. And, um, I have no affiliation with them. I just happen to like many of their products.

But, um, remember, it has to be liposomal glutathione. Like, regular glutathione is, uh, you know, is— it's not likely going to be getting into your bloodstream. In terms of the pharmacokinetics, I see some questions about intravenous vitamin C. So I'll just quickly talk about some of the— I talked about the oral pharmacokinetics in terms of if it was taken like 4 times a day, you know, you could maintain your plasma levels of around 200 micromolars throughout that whole 24-hour period. Whereas if only one high dose was taken, you sort of taper off over the course of 24 hours, and then by 24 hours, you're back to your baseline levels.

With respect to intravenous vitamin C, there's been some pharmacokinetic studies, and depending on the dose given, you can reach different plasma concentrations in the millimolar range, not micromolars, so orders of magnitude higher, right? An order of magnitude higher. The levels seem to peak at around 3 hours after the injection, and then they sort of taper off and go back to baseline at 6 hours after. So it's really a very short time that plasma levels are elevated for, are really elevated. So it's about, you know, after about 6 hours, you're back to your baseline. But, you know, the thought is that there are, you know, some lasting effects because things are getting activated.

And so there's sort of a cascade of events that happens, you know, that is happening over a period of days as well. But in terms of specifics and stuff, in terms of like some of these studies and how often they were given them and all that, that will come out with the topic page that we're gonna be releasing in the next— definitely in the next 2 weeks, it'll be out. I would say that, you know, I mentioned sort of a potential negative side effect with oral supplementation was the people that are prone to kidney stones and, you know, the potential for oxalate accumulation. With the IV vitamin C, Um, there's, there's, there's in particular, uh, high risk for people that have a deficiency in an enzyme called glucose-6-phosphate dehydrogenase, G6PD.

And, um, if you have that deficiency, you would know it's something that's like at birth because you end up having your red blood cells, you know, lyse. And so you have problems with making, um, maintaining red blood cells. Um, so that you know, is something that, you know, people with, with that deficiency cannot do IV vitamin C. But most, most clinics that are administering this will ask you if you have that. I mean, it's, it's like one of the first things they ask. The other thing is that, that patients that are, um, like undergoing dialysis or, you know, have some sort of kidney dysfunction, those are also patients that, uh, have a high risk for, um, you know, potentially having the, the oxalate accumulation.

Um, so, so that, that— those are the major things, um, with the intravenous vitamin C in terms of, um, sort of disqualifying people from using it, um, in terms of a lot of clinics. And you can find this— there's a lot of clinics around. Um, they're much more ubiquitous now than they were like 7 or 8 years ago. I mean, you can find naturopathic doctors and Um, you know, just there's a lot of, there's a lot of places, um, in, in a variety of cities that, that do this. And sometimes they call it hydration therapy. Sometimes they're giving the vitamin C with other vitamins like some B vitamins or magnesium. Um, you know, so depending on, on the place you're going, uh, there could be a variety of other, um, compounds used. I've personally done it a couple of times and I really like it.

It can be expensive, you know, it's not certainly something you'd be doing all the time, but I did take my mom there. She had come down with a cold. Basically, she had— her nose was like a faucet, you know, she had a runny nose and I felt sort of an inkling of, of the onset of something. So we went to get some intravenous vitamin C, and, um, I did not get sick, and she uncharacteristically resolved her illness within, within like 36 hours. I mean, like the next day she was like 80% better, and then the day after that she was 100% better. I mean, which is sort of uncharacteristic for her. Her sicknesses are always long and drawn out. So— You know, it is what it is, but you know, it could be placebo or it could be doing something.

And I'd say that the evidence, the scientific literature shows that IV vitamin C is definitely doing something with respect to being antiviral and also killing cancer cells, presumably through similar mechanisms as well, the hydrogen peroxide release. But there's other mechanisms as well which we'll be discussed in a topic page that will be out soon. Okay, so I'm gonna hit this last topic before we wrap this up. And this, this was sort of a big question that required a lot of deep diving and looking into the literature. So the question— forgive me, I don't remember who asked it, but the question was, does consuming protein from animal sources increase the risk of type 2 diabetes? And it's a really big question because there's just dozens and dozens and dozens of studies.

And it's one of those things where you just, again, like for a question like this where you find, you can find a lot of heterogeneity in the literature, which all that means is that you can find some studies say there is an association. Some say studies show there's not an association. And it's just like, what the heck is going on, right? I mean, like, like, clearly there's— you can both— you'll find both ways. So there's, there is something that, you know, that's going on, but there's obviously other things that are— that need to be accounted for, right? Um, and I would say, again, this is why, like, let's say, for example, you had someone who was biased in the sense that let's say they were vegan.

And they had every reason they wanted to believe that animal meat consumption increases the risk of type 2 diabetes because they're vegan and they want to justify their veganism and they want to potentially propagate it, right? So they're going to look in the literature and find any study they can that says that eating animal meat causes type 2 diabetes. And, you know, and the opposite is true. You have, let's say you have a meat eater, and they're going to go and find all the studies that show there's not an association, right? So it's one of those, it's one of those areas where you really, you just need to be unbiased. Like, if you, I mean, who doesn't want to know the truth, right? Like, like, I don't care. I either like, I'm not going to eat meat, or I'm going to eat meat.

Like, I want to know what I should do, right? Like, that's, that's how I feel. And I feel like more people should be doing that. Less— unfortunately, more and more people have an agenda, and, and that agenda is whatever it is, but it's an agenda nonetheless. And because there is such heterogeneity in, in the field of nutrition for so many reasons, um, you can pretty much find what you want to support your agenda, and that is a really unfortunate thing. What needs to be done is an unbiased approach needs to be taken. It absolutely is critical to get to the truth. That's the only way. Otherwise, you're just supporting what you want and finding the things that you want to support what you want, and that's not real science.

Okay, with that said, there are dozens of studies that do show an association between dietary protein consumption from animal sources can increase the risk of type 2 diabetes. I mean, there are so many studies, just study after study after study after study after study after study showing that there are studies that also show no association. But there's a lot of studies that show an association. However, when you start to look at every single study and you start to look at all the data, you start to see that in about 90% of every study that found an association between protein consumption from animal sources and an increased risk for type 2 diabetes, that that risk goes away when BMI is adjusted for, meaning people with a high BMI are at risk for type 2 diabetes if they have an increased intake in protein consumption from animal sources.

That's a really important thing to know. And again, it's almost, it's almost 100% of the time That holds true almost. I mean, it's just it's it's it's like beautiful. It's like okay, that's that's data, right? When you start to see that risk go away after you correct for BMI. Now there are a few instances where some studies showed that BMI did not matter if the protein intake was from red meat. And only if those people were in the top 20% of red meat consumers versus the 80% bottom of red meat consumers. So basically, some people with a normal BMI had an increased risk for type 2 diabetes if they were in the top 20% of red meat consumers. So That's kind of what I got to after my team and I just went through, I mean, dozens of studies and looking at the data over and over again.

And that's pretty much the conclusion that I've come to is that people with a high BMI are at risk slightly. And I'm not— I do not have a high BMI and I'm also not in one of the top 20% consumers of red meat. Um, so I mean, I'm not, I'm not too worried about my, my meat consumption. There's a variety of mechanisms. I, you know, I don't know what's— there's so many possibilities with, you know, the high, the top 20% of the, the red meat consumption. You know, there's, you know, NeuC, 5-GC. Um, I'm not entirely convinced of all that data, but it is some— it is something that I've been putting, you know, I've been reading about and putting together some, some information on. It is something that's specific to red meat, and you know it's quote unquote an anti nutrient.

You know, so that's a possibility. You know, I honestly don't know. I would say for the most part, it seems as though people with a normal BMI are not at a high risk for type two diabetes with increased risk of animal meat. Like that's that's the conclusion I made after like just dozens and dozens. So Walter is asking, will I post the data about BMI regarding type 2 diabetes? Yeah. I am not like this, you know, this is a— I put together some, some information, but it's— I mean, it's a document that's, that's how many pages? 10 pages long, and it's just different studies with results and, and, and some commentary and things like that. I am not posting that. I am going to eventually— we're gonna, we're gonna put together a topic page That will cover this, and it'll be in a more coherent way.

So eventually that can be posted, but it's not something I'm gonna post tomorrow. It's sort of a work in progress. And that's all I have for today. I really enjoy doing these Crowdcasts. I learn so much from people's questions. And another question that we'll— another big question that was submitted a couple of months ago that's still being worked on is the dairy consumption. Is it bad to consume dairy? It has been an enormously big task because again, it's one of those topics that just there's so much evidence showing both, like it's good and it's bad, or there's no effect.

Or so it's one of those things where you have, you have to just look at all the data and try to like, try to find things, you know, figure out things like with the BMI, you know, like, is there some kind of common thing that, you know, is happening here that can explain why there's, you know, data showing there's a negative effect and data showing no effect? So I will be getting to that and I'm not sure if it'll be next month, but it will be sometime in the next couple of months. And that's another one of those, you know, 10 to 12 page documents that we are working on right now.

So people are asking for updates on my experimentation and I'm actually getting ready to go give 17 vials of blood to like measure a variety of different biomarkers and things, So I'll keep you guys updated on some of the experiments I'm doing. But please, please ask in the Crowdcast questions to remind me to tell you. And everyone, I hope you enjoyed this Crowdcast as much as I did. And thank you so much for participating live and for submitting great questions that keep me on my toes and keep me learning more and more, and hopefully you as well. So I will talk to you guys next month. Be sure to register for the next Crowdcast. It'll, it'll be up on the dashboard. You can register on your— you can find the link on your dashboard, foundmyfitness.com/dashboard. And so I look forward to next month and you guys have a great month and stay healthy. Talk to you soon. Thank you.