Q&A #26: Do Omega-3s Raise Atrial Fibrillation Risk—and Is Acarbose a Longevity Drug?

Hello everyone. Nice to be back here. This is episode 27. No, 26. Episode 26 of our Crowdcast Q&A series. We've done this for 26 different months. That's pretty exciting. I really enjoy doing these. Q&A sessions for multiple reasons. Probably the main reason is I learn so much from the questions that are submitted. So for those of you that are new and this is your first live Q&A, typically the way it goes is I look through the questions that have been submitted on the Crowdcast website, and there are top-voted questions and oftentimes just a long list of questions. So I choose the based on a variety of factors, including the top-voted questions.

Sometimes the top-voted questions will be repeats of questions that I've already addressed in previous Crowdcasts, and in that case, I usually don't choose those again. I'll mention that this has already been addressed in a previous Crowdcast. I also go through questions that haven't really been addressed before, and/or questions that have been asked quite frequently by a number of people in some form or another. So typically we'll do a deep dive on a few of the big questions, and then I go through what I call rapid-fire questions. And those are questions that I can answer relatively briefly. Sometimes the top-voted questions fall into that rapid-fire category, so just keep in mind That rapid-fire category comes at the end of the CRADcast.

And then throughout the CRADcast, I will answer questions here in the chat that I see. Most of the time, it's nice to have them relevant to what I'm talking about, but every, every so often I'll get an off-topic question as well. So that's kind of the benefit of attending these live. You get the benefit of chatting here and having some of the questions answered live. Of course, you can always watch or listen to the replay of this video. We send out an email with a summary and time points linking to the YouTube video that you can replay. You can also download your private podcast player where you will have the aliquot, which is the private podcast feed. We have our aliquots that you can— that we've been releasing probably pretty much weekly, but you can also listen to the Q&As there.

So if you haven't downloaded that, please go to your dashboard at foundmyfitness.com/dashboard. So log in and make sure you go ahead and get that as well. All right. So I'm going to get started. The first question here on the list was kind of a— the first, actually, 2 questions were leftover From last time. And the first one was relevant to something I had mentioned with me noticing that, you know, drinking alcohol was pretty significantly lowering my postprandial blood glucose levels. In particular, it was noticeable with a refined carbohydrate treat, which I don't often do. However, there were some birthday parties and some cakes involved, and so that was something that was noticed on a number of occasions.

And so people were kind of inquiring about the mechanism, so I just wanted to briefly talk about that. So alcohol does lower blood glucose levels, and there's 2 mechanisms by which this occurs. The first is that alcohol itself can increase insulin secretion. And this happens when it's present at a moderate concentration in the blood. Alcohol can then increase the secretion of insulin in response to sugar, and this causes the sugar, glucose, to be transported into cells, either muscle, liver, or adipose cells, and that causes the blood sugar to go down. Now, one obviously would like the glucose to be transported to muscle cells over adipose cells because when you have them transported into muscle cells, that can have an anabolic effect on muscle protein synthesis.

Also can replete your muscle glycogen. Same goes with the liver. It can also— if the glucose gets transported into liver, it can be, you know, repleting the glycogen levels in the liver. When glucose is transported into adipose tissue, it's stored as triglycerides. Yeah. That's not ideal. So one of the things that helps sort of differentiate whether or not the glucose is going to go into the muscle versus the liver versus adipose tissue is the level of physical activity. So people that have already sort of depleted their muscle or liver glycogen are more likely to have the glucose being transported into those tissues versus adipose. So that's just another sort of tangent to keep in mind.

The second way alcohol lowers blood glucose levels is by actually inhibiting what's called gluconeogenesis, which is the process by which the liver can convert gluconeogenic amino acids. There are certain amino acids that can be converted into glucose or glycerol into glucose. So that is very important, for example, during a state of ketosis, fasting-induced ketosis, for example, your body absolutely needs to make glucose. Your red blood cells need it, your brain needs glucose. And so there's a mechanism, you know, that is in our body that allows us to make glucose from something other than an actual carbohydrate which has glucose. So gluconeogenesis gets inhibited to some degree in the liver as well.

And the liver basically, usually the liver will need NAD to make glucose from the amino acids or glycerol. But what alcohol does is basically the alcohol is using most of the NAD to detoxify and metabolize the alcohol. So what ends up happening is the gluconeogenesis process gets inhibited somewhat because of the lack of availability of NAD+. So anyways, I just thought that was pretty interesting and people would find that interesting as well. The next question was a question that was submitted by Frank, and this was last time, this was a top-voted question, and I said that I was going to return to it because it required some more in-depth researching.

And so the question was, Frank says, a recent study suggested that the omega-3 fatty acid DHA prevents the positive heart benefits of the omega-3 fatty acid EPA. Can you discuss this? So turns out I just filmed a podcast last Wednesday so a few days ago, with Dr. Bill Harris, who is probably one of the world's leading experts on omega-3 fatty acids. He flew out from South Dakota for the day to come and film the podcast. And it was a 2-hour conversation, would have been longer. He had to catch a flight immediately after, so we were limited by that. But we covered this question in addition to many other topics. And so I had the benefit of learning what he had to say, and it was really beneficial because I had my own interpretations, but he is the real expert.

And so it was really good to have his perspective. Let's— oh, and you know what? There was another question that was tied along to this, which was that in addition recent studies have found that very high-dose EPA may be linked to atrial fibrillation, AFib, as it's called. And so that also needs to be discussed. So let's kind of talk about some of the research here. I think there's really 3 big trials that were done. And the first trial that I want to discuss was published in 2019. This was the— it was called REDUCE-IT trial. And the REDUCE-IT trial used a form of purified EPA called Vascepa. And it was 4 grams that were used. The trial was a randomized double-blinded placebo-controlled trial.

And it found that basically 22% of the placebo group had a cardiovascular event over the course of 5 years. which they were followed, whereas only 17% of the EPA-treated group had a cardiovascular event. 8.7% of the placebo group had a heart attack, while only 6.1% of the EPA group had a heart attack. So, and there was a basically 25% reduction in cardiovascular-related mortality in the treated group. which was quite significant, and it made, you know, headlines, and it was, you know, like, wow, this is really robust, this is amazing. It also reduced triglycerides, and, you know, so there was a variety of different factors that occurred.

Within that group, so these people actually were people that had previously had a heart condition, So, they were not, you know, it wasn't— this was not like a healthy group of people to start with. They were people that actually had already been diagnosed with some kind of heart problem. Within that, there was a subpopulation of people that were given the high EPA that seemed to have an increase in AFib, in the atrial fibrillation. It was small, but it was enough to be noticeable. So the second big study, this was actually a study called the VITAL study, and it was published a year before the REDUCE-IT study. That study was published in 2018, and they gave a— it was a much smaller dose. So the last study I just mentioned was 4 grams of purified EPA. in the prescription form of Vascepa.

The VITAL study was only 1 gram of combined omega-3, and this was also for 5 years versus a placebo. And there was a variety of arms in this, different arms in this study, including a vitamin D arm. We're not going to get into that. But what the study found is that when they looked at combined cardiovascular events, all of them combined, so stroke, heart attack, you know, everything combined, there was not a statistically significant effect of the 1 gram of omega-3. However, so it was— there was a 19% reduction in all cardiovascular events, but it was not statistically significant. However, when you look at secondary endpoints, when the researchers looked at, for example, the reduced heart attack, Only, there was a 28% reduced risk of heart attack in the omega-3 group.

There was a 50% reduction in myo in the in actual in actual death from heart attack, which is quite quite robust. And there was a 28% reduction in the need for PCIs. So there was basically some pretty robust effects when you looked at, you know, specific types of heart problems. But with them all combined, there wasn't a significant reduction. And the last study, and this is the one that Frank was referring to in the question, the last study was a study that was published in 2020. And this study was called the STRENGTH study. And the STRENGTH study used an omega-3 that was combined EPA and DHA. And this trial was cut off early. So it was supposed to be 5 years, but it was cut off before that because there was no benefit that was being found in terms of the omega-3.

And so it was kind of a big failure because people were wondering why was there no— why were we not seeing any heart benefits like we saw in the other trials. And, you know, there's a variety of speculations and, you know, Dr. Harris talks about these much more prolifically than I do. But basically the population of people to start with were much healthier, so they were having fewer cardiovascular events. So it was hard to like figure out whether or not there was a benefit if there are fewer events happening in the first place. The other hypothesis was, well, this was using a combination of DHA and EPA, but whereas the REDUCE-IT trial was the 4 grams of EPA, however, the VITAL study did show a benefit with 1 gram of the combined EPA and DHA. Okay.

So it's not really known why there was no effect. Bill does not think DHA is causing a negative effect on cardiovascular health. He does not think it is negating the benefits of EPA. He thinks this trial design did not work out. And if you look at some of the meta-analyses, there was a meta-analysis published this year It showed when you looked at a range of dosages in the omega-3 between 376 milligrams per day up to 4 grams per day, the most robust effects were found in the higher dose, in the 4 grams per day. And there were 14 different trials that were looked at for fatal heart attacks and 41 different studies that were looked at for different cardiovascular disease events.

And so it was— Basically, look, combining all those studies, omega-3 supplementation was associated with a 15% reduced risk of a heart attack and a 10% reduced risk of coronary heart disease events and mortality and a 35% reduced risk of a fatal heart attack. So I think looking at the meta-analysis and combining all these studies together, there's clearly a benefit occurring from omega-3 supplementation. Why that study failed, it's unclear. People are— there was a speculation, well, maybe it was the addition of DHA. But that's just not the case for all these other 35, you know, 14 trials, you know, showing, you know, many of them having combined DHA and EPA as well. So it doesn't seem logical that that would be the explanation.

And I think if you look at the cohort, again, they were much healthier and this the study was stopped early, which I think was a big mistake because, um, because you, you know, you may have needed to take it out longer to get those cardiovascular events to happen to see a difference between the placebo and the treatment group. The other thing that did come out of that study again was a slight increased risk for atrial fibrillation. So when I talked to Bill about this, Dr. Harris, He made a really good point in that, you know, we don't know— and this was only happening, of course, when we're getting into the 4-gram range. We don't know why that is. And when you look at— so the problem, the reason atrial fibrillation is monitored is because it can lead to a stroke.

And when you look at actual stroke outcome, Omega-3 fatty acids reduce it. So it kind of doesn't make sense in a way when you're looking, well, why is there a statistically significant, you know, very small but significant increase in atrial fibrillation, but you're seeing, you know, the endpoint of what the problem with AFib is, which is stroke, being reduced. So it's really kind of unclear what's going on, and I certainly think that more research evidence, you know, we need more investigation into the AFib, you know, the potential link between them, high-dose omega-3 and AFib. But even again, it seems as though the benefit outweighs the risk because the omega-3 is reducing stroke, it's reducing heart attack, it's reducing fatalities from heart attack.

So even in a population that has a high risk, for these types of heart diseases, and probably AFib included, it may still be that the benefit outweighs the risk. So that's kind of the answer that I can give you today. I think that when we release the podcast with Dr. Harris, he goes into a little bit more detail on that. Moby asks in the chat, the live chat, hi Rhonda, thoughts on Vascepa? I think Vascepa— so Vascepa is a highly purified ethyl ester form of omega-3, the omega-3 EPA specifically, and I think it's really great people that can get— you have to meet a certain threshold for triglycerides or possibly other heart disease risk factors to get a prescription for this, which would be great because it can be— health insurance would cover that in many cases.

One thing to keep in mind with the ethyl ester is that it is— you do have to take it with food for it to be bioavailable. And so So that is something to keep in mind with respect to the Vascepa. But I do think, like, for example, my mother has high triglycerides. I've been giving her a purified form of omega-3 EPA that I get from a friend in Norway. And so I'm actually going to see if she qualifies to get the Vascepa because it would be great to get her the Vascepa. getting her on the 4 grams. Like right now she's taking 2 grams just because compliance, like for her to take 4 grams, she would have to take 8 pills. And right now it's, you know, she's taking a lot of other vitamins. So it's like it would be nice if she could get the Vascepa, which would be more omega-3 packed into a pill.

But so that's my thought. Sarah is asking in the live chat, what's my current omega-3 supplementation regimen? Currently right now I take 2 grams of EPA in the morning, and I take 2 grams of DHA in the evening for a total of 4 grams of combined EPA and DHA. Jessica's asking in the live chat about the specialized pro-resolving mediators, the SPMs as they're called. And I mean, so I think, you know, these are one really important mechanism by which the omega-3s are reducing inflammation. Metagenics that she's mentioning as an omega-3 supplement, I think that was a pretty good one that was reviewed by one of the third-party testing sites.

Just an FYI, if someone can ask in the Crowdcast for next month, I put together a spreadsheet with— our team analyzed the many different companies that have their omega-3 supplement analyzed by the International Fish Oil Standards. And so we ranked them in order of oxidation status and also concentration of EPA and DHA. And I haven't gone through that Excel spreadsheet data yet, but I will. come up with a top 5 or so list based on those— on the data from that analysis. So please ask that question next time, and we can discuss it next month after I go through the data. Alan Bishop's asking why I'm separating the DHA and EPA. Why? So, mostly because the supplement that I get comes in either a high DHA or a high EPA form. So, that's the main reason.

But I'm also just— it's kind of speculation at this point, and I don't know that there's really any reason to separate them or if there's any enzymes that may compete for some of the metabolites that are produced between the 2 omega-3s. And so I'm sort of trying to figure out whether or not there's even a real reason to need to do that. I don't think there is. But mostly it's just I'm wanting to have sort of a constant omega-3 influx into my system. And so the way to do that would be to kind of like to have it, you know, in the morning and then later on in the evening. That way it's like it's you're having, you know, blood levels that are high throughout the day. I'll tell you this, and this is like, boy, is this going to go on a tangent, but I'm really excited about it.

I was talking to Bill and and he's he just published a pilot COVID study where he found in a very small study that. that omega-3 fatty acid blood levels in red blood cells, it's called the omega-3 index, and we'll get all into this in the podcast, were associated with COVID-19-associated mortality. So people that had the highest quintile of omega-3 in their red blood cells had the lowest COVID-19-associated mortality. And this was even after correcting for like other health factors, you know. And here's where I got really excited about that There was a study that he shared with me about DHA actually keeping the spike protein, the receptor binding domain of the spike protein in what's called the closed transformation.

And here's why that's important, because the spike protein receptor binding domain region goes from a closed closed conformation to an open conformation. And when it's in the closed conformation, it cannot bind to the ACE2 receptor. It cannot attach to the ACE2 receptor. It has to be in the open conformation to do that. And so I was like super excited about that because that really suggests that perhaps having a constant stream of omega-3 in the blood would really help not only stave off infection, but also potentially help with the severity of the disease.

Because when the spike protein binds to the ACE2 receptor, it then causes a transformation, a conformation change that basically allows the spike protein to be, you know, come into the cell and it downregulates ACE2 receptor, which causes all sorts of problems. But anyways. We can talk about that in detail some other time. I'm going to move on to the next question that was submitted by Megan. And Megan asks about exercise timing for insulin sensitivity. According to the research that I've shared previously, it seems as though afternoon exercise is better for insulin sensitivity, but she's also heard that exercise Exercising while fasted or having coffee improves both, you know, fat oxidation and also blood glucose levels, which would indicate perhaps morning workout would be better.

What are your thoughts on the optimal workout time? So I would say basically any time of the day is good for exercise. It's better than not exercising at all, like hands down, whatever's like the easiest for your schedule is the best. for, you know, time to exercise. So I wouldn't get too caught up in this circadian, you know, regulation of some of the, you know, adaptations that occur from exercise. We do know that afternoon exercise gives a small increase in peak performance. We also know blood glucose control, with respect to blood glucose control, there was a small trial that was done. This was in people that had type 2 diabetes. They were wearing continuous glucose monitors. And they did high-intensity interval training at different times of the day.

So those who exercised in the morning had lower blood glucose levels after 24 hours compared to those that exercised— sorry. Oh, no. Okay. The fat oxidation was— let's start over. I have the wording here a little crossed over. So in the type 2 diabetics, they compared those that exercise in the morning and those who exercise in the afternoon basically had the lower 24-hour blood glucose levels. So the afternoon exercise lowered blood— the 24-hour blood glucose levels better than the morning exercise. Fat oxidation was 13% higher when exercising in the afternoon compared to the morning. But exercising in the morning also has unique benefits because most people tend to be fasted in the morning.

And there have been meta-analysis looking at the adaptations that occur from exercise, including mitochondrial adaptations with fatty acid oxidation. And those adaptations occur better if exercise is performed in a fasted state compared to a fed state, in which the caveat is the fed state always in these studies included carbohydrates. So basically, mitochondrial adaptations for fatty acid oxidation were better even when someone was not exercising. In other words, you're burning more fatty acids more efficiently when you exercise in a fasted state versus a fed state. So that would be one benefit to exercising in the morning because most people are typically, and this was aerobic exercise specifically, people are typically fasted in the morning versus afternoon.

However, personally, I've been, so right now I'm fasted, it's 10 o'clock. I have been eating, I've been doing a pretty long fast where I've actually been skipping breakfast altogether and taking my first meal between 1 to 2. Yesterday I had my first meal at around 2:30, and that meal was sardines and avocados. I'm now on my second day of a ketogenic diet. But anyways, I think that, you know, most people are, you know, are not going to do their exercise fasted in the afternoon for the most part. So the caffeine comes into play because caffeine was able to increase fat oxidation during a workout. Similar to what the afternoon exercise does. So, you know, most people, again, are drinking their coffee in the morning.

And so drinking the coffee, and particularly maybe even in a fasted state in the morning, may be a beneficial way to do some aerobic exercise as well. Personally, I do like doing mine in the morning, my exercise in the morning, and when I'm more fasted, and then resistance training maybe Later in like with a more fed state. But you guys can listen to the interview I did with Dr. Satchin Panda, which was released about a month ago or so. We talk about this in more detail. So Alan with an E is mentioning my— the much talked about interview on fasting. That I've mentioned for quite some time. That will be released in the next 10 days, and that's with Dr. Mark Mattson. It's a 2.5-hour podcast, so everything you want to know about fasting will be coming out on that.

It'll be coming out in about 10 days. So that's pretty exciting. Casey in the live chat is asking to hear— curious to hear about my ketogenic diet, why I'm sort of doing that, and, you know, what the benefits are, potential benefits are. Without going into too much detail, so I have noticed that my cognitive performance is enhanced if I am in a fasted state. So for example, the 2.5-hour podcast I did with Dr. Mark Mattson, And I did that completely fasted. And, you know, I think the podcast ended around— I think the podcast started around 9:30 Pacific time or so. And I was— it was just, you know, much easier for me to recall things and to— I mean, I just felt like the words were easier to access and things, you know, things were just easier.

So I've been really doing some experimentation with, with being in a fasted state when I'm doing a podcast or an interview or just really having a presentation and, or just really needing my focus to be, you know, optimal. And so I thought, you know, well, perhaps some of, there's probably multiple factors at play here. One could be the production of beta-hydroxybutyrate, which is one of the predominant ketone bodies that are produced when you're in ketosis. Certainly, there have been studies showing that beta-hydroxybutyrate itself can increase brain-derived neurotrophic factor, BDNF, which in the brain can play a role in improving cognition. I don't know how quickly that would be, if it would be like an immediate effect that I'd be feeling, you know, in the immediate.

You know, in the immediate timeframe because I do feel it like pretty immediately. So that would be one perhaps reason to try the ketogenic diet and I want to see, well, can I, you know, recapitulate some of the cognitive performance effects with the ketogenic diet? Now, I should caveat the ketogenic diet that I'm doing is largely based on getting my fat from polyunsaturated fatty and monounsaturated fat sources. So I'm eating a lot of nuts, which are a good source of polyunsaturated fat and monounsaturated fat. I'm eating a lot of avocados, which are a really good source of monounsaturated fat, olive oil, and olives also, which are a good source of both— of monounsaturated fat. I'm also eating fatty fish like salmon, and I'm eating sardines and mackerel.

So I'm doing less of the butter, dairy, saturated fat type of ketogenic diet. And so we'll see how that works out. I think the other potential reason Yeah. Just to kind of bring this full circle before I go on to the next question, why I feel performance enhancement with being in a fasted state, I think there could be the lack of a postprandial inflammatory effect, which can cause— the inflammation, you know, can— it happens when you eat food, period. I mean, it's just something that happens. It's called postprandial inflammation. And, you know, you're producing cytokines, which cross the blood-brain barrier and can, to some degree, affect neurotransmission and also cause sleepiness as well.

And so I think just eliminating that factor in and of itself, independent of the potential beta-hydroxybutyrate cognitive benefits may also just be something to consider and something that may be affecting my cognition. But again, these are both speculation at this point. Boy, these chat questions are really great. I want to just keep answering them, but I'm going to move on to the next, next big question that was submitted and upvoted. This question was submitted by David, and David asked about My thoughts on the topic of dental and oral health, specifically fluoride and flossing, oil pulling, and other things. I added xylitol to that list. So I'm going to talk a little bit about what the data show, and I'm going to add in some of my anecdote.

which don't necessarily go with exactly what the data show because, I mean, you know, who knows what's going on, but it's still kind of interesting. So I would say, you know, with respect, let's just cover flossing first and foremost. Hands down, flossing is essential. And I also think Waterpiking is. I've noticed, and so has my dental hygienist, that like my gum health and my oral health in general is improved if I do both Waterpik and floss. And if I just take out the Waterpik and continue flossing, there's a little bit of a degradation, or as you might say, in my gum health. So I've now gone back to making sure I do the Waterpik and then add the flossing in addition to that. And I think that I do Waterpik once a day and I floss twice a day.

But at the very least, doing Waterpik and floss once a day, I think, is essential. And probably if you were to pick a time to do it, it would be before bed. A lot of these bacteria are on a circadian rhythm and they're very active at nighttime when you're sleeping. So I do think that those are essential things to do. Flossing, obviously, Just like the Waterpiking gets the food out easier, flossing does as well, but also the plaque and the just physical friction force on the teeth, in between the teeth, helps with gum health and helps get the plaque out. So I think that those are just tried and true for sure. So let's talk about the fluoride. The American Dental Health Association recommends brushing teeth twice a day with fluoride toothpaste.

And there's been some concern also about the drinking with the fluoridated water, but also the American Dental Association recommends drinking fluoridated water as well. Communities that have fluoridated drinking water have 25% fewer cavities than communities that do not. And the CDC has said that fluoridation of drinking water is one of the top 10 public health achievements of the 20th century. So that's an interesting sort of piece of data. There's obviously— it's obviously possible to get too much fluoride, you know. So while too little fluoride could affect bone health and your teeth, And weaken teeth and bones. Too much can do the same thing. It can cause discoloration. It can weaken the teeth and bones and can cause joint stiffness and joint pain. How much is too much?

Well, the epidemiological data suggests that fluoride toxicity begins after long-term exposure to fluoride in the drinking water in concentrations that are 4 milligrams per liter. So the U.S. national standard is 4 milligrams per liter. Most natural drinking water sources have 0.2 milligrams per liter of fluoride. In the United States, let's see, people brush their teeth— as people brush their teeth with more fluoridated toothpaste, The recommendation for fluoridated water drinking sources went from 0.7 to 1.2 milligrams per liter. So it wasn't as high. There've been some controversy about fluoridated water and the association of a rare type of bone cancer called osteosarcoma. There've been animal studies that have shown that high doses of fluoride can increase osteosarcoma.

Human studies have failed to show this association. However, it's a very, very rare cancer in and of itself. Only 400 cases per year are diagnosed in the US. So, it could just be that there's not enough— it's underpowered to find the association. But again, it's extremely high doses in animal studies that are just not even really relevant. There have also been some studies linking intelligence, a drop in intelligence IQ quotient, with a high level of fluoridated water. So there was a 2012 meta-analysis that found high levels of fluoride in the water correlated with children that had 0.5 lower IQ in Asia. The levels of fluoride in the water in those studies were as high as 11 milligrams per liter, which is almost 3 times what the US standard was with the 4 milligrams per liter.

So, it's hard to know if that's really something to be worried about in the United States with respect to the fluoridating water or not. I personally, when I became pregnant, decided out of an overabundance of caution that I would filter my water, fluoride out of the water, and also switch to a non-fluoride toothpaste, in which case I switched from fluoride toothpaste to xylitol. And this is where, if you look at the published research on xylitol, xylitol gum chewing has been shown to reduce the amount of Streptococcus mutans in the mouth. That's the main bacteria that contributes to plaque, contributes to cavities. And it can also lead to potential heart infections in susceptible individuals.

So that sort of bacteria can actually travel in the circulation and get to the heart and cause heart problems. I personally had a— here's where my anecdote comes in, and that is I was using fluoride toothpaste Before getting pregnant, I was also not chewing xylitol gum. But when I did switch to the xylitol toothpaste and the xylitol gum, I've never had any problems with cavities showing up again since then. Whereas before, even though I wasn't eating refined sugar, I still was having like, you know, a little bit of, oh, you've got some little cavities that are showing up. So I was still once in a while having some problems with cavities. That has completely 100% gone away. It also was reversed, strangely, 2 cavities that were found on an X-ray before I was pregnant.

A few months after I gave birth, I went back and those cavities were no longer on the X-ray. It was gone. We couldn't explain why. I hypothesize it's because of the xylitol chewing gum and/or toothpaste, but I don't know for sure what caused that and why they went away, but they did. And they've not come back since. No cavities have come back since, and my oral health has been— it's just like the plaque's been really great. So I've continued to just use my xylitol toothpaste and my xylitol chewing gum. Also, the oil pulling thing, There's been some, some studies that, um, you know, the oil pulling can reduce plaque and symptoms of gingivitis, and it can reduce the, again, Streptococcus mutans bacteria in the mouth which cause plaque and cavities. Uh, previously I was doing oil pulling.

I was doing coconut oil, and I had added a variety of essential oils that I had found reduced a whole spectra of different types of both anaerobic and aerobic bacteria that live in the mouth. And still, my oral health— at the time I was doing that, I was doing fluoride toothpaste. I was not chewing xylitol gum. I was not taking xylitol toothpaste. And my oral health is much better now than it was when I was doing the oil pulling and the fluoride toothpaste. So I'm just telling you from my anecdote. I'm continuing to do what's working for me, which is like the xylitol seems to be like really— effective for my mouth microbiome, and people's microbiome, oral microbiomes are different. So that's kind of what the literature says and basically my personal anecdote.

I have been using— so Nicole's asking what xylitol gum I use. I went from using Pur. I don't know how to pronounce it. It was like P-U-R with like a little That little accent mark over the U. I was using that gum for a long time, and someone sent me something called Xylachew, and I love it. I love the consistency. I love the different flavors. And so I've been using Xylachew. I also use their mints. They have mints as well. So that's the brand I've been using for my gum. I really like it. Xylachew, it's called, and it's great. The toothpaste that I use is— boy, can I even remember the name? Oh, Hello. It's Hello, the Hello brand, and it's the— they've got different versions of it, but it's the one that has xylitol. Abigail was asking what essentials did I use in my coconut oil pulling.

Concoction that I made. I used— there was a variety that I had used. I was using thyme, oregano oil. I was using a little bit of tea tree oil, which after reading about some of the potential effects of tea tree oil on hormones and estrogen-mimicking effects, I'm not so sure that would be a good idea at this point. But at the time I was using it, and I was also using clove oil as well. Okay, so the next question was submitted by Mako, and Mako is asking about acarbose, which recently was in an animal study tested and thought to potentially play a role in longevity. A variety of supplements were tested and metformin and nicotinamide riboside failed, but acarbose passed. And so Mako wants to know my thoughts on acarbose.

So for those of you that don't know what acarbose is, it's a drug that essentially inhibits enzymes in the gut that digest complex carbohydrates. So as a result, complex carbohydrates, the carbohydrates are excreted in feces instead of being absorbed. And so it's— this Acarbose is prescribed for the treatment of type 2 diabetes. The side effect is that there's the increased load of carbohydrates to the large intestine can cause diarrhea, gas, bloating, abdominal pain, because it can also cause damage to the liver. There's a lot of routine blood tests that are done in people that are monitored— people that are prescribed Acarbose, their blood work is monitored for liver toxicity and liver problems as well. If it's taken by itself, it does not cause dangerously low blood sugar levels.

However, if it's taken in combination with other drugs that are used to treat diabetes, it can cause dangerously low blood sugar levels. So I guess that's something else that people that are prescribed acarbose, it's monitored. Clinical studies have shown that acarbose can lower HbA1c, the long-term blood glucose biomarker. It's a biomarker of your long-term blood glucose levels, in that it can lower it by 0.7. Now, let's talk about the life extension or, you know, potential longevity effects of acarbose. So there were studies conducted by 3 independent laboratories by the U.S. National Institute of Aging Intervention Testing Program. They fed mice 1 gram a day of acarbose from 4 months of age.

So Obviously, a pretty high dose if you're talking about human equivalent dose, and also it started from an early age. So this is important to keep in mind, like 4 months of age is when they started. I guess it's an early age, but in a mouse lifespan, you could, you know, I would still consider it, you know, early. Early in life, close, you know, more than I would say midlife. So let's talk about what happened. So the acarbose was shown to extend the median lifespan of female mice by 5% and male mice by 22%. So the 90th percentile of lifespan extension from female mice. So this is like basically, could it extend actual lifespan? So, female mice that were already living long, would they live even longer? And so, that's what I mean by the 90th percentile of lifespan.

It extended the— in female mice, it extended that 90th percentile of lifespan by 9%, and in male mice, it extended it by 11%. However, the maximum lifespan, so, the 99th percent, Percentile was the same for both male and female mice. So, it didn't extend— it did not extend actual maximum lifespan of mice in terms of what they're already known to maximally be able to live to. It did not go beyond that. There were no differences in the causes of death of the mice in terms of, you know, what mice die from? Hepatic lipidosis was lowered significantly by acarbose, so from 27% to 4%, if you look at the pooled data. And in mice, acarbose basically made this finding really significant. So it was more significant in males than in females.

Females already kind of have a low incidence of hepatic lipidosis, so it really didn't lower it beyond that. Limitations of this study, I would say that, you know, humans— the common causes of death in humans versus mice are quite different. The cause of death in most mice could not be established. It is known that one of the most common causes of death in mice is cancer, whereas in humans, cardiovascular disease is the most common cause of death. So, that's one important limitation. Also, there was a handful of male mice that died unexpectedly early. And so, when you remove them from the analysis, the increase in median lifespan in the acarbose group in male mice was 13% instead of 22%. So, I would say, not hugely, you know, big differences.

In females, I mean, it's almost no effect at all in the female mice. In male mice, there was a little bit of a stronger effect for median lifespan. I would say the 22% would have been more robust. But, again, when you take away those mice that died, it was 13%. Which, you know, still is something to consider, I would say, possibly. But I would say we're still just on the, you know, early, early side of understanding this and whether or not it's even applicable to humans at all. It's not something I would start to take. Of course, I'm female, and so it wouldn't make sense for me to take it, but it's not something that I'm going to get my husband on yet either. I think we need to wait for more data to really say that it really is something that could be beneficial, to be honest.

So the next question was submitted by Rachel, and Rachel asked about the topic— revisiting the topic of grains and which grains I consume and whether or not I eat sourdough bread, why or why not, how big of a factor does gluten play in the inflammatory process, and when we talk about inflammation, What are we referring to? So really a big, big question and I would say here that we're going to start with a discussion of something that is known to cause inflammation in the gut and how this may potentially be related to gluten. So zonulin is something that is released by enterocytes, which are your gut cells, either when there is bacterial overgrowth in the small intestine. You're not supposed to have bacteria in the small intestine.

They're supposed to be in the large intestine where you're mostly in the colon, so the very distal part of the large intestine, which is, which is the colon. Um, so when there's bacterial overgrowth in the small intestine, this can cause basically zonulin to be released by gut cells and And that can trigger— what that does is breaks down the tight junctions in the gut epithelial cells, and it can compromise the gut barrier very, very transiently. It happens quickly. It's resolved in a matter of minutes in most people, with the exception of people that have celiac disease or people that have a really strong— are having a really strong immune response and inflammation, perhaps people that have— other type of gut issues like IBD or even autoimmune, other autoimmune-related conditions.

So the other thing that can contribute, that can activate this very same thing is something called gliadin, which is a component of gluten. So, so gluten itself can cause zonulin to be released, which causes this transient opening of the, the, the the gut barrier, the gut epithelial cells, the tight junctions in between them. And so again, this is something that in most people does not cause an issue. It's super quick. And with the exception of people that have obviously celiac disease, that is one of the reasons why gluten is like super bad for them. But there are people that have gluten sensitivities that are that are— that don't have celiac that can be sensitive to this process as well. So the question is, well, if this happens with gluten, then wouldn't you just avoid it?

And, you know, because if there's any type of opening of these tight junctions and any type of potential inflammatory response happening, that would be bad. And so, I mean, that's my thought as well and the question is we need to look at the data because If it indeed was bad, then you would assume you would see increased markers of inflammation in people that eat gluten and you would see negative health consequences. So let's look about— let's look at some of the data. So if you look at the effect of consuming grains, whole grains, which have lots of fiber but also have gluten, and you look at the effect on all-cause mortality. So there was 2 studies that looked at whole grain consumption and all-cause mortality. between 1980 and 2010. These were large studies.

One involved 74,000 women and the other involved 43,000 men. They found that higher whole grain consumption is associated with lower all-cause mortality, lower cardiovascular-related mortality in both men and women, independent of other dietary and lifestyle factors, including vegetable intake and exercise, which would have been my major argument. Well, oh, whole grains are just biomarking Your other healthy lifestyle factors. But they corrected the data for that. So that's interesting because, you know, you're seeing a lower all-cause mortality, a lower cardiovascular-related mortality after correcting for other healthy lifestyle factors in people that consume whole grains, which theoretically they have gluten and theoretically would, you know, potentially cause a little bit of zonulin to be released, which could transiently affect things.

But again, it's super quick in most people. So that data argues, well, it's not really having a negative effect on people that are consuming whole grains because they're having a lower all-cause mortality than people that don't consume them. So the other thing would be, okay, let's differentiate, obviously, let's differentiate the whole grains from the refined grains, of course. People that are— In a study involving 11,000 women, people that consumed 4.7 grams of fiber from whole grains per 2,000 calories eaten had a 17% reduction in all-cause mortality. This was not the case— sorry, the first study I mentioned was not comparing it to refined grains. It was just eating them or not eating them. This is comparing it to refined grains.

People did not have a— people that were consuming refined grains did not have a reduction in all-cause mortality, in fact. And there was also an increase in inflammation in people that were consuming refined grains. So— and yet another study showed this, and even people that were type 2 diabetic, a lower— between 16% and 30% lower all-cause mortality in people that had the highest intake of whole grains. Another study looked at actual blood biomarkers of inflammation including C-reactive protein, fibrinogen, and other inflammatory biomarkers. And they found that after adjusting for other dietary and lifestyle factors, whole grain intake was associated with lower inflammatory biomarkers in blood cells, whereas refined grains were not. Big surprise.

So whole grains in these studies were basically oats, quinoa, brown rice, Whole grain bread, refined products were, you know, our white breads, many cereals, dessert products, and cookies, and crackers, and things like that. So the all-cause mortality data seems to suggest, you know, you'd think if it was so bad, you wouldn't see a reduction in all-cause mortality. So, you know, that's the kind of one piece of data that keeps me going, well, I don't know. Yeah. Is it that bad? I mean, there are reasons people may avoid doing it, like if you're trying to do a ketogenic diet and you're wanting to keep your blood glucose levels— by the way, I will tell you, after wearing a continuous glucose monitor for over 3 years, at least 3 years, maybe a little bit over, whole grains, if I eat, for example, 2 slices of sprouted whole grain bread and my blood glucose levels, you know, go up to like maybe 123 postprandial, go up to like 123 and then go down pretty quickly.

It's really not a huge, huge spike. You know, it's not like, it's not super detrimental. If the sprouted whole grain bread is added with some protein, that blood glucose spike is even lower by about 5, I would say 5 points. So to me, you know, it's not like a huge problem for my blood glucose levels. Now, that was something I certainly couldn't do if I was trying to do a ketogenic diet, which is what I'm experimenting with right now. But in terms of overall health, I'm not sure it's something to really obsess about. Now, with respect to like white, you know, refined bread, like white bread, the other day was— we had a long day of filming and I got a sandwich at a place that had— it was just like white bread.

And I was like, okay, well, I'm going to experiment with this and see what happens with my glucose monitor. It's a turkey sandwich with avocado, turkey, a little bit of bacon. I mean, I make these at home with my sprouted whole grain bread. And again, I told you my blood glucose levels don't— they probably go up to around 119 or so with the protein in between the 2 slices of bread. My blood glucose levels went up to like 180 with the 2 pieces of white bread. It was unbelievable. I was losing it. I was like, this is crazy. I can't believe how much of a difference. the refined carbohydrate makes with respect to my blood glucose levels. So I do kind of— there is an argument to be made with respect to that.

There was another study, the Framingham study, that followed 3,000 middle-aged adults and found after 4 years, basically, their— Diabetes. They assessed their diet, their waist size, blood pressure, blood sugar, triglycerides, HDL cholesterol. It was found that basically for every 4 years, waist size increased by an average of 1 inch in those that ate very little whole grains compared to half an inch in those that actually ate 3 or more servings of whole grains a day. So people that were eating more whole grains had, you know, they weren't having their waist size increased every year. You know, there was about a half an inch reduction in waist size increase per year.

And there was also blood sugar and systolic blood pressure benefits in people that were eating 3 servings or more of whole grains a day. There was triglycerides improvements. So these results were still significant after accounting for other dietary and lifestyle factors like alcohol intake, fruit intake, vegetable consumption. So again, you know, it seems as though you would imagine if whole grains were so bad and causing this inflammation that you would see it. And again, with that study that I mentioned, the inflammatory biomarkers were measured in people that eat— that were eating the highest intake of whole grains, they had lower markers of C-reactive protein and fibrinogen and other blood biomarkers of inflammation. You know, I can't explain that.

If it was so bad for most people, then you would expect to see data showing that, and that's just not what we see. So I think, again, it's one of those things where maybe people that have a sensitivity to gluten because they may have some underlying gut issue, dysbiosis could be one, the IBD, inflammatory bowel disease. You know, irritable bowel disease, obviously celiac disease. But you know, there's a there's a wide variety of issues that can cause you know gut problems. Perhaps that would be a specific population of people that may benefit from from removing whole grains. But other than that, it seems as though I'm having a hard time. I'm having a hard time really making the argument that eating whole grains are bad for you, especially just looking at that data.

That doesn't mean that there isn't a benefit for cutting it out and trying something like maybe a ketogenic diet, but, you know, and then there's also the potential— well, we don't have the data to look at people that are eating more of a paleo-style diet, people that are eating— healthy vegetables, you know, whole vegetables, whole fruits, whole vegetables, and, you know, lean healthy meats and maybe even some healthy types of fatty meats and fish and compare that to someone who's eating the same diet with addition of whole grains, like we don't have that data. So we don't know, is there an even more optimal diet?

Like perhaps, but I think what we can say right now is that eating whole grains along with the healthy— other healthy, you know, healthy dietary factors is not detrimental and it certainly isn't leading to a higher all-cause mortality. It's not leading to higher biomarkers of inflammation. So— and as Ella is pointing out here in the live chat, whole grains are also part of the healthy Mediterranean diet. Exactly. So, you know, I think there's an argument to be made to avoid them with maybe some people that are pre-diabetic and maybe— I mean, even at that, I mean, I think the fiber itself is beneficial and helps slow the blood glucose response. But, you know, I think— I'm not sure that it's necessarily bad. And Becky is reminding me about the other part of this question, which is sourdough.

I need to do some experimentation. I'm sort of embarrassed to say that I haven't. done it with my continuous glucose monitor. I did— one of my former colleagues, Mark Shigenaga, he's a brilliant researcher and, you know, gut microbiome, gut expert. He was doing some research back when I was a postdoc at Children's Hospital in Oakland at the research institute there. He was doing some experiments with— sourdough bread and looking at the effects, and he was using animal models, but looking at the effects on inflammation and microbiome composition. And some of his preliminary data was suggesting that because there was a high lactic acid content in the sourdough bread, that it was having a beneficial effect on the microbiome.

And that in and of itself may negate some of the negative effects of, you know, the other part of the sourdough bread, which is more refined. So the fermented part was good. And in fact, also might even have a positive effect on gut health, gut cells themselves, because as Mark showed, and I think he's just submitted this paper for publication that these short-chain fatty acids themselves, including lactic acid or acetic acid or malic acid, or their base counterparts, which would be lactate or acetate or malate, could essentially be shuttled into the mitochondria in gut epithelial cells and basically be used as energy. So the gut cells were actually healthier. And so this was actually an interesting— another interesting potential benefit as well.

So I guess what I'm going to have to do is experiment with the sourdough bread in terms of my blood glucose levels and see what effect that has, you know. And there are different types. Like I've had sourdough bread where it's like, okay, this is sour. And I've had sourdough bread where I'm like, is this white bread? I mean, is it, you know, it doesn't taste like sourdough. Are they like pulling one on me? Or, you know, so I do think that that needs to be— that's probably another issue as well. Like you might have some that are a lot more fermented and obviously more lactic acid would be better. So it's— my guess would be that it's better to have the sour-tasting bread versus the— Is this actually sourdough tasting? Is this actually sourdough bread type of bread?

So this leads me into the next question, which is kind of related. And this question was submitted by David. And David asks, how do fermented foods survive stomach acid? And is there a benefit to the microbiome when eating fermented foods? And he linked a pretty recent study from Drs. Justin and Erica Sonnenburg, who I had interviewed many years ago, about 2015. I interviewed them on the podcast. You can go back and listen to that old episode if you want. They're experts on the gut microbiome, do a lot of work on animals, but this specific study was done in people. It was a small study. And it was a 10-week study that was done in 26 adults.

So before I get into what the study showed, which is essentially that fermented foods are beneficial for gut health and overall health potentially, I want to address the question about fermented foods, which mostly would come down to probiotics in the fermented food, surviving stomach acid. And I will say that, you know, yeah, there's probably going to be some degree of, you know, you're going to lose some of that. You're going to lose some of those beneficial bacteria which are often referred to as commensal bacteria. However, a lot of the commensal bacteria thrive in acidic conditions like lactic acid.

You know, these— there are many— a lot of the fermented— a lot of the probiotics found in fermented foods are lactic acid-producing bacteria, which are, you know, which are, you know, optimal— which live, you know, in optimally acidic conditions because they make lactic acid. And part of the benefit of these types of commensal bacteria is that there are other types of bacteria that are not so beneficial that do not thrive in acidic conditions. And so One of the benefits of having a type of bacteria in your microbiome, in your in your gut, in your colon, that produce lactic acid is that that lactic acid is essentially killing off some of the other types of non beneficial bacteria that also reside in the gut. That's one of the benefits. So you know to a degree, yes, some some probably are.

You know you're going to get you're going to get. Fewer of these beneficial microbes that make their way to your gut because they have to go through the stomach acid, and they have to travel down the small intestine and make their way through the large intestine and eventually get to your colon. So yeah, you're going to lose some of them, but some of them make their way there. And as this specific study showed, we'll talk about right now what they showed is that people that ate fermented foods including yogurt, kefir, fermented cottage cheese, kimchi, and other fermented vegetables, and also vegetable brine drinks and kombucha, they had experienced an increase in overall microbiome diversity. And there was a dose-dependent effect.

In other words, people that were eating larger servings of these types of fermented foods that I just listed off, they had a more robust increase in microbiome diversity in their colon. They also found that people eating these types of fermented foods had levels of— there's different biomarkers for inflammation that were measured. 19 different inflammatory biomarkers were measured. And people had— people eating the fermented food had lower levels of these 19 different inflammatory biomarkers, which was kind of astonishing. By contrast, there was a group of people that were given foods that are high fiber, high in what are, you know, what are often referred to as prebiotic. You know, these are things that feed the already existing beneficial bacteria in the gut.

So they were eating legumes, they were eating seeds, they were eating whole grains, they were eating nuts, vegetables, and fruits. And on average, those individuals' gut microbiome over 10 weeks remained pretty— their diversity of their microbiome remained pretty stable. So they didn't have that boost in microbiome diversity after 10 weeks. And they also didn't have the lowering of the 19 different inflammatory biomarkers. Now, this is a 10-week study and it takes a lot of time. Like, you know, your microbiome is pretty stable and it does take time to change those, you know, the bacteria in the gut to a significant level where you start to have effects where you can measure them.

And so I would predict that because it was a short study, 10 weeks, that The boost that was seen in the fermented food groups was pretty apparent because you're already giving the probiotics, you're seeding the probiotics into the gut. So it's much quicker than eating foods that are high in these prebiotic fibers which take a much longer time to increase the microbiome numbers and then perhaps which would translate to effects on inflammatory biomarkers as well. So— And that's what the Sonenbergs speculate as well, basically, you know, that they basically would have to do this study, you know, do it much longer, perhaps for 20 weeks instead of 10 weeks.

But I do think this study is very exciting in the sense that, you know, it seems beneficial to eat fermented foods and a wide variety of them and even ones that are dairy, you know, so yogurt, kefir, the fermented cottage cheese, kimchi, the vegetable brine drinks, even kombucha. So I think that is a great study. We need larger studies to really confirm these effects, but I think it's great, a great sort of proof of principle and also reason to potentially add fermented foods to your diet. I know that's something that I have been doing and will continue to try to do. Joe asks about prebiotic supplementing versus probiotic be better. There've been some studies that have looked at prebiotic supplementation and that while prebiotic supplementation can increase some types of bacteria.

The one concern with that is that it sort of increases one type of bacteria that lives off of that type of prebiotic. And so diversity, you know, is something that occurs when you have different types of prebiotics. And so the one concern would be like if you just take inulin, that you're going to be— overloading your gut with the type of bacteria that, you know, consumes inulin. And so you might have the opposite effect. They do— there are benefits that have been seen with, you know, doing prebiotic supplementation as well as probiotics as well. And someone in the chat, in the live chat, is asking about also probiotic supplementation and, you know, like, would you have the same effects in Yeah.

You know, I think there's something unique about the fermented foods because we don't know exactly all the different types of bacteria that are on these fermented foods. I mean, we know some of them that we're measuring, but there may be a whole bunch that are there that we just aren't even measuring. In addition, You know, these fermented foods have the lactic acid or acetic acid or malic acid in them. And I think Mark Shigenaga's data argues that those short-chain fatty acids themselves are having a beneficial effect on the gut. And that's not something you're going to get from a probiotic. That's not something you're going to get. Now, it is something you can get from eating Maybe a sour apple or, you know, a sour type of fruit which has high levels of malic acid.

But it's not— I mean, the fermented foods have high levels of these short-chain fatty acids. And I can tell you, I know, like, you know, this data is not— it's unpublished and it's mostly coming from a former colleague of mine who happens to be a friend of mine as well. And I mean, his data is pretty clear. I mean, when he, like, just gives these short-chain fatty acids— There are beneficial effects on inflammation and on gut health. So I think there may be some sort of combined, maybe additive, who knows, maybe even synergistic, we don't know, effect where you're getting not only the bacteria themselves in the fermented foods, but you're getting high concentrations of these short-chain fatty acids, these what we call short-chain fatty acids, but lactic acid, malic acid, acetic acid, the things that are in the fermented foods.

Those are beneficial in and of themselves, and so I think there's something magical about the fermented foods that you're not going to get from a probiotic supplement or a prebiotic supplement, or even the whole food from themselves because you're not you know you're not going to have such high levels of of you know those those fermented fermented fatty acid. You're not going to get those those the lactate lactic acid or the acetic acid or the malic acid at such a high concentration that you would. in a fermented food. So that's the long answer. Okay. I'm going to get to some rapid-fire questions. Any concerns with long-term berberine supplementation? Many sources recommend temporary berberine use only. We have a topic page on berberine.

Please go and read it, read through it, because it goes through berberine safety. And, you know, I think— so this is on foundmyfitness.com/topics, or just go to foundmyfitness.com, click on the topics on the toolbar, and it'll take you to the topic pages, which are alphabetized, and you can click on B for berberine and find it. And read all about it because essentially, if you're looking at like toxicity studies in animals, it showed that the dosage required to kill 50% of the mice was 2.0 grams per kilogram per day, which is about 100 times more than what's been used in clinical trials. There's been a meta-analysis of 27 studies evaluating the efficacy and safety of berberine, did not find any adverse effects from berberine supplementation.

in those 27 studies, but the timeframe was basically either 2 weeks to 4 months. So 4 months was the longest timeframe that was studied. And the dose of berberine ranged from 0.6 grams a day to 2.7 grams a day. So at least in the case of like 4 months, I think it seems as though it was not something to be too concerned about with respect to toxicity. I personally, You know, would still probably want to, you know, look into the cycling of it perhaps if I were going to supplement with it as well, just to be on the safe side. But please do go see the topic page. N-acetylcysteine, or NAC as it's called for short, has been suggested for my son. I've been reading about it and it sounds like it can increase glutathione production. Is that correct? What other benefits are there for taking NAC?

Is there a reason why you removed it from your supplement list? So N-acetylcysteine can increase glutathione production, and it can have some benefits specifically in the lung with respect to like asthma or even inflammation in the lung with like respiratory illness as well, which is one reason I sort of was temporarily adding it to my regimen. The reason I stopped it is because There were 2 animal studies that showed giving N-acetylcysteine, granted it was much higher doses than something that I was taking, caused lung tumors in animals that were healthy. Didn't have— these weren't animals that were supposed to get lung cancer. That scared me. And so I sort of Yeah.

So I stopped taking it because I didn't understand what was going on and that was enough for me to go, okay, wait a minute, something might be going on here that we need to understand. So that's the reason why I stopped it. I think there are some specific illnesses and diseases where N-acetylcysteine is recommended in the short term and certainly, you know, maybe something to talk about with the physician and there may be some benefits to taking it in those in those cases. But I'm still sort of— our team is— that's on our list to investigate and do a topic page on N-acetylcysteine and see if that's something that we really should be concerned about. Dan asks about my thoughts on Athletic Greens as a supplement or multivitamin.

It's been recommended by a lot of experts, he says, but it seems to have a lot of proprietary blends, which is a bit of a red flag. I've never tried Athletic Greens. I looked it up a couple of months ago when one of our top subscribers, which comes to our— we have a Google Hangout that happens on the first Sunday of every month where we have a discussion about all sorts of things, and one of the questions was about Athletic Greens. So I looked into it and I saw that it had the blue-green algae, microalgae. And that's always a red flag for me because blue-green microalgae is potentially really a big source of the liver toxin microcystin. And so, I told her, you should reach out to them and ask them to look at their microcystin data. And she did.

And they said, no, we're not going to share that data with you. And to me, I was like, well, That sounds like something I wouldn't take. So that's my thoughts. Cameron is asking about EMF, my thoughts on EMF exposure. I did a pretty detailed review on EMF exposure in Crowdcast number 9 at the very start of that episode. You can go back and listen to that Q&A in your private podcast player, which we call the Aloquat. If you have not gotten that, please go to your dashboard and get it, foundmyfitness.com/dashboard. Listen to that Crowdcast. I'm not going to go into the details. Crowdcast number 9. At that point, which was about a year ago, my review of the data did not have me concerned about my own exposure in my home. All right, another question.

This was a repeat question from multiple women. Simone and others asked, hi Rhonda, I'm a first-time mom-to-be and I'm trying to sift through all the research when it comes to childhood vaccines. Is there a specific vaccine schedule you adhere to with your son? And some people were asking other sort of variations of this question about my using singles and things like that. So basically, I made my vaccine decisions based on the fact that I did not have my son in any type of daycare or childcare settings. In other words, he was not around and exposed to a bunch of other potential viruses through the other children, which are often viral vectors.

If my son was going to be in a daycare or childcare setting, You know, I may have changed the type of vaccines that I had my son get because of the potential risk of being exposed to those illnesses. So that is a very important thing to consider is whether or not you're putting your infant and/or toddler into a daycare setting where they potentially will be exposed to illnesses that could cause harm. So with that in mind, that was not the case for me. I decided to go with the vaccines that are required for kindergarten in California. So that includes polio, the DTaP, which is diphtheria, tetanus, and pertussis, and measles, mumps, rubella, the MMR, hepatitis B, and the varicella, which is chickenpox vaccines. I did those.

When I said that I have done them, decided to do them in singles, what I meant by that was essentially you can have the option of combining the polio vaccine with the DTaP, and I decided not to combine all those things. It was like, well, DTaP has enough stuff in it already. So I was doing each of these by themselves. That's pretty much what I did or decided to do. Another rapid-fire question was from Gal, who says, sorry for more COVID questions, but as Delta is becoming more prevalent, I'd love to learn any info on outdoor transmission. While earlier strains are much harder to catch outdoors, Delta is Much more transmissible, so I'm assuming outdoor risk might be more of a possibility too.

She says she's weighing how many outdoor activities to do with friends, playground visits, things like that, going to the zoo. So trying to weigh risk versus, you know, basically looking at their level of risk. So there is a greater viral load And which means transmission is much, much higher with the Delta variant. So like the original, if you can call it original, the original strain that was circulating in the United States when this pandemic first started, there was an R-naught, which is what is the jargon that's used to define the transmission rate, like how many people become infected from a single person that that's infected. So the R-naught was 2.5. In other words, for every 1 person that was infected, they would infect 2.5 other people.

Now the R-naught is between 5 and 6 for the Delta variant. So for every 1 person that is infected, they go on to infect 5 other people, perhaps even 6, 5 to 6 other people. So in each of those 5 to 6 people then go on to infect 5 to 6 more people, which is why the caseloads are going up quite rapidly. So there is more viral transmission, and that also is linked to the fact that there's more viral load. And so in any case where there's more viral load, viral transmission goes up. And so the thing about being outdoors is obviously that's diluted. I mean, when you're outdoors, the amount of viral particles being expelled into the air is diluted greatly.

Personally, I still think, you know, being outdoors is, for the most part, you know, safe as long as like someone's not like coughing on your face or sneezing on you, or you're not in a like crowded packed concert kind of thing where you're just really close to people that are like breathing on your face and stuff. You know, so I'm, I am right now avoiding you know, situations like the zoo or going to like an amusement park or, you know, places that are much more crowded while there is a surge in cases and with a Delta variant. I think it's just probably safer to stay out of those situations. I still feel pretty safe having people come outside. And again, You know, the effects of the virus on, like, surfaces is also a whole different topic.

You know, we know that most of the transmission is not coming from catching it from a surface like you do, for example, rhinovirus or influenza, where it stays on surfaces for a long time, and that's, you know, particularly where people are catching it from. It's mostly this aerosolized transmission that's happening with— With the SARS-CoV-2 virus, the UV sensitivity of the SARS-CoV-2 virus is much more sensitive than influenza. So, for example, SARS-CoV-2 is 3 times more sensitive than influenza, and 90% of viral particles on a surface are inactivated after 30 minutes. Inactivation of the viral particles starts at around 10 minutes. And so, like, if you're talking about things like playgrounds and stuff, they're just being— the viral particles are just being killed.

Killed by the UV in the sun. But I would still be careful personally with playgrounds because you never know if 2 children are up close to each other and one coughs right in the face of another child and stuff like that. That's kind of hard to control. Things like that happen. And that's, I think, the biggest reason to be more cautious at this time. But I still feel pretty safe that outdoors is definitely safer. Another question. This is very rapid fire. Santosh asked about mushroom supplements, how they— some of them contain lead. Are there any brands that I like and I think are safe? I personally take Layered Superfood Performance Mushrooms.

And the other one I had previously taken that was pretty good was this Four Sigmatic, but some of their mushrooms, like powder stuff, have like too much sugar and they were raising my blood glucose. So I stopped using their products. And last question, rapid fire on my list, was from Eddie, who was asking about consuming organ meat, liver, kidneys, which types? How often to take them, if they're safe and effective. So personally, I think— so there's a lot of great micronutrients that you can get in a variety of different types of organ meat like liver, heart, and kidney. But there's also like you can get too much of them like if you're eating them like every day. So you don't want to get too much of the copper or the vitamin A or— or iron. That's really hard to do.

I mean, you'd have to be eating a lot of them every day. But personally, what I do is I like to do like maybe once a week and I order a type of ground beef from US Wellness Meats that has liver, kidney, and heart in it. And it's like hard to really taste it, especially if you like, you know, mix it up with like a sauce and— or you're making like a chili with it or things like that. Or you're making spaghetti with lentil noodles or something like that. It's a great way to get the organ meat in family members that will just not eat it otherwise. So that's sort of my thing, but again, I typically have a very micronutrient-diverse diet, getting a lot of micronutrients from plant sources.

So people that do not do that may consider eating, you know, the liver, heart, kidney on a more, maybe more frequent basis than I do. Some of the questions in the chat here. Sverdu is asking about out of the 3 vaccines available in the US, Which one did I take and why, and what would be the best option for a healthy male in their 30s? I'm personally—I was personally wanting to take either the Pfizer or Moderna mRNA vaccines. I got the Pfizer because that was what was available to me. But now looking at some of the data on the protective effects of both of Moderna or the Pfizer vaccine on the Delta variant, it seems as though Moderna seems to be more protective.

And so perhaps if I was not vaccinated but, you know, going to get vaccinated at this point right now, I would probably try to get Moderna because it looks as though it might be a little more protective. But it's unclear. So I will say this. There was a really big study that was published out of Israel that looked at thousands of healthcare workers and these so-called breakthrough infections. Of course, in Israel, they used Pfizer, so this was the Pfizer vaccine. They looked at breakthrough infections, and they measured antibody levels and found that the breakthrough infections were occurring in individuals that had a much lower neutralizing antibody titer than individual healthcare workers that had higher levels of antibodies and were not getting these breakthrough infections.

They were not getting infected with SARS-CoV-2. This was before Delta, but still, the proof of principle is that, you know, the antibody titers were absolutely linked to breakthrough infections. And, you know, what we know now is that these— the neutralizing antibodies do wane over time. And, you know, 6, 7 months out, that, you know, you're having much lower levels than you did, you know, 3 months out. But in addition to that, there are many different individual responses to antibody production from a vaccine. For example, older people have a much more blunted antibody response than younger people do. Things— dietary lifestyle factors affect it as well. Like one night of, you know, like lack of sleep can like lower your antibody titer by like 50%. I mean, it's insane.

So there are available antibody tests. I know Quest does one. LabCorp as well. People can measure their antibody levels. Right now, the government recommends not doing that for this purpose of trying to figure out if you have high enough antibody levels to be protected from SARS-CoV-2 infection. However, in the future, that may change. The CDC and other— the FDA may decide, oh, maybe this will be a good thing to do to see who might who should be available for a booster shot versus who still has higher levels. Just as an anecdote, I'll tell you, I've got these at-home antibody tests that I do, IgG and IgM, and they're very— it's like a pregnancy test where a line shows up if you have them versus not.

And, you know, you can see like there's the concentration, you can see like visually see differences. Now, if you do an actual blood test from LabCorp request, you'll see, like, you'll quantitatively get a number, which is much better. But, um, I, I myself, um, my husband and my mom, we've all been vaccinated with Pfizer. And, um, my mother was fully vaccinated at the beginning of March, and my husband and I were fully vaccinated mid-May. And, um, we did this antibody test like a week and a half ago, and my husband and I's IgG antibodies were like We had a very strong signal, and my mom's signal was extremely hard to pick up, which made me a little worried. But, again, anecdote, not quantitative, visual only, you know, so there's no telling what could be going on there.

But we do know from the Israel study that people with lower antibody levels were much more likely to have a breakthrough infection. So just an interesting, I think, Yeah. You know, little piece of data. I'm just looking for any more questions in the chat here. I see some people asking about the omega-3 to omega-6 ratio. You're going to be so happy we get all into that in the podcast with Dr. Vilhara. So that will be coming out soon. And I also see someone asking about fish oil and potentially, you know, lowering your dose before surgery or like, for example, a pregnancy— sorry, giving birth. We also get into all of that, and Dr. Bill Harris thinks there is no reason to do that, and in fact, it might be protective to actually have the fish oil. So he gets into all that as well. Wow.

And so that's something you guys will really enjoy this podcast. It was really, really good. Mary's asking which at-home antibody test I use. I got it when the pandemic first started from a friend that works at a company, and it's not something that's like commercially available. So they work in China. It's Lungene. Lunggene is the name of it. And I got it at the start of the pandemic from a friend. So, but on that note, I will say I did also buy a bunch of rapid tests to do, to have at my house if someone is coming over and they've been traveling or they're not vaccinated. I think the rapid test is a great thing to have to give you sort of peace of mind that they aren't currently infected with SARS-CoV-2. All right. I think that wraps up this Crowdcast.

Really, really, really interesting Q&A session today. A big thank you to all you guys who submitted really interesting questions, and an even more big thank you to all of you that are here live today because The chat questions today were exceptional. They were just—they were—they were superb. I really enjoyed them. Again, please make sure if you want to catch a part of this this episode again to to make sure you have your private podcast player. You can find that on your on your dashboard, foundmyfitness.com forward slash dashboard. We'll be sending out an email summary. With a link to the YouTube video and also links to different time points in this episode, which are also available on the private podcast player as well.

When you open up that episode, you'll see links to it in the description area. And please submit your questions for next month in the correct area, which is the Ask a Question area. Make sure you scroll through the questions that have already been submitted so that you can vote on them and we don't have repeats. And the chat itself, I do see people like to post questions there, but the chat itself is really for the day of the Q&A. That way I can scroll through these and answer all the questions. So, okay, that's it for this episode. Thank you so much. I will talk to you guys next month. I, in about 10 days, will be going on Joe Rogan's podcast talking about all kinds of interesting stuff. So that's something to look forward to, to hear me talking again for, you know, another 2 to 3 hours.

3 hours, I guess, is what his podcasts are. So you guys can hear from me then. We got these great podcasts coming out. Mark Mattson, Got another one coming out with Dr. Ashley Mason, who is a collaborator of mine on sauna research, and this Bill Harris podcast on omega-3. So, talk to you guys soon.