Q&A #30: Can Rapamycin Extend Lifespan—and Should You Take Daily Aspirin?

Hi everyone, nice to be here. Welcome to Crowdcast number 30. For those of you who are new, we have these Q&A sessions once a month, usually on the first Saturday of the month. People submit questions, usually in the Ask a Question section here, and others can vote on those those questions that were submitted. I go through the questions and choose questions based on a variety of factors: interest, votes, as well as how many times I've been asked the question, maybe my own interest and whether or not I want to dive deeper and learn more about that. So that's kind of how I choose the questions. Today, what I do is I go through and we do a deep dive on a few questions, and then I also, towards the end of the Crowdcast, I will answer some rapid-fire questions.

These are usually things I can sort of quickly answer in sometimes a couple of sentences or one sentence or even a word. The live chat is great. People can ask questions, you know, live based on a topic that we're already discussing. These are recorded and available for view and audio listening later, so you can You can listen to the audio on your dashboard, your members dashboard. You'll find that at foundmyfitness.com/dashboard. So you can listen to it directly on the dashboard. You can also, if you've downloaded your private podcast feed player, you can listen to it there. We send out an email summary with a timeline and some links to references of some of the studies discussed, and with a link to the YouTube video if you want to go ahead and watch the video as well.

So that's all available to you guys. So for those of you that can't make the live chat, a lot of members will just watch it later or listen to it later. I like to answer some of the questions in the chat along the way, so I'll take a look as we go. So I'm going to start today with a a question about taking daily baby aspirin. So HC asks, do you think daily baby aspirin is beneficial for health? So just as a reminder, I'm not giving any medical advice or medical recommendations in these Crowdcasts. So this is me and my team just doing sort of a literature review, talking about what the current data says, maybe what the old data said, if there's been any changes.

Sometimes it's my opinion, my thoughts, but it's certainly not medical advice, and you should always speak with your physician about any type of lifestyle changes or medication changes that you're going to make. So the daily baby aspirin story is kind of an interesting one because for quite a while now, it's been recommended by physicians for prevention of heart attack or stroke, but there's been some recent evidence that have come out over the last couple of years that have suggested maybe there could be a harm versus benefit in terms of taking a daily baby aspirin in some people. So daily baby aspirin, and this is like baby aspirin is kind of a way of just saying low-dose aspirin.

It was recommended by the US Preventative Services Task Force for all adults ages 40 to 59 to reduce their risk of a heart attack or stroke. And this was really based on evidence from it reducing the risk of a second heart attack or stroke in people that had previously had one. So this recommendation has now changed this year because data showed that there was some life-threatening bleeding that was nearly equivalent to the benefit of preventing heart attacks or ischemic strokes. So the number of people needed to treat or prevent one major cardiovascular event over a 7-year period is 284. And by comparison, the number of people needed to treat or cause one life-threatening bleeding is 299.

So the— now the U.S. Preventative Services Task Force recommends that if you are 40 to 59 years old, you should have a conversation with your physician about starting daily baby aspirin. And the benefits of taking daily baby aspirin could still outweigh the risks of bleeding in some people with certain risk factors, such as those that have had a previous heart attack or stroke. However, it may not be the case, you know, for people that have never had one of those. Maybe they don't need to actually start taking daily baby aspirin as a preventative measure. The American College of Cardiology and American Heart Association have similar recommendations, but they extend it up to adults 70 years old.

So those over 60, according to the U.S. Preventative Services Task Force, or 70 according to the American Heart Association, are recommended not to take daily aspirin, and these are people that have not had a previous heart attack or stroke. In addition to the the bleeding risk, there's been a recent meta-analysis showing an association between aspirin use and the development of heart failure. So aspirin use was linked to a 26% higher risk of heart failure in people that had at least one predisposing condition, and the predisposing conditions were smoking, obesity, high blood pressure, high cholesterol, diabetes, and cardiovascular disease.

So people that had just one of those and took daily baby aspirin had a 26% higher risk of heart failure compared to people that didn't take daily aspirin that had one of those predispositions. People that took daily baby aspirin that did not have any of those conditions, there wasn't an increased risk of heart failure over the time studied. So I think, you know, that was an observational study. Really, randomized controlled trials need to be done to really definitively improve a causative you know, factor there with the daily baby aspirin. But I think there's enough evidence to really sort of have, you know, some awareness that maybe, you know, this daily baby aspirin should be discussed on a case-by-case basis with your physician.

It's something that necessarily isn't a blanket overall good thing for everyone to do. So additionally, there was another large randomized controlled trial. This was over 19,000 people from Australia and from the United States. That study found that older adults that took 100 milligrams of daily aspirin a day were more likely to be diagnosed with advanced metastatic cancers, and they were more likely to die from cancer compared to those that were taking a placebo. So this is a randomized controlled trial. This is, this is different than an observational study. It is able to to some degree establish causation. It's important to realize though, the— there was no difference between people taking the 100 milligrams of aspirin daily in terms of just new cancer diagnoses.

The difference was that the people that were diagnosed with cancer, it was late, it was already like metastatic, it had already— it was more likely to have spread to other tissues. Maybe this has to do with the effect of aspirin on You know, the blood clotting and stuff like that. So, you know, I don't— the mechanism isn't quite known, but what was definitely clear was that there was an increase in metastatic cancers and also in the risk of dying from cancer. So I think, again, it's just— it's one of those things where, you know, if you're already taking daily baby aspirin on Per a physician's recommendation, that would be something not to stop doing, but to discuss with your physician. Again, some people do have benefits from taking daily baby aspirin.

So it's not, you know, this isn't something that it's like, oh my gosh, no one should ever take it, or if I'm taking it, I need to stop. It's just something that, you know, well, there's some new data out and there's been some new recommendations. Doesn't apply to everyone, but it is something to bring up to a physician, you know. when, if appropriate, basically. Chad is asking in the chat, besides the risk of bleeding and heart failure, does aspirin have the same negative effects of other NSAIDs or nonsteroidal anti-inflammatories, as I've mentioned before, like ibuprofen? So generally speaking, no, the data has shown that aspirin does not have the same negative consequences on increasing stroke risk because aspirin is not necessarily a what's called COX-2 inhibitor.

It does affect COX-1, but not COX-2. So classically, a lot of these nonsteroidal anti-inflammatories like ibuprofen and some of the stronger ones like naproxen, They affect— they are inhibiting a pathway called COX-2, which affects nitric oxide produced in your blood vessels. It affects a variety of, you know, prostaglandins produced and things like that. And it is part of the anti-inflammatory effect, but to some degree, it may be a little bit overkill. So it is different in that regard from other classical nonsteroidal anti-inflammatories. Okay. I see someone asking in the chat. This is Jim asking about the omega-3 effects on COVID health that I have discussed in previous Crowdcasts.

I don't know which Crowdcasts off the top of my head, but those are available with timelines on the YouTube video, and also we send out these emails. So if you've been a member and have been receiving the emails, then I would search your email. But in a nutshell, some of the stuff that I've talked about was preliminary data showing from Bill Harris's group that the omega-3 index, which is a marker of omega-3 fatty acid content in red blood cells, that was associated— so a higher index, meaning the more omega-3s you take in, higher omega-3 index, the lower the severity and mortality from COVID-19. I mean, it was pretty severe, like, reduction in mortality. I mean, it was like 70% or something lower mortality rate.

Some of the other data was not human data, but it was some interesting in vitro data showing that DHA— no, EPA could basically keep the receptor binding domain of the spike protein in what's called a closed conformation. So there's about 26 spike proteins on the surface of a SARS-CoV-2 viral particle. And each of those spike proteins have receptor binding domains. And the receptor binding domains, they kind of— you can think of them as a door. They kind of swing open and shut, open and shut. And much like a door, in order to enter, you have to have the door open. Well, the receptor binding domain has to be in an open conformation for it to bind to the ACE2 receptor, which is the receptor that the spike protein binds to.

So the omega-3 fatty acids, EPA, was shown to keep the receptor binding domain in a closed conformation, rendering it unable to even latch onto the ACE2 receptor. Again, this is in vitro data. We don't know how relevant this is. Personally, I found it fascinating, absolutely fascinating. So that was some of the stuff I've talked about in the previous Crowdcasts. Okay. Okay. The next question, deep dive question, was about rapamycin. And HC also submitted this question. So sometimes I choose questions that I kind of want to dive into, and this is one that I was interested in. So the question HC asked was, can you tell us your thoughts on rapamycin? I keep hearing how amazing it is. It is easy to get, or is it easy to get? Any opinions here?

So, I personally have also been quite interested in rapamycin for some time. For those of you that aren't familiar with it, rapamycin—there's also—it's also sometimes called sirolimus. Sirolimus—it's an analog, and its analogs of it. There's some other analogs of rapamycin that they basically. Are used to prevent organ rejection in kidney transplants, people that are getting a kidney transplant. Rapamycin is also used in stents to reduce the risk of blood clotting, blood vessels clotting off. There's another analog called everolimus. That's an analog of rapamycin that's also used in the treatment of renal and pancreatic cancer. So there are several mechanisms. It acts as an immune modulator by inhibiting IL-2 transcription. So then it has a downstream effect of blocking T-cell activation.

This prevents kidney transplant rejection, among other things. Also, you know, it's sort of a very strong anti-inflammatory. In other cells, it can inhibit mTOR, which is an anabolic pathway that you want active in certain tissues like your muscle because it plays a role in muscle growth. in strength. But in other tissues, you also— mTOR can be activated, you know, and basically allow cancer cells to continue to grow. So it can play a role in cancer. Turning off mTOR can also stimulate autophagy. So sort of a fasting mimetic sort of effect there. And it's also been shown to increase NRF2. Which is the major pathway that sulforaphane increases.

Animal research has shown that rapamycin, when given to a wide range of lower organisms, yeast, nematode worms, fruit flies, it extends their lifespan. It also extends the lifespan of mice. It extends their average lifespan, so it does not increase their maximum lifespan. So the maximum lifespan of a rodent Of a mouse is about 3.5 years. So, it doesn't allow mice to live longer than 3.5 years, but not every mouse makes it to 3.5 years. So, it does increase the average lifespan, meaning more mice are making it to that maximal lifespan, which is interesting. It really seems to affect healthspan. It has more of a robust effect in female mice than it does in males. And, you know, I would say that it's a slight increase, and it's certainly interesting.

Dr. Matt Kaeberlein is doing a lot of rapamycin research on dogs. He has done a small trial where he showed 24 dogs given rapamycin had improvement in their heart function. He's currently doing a larger trial with about 350 dogs to learn more about its effects on delaying aging. So that's something that I will continue to follow. There's no human data showing that rapamycin can prolong lifespan or delay aging even in healthy adults. Healthy adults. So there is an ongoing trial called the Participatory Evaluation of Aging with Rapamycin for Longevity Study. It's the PERL study for short. And this is something that's ongoing. And, you know, I think that as we get data in from this study, it'll kind of add a lot more.

It'll illuminate, you know, this idea as whether or not rapamycin is something that will extend human healthspan or extend human lifespan. There are a variety of side effects with you know, taking rapamycin or one of its analogs. We have a lot of data from people that have undergone kidney transplants that have been on rapamycin analogs. Nearly all renal transplants receiving rapamycin have some sort of skin side effect. The most common ones are hair loss. I have friends that have had, you know, siblings that have taken Right. Taken Cermolius for kidney transplant, and they had significant hair loss, and they were, you know, in their 20s. It leads to acne, fungal nail infections, swelling, mouth ulcers, nose bleeding.

There's also some rare metabolic side effects like low white blood cell counts, low platelet counts, anemia, high cholesterol, diarrhea, new onset of diabetes, and decreased sperm quality. It is technically immunosuppressant, but it doesn't seem to raise the risk of getting more, for example, viral infections. And kidney transplant patients typically take between 2 to 5 milligrams of rapamycin a day. Dosing for any potential anti-aging effects in humans has not been established. And it does not— it's really, you know, it's not known if the side effects will even occur at extremely low doses. It's possible that extremely low doses will, you know, get rid of these side effects. I do— I'm personally— my thoughts are I'm still personally following the research. I'm interested in it.

I'm not convinced that it's the end-all be-all aging. I'm not convinced that I need to start taking it. I think that looking at the mechanisms, some of the low-hanging fruit that can really do similar things to to what rapamycin is doing. For one, you know, the massive anti-inflammatory effect of omega-3s. I mean, you're talking the resolvins, you're talking about the pro-resolving mediators, you're talking about like affecting multiple like resolution of inflammation pathways in addition to lowering inflammation as well. I think there's a lot of potential that has not been unlocked there, and the side effects for omega-3 are, I mean, just so little. I mean, it's just for most people, so little for most people.

So personally, I am currently taking 3 grams a day of omega-3, you know, and again, I don't, you know, I don't know, you know, I don't know whether or not This is very experimental, so I'm not telling you to do that. I also think the sulforaphane, which I take, activating the NRF2 pathway, sulforaphane is very robust at doing that. And then for the autophagy, you know, I'm not necessarily convinced that I want to, like, inhibit mTOR full stop because, you know, it's kind of like that IGF-1 trade-off where, like, you do want some mTOR. So, you know, doing some intermittent fasting, polyphenols, a lot of coffee polyphenols and tea polyphenols. Have been shown to activate autophagy. You know, so I try to do what I can with the low-hanging fruit that I know is at least safe.

Is it going to have the same— we don't know what rapamycin is really going to do in humans. And, you know, perhaps it'll be awesome, but we don't really know. A lot of people were real fired up about metformin. A lot of people started taking it, and healthy individuals that did not have diabetes were taking metformin. And lo and behold, a bunch of new data started coming out where Metformin was not necessarily great for healthy individuals because it was blunting exercise-induced adaptations, which are extremely beneficial for health and for increasing healthspan. So is that possible with rapamycin? Absolutely. Is it possible that rapamycin may be awesome and extend healthspan? Yeah, it is, but we just don't know. So those are kind of my thoughts.

Someone in the chat's asking about what I think about alpha-ketoglutarate and longevity research. I would say that it's like almost non-existent data that has convinced me that it really does anything beneficial. I think there's so little data to make any conclusion with an alpha-ketoglutarate. Anti-Aging Girl, she's bringing us to COVID. She wants to know if there is any data on the difference between Moderna and Pfizer booster shots. So I will give you sort of just a couple of my thoughts. One, we do know for sure that the Moderna booster is— they've reduced what the third shot isn't as much mRNA as the first 2. So Moderna booster shot's 50 micrograms of mRNA, and the Pfizer booster is 30 micrograms.

So Moderna is slightly more mRNA, meaning you potentially could have more of a robust neutralizing antibody response. Because the more mRNA you have, like, the more robust of an immune response you're going to have. And that's been shown at least with the first 2 shots with comparing Pfizer versus Moderna, because Moderna was 90 micrograms in the first 2 shots and Pfizer was 30. So it's 3 times as much. And so it wasn't that surprising that people that had gotten Moderna for the first 2 vaccine doses had much more antibodies, and they had them for a longer period of time, and they were more protected from other variants like Delta variant, for example. I will say this.

Interestingly, I kind of met someone recently who worked for— he's doing some cancer chemo drugs like CAR-T stuff and PD-1 inhibitors and stuff, but it's with Moderna. And He was telling me that Moderna doesn't actually make the vaccines, that they like, they sort of farm it out to like a lot of different other companies. And kind of thinking about this in my head, and this is totally just a thought, is there's no data to show this, but there certainly have been a lot more side effects with Moderna compared to Pfizer. One could be because it is a higher dose of mRNA. And I think that's absolutely probably one contributing factor.

The other is, have a bunch of other little companies making these vaccines, and there has been some links to certain lot or batches of the vaccines having more adverse effects. So maybe it's not like a standardized— you don't have these vaccines being made at a standardized place, a bunch of different pharmaceutical companies making it, and you may just be getting some variation there with, in terms of like something wasn't quite right. I don't know. So to me, I'm a little more prone to wanting to get something more standard like Pfizer. And that's what I got for my first 2 and what I will likely get for my boosters. Just as a little tangent, not to go too far into the COVID world, but I went ahead and got my antibodies levels, my antibody spike antibody anti-S levels measured by LabCorp.

And I think this may have actually been a question Someone was asking in the Crowdcast. Yeah, so I'm going to go ahead and answer this question now. It was Lanice. She said, hi, Rhonda, question on COVID booster shots. I'm here in Colorado and everyone is approved to get booster shots. I'm also pregnant. I'm curious what the data have to say and your opinion on COVID booster shots and getting booster shots while pregnant. I can't find a ton of data on pregnant women getting booster shots. I got my first 2 Pfizer shots in March and April, so according to the CDC, I'm due for a booster. Again, Talk to your physician about whether or not a booster shot is a good idea for you. I'm going to give you a little bit of anecdotal data here first.

I got my antibody levels measured and the test that they used, it was called the Roche ELISA anti-SARS-CoV-2 assay and it was from LabCorp. My levels were 127 units per mL. The assay that was used has a detection range of 0.4 units Yes. Per mL to 250 units per mL. And that's after like some 1 to 10 dilutions of plasma. So people that have 0.8 or less, they're considered negative. So if you have above 0.8 units per mL, you're considered positive for antibodies. I was 127, as I just mentioned, and the detection range goes up to 250. I have not had COVID as far as I know. Looking at some data, you can see that the high-end people that have been previously infected with SARS-CoV-2, that you can get up to 1,000 units per mL. So you can get quite high.

But what I did was I looked at some data from— this was a Nature Medicine paper by Miles Davenport's group. And what his data showed was that in order— they estimated based on looking at a lot of different data that to have 50% protective neutralization, that was roughly equivalent to 54 units per mL. So 50% neutralization was effectively equivalent to about 54. And mine is 127. Yeah. to me, if I'm interpreting that correctly, it sounds like I'm in pretty good shape. I'm probably still going to get a booster. I'm just kind of waiting to see what's happening with this new variant, the Omicron variant. But to me, it looks like my antibody levels are quite good. Even my— I got my last dose of Pfizer back in May.

So I'm having a couple other people get their levels measured to kind of test for that. I did do another blood test as well from LabCorp. The test was a nucleocapsid antibody test. That test is able to differentiate between antibodies that are generated from SARS-CoV-2 infection versus antibodies generated from the vaccine. According to that test, I was negative for nucleocapsid, which would suggest that I was not infected with SARS-CoV-2, meaning I did not have COVID-19. However, I don't— a negative, whenever you have negative data in science, it doesn't necessarily tell you anything. It just means you're not getting— you're still at it. Well, I still could have had COVID and I was outside. Maybe this antibody is only detected for 2 months and I had it, you know, 3 or 4 months ago.

You know, so like a negative result doesn't necessarily give you confirmation. With respect to the pregnancy question, You know, again, this needs to be discussed with someone's OB-GYN. I think there really isn't any data on boosters in pregnant women. We do know that women that have had 2 shots like Lanise are protected mostly from any severe consequences of COVID which is really good. So, For me, if it were me, I would probably wait to get a booster until after I had my baby. If I had not had any COVID shots and I was pregnant, that would be a dangerous situation. We now have ample data that suggests that getting infected with SARS-CoV-2 during pregnancy and being unvaccinated can lead to severe outcomes and also other problems with the baby.

So it is certainly a risk to be unvaccinated and pregnant. Okay, so that was the big, big, big tangent. Andrew was saying in the chat that Peter Attia on JRE said he thinks we should combine mRNA and another type of viral vector like adenoviral I'm personally not a big fan of adenoviral vectors. There's been some preprint data. So the adenovirus can get into the nucleus of your cell, and inside of there, it can get spliced up. And there's been some preliminary data that there can be some alternative spike protein pieces that lack what's called a transmembrane domain. So when you make— when you have the mRNA vaccines, the mRNA is, you know, the vaccine's delivered to your muscle, and the mRNA cannot get inside of the nucleus of the cell at all.

And so the mRNA is made in the cytosol, and a spike protein is made, and the spike protein has a transmembrane domain, which keeps it stuck at the surface of the cell. It's like a big sticky thing. It cannot leave the cell. If you were to cut that transmembrane domain off, the spike protein would be free to float around in circulation. And so there's been some evidence that that does happen. We had no idea that there was these, you know, some of these enzymes in the nucleus, you know, region are splicing up the spike protein in some of the adenoviral-based vaccines. This is all preliminary, not peer-reviewed. So, you know, again, it's just, for me, a sort of like, okay, we need to follow this data a little bit more. We need more data before we jump into it.

So personally, I'm not a huge fan of taking a risk like that when the mRNA vaccines seem to be much safer in that regard. So that's kind of my, you know, 2 cents. Also, there's been a recent study, I think it was either August or September that came out that had injected the mRNA vaccine. This was mRNA vaccine. It injected either into muscle tissue of mice or into the vein, so intravenously, and intravenous injection, when it was free to go get into the circulation, caused massive, like, heart problems and cell death in heart cells and myocarditis and pericarditis, whereas the muscle injection did not do that. So I'm a little concerned about that stuff getting into circulation where I know that transmembrane domain keeps the spike protein in the muscle cell.

And so that's kind of where I feel the data is strongest for safety, in my opinion. But again, that's all just opinion, and we just—you know—the data is all coming in so new, and things change. And so, I think we just don't know. Okay, I'm going to move on to the next question from the crowdcast, and this question was submitted by a couple of people had asked. The same thing. So Alex and Chad had asked, Rhonda, could you please talk about the effect of intermittent fasting and prolonged fasting on testosterone levels? So let's start with intermittent fasting. There was a small study, and it was a long—it was quite quite some time ago. It was back in 1993. It inadvertently answered the question using college wrestlers.

The study was trying to answer why previous studies showed that testosterone levels rise after a sporting competition in most athletes. Athletes, except for wrestlers. So researchers hypothesized that the difference was that wrestlers are often in a fasted state prior to competition because of the pressure to meet the weight requirements. So what the researchers did was they followed a team of college wrestlers for a season and they measured their salivary testosterone levels the day prior, a couple of days before a match, and a couple of hours after a match, and then the day after a match. So they had multiple time points. They used heavyweight athletes as controls because they do not fast prior to matches.

And what they found was that in wrestlers who fasted, their testosterone levels dropped the day of their match, which is, I think, usually when they are fasted. In addition, the heavyweight wrestlers who did not fast saw an expected increase in their testosterone levels. The day of the match. Which was even more interesting was that their testosterone levels the day after the match, looking at the wrestlers who had fasted, their testosterone increased back towards their baseline, where the wrestlers who did not fast saw their testosterone decrease back towards their baseline.

So if you remember correctly, the wrestlers that fasted had a decrease in testosterone on the day of their match, But then the next day after their match, their testosterone levels increased back to their baseline levels. The wrestlers who did not match— sorry, did not fast had an increase in their testosterone on the day of the match. And the next day, their testosterone decreased back to their baseline. So everyone went back to baseline the day after the match, essentially suggesting short periods of fasting may temporarily affect testosterone, but not in the long term. You know, fasting the testosterone went back to baseline, so it wasn't like testosterone was decreased and stayed low.

Time restricted eating: there have been several clinical studies that have shown that time restricted eating does decrease testosterone levels in the short term. So while while the time restricted eating is happening, and this is more of a pretty pretty, um, like eating within, within 8 hours and then fasting for 16, or eating within 6 hours and fasting for 20. Uh, none of the studies have gone and measured testosterone levels like at multiple time points. Uh, so that's something that needs to be done. But the good news is that none of the participants— so these— so some of these studies are, um, in mostly active adults, physically active adults. None of those participants actually lost any muscle mass.

So you'd think if they were like, if there was a long-term effect with testosterone, you'd sort of see that represented in their muscle mass, and that wasn't seen. Prolonged fasting. It seems like the most important factor that predicts a drop in testosterone during a prolonged fast is the pre-fast fat mass level. And it seems as though people that are Obese do not have any change in their testosterone levels after a prolonged fast, whereas people that are lean or even just moderately overweight do have a decreased testosterone level if they do a prolonged fast anywhere between 3 to 10 days. Again, we don't really know if this is just a short-term thing like I talked about with the wrestlers.

Or if they're— I would tend to think that it's probably a temporary thing where it's just happening while you're doing it and then it goes back. Okay, we have a couple of questions. that are related to sort of women issues. One was a mammogram question, and I didn't have the person's name here for some reason, but there was a lot of upvotes on it. And the question was, Hi Rhonda, Dr. Greger's series on mammograms recommends it is not really helpful in saving women's lives by early detection of breast cancer. What are your thoughts on this? If you recommend all women to undergo mammogram screening, when they should start? How often should it be done? Thanks. Again, I am not a physician. This is not medical advice. Women interested in mammograms should speak with their physician about that.

I'm just going to talk about some of the data and speak specifically to what some of the claims that Dr. Greger, or I think it's McGregor, made in his video. So the US Preventative Services Task Force breast cancer screening recommendations are that mammograms should be given every other year starting at age 50 and up until age 75. For women before the age of 50, it's recommended the decision to start screening via mammogram is something that should be on an individual basis and something that should be discussed with your physician. Obviously, Some women have genetic, you know, there's a genetic or family history of breast cancer. Those would be people that, women that are at high risk and, you know, absolutely should undergo screening.

And there's also women that have a lot of high-risk factors, which we'll talk about in a minute. But let's talk a little bit about the argument that Dr. Greger makes in his mammogram video. He states basically that, in a nutshell, widespread screening for breast cancer leads to an overdiagnosis of breast cancer that could otherwise— that would affect a person's life. Excuse me. A similar argument could be made or seen with prostate cancer, where the trend is to do less screening because of the issues of overdiagnosis. So Dr. Greger states that he says up to 90% of breast cancer caught during a mammogram screening would not lead to death from breast cancer, but rather death with breast cancer.

So if 90% of breast cancers are caught on screening didn't actually need to be treated, Is it even worth screening? And I really— that's a really difficult question to answer because a woman doesn't know at the time of diagnosis of breast cancer if she's going to be in the 90% that dies with breast cancer or the 10% that dies from it. So without knowing which group you're going to be in, you have to ask yourself, okay, are you willing to take the risk? Are you willing to accept the consequences of being wrong? So, you know, death from breast cancer is— it's slow, it's painful, it's debilitating. Once it spreads to the brain, you lose cognitive abilities, you know, all controls over your body. Late stages, you start to like forget your loved ones.

I mean, it spreads to your bones, it can lead to intense pain, it can lead to a lot of problems. It's terrible. So Sorry, I've got something in my throat. But that's not to say that actually, you know, the consequences of chemotherapy also are devastating, you know, causes fatigue, weight loss, hair loss, neuropathies, heart failure. I mean, and probably there's all sorts of long-term effects that we don't even know about. Surgery also has complications. There's scars, loss of breasts, you know, arm swelling, lymph node removal. I mean, You know, radiation has problems. So it's sort of a catch-22 in a way, and I don't know that there's a real simple answer. I think that universal breast screening is not perfect. I don't know necessarily if it should be completely abandoned either.

So, you know, perhaps there's a middle ground and discussing it with your physician and knowing— I think knowing your modifiable risk factors are important. So we know Obesity, the risk for postmenopausal breast cancer increases about 6% for each 10-pound increase in a woman's weight. So this corresponds to a 26% increased risk for breast cancer when you're 40 pounds overweight. Exercise, women who do large amounts of vigorous physical activity such as running or cycling have around a 17% lower risk of premenopausal breast cancer and a 10% lower risk of postmenopausal breast cancer. than women who do low levels of vigorous physical activity. Alcohol, women who drink 1 standard glass of alcohol each day have a 7% higher risk of breast cancer than women who never drink alcohol.

Hormone replacement therapy, for every 10,000 women on hormone replacement therapy for menopause, there would be an additional 8 cases of breast cancer per year than if they were not taking hormone replacement. Birth control, the risk for breast cancer in women who are currently using combined oral contraceptive pills increases by about 7% for every 5 years of use. That risk goes down when a woman stops using the oral contraceptives. And breastfeeding— the woman— the longer a woman breastfeeds, the lower her risk of breast cancer. The risk of breast cancer decreases by about 2% for every 5 months that a woman breastfeeds. This is equivalent to a 5% decrease in the risk for breast cancer for a lifetime of 12 months of breastfeeding.

So there's a lot of modifiable risk factors, obviously knowing family history and even doing genetic screening. There's a lot of well-known breast cancer risk genes. I think these all sort of working with your physician and instead of just blindly saying, I'm going to do a mammogram because I'm age X, maybe doing some of these other things and talking about some of the risk factors and looking into genetics and Like all these factors, you know, it's good to kind of like take a comprehensive approach and certainly keeping the physician involvement in it is important. So, you know, and maybe there's another middle ground where once you reach the age of 50, you know, you kind of come up with a screening plan that works best for you after speaking with your physician about it.

So that's kind of— What I have on on the breast cancer mammogram question, and on a related topic, estrogen. So this was this was. submitted. I think a couple of people were commenting on it too. So the question is, I keep hearing it's a good idea for women to use an estrogen patch or cream during the first 5 years of menopause for long-term brain, heart, and bone health. Could you please give some recommendations for which types of estrogen are best? It would be very useful for women, you know, going in Are entering menopause or going to enter menopause. So let's talk a little bit about, again, this is, there's no recommendations I can make here, but I can just speak to some of the medical literature and talk about some of what some of the data says.

The patch or cream gets absorbed into the bloodstream and it has systemic effects. So the symptoms it best treats are hot flashes and night sweats. Women may also experience improvement in other symptoms like vaginal dryness, pain during sex, sleep problems, anxiety, and depression. For symptom control, the goal is to use the lowest possible dose for the least amount of time with estrogen patch. Estrogen with or without progesterone? If a woman still has their uterus, then they maybe will be given an estrogen patch with the progestin in it as well. Because estrogen alone can increase the risk of uterine cancer.

There are some other benefits as well with the estrogen and estrogen plus progesterone patches in terms— in addition to the menopausal symptoms, there's some effects on reducing other types of cancers and maybe even some all-cause mortality as well. It does seem to protect bones from the loss of bone density that occurs during menopause, but it's not really recommended usually for that because there's other ways that are safer for increasing bone density. There's really no good evidence that it prevents dementia. There is an increased risk of breast cancer that lasts 3 years from when hormone replacements were last used. It is not safe for those with a history of breast or endometrial cancer, liver disease, stroke, heart attack, or blood clots.

For those who have cardiovascular disease, treatment options depend on a 10-year cardiovascular event risk. So it seems like in terms of like finding the right patch, they all sort of work similarly, but products that have compounded bioidentical hormones should be avoided. These are hormone cocktails that are compounded by a pharmacist using doctor's prescription, but the end product is really not FDA regulated and the actual doses can be significantly different. From what is actually advertised on the package. So, like things that are not FDA regulated, you'll often find like with vitamins, it'll say a concentration on the back of your vitamin pill container. But when you actually measure the dose, it's oftentimes either much lower or much higher. I mean, it varies.

Things that are not regulated, that's often the case. So, it's really kind of getting these bio— getting the patches that have the compounded bioidentical hormones may not be a good idea for that reason. There was also a really large meta-analysis involving over 22 studies. And the conclusion of that meta-analysis was that, you know, women with intolerable menopausal symptoms may want to weigh the benefits of symptom relief against the small absolute risk of harm rising from short-term use of hormone replacement therapy. It may be unsuitable for some women, especially those with an increased risk for cardiovascular disease, increased risk for thromboembolic disease, and increased risk for certain types of cancer. So that's kind of the estrogen patches in a nutshell.

Myrick is asking in the chat, is spermidine in big amounts in yellow cheese? Is it even worth it to buy while there are so many good sources in food? The amount of spermidine in fermented cheeses is quite low. You're much better off eating natto. I once put together a— I think actually we went through foods that were high and lower in spermidine in a previous Crowdcast episode. I can't remember which one. Crowdcast maybe 13, Crowdcast 19. I think I also talked about it as well. So, if you guys want to check out those Crowdcasts, that would be the place to find more information on that. But I do think that I'm interested in the spermidine supplementation because spermidine does increase autophagy. So, at least in preclinical studies.

And there's a lot of evidence that people, you know, when you look at spermidine intake in people, there's, you know, all sorts of healthspan benefits and cognitive benefits that Yeah. So, spermidine is certainly a very interesting topic. Since we talked, I mentioned bone health briefly a moment ago, there was a question A couple of Crowdcasts ago by Susan. Susan says, hi, Rhonda. I'm interested in your thoughts on nutrition to support bone health. I've read conflicting reports regarding the effectiveness of calcium, magnesium supplementation as opposed to getting these minerals through dietary sources. What does the research say about the best sources to promote optimal bone health? So calcium participates in many aspects of human health. It's best known for its role in bone health.

The body maintains very tight control over calcium circulating in the blood at any given time. So protein exerts variable effects, both good and bad, on a person's calcium balance depending on their dietary calcium. For example, dietary protein promotes the production of insulin-like growth factor, a growth factor involved in bone formation. But protein also increases urinary calcium losses, which can also harm bone health. The current dietary guidelines recommended— that are recommended for older adults are 1,200 milligrams of calcium per day and 0.8 grams of protein per kilogram of body weight per day. I think, you know, the protein sort of varies based on a person's physical activity, you know, and so that's That's something to keep in mind.

There was a 2-year randomized controlled trial involving more than 7,000 adults that were elderly. So, they were in their 80s. They were living in a variety of different residential aged care facilities, and they were all vitamin D replete. So, they had been, you know, given vitamin D, which is one way to dramatically increase your dietary calcium absorption. By up to 40%. So having optimal vitamin D levels, or basically not being vitamin D insufficient or deficient, is a great way to make sure you're maximizing the amount of calcium you can get from your food. So back to this randomized controlled trial, half of these participants supplemented with about 1,200 milligrams of calcium and 69 grams of protein per day.

The other half maintained their usual menus, providing residents with about 700 milligrams of calcium and 58 grams of protein per 0.9 grams of— 0.9 grams per kilogram body weight per day. The data found that residents who consumed the high calcium, the 1,200 milligrams of calcium per day, and the high protein foods were 33% less likely to experience any type of fracture. They were 46% less likely to experience a hip fracture. So I think the take-home here is, at least with older adults, getting protein and calcium is really important for preventing fractures and hip fractures. And once that happens, I mean, everything just spirals downhill. So, you know, personally, I think having the vitamin D levels optimal is number one key.

And then, you know, making sure that you're meeting your dietary requirements for calcium of about 1,200 milligrams a day. If you're not meeting that, then calcium supplementation in addition would be a good option. But again, remember, you are— when you're vitamin D sufficient, you are absorbing 40% more dietary calcium. So, it's really important to make sure your vitamin D is sufficient. And then you also are absorbing more phosphorus as well. And then exercise. Exercise is really, believe it or not, really, really good for bone health as well. So, I think those are some of the main factors that seem to be great for bone health.

I think, you know, some of the data with conflicting calcium-magnesium supplementation, I think the biggest confounding factor is people don't measure vitamin D levels in those And with 70% of the US population, almost like 99% of elderly people where these studies are done are vitamin D deficient. Like, you know, they're not absorbing their dietary calcium. It's just being excreted. You know, so I think that's a really important point to consider, as well as the protein intake. You know, a lot of these studies are in elderly people that don't, you know, like they're just not eating enough protein as well. I see people talking about saunas in the chat wondering if blanket saunas are worth it. And so, Myrick is asking if blanket saunas that get up to 180 Fahrenheit Are worth the buy?

It's far infrared, and I'm wondering if it's a waste of time. So I you know I think that for people that cannot get a regular dry sauna or regular sauna in their in their house, that I do think these the sauna blankets are are worth it. I do think there have been some there's been some interesting evidence coming out of Dr. Ashley Mason's group, who uses they she uses a sauna tent. But also some interesting evidence with the sauna blankets, like some of these Japanese people are using the far infrared and also just infrared studies where there's been some beneficial effects on heart health, for example, using some of these things. And I think, you know, at the end of the day, even hot baths are a good alternative to the sauna as well.

Is there a danger in over-supplementing with calcium if vitamin D levels are optimized? I would tend to say yes. There's always a possibility of over-supplementing. I mean, some people think because vitamins are good, more is better, and that's not always the case. More is not always better. There's an optimal range because vitamin D does dramatically increase your absorption of calcium. Oversupplementing with calcium might be a problem because you might end up with too much calcium in the bloodstream, and that can precipitate, and, you know, it can lead to all sorts of vascular problems. So another sort of probably something I should have mentioned, another thing that I like to do is supplement with vitamin K2. A lot of you know this already.

But that's sort of insurance for making sure that the dietary calcium is going to the bones. And in fact, I definitely should have mentioned this with respect to the question because there have been studies linking bone health to vitamin K2 levels. And I think that largely has to do with the fact that vitamin K2 is activating some of the proteins that are transporting calcium out of the bloodstream and bringing it to the bone. And so making sure you're having enough. Vitamin K1 can also do it, but I think that vitamin K2 is a good sort of backup insurance to cover that. And so having the calcium, vitamin D, and the vitamin K2 is really a good trio, but not over-supplementing. I mentioned 1,200 milligrams per day for calcium.

Now, you know, a lot of these studies, you know, I think for the recommendations that that's in the background of a vitamin D sufficient person for the most part. But when you start to look at these randomized controlled trials, oftentimes they'll do a calcium supplementation trial and they don't measure vitamin D at all. And it's like, well, maybe that person was deficient, so the 1,200 milligrams didn't do anything. So, definitely, there is a danger in over-calcium, in over-supplementing with calcium with someone who is very, you know, has optimal vitamin D levels. So, I certainly appreciate you asking that question, Abby.

And, you know, measuring calcium levels, you know, there's a routine blood test where you can do that, would be another option to really sort of Fine-tune your levels and figure out if your dietary regimen is optimal and whether or not you're, you know, if you have to up your supplementation or not. Maria is asking what vitamin K2 dose would be optimal. We've covered this in a variety of other Crowdcast episodes. Off the top of my head, I remember not seeing a benefit above 45 micrograms of MK-4 per day. It wasn't like you had an added benefit by taking more than that, but that seemed to be the sweet spot. So that's pretty much what I can remember off the top of my head, but you can always go back to the previous Crowdcast to find where we covered that information in depth.

So there was a question about— this was submitted by Melissa, and Melissa was essentially wondering whether or not someone with an APOE4 allele, which increases the risk for Alzheimer's disease, has to completely eliminate alcohol from their diet. For example, Dr. Bredesen's Alzheimer's Prevention Protocol calls for them to completely eliminate alcohol from the diet. And it's something that I've been interested in in the past and really What I can come up with looking at the data, because there's really inconsistent data, you'll see data showing that alcohol consumption dramatically increases the risk for Alzheimer's disease, specifically in people that have APOE4 alleles, whereas it does the opposite for people without it.

In other words, people that are drinking like moderate alcohol, so anywhere between 1 to 7 drinks a week, People without an E4 allele actually had a protective effect on dementia and Alzheimer's disease, where people with an ApoE4 had a much higher risk. And so you'll find studies like that, but then you'll also find studies where alcohol has no effect on increasing the risk for Alzheimer's disease even more in people with ApoE4 than just having the E4 allele already does by itself. And so, you know, kind of trying to look at the data a little bit, there is some differences in terms of what people are defining as low versus moderate versus high alcohol consumption. And it seems as though the sweet spot maybe, maybe is key for people with ApoE4 is no more than 4 drinks a week.

And even that, it seems like You know, on the safe side, maybe it would be more like 1 to 2 drinks per week to kind of save it, make it on the safe side. And that seems to be maybe in the context of lowering all the other modifiable risk factors that can increase the risk of Alzheimer's disease in ApoE4 carriers. So some of the things that we know that are really important is physical activity for ApoE4 really seems to lower the Alzheimer's disease risk. getting good sleep really lowers the Alzheimer's disease risk in E4 carriers. Keeping homocysteine levels low, particularly for E4 carriers, really important for lowering Alzheimer's disease risk. Getting enough omega-3, very important for E4 carriers.

Vitamin D levels also seem to be strongly related to vitamin D, having levels above 30 nanograms per mL. So somewhere between 40 40 to 60 is best. Also, getting a lot of polyphenols from— and flavonols and these types of phytonutrients from foods seems to really lower the risk of Alzheimer's disease. So, you know, tea and berries and, you know, some of the antioxidants in some of these plant compounds as well. Some other things, keeping cholesterol in check for E4 carriers seems to also be important. But I think the way I look at it is avoiding hypertension also seems to be— if you're doing all these other things, then do you need to necessarily never ever drink? A glass of wine on the weekend with your family or your friends.

You know, I just, I don't know that that's necessarily the case. You know, I think modifying all these other really important risk factors that, you know, it might be okay to be a weekend glass of wine kind of person when you have an ApoE4 allele. That's the way I've been viewing it for myself. To be honest, so until there's more research that comes, more definitive research that comes out that shows otherwise, I'm not sure that you have to 100% avoid alcohol unless maybe there is a family history of Alzheimer's disease and you have ApoE4, and maybe you have two alleles of ApoE4. I think two alleles of ApoE4. There's a there would be a good argument to avoid alcohol full stop. Phillips asked, asking if I have any opinion on fish oil versus krill as a source of omega-3. I do.

I think fish oil is superior, even though krill oil has phosphatidylcholine. So it has that form of omega-3, which is more bioavailable, also more bioavailable to the brain. The amounts are so low in comparison to what's found in in high-quality fish oil. And honestly, just getting more than 2 grams a day of the fish oil, I think, is just stellar. I really think it's really good. And the krill oil, it seems like it's really hard to find a reliable source. It all just seems to smell so rancid. I have not found a really good source of krill oil. So, Personally, I think the fish oil is better. I've gone through my list with you guys in terms of some of the brands that I like based off of the international fish oil standards. And that was in a previous Crowdcast as well.

So please go back and see that. I know one that off the top of my head that I really like is Barleans, B-A-R-L-E-A-N-S. Now, I was sorting this based on high EPA levels. So they also have DHA. Yeah. High EPA, low oxidation, low mercury, low contaminants, and stuff like that. So I do think that taking, you know, for me, like I said, I'm taking 3 to 4 grams a day. Actually, I take 2 grams in the morning. For the most part, I take 2 grams in the morning and 2 grams in the evening. I do EPA in the morning and I do DHA in the evening, so I'm actually getting a total of 4. On days that I forget to take it in the morning, I get 3 grams of my omega-3. So I either get between 3 to 4 depending on how strict I am on remembering to take my morning ones.

Alan's asking if there's any vegan omega-3 fish— omega-3. I think some of the best ones are microalgae oil, that would be— and Nordic Naturals has a really higher omega-3 dose of the microalgae omega-3. I found that they have a pretty decent one. They're not the best for fish oil, but for their microalgae oil, I found a pretty good one that seems to be high in concentration. So there's some rapid-fire questions that I'm going to hit up. So Chad asks, with regular intermittent fasting, is there any evidence that metabolism will adjust down due to the shorter eating window as a way to reach homeostasis. A nutritionist suggested that this downregulation of metabolism negates the benefits of intermittent fasting long-term and can actually lead to feeling worse. Is there any truth to this?

No, not that I could find. And in fact, with that logic, the converse is true. Eating more food would increase your metabolism and you would reach a new homeostasis and That's just not true. Overeating makes you gain more weight. When you're fasting, what we do know happens is that you become metabolically flexible. You start to get this metabolic switch where you're able to metabolize fatty acids and you start to get better at doing it. If anything, it seems to make people more fat adapted. It seems to make people more metabolically flexible. Being able to like, you know, oxidize fats better than they otherwise would have. So I think that's something— the basis of that, I mean, who knows? Who knows where that's coming from? But I personally don't buy into it.

Owen's asking, do you use any type of water filtration system in your home? Do you prefer any particular bottled water? I use a Berkey water filter and I've got Like four filters. I do all the chlorine, fluoride, and all the all the standard stuff. I I do really like their filters. I do like the bottled water I like is Mountain Valley water. I also like their their sparkling water, and another one I like is I think it's like Geinstein's or something like that. That's another sparkling water that I like. So John asked, for activating NRF2, how much Kulikuli moringa powder would be roughly equivalent to the higher-end dose of sulforaphane? We don't have a head-to-head comparison, so I couldn't tell you that for sure. I can tell you what I use.

I use a heaping tablespoon of Kulikuli moringa powder. So that's all I got. She says, I am a middle-aged woman with Parkinson's disease, and along with the gold standards, She takes supplements and follows a vegan diet, tries to exercise, has started sprouting broccoli seeds. Can I talk about anything relevant for Parkinson's disease and sulforaphane and whether or not sulforaphane disrupts thyroid function? So it's interesting that Missy asked this question because about a month ago, new evidence suggested That sulforaphane may prevent the loss of dopaminergic neurons. Like, there seems to potentially be a Parkinson's benefit for sulforaphane. My father was diagnosed with Parkinson's a few years back.

He's doing quite well right now, but he's, you know, he's only had Parkinson's disease for about 5 years. So, or diagnosed, he was diagnosed with it about 5 years ago, still kind of early in his progression. I just got him Prostafane and I started telling him, okay, you need to, at the very least, you need to take one of these with your meal every day. So I haven't talked to him since I gave him that. I think it was last week he came, or 2 weeks ago he came over. I haven't talked to him about it, but when he comes over this weekend, I'm going to ask him how it's going. So I do think that's interesting and something that I am now including in my father's regimen. With respect to thyroid function, really, it's not— it shouldn't disrupt thyroid function.

It's the compounds made by sulforaphane. There are other ones in other cruciferous vegetables like cabbage. That can potentially do that when someone's iodine deficient. Iodine deficiency is the main thing, but there are people with hypothyroid that should check it out. You know, I've been taking sulforaphane for years and years and years and never have any problems with my thyroids, but that doesn't mean that you won't. I don't necessarily know what to say other than, you know, get your blood test done and do it. Before and after supplementing with sulforaphane. For someone that's already having thyroid problems at the baseline, seeing if sulforaphane augments that even further would be important.

There was animal evidence showing that in animals that were induced to have hypothyroid, giving them broccoli sprout extract actually benefited them, not harmed, benefited. That's an animal study. Who knows with the humans? So, You can talk it with— talk over with your doctor and do the experiment yourself. Get your thyroid levels measured, start taking your broccoli sprouts or sulforaphane, and then get your thyroid levels measured again and see if there's any effect. Couple more rapid-fire questions here. Brock asks, hey, could you talk about some of the foods you started introducing to your Your kid at young ages, like under 1 year old, essentially wondering if you sort of have top foods to start feeding your baby when they start on solid foods.

So when I started solid foods at 6 months, so my son was still being breastfed, but I introduced solid foods. Some of the foods that I did was pureed cooked salmon along with cooked blueberry kind of mixed together in a puree. So it was like a cooked blueberry salmon puree. I switched around the cherry and the blueberry sometimes with that. And then I also did pureed cooked chicken and cooked cherry and made a puree. So it was like a chicken cherry, cooked chicken cherry puree, or I would switch it with a cooked chicken blueberry puree. I also did pureed avocado and cooked spinach together. And I did pureed cooked sweet potato. Those were some of my go-tos. Lynell asks, she says, hi, Rhonda, thank you for all you do.

I recently heard an interview about urolithin A, which stimulates mitophagy and renewal of healthy mitochondria. I know your clever mitochondriac t-shirt, which she has, and that I'm interested in healthy mitochondria. I guess the Buck Institute for Research on Aging just received a large large grant to study this molecule and potentially commercialize it. It looks like it's promising and wondered if I was familiar with it. Yes, I'm very familiar. So for people wanting to know what this is, urolithin A is a compound. It's mostly found in pomegranate, like the skin part of it is really the highest of it, you know, the part that's bitter. And that's like the major source of it, and it affects the gut microbiome.

And basically, it stimulates what's called mitophagy, which is— it is the recycling of damaged old mitochondria. So you basically are getting rid— it's like cleaning house, like you do when you're fasting, and autophagy, you know, you're It's recycling other parts of the cell, like the other organelles and stuff. Well, this is specific to just the mitochondria. So it's a really cool way of cleaning out old damaged mitochondria. So I'm super interested in it. I do eat pomegranate, although my glucose monitor tells me not to eat it too, too much or not in the quantities that my son— my son loves it. Like, he eats pomegranate every single day. And with the pomegranate, you get a little bit of, you know, the skin.

And there is some in the arils, you know, the little seeds that we eat, but it's really concentrated in that terribly tasting bitter part. So you want some of that? Eat it. That would be my suggestion. Nilesh is asking in the chat, any advice for adult ADHD improvement? We actually covered this Like 2 or 3 Crowdcast episodes ago. So go back and listen to that Crowdcast. Look at the timeline because we did cover that Crowdcast and we talked about a lot of things that could be done for ADHD. Looking through some of these chat questions, Myrick's mentioning about Charles Poliquin, who used to recommend taking up to 30 grams of omega-3 per day, had no adverse effects. That's quite a lot. That's extremely experimental.

I really can't speak to that kind of dose, but again, I take 3 to 4 grams a day. And we do have our video with Dr. Bill Harris coming out this coming week, and it's really a stellar video. And he's the omega-3 expert, and it's just great. It's a really great video. We have wonderful slides, a lot of extra information on the video. I think you guys are going to love it. We have a summary show notes page coming out. We're going to send you guys an email which has great information in it as well, along with a discount code for the OmegaQuant test they do, which is the omega-3 index I was talking about. Dan, my husband, just did a test, and I have one sitting on my desk. I just need to like remember to do it. I'll probably be doing it this week.

I don't have any affiliation with the Omega-3 Quant. He just offered it for a discount for for viewer or our audience, basically. So you guys can try that out and see. I really like measuring the omega-3 index versus a standard omega-3 test, which is looking at omega-3 in plasma, because it's really just the plasma, you know, looking at the phospholipid levels is really just a reflection of what you ate like the last couple of nights versus a long-term effect, because the omega-3 levels in red blood cells are there for like I don't know, 33 days or something like that. So it's really indicative of a long-term— your long-term omega-3 levels. And, you know, Bill has wonderful data looking at all-cause mortality and omega-3 index. I did have my omega-3 index measured.

So it was measured by another company, and they did do RBC, and I was 11%. I was on the high end of what the Japanese— so like Japanese People eat a lot more fish. They on average have a 5-year increased average lifespan or life expectancy compared to people in the US. And their omega-3 index is generally between 8% to 11%. And in the US, the average is like 4% to 5%. So I was 11%. And I'm going to go ahead and do omega-3s test to see if it's the same. Yeah. The last time I had my omega-3 level, my red blood cell omega-3 levels measured was March 2020. It was like right before everything shut down from the pandemic.

So yeah, you guys should, if you're interested in knowing your omega-3 index, get the omega-3 index done and aim for that at least 8%, because I think that just looking at the all-cause mortality data, There's evidence that, you know, it's up to a 5% increase— I'm sorry, a 5-year increase in life expectancy, which is pretty awesome, if I don't say so. So I think that's all I have for today. I'm going to go have an arts and crafts party for my 4-year-old. We're going to paint a bunch of Christmas ornaments and do a bunch of fun arts and crafts. Stuff and play some games. So I'm looking forward to that. Thank you guys so much for all your support. I really enjoy doing these Crowdcasts. I just love doing them. Don't forget to submit your questions for next time.

Again, I do archive, as you saw. I went back to a question from a couple of months ago on the calcium and bone stuff. So I look forward to all the questions you guys are going to submit. For those of you that are new, I hope you enjoyed it. Go back and listen. You'll get a timeline with references if you want to do some more digging into it as well. Have a Merry Christmas, happy holidays, happy Hanukkah, all the other things that you may celebrate around the world. Just enjoy time with family and friends. We will be continuing to cover some COVID stuff as more data comes out with respect to boosters, with respect to young children age 5 to 11, and with respect to the new variant. So please submit your questions, but know that we are definitely following that as more data comes out as well. Bye, everyone. Look forward to seeing you guys next year. Man, hope it's a good year. I'm looking forward to starting off with a bang. Bye. Thank you.