Welcome to Crowdcast number 37. And for those of you that are new, welcome. Happy to have you guys here. The way this works is that I usually go through and I choose questions based on whether or not I've covered the question before, based on whether or not, you know, there's interest from the audience, from subscribers, and also sometimes just my own interest if I want to dive deeper into something. So typically I'll dive deeper into a few questions and then I also go through what I call rapid-fire questions. So these are questions that I can answer in a sentence or 2 or sometimes even a word. So that's kind of how it works. This episode I am going to go back and address what I did not get to last time. So there'll be some questions that I did not address last time that I'm getting to.

And I did see that people submitted some of the same questions from last time, and I happen to be addressing those. So people will be happy about that. Also, I think I, this time around, have a little bit of a mishmash of my deep dives and rapid fires. Usually I like to repeat the rapid fires at the end, but because I'm addressing some questions from last time, they're kind of mishmashed in there. So I'll get started in just a minute, but also I have seen in the chat and also people have submitted this a couple of times where they can find whether or not what the archive of questions from the previous Q&As are. So for example, this is Crowdcast number 37. We've done these 37 times. It's quite a few times.

So right now the best way to find questions that were submitted previously is to either go onto your dashboard or to go into your private podcast player. So wherever you're listening to the Aliquats or these Q&A episodes later after, you know, after they've been recorded. And if you go into your dashboard or your private podcast player, you know, feed, there's a summary or a description section. And in that section, we have, we have bullet points sometimes with timestamps of the questions and topics that were covered. So right now, that's the best way to go back and look at that. So either dashboard or private podcast feed. We do want to get those archived on the website. It's an— it's a monumental effort to do anything on the website.

I can't explain it, but like development and doing all that takes an enormous amount of work, more than you would think. I wish it was as easy as it seems. So it is on the list to do, but for now, the best way to do that is to go to the dashboard or your private podcast feed. podcast player, go back to the previous episode, Q&A episodes, and then look at the description summary section and you can see the questions listed there. So with that, we'll get started. And the first question was that I'm covering in this Crowdcast was submitted by Libby, and Libby was asking whether I could provide any information or research on alpha-lipoic acid Its effectiveness, how it can control blood sugar, the R versus S, and reliable brands.

So this is a question I haven't really covered, so I kind of just want to you know cover a few of the the background basics just to start with. You can find alpha lipoic acid in foods, so it's it's found in animal tissues like kidney, animal organ tissues. So that the kidney, heart, and liver are pretty high in alpha-lipoic acid. You can also find it in some vegetables like spinach and broccoli. Then there's the supplemental form. So, um, you can find alpha-lipoic acid in typical supplements. It'll— it's literally like 1,000 times greater than what you would find in food. And the recommended doses usually are anywhere between 200 to 600 milligrams a day, you know, depending on what the outcome is and what the research has shown on that outcome.

There is an oxidized form of alpha-lipoic acid and a reduced form. They kind of cycle between the two, much like vitamin C. There's been a lot of interest in its free radical scavenging capabilities. So it can basically help prevent DNA damage, damage to proteins and lipids in our body. It neutralizes reactive oxygen species. It's also been shown to protect cells from UV-induced damage. And the alpha lipoic acid recycles between its oxidized and reduced form. It also regenerates vitamin C and vitamin E. So vitamin C and vitamin E also become oxidized, and they go through, for example, vitamin C goes through like four cycles. Well, alpha lipoic acid can help regenerate some of that vitamin C, so it kind of prolongs the half-life of it.

Interestingly, alpha lipoic acid also has some interesting metal chelation properties, so it can. It can chelate some free metal ions, so iron, zinc, and copper, for example. So when you have those metal free metals floating around in cells, they can induce oxidative damage. So what alpha lipoic acid does is it binds to and chelates these free metals, preventing them from inducing oxidative damage inside of cells. It also has been shown to reduce advanced glycation end products. So these are damaging products that happen when you have a combination of fructose plus either protein or, you know, fructose with protein or lipids and DNA. And so the advanced glycation end products can bind to the lipids and DNA and protein, sort of cross-link them, and it can damage them.

You can find a higher proportion— people consume, actually consume advanced glycation end products from really deep-fried foods, from barbecued and grilled foods, hamburgers, hot dogs, for example, really, really fried foods like French fries, crackers, chips, you know, processed foods, like those are really high in advanced glycation end products. So alpha-lipoic acid has been shown to decrease or reduce the formation of advanced glycation end products. It also has been shown to play a role in brain aging. So it increases the production of anti-inflammatory genes and genes that can respond to oxidative stress as well. It's been shown, interestingly, there's been some animal studies showing that alpha-lipoic acid can mimic some aspects of caloric restriction in the brain specifically.

So again, it's like inducing a lot of the same genetic pathways in brain regions like the cerebellum. That caloric restriction induces. So that's also pretty interesting. Now, where the blood sugar stuff comes in, there's been a variety of studies showing that alpha-lipoic acid can improve insulin sensitivity and it can lower blood sugar levels. It's also been shown to play a role in diabetic neuropathy. So, you know, this is a big, big problem with people that have type 2 diabetes, for example. 600 milligrams of alpha-lipoic acid per day for 3 weeks was able to reduce symptoms of diabetic neuropathy. And it's also been shown to play a role in aging skin, which also has piqued my interest. So, you know, collagen is one respect that it's been shown to play a role.

So alpha-lipoic acid can increase the production of type 1 collagen in the skin. It also increases the expression of an enzyme, a gene that produces an enzyme called prolyl hydroxylase that's necessary to produce collagen. Also has been shown topically to play a role in lowering the production of melanin in the skin. So it's been helped to show treat— what's it called— the hyperpigmentation in your skin. So that's another interesting aspect of alpha-lipoic acid. I think that the combination of the R&S brand's Pure Encapsulations makes a good one. I will go through my supplement list today because that was another question, but I'm sort of interested in experimenting with it. I did place an order for my mother to have it, so it might be something that I'll be adding to my list.

So if you guys want to check back again with my supplement list again soon, then, you know, I may be trying that as well. I see some people asking in the chat about Athletic Greens. I have covered that in a previous Crowdcast. Personally, I'm not, you know, I think that there's a lot of the blue-green algaes in there, you know, that are in some of these supplement powders, including the Athletic Greens, I'm just not a big fan of. There's heavy metals that are piggybacking in those, but there's also the microcysteine. And so I just, I don't really, I don't see a benefit of taking those powders above and beyond taking your multivitamin supplement and then getting a good diet and having some vegetables and stuff as well.

Xavier was asking about urolithin A. He says, a lab I work with told me— so urolithin A is something that there's a precursor compound found in pomegranate, specifically, I mean, pomegranate that can, that, you know, is transformed into urolithin A in the gut. And urolithin A has been shown to improve mitochondrial function, improved endurance in people. improve memory. So there's a lot of functions that it seems to benefit. So Xavier is asking about how it can be conjugated when absorbed in vivo, inside the body, and it can lose most of its efficacy. So he was wondering whether or not that, you know, I could, you know, look into this and see whether or not I agree.

I do see that You can have a loss of efficacy with urolithin A due to this conjugation, but that happens under inflammatory conditions when LPS is released. So again, that might be something to consider. LPS obviously is released under a variety of inflammatory conditions and people that have any type of intestinal permeability, commonly known as leaky gut. that, that could be an issue. Food itself, just the act of eating, also can release LPS. And so that kind of makes me think maybe it's better to take your L-lysine A on an empty stomach because then you're not having the LPS release with food. I mean, that's just a theory, but it does seem as though it's the inflammatory conditions like LPS that are conjugating the urolithin A to become ineffective. Rapid-fire question from Urban.

Urban asked, is it okay to have kefir and kombucha on the same day or week, or will it start a culture war? And I would have to say I think it's fine. Both Chuck and Steve submitted a question last time saying that ConsumerLab sent out an email, and the email said that higher blood levels of vitamin C were associated with an increased risk of death over 10 years in a recent study. And they linked the reference. They wanted to know my thoughts. First and foremost, I'm going to tell you ConsumerLab is good for third-party testing. In other words, they take a variety of brands out there and they measure things, data, hard empirical data. That I think ConsumerLab is great for. What I do not think ConsumerLab is great for is scientific analysis. In analyzing actual data.

I don't think I've been— I haven't been impressed in any way, shape, or form with their analysis of data. So those are 2 separate things. I mean, it's one thing to measure things, have numbers, and say, look, this is what our numbers show, and this is, you know, these brands have higher levels of cadmium, for example. Like, you can't go wrong with that. But when you get people then trying to review data and they might just not have the knowledge necessary, you know, and be the capacity to look at all the data and the totality of evidence, then you might get some inaccurate data. So this is one example. So basically, this email they sent out was on one prospective study. If you look at a meta-analysis of 69 different prospective studies on vitamin C, it's the exact opposite.

In fact, So higher blood levels of vitamin C and also higher dietary intake of vitamin C was associated with a lower disease-specific mortality and a lower all-cause mortality. So one prospective study versus 69, I'm definitely going to go with the 69. So this question was submitted by JQ, and I also saw this question in one shape or form this Q&A submitted by this Q&A, and it has to do with ApoB and lipoproteins. So I've definitely covered this topic in detail in previous Q&As. I probably cover it once every year and a half or so, or something like that.

So the question has to do with ApoB and LDL cholesterol and those numbers being quite high, eating a fairly healthy diet or, you know, being relatively healthy, eating mostly low carb, exercising, being at a healthy weight, but still having high ApoB and LDL? And basically, is there anything to address? And I think first of all, understanding, look, ApoB is a protein that's produced in the liver. It provides structural support for lipoproteins, particularly VLDL. So that's the precursor to LDL. ApoB is a marker of cardiovascular health for a couple of reasons. First, it's a more direct way to measure LDL particle number, which may be more relevant for cardiovascular health than total LDL cholesterol.

Second, ApoB is what is likely to insert into arterial walls, which then basically allow the LDL lipoprotein to not be recycled. They sort of start that cascade of inflammation and foam cell formation. So ApoB is relevant. And there's a lot of interest in the regulation of ApoB. It's mostly regulated through degradation and not synthesis. So it's regulated mostly in getting rid of it and not the production of it. Your liver is really constantly making ApoB to some degree. And we do know that there is one factor that regulates synthesis or production of it, and that is inflammation, and particularly cytokines like TNF-alpha and interferon.

TNF-alpha can be dramatically increased again under like conditions of intestinal permeability, and I talked a lot about this in a presentation I gave a couple of months ago, and there are a variety of factors that can regulate intestinal permeability: stress, alcohol, diet, particularly a very, very high-fat, refined carbohydrate diet, but even a high-fat, low-fiber diet in some cases can increase intestinal permeability. Interestingly, we know that omega-3, particularly the marine omega-3s, DHA and EPA, so fish oil supplementation has been shown to decrease ApoB levels in people with dyslipidemia and also in people with normal lipids. The dose was about 1,500 milligrams of EPA and 1,000 milligrams of DHA.

That was shown to decrease ApoB, possibly through this inflammation, you know, related mechanism or maybe other mechanisms as well. We know that omega-3 has been shown to reduce TNF-alpha, for example, and in fact, omega-3 has been shown to reduce lipopolysaccharide induced from a meal. And again, lipopolysaccharide— when lipopolysaccharide makes its way into circulation from the gut, it increases TNF-alpha. I think there's a lot of potential synergistic effects going on there with omega-3 where it's stopping the LPS release, and so that's one way it's reducing inflammatory markers like TNF-alpha. And it's also just resolving the inflammation quicker and lowering the inflammation.

So I think that— The omega-3 is probably one sort of low-hanging fruit avenue to explore with respect to ApoB reduction. Fish has also been shown to lower ApoB synthesis. So another study found that even higher dose of fish oil, so 1.8 grams of EPA and 1.2 grams of DHA, Was able to lower ApoB production by 29% in people with normal blood lipids. So that's pretty cool. There was also a decrease in the VLDL pool size by 43%. So that's the sort of supplemental side of the story. And again, you guys already know, and you'll hear more about my supplementation routine in a minute, but you already know I'm a huge, huge fan of omega-3 supplementation.

And I've also seen a variety of questions submitted in this Q&A about fish intake and concerns about heavy metals from fish intake and if there's a trade-off or not. So I will say this, yes, to some degree, you're going to get some contamination from fish. And the best thing you could do is go for the fish that are known to be lower in heavy metals and contaminants, right? So those are the wild Alaskan salmon, sardines. You got to find— obviously, there could be some contamination with arsenic with some of the sardines. But finding the smaller fish that are not accumulating these heavy metals as much. But also keep in mind that there have been studies done, particularly in pregnant women where pregnant women eating fish— in fact, the biomarker for fish intake was mercury.

So they knew the women were eating more fish because their mercury levels were much higher than women that were not. And the omega-3 fatty acid content in the fish protected the developing fetus and not only protected the developing fetus, there was benefits from it. Yeah. In other words, not getting the fish even though there was lower mercury was worse for the fetus, which is more sensitive, by the way, to heavy metals than an adult is. So they were more sensitive. So they're more sensitive to the heavy metals and yet having the higher heavy metals was better because of the omega-3.

So it's like the omega-3 is negating some of these potential adverse effects from from these heavy metals, not to mention again, excreting some of these heavy metals through sweat and also through things like beta-mercaptans from garlic, which helps excrete it through urine, also helps. I personally choose to eat fish, but if you're super, super concerned about heavy metals and you get your heavy metals measured, that's something to keep in mind is also having your omega-3 index measured and how high is your omega-3 index. That should really tell you something, not to mention the fact that, you know, you can also obviously supplement with a higher dose of omega-3 and maybe cut down some of your fish intake if that's also a really big concern.

For me, I personally like to eat the fish in addition. There's other micronutrients that are also present in the fish that are beneficial as well. So— I think that that's kind of my take on that. And that was a big tangent. I'm going to get back to the ApoE here— I mean, to the ApoB story here, because there's also a story to be told with respect to diet. And I know that a lot of people follow a low-carb diet, and JQ had mentioned it in his initial question. And there's been some really interesting research, a lot of it from my friend and former colleague, Dr. Ron Krauss, who's done a lot of work on this, looking at how different types of diets, low-carb versus low-fat, and how they affect— ApoB and how they affect other risk factors like small dense LDL, for example.

And it's interesting because it really— the dietary effects on ApoB and small dense LDL really come down to where a person is at their baseline in terms of their phenotype. So there's a big genetic predisposition to whether or not a person is a phenotype A versus a phenotype B. In other words, whether or not they're making more of the small dense LDL products versus not. And so starting out on, you know, someone that's already genetically predisposed to making a lot of small dense LDL is something that's important to consider when making dietary changes. So for example, looking at a high-fat versus a low-fat diet and then switching, you know, doing a switchover. So men that did either a high-fat or low-fat and then they switched the diet.

After doing the diet, after the high-fat diet, the individuals were classified as either phenotype A or phenotype B. And then if they were following a low-fat diet, all the phenotype B individuals stayed phenotype B. But about 36 of those people shifted from a phenotype A to a phenotype B, whereas about half, like 51 of the people, remained phenotype A. After the low-fat diet, phenotype B subjects had a greater decrease in their total cholesterol and also they decreased their ApoB. Whereas phenotype A— compared to phenotype A. Whereas phenotype A people had reductions in their total cholesterol, but they also had no change in their ApoB.

So it seems as though a low-fat diet may be more beneficial for people that already are phenotype B, already are people that are genetically predisposed to making small dense LDL. So phenotype B people are predisposed to higher small dense LDL, higher ApoB than phenotype A. So a low-fat diet may not necessarily benefit people that are phenotype A that already sort of are not genetically predisposed to that, but it may benefit some of the people that are phenotype B. And that would be something to sort of explore through some self-experimentation. There's another study that showed people again that are phenotype B that are put on a high saturated fat diet had a significant increase in ApoB and also a significant increase in small and also total LDL particles.

So again, it might— this might mean that people that have a phenotype B type of lipid profile might not do well on a very low-carb, high-fat diet. And that is— I also think this is also something where looking at the conflicting data, this is— there's a genetic component in there. And I think that that's not usually considered. But if a phenotype is measured at the baseline, is this person phenotype A or phenotype B, then you can kind of maybe say, well, maybe I'm phenotype B. Maybe I should not be doing so much of a high-fat, low-carb diet. Maybe I should be eating more fiber and eating more mono and polyunsaturated fats and less of the high saturated fat.

And this was also asked by Bernardo who asked if there was any recommendations for a low-carb diet with the problem again of elevating ApoB due to the consumption of high quantities of fat. And he was talking about doing keto for years and his LDL going just through the roof. And his ApoB also going really high. So again, I would say many low-carb or keto eaters do eat a lot of saturated fat, and some of these people that are already ApoB to start with might consider doing a low saturated diet sort of fat, like a low saturated fat diet, and to see how that affects lipids. So low dairy, low cheese, low butter, low red meat, low coconut oil, low palm oil, like basically very low, or if any of those.

Replace those things with avocado oil, with olive oil, with avocados and oils and nuts and fat from like salmon. And if you really, really, really want to do the keto version of it, again, like you can do a keto diet, but instead of doing all the saturated fat, you do mono and polyunsaturated fat. And that would be something to really check because there are, again, people that are already phenotype B that can increase their ApoB and do worse with a low-carb, high-fat diet, particularly when it's low-carb, high-saturated fat. How do we know if we're phenotype A or phenotype B? So I typically do WellnessFX tests, lipid panel tests, and they will tell you that you're phenotype A or phenotype B. That's something you can also ask your physician to do as well. measure what your phenotype is.

But again, I just go through WellnessFX and, you know, it's— I forgot what the price is, like $150 or something, and they do the whole lipid panel and they measure a variety of other things as well. Even if you just do their baseline test, which is the lipids and I think they do it with the baseline test. You might want to ask them if their baseline test also does. I know their— Their performance tests and other tests definitely show the phenotype. They measure the phenotype for you. So that's always how I've gotten my phenotype is through WellnessFX. But you might even just be able to ask your physician as well. Lori's asking in the chat, what if you're already on low-carb, high-fat and may not be at baseline? How long would you follow a higher-carb diet before taking the test?

I would say like minimum 3 weeks. It seems as though you'll see some changes after a minimum of 3 weeks, ideally probably 6, but some of these studies were 3 weeks, and so I would say a minimum of 3 weeks would be good as well. John is asking about Lp, whether or not it influences the phenotype A or B. You know, I don't remember off the top of my head all of the factors that influence ApoA or Apo— I mean, phenotype A or phenotype B. So I can't answer that off the top of my head. But again, you can get that measured. And most of the time, like the phenotype, it's really— there's a big genetic component that does determine it.

And so, you know, getting that test done, you can really see that just from— from doing the, you know, all the parameters that are measured for determining the phenotype A and phenotype B. Most often, if someone is phenotype B, they, you know, changing the diet, in many cases, actually lowering the saturated fat and increasing a little bit of the complex carbohydrates like dietary fiber and shifting to monounsaturated and polyunsaturated fat and a lot of omega-3 might help shift that pattern more to phenotype A. So if you guys are more interested in some of these phenotype A and B questions and diet, the effects of diet, please submit them next time so I can go into more detail. Chris asked about my smoothie that I was making.

I was making a pomegranate smoothie and, you know, how much urolithin A is produced. Like, I don't really know how much is produced. I know I was using the white part of the pomegranate, so under the skin where all the seeds are. That's like the highest in the polyphenol precursor to urolithin A, and it's also the bitter part. And so I was making smoothies with those and then adding a few strawberries to kind of counter the bitterness of it. And it's much cheaper than buying MitoPure, which is what I was supplementing with. It's so expensive. It is incredibly expensive. I also just think that making the pomegranate smoothie is really just beneficial for the gut as well and also adding some of the seeds in there.

There's been studies showing that pomegranate juice, for example, improves intelligence in offspring of pregnant mothers. It improved intelligence in older people that take it. Again, is that from the urolithin A? There's a very good chance it is because other studies show that, again, that urolithin A itself can do that. So I just think there's a good argument for just making— adding the pomegranate or drinking a pomegranate kind of smoothie with that bitter-tasting component in there as well because that's really high in urolithin A or the precursor, the polyphenol of urolithin A. Okay. Yeah. Liawei and Barbara were asking about the olive leaf powder extract, how I was using Dos Alquimistas and how that's not found in the US anymore, and to find a good brand. I would look into ConsumerLab.

I think they've looked at olive leaf extract. Again, they're great for analyzing actual empirical data that they generate from testing, but I would leave the literature reviews to, you know, not ConsumerLab, definitely. They do not oftentimes get things right. But they are great for testing things like contaminants in supplements and powders and stuff. Malisa was asking about sauna use and mastectomy. She was told to avoid the sauna because of the risk of lymphedema. I would, I kind of looked into this and there does, it does seem there is a study showing that it might be a risk factor.

So it's probably, you know, best to avoid that or talk to your physician and see if like doing the hot tub is safe, if you can do hot tubs, because there's a, you can get a lot of benefits from the heat stress of a hot tub as well. But it does seem like there is a risk of lymphedema, you know, with respect to, um, to that specific factor. So I would, I would definitely, you know, be cautious and talk to your physician about that. Simone was asking about medicine alternatives that I give my son for pain management. She says, I read you shouldn't give your kids Tylenol because it can deplete their glutathione. Is this true? So I've never had to give my son anything for pain management. I've been just, I guess, really lucky. I don't know.

I've— if he, you know, whenever he's had a fever, I've really just— when he was really young and I was still breastfeeding him, breastfeeding always helped. I mean, breastfeeding took away every problem ever. So if they're young enough, to still be breastfed, that was always my go-to. But now that my son is older, like when he's had a fever, I just basically give him like a homemade popsicle or a cool rag. I strip him down and he's pretty much fine. He just kind of sleeps it off or— So I've never really had to give him any anything for pain management. And so I just haven't gone there. And I'm not sure, you know, again, those things aren't used to like make them better. It is just to help with pain management.

So I guess that would be kind of at your discretion whether or not you think the pain is just so great. I haven't reached that point. So I've never had to do it. Okay, a couple more rapid-fire questions from last time and then we'll move on to this some of the bigger questions from this crowdcast. Fitz asked about my thoughts on fasting and keto for long COVID for the autoimmune perspective. I think it makes sense. I think, you know, both fasting and ketogenic diets have been shown to improve autoimmune disease biomarkers and in some cases some symptoms of specific autoimmune diseases. Additionally, you know, Beneficial, you know, compounds for the gut, like prebiotic fibers and stuff, also have been shown to increase regulatory T cells.

So it does make sense that that may, in theory, could be beneficial for long COVID. All right. Chris asked about the sauna and exercise. So he says, you've previously mentioned that sauna plus exercise is better than either alone. But running the thought experiment of using 30 minutes in the sauna and matching exercise for heart rate in the sauna, do you think sauna would have additional benefits over that time just to exercise? So the health benefits of exercise, you know, they do follow a diminishing return pattern. So like when you get to the extreme athlete level, so those who are not active at all benefit most by doing some exercise. And then the 75 minutes of vigorous exercise per week or 150 minutes of moderate exercise per week. You know, are the guidelines.

So when you get— there's a reduction in all-cause mortality by 31% if you meet those guidelines compared to no exercise at all. More exercise beyond those guidelines are— they yield really small increases in health benefits. So the maximum decrease in all-cause mortality plateaus at 39%. So, and that was achieved by 3 to 5 times the CDC physical activity guidelines. Which is quite quite a bit to get to for an eight percent increase. You know, basically going from a thirty-one percent decrease in all cause mortality risk to thirty-nine percent decrease in all cause mortality risk.

You know, so I mean, I I do know that there's been shown there have been studies that have shown that sauna more robustly activates heat shock proteins and also leads to more sweating, which you get excretion and detoxification of certain heavy metals that are really. you know, robustly excreted through sweat, things like cadmium and aluminum, for example. So I do think there is, like, unless you're going to be doing, you know, are you going to be doing 3 to 5 times what the CDC recommends, which is 75 minutes of vigorous exercise a week or 150 minutes of moderate exercise, so 3 to 5 times that, or are you just going to, like, sit in the sauna for an additional 20 minutes on top of that and get benefits.

Because if you're only going to— I think that there's an argument to be made to do both the sauna and exercise. Not to mention, the sauna really robustly increases growth hormone because it is a very big stressor on the body. And growth hormone supports collagen synthesis in the tendons and muscles, joints. And that is really good for strengthening muscles, preventing injury. And I think it's just— It's good for joint health in general. So I think there's an argument to be made for that as well. And let's see, last couple of questions, rapid fire. James asked, what do Yamanaka factors do in the human body? We aren't a species that typically despecializes our cells after they form. Is there a purpose for these genes naturally? So the Yamanaka factors are transcription factors.

There's 4 of them. What they're doing during— they play a very— they're transcription factors that are coordinating the activation of many different genes at specific times during development. They're very important for basically telling different cell types to become this type of cell and that type of cell and so on. And so, they play a very, very, very important role for determining cell fate during development. Beyond that, they also can play a role when they become activated too much in cancer because there's a lot of overlap between, interestingly, development, like stem cells, cancer, and aging. and reversing aging. And it's like the interface of these— this overlap that it's fascinating to me.

We don't understand it, but there's something going on there between, you know, reversing aging and basically making a cell become a stem cell, or even just making a cell and wiping out its epigenome and making it young again, and development. So, there's a big correlation between these things. Like, there's some kind of program, almost like aging is a program. But then on the flip side of that, there's something also going on with cancer that correlates with these same things that are regulating, you know, the development process. So a lot of interesting work to be done there. Heather asked about kids and COVID. I discussed my protocol, so she kind of wanted to know what I did. For my son when he had COVID. So what I did was I did vitamin C chewables by Swanson, 500 milligrams.

I did it like every 2 to 3 hours. I also did zinc lozenges, the little tiny ones, but the orange-flavored ones by Life Extension. And I did— I was doing up to, um, like 40. I think it was like 40 milligrams a day. And, um, And then I was doing the omega-3 gummies, the zero sugar one from Pure Encapsulations. And what else was I doing? I think those were the main ones I was doing for my son. Yeah, those were the main things I did. And then his multivitamin on top of that. All right. So big question from Isabel this time around was about my supplements. Richard's asking whether or not my son was vaccinated. No, no, he's not vaccinated.

He's still 4, and I'm not sure that I would or would— will vaccinate him ever, because I think there's been increasing evidence coming out, first of all, that vaccines are no longer really effective against, you know, Omicron and all the subvariants of Omicron, whereas they, they were much more effective against the Beta variant and even somewhat still effective against Delta. They're just Omicron and all the subvariants of Omicron are completely escaping vaccine immunity. Vaccines do seem to be beneficial for older at-risk people with comorbidities that might have a risk for severe COVID.

Most children do not have a risk for severe COVID, and so I don't really see an argument to be made to vaccinate To be honest, I just, like, if this was the beta variant, there I could see an argument to be made. It was actually preventing people from getting, you know, SARS-CoV-2, but that's just completely not the case anymore. It's a new virus. You know, we have to always reevaluate new data. And on top of that, the myocarditis risk, particularly in young boys, concerns me. There's just been more and more and more evidence that has come out over the past year that has convinced me that the risk is not worth the very, very, very small, if any, benefit in children. So that's kind of my stance on the vaccines.

Again, as soon as Omicron sort of dominated last— what was it, last Christmas, last December, January, started to come, started to really take over. And with all that new data coming out where vaccines were no longer protecting against getting infected. I just didn't feel that there was any real benefit to getting vaccinated unless perhaps a person who is, again, comorbidities, old, at risk, just autoimmune, you know, immune compromised. Like, I think there's an argument to be made for those people that, you know, vaccination may help prevent a severe type of COVID River's asking about loading creatine. No, Stuart Phillips said that is complete garbage. You do not have to load creatine, like, at all. So, you know, I definitely wouldn't be loading the creatine.

But that kind of leads me into my next topic on my supplements. So Isabel asked update on my supplements. So here's the update. And I kind of like— I do kind of every couple of months kind of swap out and try new things. So it is kind of good to ask. First and foremost, I am taking my— I take 4 to 6 grams of EPA and DHA daily. If I'm doing the 6 grams, I get— I'm getting 3 grams of EPA in the morning and 3 grams of DHA in the evening. If I'm doing more on the 4 grams range, then sometimes it'll be just one or the other, and I alternate. Like, I'll do 4 grams of EPA one day and 4 grams of DHA the next day. So I'll alternate, or sometimes I'll do 2 and 2 of each. the same day. So, I kind of go between 4 to 6. I take, for my multivitamin, I kind of do one month.

I alternate one month between 2 different multivitamins. I do one by Pure Encapsulations and then I do 2 Basic by Thorne. So, I kind of switch between those. I do my vitamin D supplement. I usually do Pure Encapsulations for that. And in the summertime now, I usually am, you know, like in winter, I'll do 5,000 IUs, but right now I'm doing 2,000 IUs. Because I'm also getting some from my multi as well. I do vitamin K2, 45 micrograms of MK-7 by Life Extension. I do a magnesium citrate malate combo by Pure Encapsulations. I take ubiquinol, 200 milligrams. I also take CoQovia, the cardioprotective version of it. And then I've shifted my sulforaphane from Prostaphane, which is kind of increasingly more challenging and annoying to get, to the Brock supplement, which is the same as Prostavane.

It's like the same company now that's like, they're making it in the US. And so I've started ordering that. And then I'm taking Autophagy Renew mostly to get the luteolin from it. And I'm getting that by Life Extension. And so that's got about 165 milligrams of luteolin in it, which is really good for the brain. And then I also am sometimes taking Brain Reset, and that has— that's from Pure Encapsulations, and that also has luteolin in it, but it also has lion's mane, and it has some other things in it as well. So, like, I'm kind of experimenting with that recently. And then I ordered my creatine, which I got in from Thorne, and I think I'll probably be getting 3 to 5 grams of that I'm going to be experimenting with as well. And then at nighttime, I do take a high dose of melatonin.

And that is, again, because I— it's like it treats my night terrors. So I take anywhere between 10 to 20 milligrams of melatonin. For the— with respect, people in the chat asking about summarizing the supplements, I can in the email that we send out. I'll have the bulleted list of the supplements. Okay, so the next question that was also— there was a big interest in this question that was submitted by David. David says, I keep hearing more studies associating egg consumption with overall mortality despite the valuable nutrients they contain. Can you give a summary of where the research currently stands on egg consumption and health outcomes? Is there any safe number of eggs per week? Or type of egg that is deemed safe and not controversial? Thanks. Okay.

So I did cover egg consumption and cardiovascular mortality, which is sort of the big concern with egg consumption. I covered that in Crowdcast number 25. I will go into it a little bit again. I'll say this, with respect to the number of eggs that are safe, you know, per week, per day, That's not controversial. That has been sort of spelled out by the American Heart Association. And so they think that 2 eggs per day are safe, and not only safe, but reduce stroke risk. So I would say that 2 eggs per day is pretty non-controversial if the American Heart Association is currently saying that that is safe. There was a study that came out of Australia that found eating up to 12 eggs per week for a year did not increase cardiovascular risk factors in people with prediabetes and type 2 diabetes.

In general, like, so there was a huge study that came out. This was, again, from the American Heart Association. It was a science advisory meta-analysis. And they found, in general, egg intake was not significantly associated with cardiovascular disease risk. With the stroke meta-analysis data they analyzed, in fact, the high egg consumption, so more than 7 eggs a week, was significantly associated with a significantly lower risk of stroke risk compared to a low intake of eggs, so 1 or less than 1 egg per week. And with coronary heart disease, there was no significant association observed between egg intake and coronary heart disease. However, among individuals with type 2 diabetes, there were 2 out of 3 studies that reported an association.

So it seemed as though there was something going on between people that had type 2 diabetes, potentially had type 2 diabetes, and were eating eggs. A meta-analysis of 17 different intervention trials reported an increase in total cholesterol. It was very minor. So there was an increase by 11.2 mg per deciliter. And an increase in LDL cholesterol, 6.7 mg/dL, and an increase in HDL cholesterol of 3.2 mg/dL compared to the control group. And the intervention group included studies that basically— I mean, it was basically equivalent to consuming between 3 to 7 eggs per week or about 0 to 2 eggs per day. I would say that like generally, again, 2 eggs per day is what seems to be pretty safe and non-controversial.

The ones— this one kind of study that made headlines, I think it was 2019 study, and, you know, it had found an increased risk in cardiovascular mortality with egg consumption. But then when they started to do all this covariate and adjustment for different types of other lifestyle factors, again, a lot of those associations were no longer significant, you know. So when you start to look at, oh, people eating processed meat and also then eating eggs, then the association with cardiovascular-related mortality went away. Or, you know, when you started to take in other cholesterol components The cardiovascular mortality went away. So I think that there, you know, again, some of the conflicting data does really come from the fact that like, okay, does this person have type 2 diabetes?

What else are they eating? Are they eating a stack of pancakes with syrup along with their eggs? You know, I think there are important things to consider when you're looking at a lot of these studies. And then looking at meta-analyses, and that's really important because like when you're looking at the meta-analyses, they're looking at many, many, many different studies compared to just one study that comes out, even if it's a big study. You have to look at the totality of evidence. And so, you know, I do think that the totality of evidence is really important. Generally speaking, dietary cholesterol, it's not really like the amount of dietary cholesterol that's actually converted into cholesterol, like, it's so minuscule, it's almost just not even important.

And that's really just an outdated sort of view of, you know, dietary cholesterol intake. Like, that was like back in like the '80s, you know, '80s and '90s. And we've now learned that our body's making cholesterol. And in fact, saturated fat is a much more— larger component to regulating our cholesterol levels than actual eating dietary cholesterol, which is relatively high in egg yolk. It could be, you know, up to like 300 milligrams or something like that. It can be found in eggs. I will say this, if you're wanting to be on the safe side, again, 2 eggs per day is pretty non-controversial. And so I think that kind of answers an important part of David's question there, which is like what amount of eggs per day is considered safe? And I would say, 2, for sure, 2.

When you start to go beyond that, then, okay, then we maybe start having to consider all these other factors. What else are you eating? Are you sedentary? Are you overweight? Do you have type 2 diabetes? There might be other things to consider that may, a big emphasis on may, influence cardiovascular disease risk. And I still think that it's a big may. With that. So eggs are really great because it's an easy way to get protein with your breakfast, which is, I think, a really important thing to get with each meal after the Stuart Phillips podcast particularly. I'm pretty convinced. And there's also a lot of lutein and choline and other things that are really beneficial in the egg yolk specifically. So I do think that That eating 2 eggs is definitely safe.

I honestly, most of the time, I actually eat 3. I personally am eating 3 eggs a day. So obviously, I'm not feeling concerned over eating 3 eggs a day. And again, I think there's so many confounding factors when it comes to nutrition studies. Yeah. And when you look at the actual intervention trials where they're actually controlling for things, it's not just a dietary recall, they're saying, okay, eat these many eggs, and they're eating them for that designated time, you actually start to see a reduction in like stroke disease risk, stroke risk and stuff like that. So I find intervention trials a lot more compelling, and intervention trials seem to by and large be very positive for— with respect to the egg consumption data.

I also try to eat pasture-raised eggs because they're much higher in a lot of these carotenoids like lutein and they're just better. I mean, you can tell the difference in the egg yolk when you— my favorite brand is Happy Eggs. Those Happy Eggs, they have really, really just orange and brilliant colored egg yolks compared to if you just get your standard white egg that's non-pasture-raised. So I do think that if you can— I mean, food is so expensive these days too, though, unfortunately. It's kind of hard to— you kind of have to choose your battles. I don't think that eating a non-organic egg is going to be terrible for you. So I think that's okay. So, the next question that was of interest was submitted by Chad.

And Chad was asking about any concerns with vitamin K2's negative effects on lipids. He linked a study that was for MK-4, and he wants to know if it would be MK-7 as well. So, I'm not concerned. I wouldn't generalize the results from this study to humans because it was an animal study in genetically modified mice that were fed a very Western high-sugar, high-fat diet. And the effect of vitamin K2 on blood lipids was really not even the purpose of the study. It was designed to act, you know, assess whether or not vitamin K2 could reduce calcified aortic valve disease. So, in fact, in a small study on people that were on dialysis, vitamin K2 was shown to be beneficial for blood lipids. It reduced It actually significantly reduced total cholesterol and LDL cholesterol.

So I'm really not concerned with the genetically modified mice that were on a very American Western diet. Cynthia asked about cautions against hormone replacement therapy for menopausal women, still based on what she called a flawed women's health study. And then she mentioned someone's book, Dr. Bluming's book on Estrogen Matters. But would like to know my insights on it. So for background, the Women's Health Study, it's an ongoing observational study run out of Harvard and the Brigham Hospital. It consists of over 30,000 women. It started in the 1990s and has resulted in over 600 publications with a focus on preventative medicine. I wouldn't say that the Women's Health Study is flawed so much that it has limitations because of the nature of its design.

It's a prospective observational study. study, which means it's susceptible to observational bias. It's susceptible to recall bias, response bias. So there's a lot of limitations with observational prospective studies, which again, the egg study, one of the egg studies we just talked about that hadn't showed an increased risk for heart disease was one of those types of studies. There have been several blinded randomized clinical trials that have sprung up from the original observational data from the Women's Health Study. And these randomized controlled trials, they've identified that combination estrogen hormone therapy increases the risk of heart disease, which was previously thought to be cardioprotective.

And it also confirmed an increased risk of breast cancer, venous thromboembolism, and stroke. In fact, the studies were stopped early because of these concerning findings. The publication regarding hormone replacement therapy and breast cancer though, there was a subset about almost 18,000 women who were followed for 6 years and they found 411 cases of breast cancer. So it found there was a 37% increased relative risk of breast cancer incidence in those who used estrogen progestin therapy compared to the control group. Now, I haven't read Dr. Blooming's book, but there's a point to be made that, you know, these findings are all relative risk. So it's very different from absolute risk, right?

So the absolute risk for breast cancer was about 0.1%. So you could make an argument that relative risk is really not as important because the absolute risk is so low. So in other words, for every 1,000 women that were treated with hormone replacement therapy, 1 additional woman would get breast cancer, 1 additional woman out of 1,000. And you might go, oh, that's kind of a low absolute risk. I think the more important thing to think about with absolute risk is what is your personal absolute risk for breast cancer? Is there a family history? Do you have genetic predisposition? Are you overweight, obese? Do you consume excess alcohol? Those are really big factors for breast cancer. So I think there are things to consider.

The observational data has been followed up with randomized placebo-controlled studies. There was one with 27,347 women. It found similar results. In other words, estrogen replacement or estrogen progesterone replacement therapy increased the relative risk of breast cancer by 24%, but the absolute risk was only increased by 0.1%. So I think, I think in conclusion, hormone replacement therapy used to be viewed as completely harmless and it was prescribed liberally to many post— most postmenopausal women. Since the Women's Health Study and a variety of actual randomized placebo-controlled trials, there's, there's been a little bit of a swing in the pendulum. In other words, now doctors are a little more hesitant to prescribe it.

And they use a lot of medical guidelines like, okay, let's do the quote-unquote least amount of hormone supplement necessary for the shortest amount of time. So I do think if you look at the data more closely, it does seem that the risks of hormone replacement therapy— there's a real risk, but it's small. It's a small risk. So ideally, I think women should talk to their physician, have a very open and candid conversation about their own their own already risk for breast cancer and whether or not the absolute risk, the 0.1% increase in absolute risk, is something for them personally to be concerned about.

And so this is a much more personal approach to take with the physician and figure out whether or not having hormone replacement therapy would be even a big concern for for someone personally. There's a lot of questions in the chat about other factors for hormone replacement therapy, which I cannot answer off the top of my head. I do recall also covering hormone replacement therapy a little bit in another episode of— another Crowdcast episode. But again, if you have some more questions that you'd like to specifically be answered, submit them for next time. You know, I haven't had to really— eventually I will have to face that question as well. And, you know, for me, there's not a history of breast cancer. I don't have risk factors.

I don't have genetic risk factors or lifestyle risk factors for breast cancer. But, you know, breast cancer is a scary concern. So, you know, I think it is a little bit— it does make me feel better that the absolute risk for breast cancer was so small. So for every 1,000 women treated, there was one person, you know, was getting breast cancer. A 0.1% absolute risk is a pretty small absolute risk. So that does make me feel a lot better with respect to the breast cancer concern. There have been some people asking about this low-level laser therapy for reversing hair loss. So Sam from Hong Kong asked the question, says Dr. David Sinclair recently said on his podcast that is— that it is legit, to his own surprise, and a hair specialist on Dr. Peter Attia's podcast also endorsed it.

The high-quality version of this is very expensive, and I'd appreciate if you weighed in and had a look at the data as well. I previously talked about low-level laser therapy in Crowdcast number 29, so you can go back and look at that in depth. There was— there's a lot of marketing that has gotten ahead of the research, I will say that. And at that time, there was very little human data, and I wasn't super convinced. Since then, a new paper came out, and it was a systematic review and meta-analysis of randomized controlled trials in the United States Uh, it says Food and Drug Administration approved home use low-level light laser therapy devices for pattern hair loss.

So this study, the researchers searched through the available literature and compiled all the data from studies that had a sham control, and they found that there was a small but consistent benefit to laser therapy. Um, I don't know which commercial products work though. I wouldn't be fooled by the, the FDA-approved title. So a lot of companies will advertise that they're FDA approved, but it's really misleading because they're FDA approved for safety, not efficacy. So in other words, they're FDA approved to not harm you, but they're not FDA approved to actually regrow your hair. So there's, there's no light therapy that is FDA approved for actual hair growth. That's really all I have. It's, you know, I think there's a possibility of it.

And, you know, it's just there was a small benefit, you know, so compared to the sham control. So it's interesting. It's certainly interesting. And for people that it's relevant for, maybe it's worth a shot. Really, like, on the same topic of hair loss, this has been a question that has come up quite a bit with respect to to creatine monohydrate supplementation. So I mentioned that I'm, you know, I actually ordered it for myself. I ordered it for my mother and my father. And the biggest concern I had seen, you know, I'm very interested in the effects on the brain and the positive— and this is, you know, beneficial effects on the brain in humans and also in And muscle. So, so I'm, I'm, I've gotten really interested in taking it.

But then once I— because we've got a topic page on it, you know, you can go and read about it. But also after having Stuart Phillips on, who also talked about benefits and said it was really safe, a lot of people have reached out to me and said, oh, they're concerned about some kind of hair loss, creatine supplementation causing hair loss. And so So the question really has to do with, with the hair loss and the side effects, and is it, is it a concern? I would say I think it's pretty safe. And the vast majority of the speculation regarding the relationship between creatine supplementation and hair loss and baldness really stems from a single study.

And the study was, was by Vander Mirway, and it was basically where college-aged male rugby players, they supplemented with creatine and they had— they did this loading phase, which is absolute rubbish. You do not have to do a loading phase. They were doing 25 grams a day for 7 days and then followed by 5 grams a day after for an additional 14 days. And they experienced an increase in serum dihydrotestosterone. DHT, and specifically the DHT increased 56% after that loading phase. So after that 25 grams a day for seven days, and then they remained elevated above baseline for 40% above baseline for that 14-day maintenance period where they were doing five grams a day. The results were statistically significant compared to when the other participants consumed a placebo.

And so that— so the DHT, again, it was elevations in DHT which have been linked to some but not all occurrences of hair loss and baldness. And the theory is that creatine supplementation may lead to hair loss and baldness because of that elevation in DHT in that one study. And again, the one study where they were doing 25 grams a day For 7 days and then followed by 5 grams a day. DHT is a metabolite of testosterone. It's formed when the enzyme 5-alpha reductase converts free testosterone into DHT. So in males, DHT can bind to androgen receptors in susceptible hair follicles and they can cause the hair follicles to shrink, ultimately leading to hair loss. That's the whole sort of mechanism. But the DHT, again, is formed from free testosterone.

To date, there have been 12 other studies that have investigated the effects of creatine supplementation ranging from 3 grams a day to 25 grams a day on testosterone. 2 studies reported physiologically insignificant increases in total testosterone. While the remaining 10 studies had no change in testosterone concentrations. 5 of these studies looked at free testosterone, which the body uses to produce DHT. And again, no increases were found. So I just don't know whether or not the concern is real when you literally have like 12 other studies, none of them have found any changes in testosterone at all. And you'd think that if DHT was going, you know, through the roof, that you would see those changes in the testosterone as well.

So I think that one study is sort of what sort of sparked this whole concern over hair loss. And I don't know how much of it is really just paranoia and wives' tale versus actual, like, fact. You know, because if it was actual fact, you know, creatine sup— people are using creatine supplements and there's so much data on creatine supplementation. Like, you, you'd think that would be found and that would be replicated more than just that one study. So, um, I really think that's, you know, take it with a, a huge grain of salt. So there were some other questions in the chat on— Mary Ann asked about collagen supplementation and recommendations for, you know, creating a plan of collagen supplementations.

I would say look at our topics page on hydrolyzed collagen because we cover a lot of, of the human studies and clinical trials on hydrolyzed collagen supplementation for a variety of different purposes. And I think that that's like right now the resource that I go to and the best the best resource that I've seen with respect to high-quality data on collagen supplementation as well. And again, I do use the Great Lakes brand of hydrolyzed collagen for my collagen supplementation as well. All right. So with that said, I think I've gone through all of the questions that I was going to get through today. Thank you guys so much for all of your amazing questions and for all of your support and for attending these live. I really enjoy the live chats.

They're really fun to know that people are here and interested enough to like take time out of their Saturday to come spend it with me and with all you guys and, you know, dive into some of the science stuff. Again, Ask a question section is where you should submit your questions. Ask them, you know, for next round, and we'll get into as many of the deep dives and rapid-fire questions as usual. And as you guys see, I do go back and answer questions from previous Crowdcasts. So if you want to resubmit your question, if I didn't get to it, you can always resubmit it again. But don't worry, I also do go back and I go through some of the archives as well. So make sure you, you know, if you want to submit the question I didn't get to, make sure you go to the Ask a Question and submit it again.

And if you guys enjoy these Crowdcasts, please tell a friend, share it with anyone you think that could benefit from them. It's always great to share, you know, this information. And hopefully we'll have some amazing questions next time. I look into— I look forward to diving into them. I learn so much from these Crowdcasts as well. They're a lot of fun for me. So you guys have a great weekend, and I will see you guys soon. So we'll we'll be talking on the first Saturday of of August. So sooner sooner than later. All right, bye everyone.