Hi everyone. Welcome to Crowdcast number 41, November edition. A little bit late. I've been traveling, but got back late last night, avoided a hurricane in Florida. All is well. For those of you that are new, typically I go through questions that were submitted in the submit a question section at the bottom of the Crowdcast toolbar. And I choose top-voted questions. I choose questions I have not answered before, questions that'll be interesting to the audience, questions that I'm just interested in doing a deep dive in. Typically, we do a few deep dives depending on the pool of questions. We may do more deep dives one month and fewer the other. And then I go and do a variety of rapid-fire answers to questions.

These are questions that don't involve a really deep dive research analysis, and so it's something I can answer in a sentence or 2 or something like that. I like to try and answer questions in the live chat section, and that's sort of the benefit of attending these live is that you get to submit a question in the chat section. And I already see that there's quite a few people that were submitting some Keep in mind that typically I'm not going through the chat until I'm here live, and at that point I start at the end of the chat, and so your question may not— may have been overlooked if you didn't put it in the submit a question section. I do see a couple of questions in that chat section that I will be addressing. For example, ApoE4 and omega-3.

We're going to be talking in detail about ApoE4 today. It's been a while since I've done a deep dive on that, so it's always good to kind of do a literature review and see what's new or maybe what's changed in terms of, you know, the scientific literature. So I'm going to go ahead and get started. And for those of you having, you know, if you can't hear anything or something, most people are hearing it, so there's probably something wrong with your setup. So just go ahead and try to Try to troubleshoot that. I'm going to go ahead and continue. You guys can always download the video again, watch it on YouTube. We send out a summary email with timestamps, and we also then post it to the Aliquot Podcast, which is our private members-only podcast.

We just released a new episode last week, sent out an email this morning. So you we we usually release episodes about once a week. So make sure you have if you haven't already. Downloaded your private podcast feeds, you can find that on your dashboard at foundmyfitness.com/dashboard. And you can listen to the aliquot right there on the dashboard, or, or you can download your private podcast feed so that you can just download episodes and have them notify you when they come out. So one of the, one of the first questions that was also one of the most top-voted questions was submitted by Lisa, and Lisa was asking about what topics my viewpoints have changed on most significantly over the past couple of years.

And I would say probably at the top of that list, pandemic-related stuff aside, would be my thoughts on protein consumption and aging. And I think that, you know, we've had a couple of really in-depth conversations about this over the last couple of Crowdcasts. We did a real deep dive one, like, 3 months ago or something. So I'm not going to go and rehash all of that. But essentially, you know, when I was in training and, you know, a young training scientist, and particularly You know, in the aging field and just also being, you know, interested in reading all the latest studies, you know, coming out, you know, over the past 20 years, you know, 20 years or maybe I should say more like 15 years.

I would say that it was really dogma that low protein intake or, you know, basically decreasing protein consumption was the way to go for healthy aging, longevity. It was, you know, at the molecular level activating, you know, stress response pathways, and it was also suppressing mTOR activation, which was largely thought to be beneficial because mTOR can play a role in cancer. It can play a role in cancer growth. And And so there's just a lot of animal data out there showing that if you restrict protein consumption, animals' lifespans are extended, their healthspans are extended. And again, we've talked about this a few months ago.

So I think over the years, as I started to shift more to, you know, first of all, doing clinical research in my postdoc and then understanding clinical research and understanding differences between a lab animal in a sterile environment, in a very controlled environment, and human aging, I realized that even though there's these molecular mechanisms that are probably still conserved to some degree between, you know, for example, a rodent and a human, like mTOR, the environment is very different. And it's not just about it, you know, I think people always want it to be Either black or white. There's no shades of gray, and unfortunately biology is all shades of gray. There's tons and tons of nuance. Nuance never goes viral. Goes viral is this or that, right?

But the reality is is that there's always nuance, and you know, with respect to mTOR activation, it's another one of those areas where you actually—it's not that you don't want mTOR activated; you actually really want it activated in your muscles, your skeletal muscle, and muscle mass is so important for aging. And protein intake is one of the 2 signals that is essential for activating mTOR. And so I think that's probably one of the biggest— one of my biggest viewpoints that has changed over the years.

And there's a lot of, you know, there's a lot of really good scientists, Valter Longo, for example, who is really— he's an advocate of low protein intake and he's got, you know, really well-done controlled animal studies beautifully showing causation and mechanistic causality and how low protein consumption basically can extend lifespan and healthspan in mice. And then with the epidemiological data, it's always observational data and it's always comparing vegetarians to omnivores. Meat eaters. And again, it's just— you just can't compare apples and oranges because you have meat eaters and then you have meat eaters that are physically active. You have ones that are not eating refined sugars.

And those aren't the same as people eating meat that are sedentary and not, you know, not avoiding refined sugars. You know, so they're all lumped together in the same category. So I— it just doesn't fit. I don't think the big picture is, oh yeah, we should reduce our protein intake. I think the big picture is We need to be physically active. We need to take in enough protein to maintain and sustain our muscle mass. And particularly as we're aging, I mean, it's— we're staving off atrophy. And we need to avoid, you know, eating refined sugars and refined carbohydrates. And I think to a certain degree, a lot of processed meats as well. I think there's really been a lot of mounting evidence that processed meats aren't really great.

So I think that, again, that's my biggest probably paradigm shift over the years is protein intake. And I think that it's really not bad to take in more protein. And in fact, it's good. But you have to be physically active and you should be physically active. And that is— I think that's the key is just being physically active. So, so that's one of the biggest, my biggest paradigm shifts over, over the years. And then I think of late probably would be a little bit of my stance on, and I don't want to like emphasize this so much, but like the COVID vaccines, as, as the COVID as the SARS-CoV-2 variants started to shift and we went from, you know, Delta variant to Omicron, and now we're in tons of different Omicron subvariants.

The shift from Delta to Omicron was really a new virus in a sense, in many ways. And so, you know, with the new virus, it being, you know, 70 to 100 times less likely to go deep into the lungs, and, you know, people are not going on ventilators like they were, it's just not as severe of an illness in most people. people. There's always exceptions. There's always immunocompromised people and people obviously that are susceptible still to severe COVID. But generally speaking, it's a different virus. And as that virus changed from Delta to Omicron, the vaccines no longer were doing really anything for preventing the spread. And I think it's like, well, now we're talking about essentially a flu vaccine in a sense where flu vaccines don't prevent the spread. Flu vaccines are optional.

They're for people that probably get a severe flu and are at risk for severe flus, which can be severe in people. And so the COVID vaccines have now kind of shifted to that category. I mean, they shifted a while back, almost a year ago, actually. And I think Before that time, I wasn't—it wasn't that I was so, you know. I—I think I was against particular pieces of information that were floating around that were just inaccurate, and I was trying to counter the inaccuracy on those. And that kind of got blown up into a Rhonda's just pro-vax, and it's like, well, not necessarily. I—you know—never was like all people need to be vaccinated. I just was against. inaccurate data and people misrepresenting things.

And so, um, and I do think that there's new data that have come out over the past year since I've talked about it a little more publicly, uh, with respect to the myocarditis issues. And I think there's more and more evidence that myocarditis certainly is an issue in young, healthy men and boys as well, boys and men. And I think that That's pretty alarming for young, healthy men, young, healthy boys who are not a— I mean, you know, COVID's just kind of like a bad cold. And so why would they put them— why should they put themselves at risk for, you know, potentially more dangerous disease or, you know, transient disease? I don't really know. We don't really know exactly if there's long-term effects with myocarditis.

So that's another area I would say has shifted because the data has shifted, right? We've got new viruses, the vaccines are different, they're not doing what they were doing when we had the original strain or even the Beta variant and Delta variant. So those were my biggest paradigm shifts as well. I see a couple people here in the chat from Florida. I saw Fort Lauderdale and Orlando. I was with you guys through Hurricane Nicole. I was in Palm Beach. I gave a talk, really a large event Tony Robbins put on. There's about 9,000 attendees. I talked all about sauna and cold therapy. And literally the hurricane hit like 2 days after my talk and we were heading to Orlando to go to Disney World. And so glad everyone is okay there and I made it out of the hurricane.

Being from California, that was definitely a different experience for me. James is talking about chronic illness from having COVID-19. And again, that's also something not to be ignored. I will say this. I think that COVID-19 is not the exception. Respiratory illnesses in general cause long-term illnesses. They also unlock— you know, type 2 diabetes or even type 1 diabetes in people. I think that COVID has been under a global magnifying glass. And so people are much more aware of the fact that infectious diseases can really, in some people, cause long-term effects. I don't know that this is just, you know, isolated with COVID I mean, I think there's— infectious diseases in general do this in some people.

Infectious diseases can be, you know, long, long-lasting, and, you know, the SARS-CoV-2 virus is no different. So I do think that, of course, there's always the risk for, you know, lingering effects with COVID or any other infectious disease. I don't know if we have real evidence to suggest that getting an mRNA COVID-19 vaccine with now the Omicron subvariants that we have, if that's doing anything to protect against long-term COVID. It might, or it might not. I think, you know, it's really, it's just hard to know. There may be a little bit of a, A reduced risk for long-term effects. I mean, in some cases, the more severe the illness, the more— the higher the risk of having a long-term effect, but that's not necessarily always the case.

In some cases, some people can have a mild case of COVID and still have, you know, lingering effects for many months. So, um, so that's, that's something to also consider. And Roman's talking about COVID risk, COVID-causing myocarditis, and that risk for myocarditis being higher from COVID-19 versus vaccination. And again, it's one of those things where everyone wants to say it's either that or the other, which would be no, vaccination's giving you a higher risk for myocarditis. But guess what? There's so much nuance and data shows both.

And there's probably a lot of little things that we just still don't understand about that, like certain subpopulations of people perhaps are higher at risk for COVID-related, COVID-19-related myocarditis, where other populations of people are at risk for COVID-19 vaccine-related myocarditis. Or perhaps people that were vaccinated and never got COVID, maybe if they had gotten— if they were vaccinated and they got myocarditis, perhaps they would have gotten myocarditis even worse from COVID-19. There's a lot of nuance. We don't really know But at the end of the day, the reality is that both COVID-19 and COVID-19 vaccinations, particularly the vaccinations are really in young men and boys, they're causing a myocarditis risk.

And so I don't think the data is clear enough to make the blanket statement that if you get vaccinated, you are going to protect yourself from myocarditis because COVID-19 is going to give you worse myocarditis. I don't think there's data to suggest that. suggest full stop that. Now, there is, again, you'll find one study that shows that and you'll find another study that shows the opposite. Usually when you have conflicting data like that, it's because there's nuance. There's things that we don't understand. There's confounding factors. There's other little subgroup things that are going on. There's something happening and we just don't know exactly what that is. So I don't feel comfortable making a blanket statement. I don't think that there's data to suggest it either way.

I think what we know is that Both of those things can increase myocarditis risk. And at the end of the day, you know, you got to pick and choose your battles. I think that most people have had COVID-19. If you've already had COVID-19 and you didn't get myocarditis, then you're probably okay and don't have to worry, you know. So, for example, my family had COVID-19. I was vaccinated and I've also had COVID-19. I don't plan on getting any other vaccinations. My son had COVID-19. He was not vaccinated, and I do not plan on vaccinating him. I do not want to put him at risk for potentially myocarditis. He probably wouldn't get it from a vaccine, but there is a risk, and he's already had COVID, and it wasn't a big issue at all for him. In fact, it was almost like he was sick for maybe one day.

I mean, it was really mild for him. And he had no long-term effects or anything like that. So I'm really not worried at this point. point. So I really think that it's really a personal decision. I do think, again, I think the myocarditis risk, particularly for young boys and young teenagers, and even young, young men, like 30 years old, young healthy men, obese, unhealthy guys, type 2 diabetes, people with these comorbidities, COVID-19 may be a little bit more severe. And so perhaps— the vaccination could outweigh the risks for that. But again, COVID-19 is different than it was, you know, a year and a half ago. So it's really much more mild, and I think that it's something that people, you know, as data changes, our, you know, our understanding of things needs to change as well.

So certainly mine has, and I'm sure many of yours has as well. A lot of the data out there, you'll see headlines like COVID-19 leads to brain atrophy and Alzheimer's disease risk. Again, this is all data from early, early variants. This is data from the, you know, original strain, the beta variant, a lot of it from the beta variant, and even some delta. A lot of it, mostly, most of the Alzheimer's disease risk stuff is from pre-Omicron as well. So you'll see these study headlines, and again, it's almost— it's like it's a new virus in a way, in many ways, you know, where it's just the Omicron virus is so different from what the other, the parent variants were.

So it's one of those things again where it's like, okay, this headline comes out because, well, People get clicks when they have a really strong headline, and, you know, no one's paying attention to the fact that this Alzheimer's disease risk, they should probably put it, you know, in bold that this was the, you know, X, Y, or Z variant. That way people can understand we can't generalize it to every COVID-19 variant as well. So anyways, that's— I won't spend too much time talking about all that. But, but that's, that's generally my, my, uh, some of my paradigm shifts over the last, I would say, um, 2 or 3 years. So we're gonna do some really, um, we're gonna do some deep dives today. One in particular is gonna be on the ApoE4. But first, I'm gonna hit, uh, the question.

There was a couple of questions on hydrolyzed collagen powder. So Hillary and Angela both Both asked about hydrolyzed collagen powder and how it's different from getting amino acids from just you know whole protein. And I would say that starting out, it's important to understand that collagen there's really three very abundant amino acids in it, and it's a tripeptide. So it's three amino acids strung together. So they're They're they're bound together, and those three amino acids are glycine, proline, and hydroxyproline. Now there are different types of collagen. So for example, type three collagen contains more hydroxyproline compared to types one and two. And you know, so you'll find a little like subtle differences between types one, two, and three collagen. But generally speaking.

The major difference between amino acid composition and collagen and just whole protein is the glycine-proline-hydroxyproline tripeptide. There's been some studies by the Protein Digestibility Amino Acid— there's like a corrected amino acid score. Collagen protein lacks one indispensable amino acid, which is tryptophan. And so it's actually categorized as an incomplete protein source because of that reason. It's also low in a few other amino acids like cysteine and methionine, for example. But if you're getting your whole protein sources, they're very rich in those cysteine and methionine, for example. Whole protein is actually— like, if you're eating a protein source that's animal-based or plant-based, you are not getting significant amounts of glycine, proline, hydroxyproline.

Those are not in abundant quantities in whole protein. And in fact, there's been some studies looking at whether or not it would be beneficial to supplement collagen peptides in a sort of whole, like, whole protein, with whole protein. So if the standard American diet was replaced with 36% collagen peptides, There's been some analysis showing that it would actually be more nutritionally balanced and beneficial because it's nutritionally balanced. And I thought that was kind of interesting because it suggests that really, it really may be beneficial to supplement with the hydrolyzed collagen powder. And so, I kind of like go through these like peaks and troughs with my collagen supplementation.

For whatever reason, sometimes I'll fall out of habit and then I'll like get reignited because I'll read a study or something and I'm like, oh, that's right here in my pantry. Why did I forget to do this for the last month? And so I do think that the collagen supplementation is beneficial. I would— so Luane is asking about supplementing with one type of collagen versus another for, for example, skin or tendons. And we have a collagen, a hydrolyzed collagen topic page that kind of goes into the details on all this. And I would say thousand-mile-high summary really is I don't think there's like— I don't think you really need to pay attention to all that.

Like, I think getting something like the Great Lakes hydrolyzed collagen powder, which is what I use, is gonna cover your bases— skin, tendons, and all that. And so I wouldn't really worry about trying to find type 3 collagen and all that because, first of all, there's also not a lot of research, a lot of, you know, looking at the different types of collagen powder on skin versus tendons, for example. So often what you'll find is, oh, they got funding from this source that happens to use collagen type 1 or type 3 powder, and so that's what they used, you know. LP is asking about vegan collagen supplements. I am not aware of that. How, you know, that would be interesting.

The closest thing that I would, that I've suggested for people that are sort of vegan-like, not necessarily vegan, but more pescatarian would be the marine-derived collagen powder, which also is beneficial. But I don't know that there is a real vegan source of collagen because it by nature is not. It's coming from an animal. So I don't know about that. I think that You know, it would be nice if vegans could take collagen powder. I do think those amino acids are very beneficial. And interestingly, there was a question in the chat about things to help with photo skin photoaging. This is a rapid fire question. I'm just going to throw it in right now because it's relevant.

And it's interesting because as my team and I were looking into some of the collagen research again, you know, we kind of do a a literature review every so often, um, it showed up that there's, you know, there's really some evidence that supplementing with hydrolyzed collagen powder helps protect against UV, you know, damage in the skin and photoaging— photoskin aging, sorry. So, um, again, that was one of those things for me that was like, oh yes, I got to get my collagen back, my collagen powder, because, um, I do— I often am pretty good about taking it, but for whatever reason, like the last I would say a couple of months, I just really haven't been taking it. I haven't been putting it in my coffee or anything. And so I started doing that again recently. I'll try to stick with it.

And if you haven't read our topic page on hydrolyzed collagen powder, it's on the foundmyfitness.com website. Click on the topics tab in the toolbar in the upper part of the page. And then you can skip down to C for— or no, H for hydrolyzed collagen powder. It's a really good topic page. You can look at the table of contents and sort of look and see what you're interested in reading about, but it's really good. I recommend you guys look at it. So the next sort of deep dive question was— it was a real deep dive actually, and it's something that I know a lot of people are interested in.

And for those of you that do not have, or, you know, aren't aware that you have an ApoE4 allele, I think— I still think listening to this section will be beneficial because it still covers APOE4 non-carriers as well. But the question was, and this was submitted by multiple people, can you review dos and don'ts specific to APOE4 carriers? And this was actually from last month's Q&A, and I said I would go over it next time. So we're going to start off with, and this was an interesting one to kind of revisit, Physical exercise. Physical exercise, there's no doubt. I mean, it's like the most beneficial thing that you can do to age better, period. I think like above diet, everything else, I really think physical activity is the best anti-aging drug that we have. Nothing compares. Nothing.

Nothing compares, period. So, there's every reason to, to be physically active. But let's just talk about some interesting details when it comes to physical activity and protecting. So people with APOE4, um, one allele have a twofold higher risk of— for Alzheimer's disease. They're also at risk for higher LDL cholesterol. They're at risk for, you know, of course, higher LDL cholesterol can also be associated with increased risk for cardiovascular diseases as well. So there's a risk for cardiovascular disease and Alzheimer's disease in ApoE4 carriers. People that have 2 alleles, so about 25% of the population has 1 allele, it's much more rare to have 2. I mean, it's very uncommon, but 2 is associated with a 10- to 11-fold increased risk for Alzheimer's disease. It's really, really high.

With respect to physical activity, it's really the thing that— the takeaway here that was very interesting to me was that looking at, you know, multiple studies, it appears as though, yes, being physically active does protect against the neurological problems of having an ApoE4 allele, particularly, you know, increased risk for cognitive decline and dementia and Alzheimer's disease. However, it really seems to be more beneficial if the physical activity starts earlier in life. In other words, if you have an APOE4 allele and you're already 50, 60, 70 years old and you've been sedentary your whole life, is it a good idea to start exercising? Absolutely.

There's tons of data showing that, I mean, you know, men even experience, if they start work, if they start, you know, becoming physically active, even in their 70s, they have like a 30% lower risk of, you know, heart disease in their 70s. You know, they're literally sedentary all the way up until their 70s. So it's always a good time to start. But if you're looking for protective effects, strong protective effects against Alzheimer's disease starting at a younger age is clearly more beneficial for people with APOE4. And the younger, the better. So if you're— if you've been physically active since childhood, you've got an APOE4, essentially, I mean, I would say that, you know, some studies show even a pretty similar risk for Alzheimer's.

So physical exercise upregulates brain-derived neurotrophic factor. And it also seems to really— and whether or not it's just the BDNF that is affecting the cognition, or there's probably many other things as well. But again, being physically active, 70 to 80% maximal heart rate, even 1 hour, 3 times a week. So essentially 3 hours a week, you know, really is beneficial for ApoE4 carriers with respect to benefits on cognition, less cognitive decline, less hippocampal atrophy. So that means, like, you know, dying neurons in the hippocampus region of the brain, which is important for learning and memory. And this is— you'll find comparisons that, you know, ApoE4 carriers that are physically active compared to ApoE4 carriers who are not physically active.

In some cases, starting physical activity early on can even just give you the same risk as an ApoE4 non-carrier. So again, that seems to be why it's so important to start early in life. And there's some inconsistencies in the literature, but again, it's also, you know, when you start to look at people that are starting in their 70s, it's not as beneficial. You know, you're already at a point where you've had, you know, a lifetime of, you know, ApoE4-related things going on in the brain, and you weren't physically active to kind of help, you know, buffer that. But again, it's never too late to start. So don't take that as a, oh, well, you know. I'm in my 70s, I have ApoE4, and I'm sedentary. I shouldn't— why should I start exercising? You should. It is beneficial. It is.

But it's more beneficial to start earlier. People without ApoE4 allele, same thing. I mean, not same thing in the respect of, you know, more beneficial earlier. I mean, I tend to think that, yes, anyone that's going to start exercising earlier in their life, they're going to reap— I mean, it's a compounding effect, right? You're going to build up your muscle reserve. You're going to preserve your bone density better. All these things, there's lots and lots and lots of, you know, cancer risk. All these things are going to be improved. So obviously, earlier is better. But ApoE4 non-carriers also have improved executive function. They have improved, you know, markers of cognition, and they have less brain atrophy. They have less dementia risk. They have less Alzheimer's disease risk.

Whether or not you're an ApoE4 carrier, physical activity is the king with respect to brain health. Like, if you're physically active, it's the best thing you can do to protect your brain from aging. And ApoE4 carriers really need to protect their brains from aging. So it's even more important for people with ApoE4 to be physically active. Should ApoE4 carriers abstain from wrestling and/or combat sports? Obviously, that's a personal decision. I would Personally, I would if I were someone that was into it. The risk, and the reason that Al's asking this is because traumatic brain injury is so much more pronounced in ApoE4 carriers. So, people that have one ApoE4 allele, one of the problems with ApoE4 is the repair mechanisms in the brain aren't as robust as having 2 APOE3.

So people with one APOE4 still have one APOE3 version. So they have one version that's still able to repair, but the APOE4 doesn't repair as well. And so what ends up happening, if you're looking at, you know, a lifetime of just normal brain aging, you know, obviously, there's repair mechanisms that are at play throughout, you know, throughout the lifespan. And, you know, so having a lower repair mechanism is already— you're already at a disadvantage. But when you're actually adding insult to your brain and you desperately need it, I mean, it's critical, the repair is critical, then you're talking about not even being able to, like, get above your head above water, right?

So I really do think that engaging in combat sports or any type of, of sports that, that has a high risk for TBI, soccer included, uh, or I guess football if you're in another— if you're in Europe, it's called, um— I, I think there's, there should, there should be some serious consideration. Obviously, like, there are people that have passions for it and it's going to bring them great happiness and joy in life. And, you know, obviously there's, there, there are things, there, there are things to There are pros and cons, right? So, you know, I certainly wouldn't say no, no one should ever do combat, any sort of combat sport if they have an ApoE4 allele, but they should definitely— I mean, is this just— is this your life's passion?

Is this, you know, or is it just something— can you— is there something else you can do that'll give you as much joy and that you can practice and spend a lot of time, you know, you know, mastering a skill maybe that doesn't involve a combat or a risk for TBI. So, um, I would, I would, I would say, yeah, I would definitely weigh, weigh the risks because the risks are really high for the, the TBI stuff. I mean, TBIs are bad in general, but for ApoE4, you're talking about— in some cases, I mentioned, um, you'll find some studies, and really it depends also on the level of TBI, right? There's different levels of it.

But you can take someone who has one ApoE4 allele, and as I mentioned, they have a, let's say, on average, generally speaking, a twofold increased risk for getting Alzheimer's disease compared to someone that has no ApoE4 alleles. And you can take that person, you go, okay, well, I have a twofold risk. I'm going to be physically active. I'm going to lower my— I'm going to get my risk down to what it's like to have no ApoE4 allele. And you can do that. But then let's say your physical activity is, you know, you're doing wrestling or, you know, or some other sort of combat sports, football, for example, American football, then you could get one TBI and that risk now goes up to like having 2 APOE4 alleles. Like it goes up to like tenfold with just one TBI.

And as you get more TBIs, you're almost guaranteed that you are going to be cognitively demented, not— and it's, and it's going to happen earlier in life. It'll be an earlier onset. So it's quite risky for people with APOE4 to get TBI, which is traumatic brain injury. Thank you. Uh, okay, so let's move on to some more. I saw people asking about alcohol as well, and we're gonna get to that. So that was the physical activity. Um, The other sort of interesting aspect was diet. So there's been some studies looking at a lot of observational data, which again is it's useful, but it's not like the end-all be-all, like we should make you know clear lifestyle changes based on this data kind of data, right? So there's evidence that have shown that high-fat diet.

increased total cholesterol, reduced micronutrient intake, so thiamine, folate, vitamin C, vitamin E, B6, choline, and several antioxidants, increased consumption of trans and saturated fats, as well as lower omega-3 fatty acids could predispose people to Alzheimer's disease and with ApoE4. And in fact, the highest The highest, one of the highest risk factors, interestingly, for Alzheimer's disease is lipid metabolism dysregulation. There's a lot of inconsistent data, so we're going to talk a little bit about it. I think the inconsistent data with respect to how diet affects cognition, generally speaking, could come down to, oh, did you do a subgroup analysis and only look at ApoE4 people? Because ApoE4 people can respond differently to different diets than people who have no ApoE4 allele.

And that may sort of make the data inconsistent where one study finds this, but the other study finds that. And you're like, well, is it this or is it that? And it's like, well, it's actually this and that. It depends on if you have this genetic variant. So Let's talk about one study. This was a study. It was a blinded random study. It was blinded in a random fashion. And it was about 50 adults, close to 50 adults. They either had cognitive impairment or they had normal cognition. The diet was either what was considered a low diet. So it was low fat. It was 25% total fat. 7% saturated fat and a GI less than 55. So that would— that just being a marker of carbohydrates. It wasn't like necessarily bad carbohydrates, it was just carbohydrates.

And then there was the high meal, which was considered high fat. So it was 50% total fat, 25% saturated fat, and then Interestingly, they also had a higher glucose index as well. But the cognitively normal ApoE carriers, so these are people that are not cognitively impaired yet, but they do have an ApoE4 allele, had improved cognitive performance after a meal with increased levels of total fat. saturated fat and glycemic index. So, um, they actually did better on a high-fat meal than a low-fat meal. These are ApoE4 carriers, by the way, carriers. Cognitively normal ApoE4 non-carriers. So we just talked about cognitively normal ApoE carriers. Now we're talking about cognitively normal no ApoE4 allele had the opposite relationship. That was very interesting to me.

So people with no ApoE4 allele, no cognitive impairment, actually had better cognition on a lower fat, lower saturated fat, and higher glycemic index meal, which is— it was quite interesting to me. Cognitively impaired ApoE4 non-carriers actually had the opposite as the cognitively normal non-carrier, ApoE4 non-carrier. So cognitively impaired people with no ApoE4 allele did better on a high-fat meal. And then cognitively impaired ApoE4 carriers had no effect with any meal, like they were the same with both meals. In other words, there was nothing that was improving them at that point where they were already cognitively impaired and they had ApoE4. So there was also a subgroup— there was a subgroup analysis in that already cognitively impaired ApoE4 group.

Their executive function was improved if they were able to— if they had the high meal. So Yeah. It's a little confusing, to be honest, and I don't exactly understand what's happening here, but it just goes to show that there's a lot of genetic influence on the way people respond to different macronutrient concentrations. And so at one time, I think it's thought, oh, well, ApoE4 carriers should avoid high fat and high saturated fat because of their LDL sort of, you know, their LDL recycling mechanism is a little bit dysregulated. There's also been some data looking at actual ketogenic diets. So this would be either a low-carb or a ketogenic diet.

enhancing cognition for ApoE4 as well, and also protecting the brain against glycation, which is something that happens when you're in a high glucose state. And particularly when you have an ApoE4, it seems as though ApoE4 can contribute to higher glycation. And so, you know, basically what ends up happening is The glycation can impair the ability of cholesterol and lipids to traffic in the brain. And so cholesterol— and it's very important, like this is very important in the brain. And so the lipid and cholesterol trafficking stuff going on in the brain, which depends on ApoE4 and other— there's other players as well, gets kind of wonky when there's too much glycation. And again, A low-carb, more ketogenic-like diet can lower glycation.

And so that is something that is sort of interesting for people that have an APOE4 allele. There's also some data that a Mediterranean diet is beneficial as well. I mean, there's lots of data out there showing Alzheimer's disease risk is lowered, disease progression is lowered in, you know, in people that follow a Mediterranean-like diet. And carriers of ApoE4 who live in Italy and presumably eat the same sort of Mediterranean diet as all the other Italians there, you know, for most of their life, they basically have the same life expectancy as ApoE4 non-carriers. They have the same Alzheimer's disease risk as these non-carriers. Interesting. And so that's also very interesting.

There's been a lot of research looking at actually olive oil and the polyphenols in olive oil and how those may actually protect. They may play a— I think there's— I wouldn't say there's overwhelming data, but I think there's enough data to make a plausible hypothesis that the polyphenols in olive oil could play a protective role. in ApoE4 carriers specifically, and in most, in all people, but specifically also in ApoE4 carriers. There's some neuroprotective phenolic compounds that are high in olive oil. And if you guys, if someone reminds me in the questions for next time, there's a new, there's a brand of olive oil. I can't remember it off the top of my head, but it's like really high in a couple of these compounds.

And I'm getting ready to order some so I can tell you guys about it next time if you remind me. So anyways, olive oil polyphenols seem to be beneficial as well as, you know, basically protecting the blood-brain barrier. And then we'll get into the omega-3 stuff, you know, next. But I think overall, here's my conclusion because that diet stuff is kind of confusing and I would say that The diet stuff is always confusing. I mean, there's nothing non-confusing about diets because it's really hard to tease apart what's— diets are very complex and genetics adds another layer of complexity that most studies are not sort of unveiling, right?

So I think generally speaking, what I have concluded from looking at the literature with respect to ApoE4 carriers is I think there is a benefit to being in a mild ketotic state for neurological health. And the way to achieve that ketotic state, I would say, one, obviously, is time-restricted eating where you're, you know, you're getting a good 14 hours of— Of ketosis. You're getting a good 14 hours of not digesting your oxidizing fatty acids, but not skipping meals. You want to make sure that when you're, you know, if you're doing your 10-hour window or even 8-hour window and you're doing a 16-hour, you know, getting a 16-hour not eating period, you want to make sure you're getting all your protein intake for the day.

You want to make sure that you're getting your micronutrients and everything. You're not just skipping meals because you don't want to just be in a caloric deficit either. It's really hard to grow muscle mass in a caloric deficit. The other way would be to do a sort of, I think, Mediterranean-like ketogenic diet. And this is going to be my new— I did a whole exercise month, my Everyday October, if you guys were following me on social media. I exercised every day. It was awesome. I will say this, recovery is so important. I definitely don't recommend exercising nonstop every single day without taking, you know, recovery days because that definitely is important. But I'm going to be doing something similar with a more ketogenic, a Mediterranean ketogenic-like diet.

Even just cycling it as well, you know, it is really hard to adhere to a ketogenic-like diet and also maybe even doing a more modified higher protein version of it. So I think you can, you know, experiment with ketosis, like you have ketone meters you can measure. I still use Precision Xtra. I think Keto Mojo is like the newest one that's the best. I still haven't gotten that one yet, but, um, you know, measuring your ketone levels, I think, you know, is a, is a good way to figure out how you're responding. And so I'm going to try to, I'm going to try to sort of do a little bit of a higher protein and, um, you know, more fats from olive oil. I'm going to do a lot of olive oil.

I again think that actually even just olive oil itself is what's really beneficial So I do think that being in a little bit of a mild sort of ketogenic-like diet is— could be beneficial for ApoE4 carriers. But again, you also need to do some blood lipid panels because you could be that person that doesn't respond well. And there are the other genetic factors and things like that as well. So definitely important to look at that. Marius is asking in the chat, what's my current take on daily 16-hour What's the best way to do intermittent fasting? Intermittent fasting, or 20-hour fasting versus 2 full days per 7-day week? I think this goes along with, you know, I think, you know, it depends on what someone's goals are.

So, you know, someone who's obese and overweight needs to like reduce their calorie intake. They're trying to get to their target, you know, body fat percent and lean mass, etc. I think that Yeah. You know, fasting more aggressively and reducing calorie intake is great and a way to go. Someone like myself, someone who's lean, who is trying to maintain muscle, grow muscle, but also kind of get those repair mechanisms active, which happens during a fasted state, right? You need to basically not be digesting food. I think it's good to have, you know, I think the 14 or 16 daily time-restricted eating without restricting calories, without skipping meals, without skipping protein is probably beneficial.

Once in a while, I think it's good to do a reset where you're maybe fasting for a day, like, or perhaps 2. I wouldn't do that every week, no way, unless you're a really obese person, again, trying to That can be a very effective way to lose fat. But not so much for just normal weight people that are trying to optimize their health and maximize healthspan. I don't think that is something that is beneficial and, in fact, could be counter because, you know, getting in such a caloric deficit and you're losing, you know, the protein for a couple of days that I don't— I just don't think that is— the way to go on a weekly basis. All right, back to the ApoE4 deep dive. Fatty fish and omega-3.

I would say, again, it's in one of those areas where you'll find all sorts of conflicting data because everything is complex. Just lots of data that I would say with respect to ApoE4, I have a lot of stuff here, but let me just give you the take-home. APOE4 carriers probably need much higher doses of omega-3, especially DHA, because they oxidize DHA more readily, which means they're using it as a fat source rather than the beneficial Metabolism of DHA making the resolvins and the maresins and the SPMs, you know. So like the the the really beneficial parts of the omega three is be it comes down to you know it's it's you know the way it mediates resolving inflammation and because ApoE four carriers seem to oxidize it. More readily and use it as a fat source.

Again, it'd be interesting to also see a study where they're giving ApoE4 carriers a higher fat dose, like ketogenic, more like a ketogenic-like diet, and then supplementing with the fish oils. Like, well, they're having so much fat, why would they need to oxidize the DHA, uh, beta, you know, undergo beta oxidation, which is the basically— it's, it's the, it's the way our body uses fat for energy. It's called beta oxidation. Maybe they won't, but the reality is the data shows that if you take an APOE4 non-carrier, so someone who doesn't have the allele, and you get a carrier, someone that has it, you give them the same exact dose of DHA, someone that has the APOE4 allele will use a certain percentage of that DHA as just energy, whereas the person without the APOE4 allele does not do that.

They're just making all these anti-inflammatory and inflammation-resolving compounds. So I think that is something to consider with respect to dose. You guys know I take an unusually high dose. I'm taking on a day— I would say anywhere between 4 to 6 grams a day of total omega-3. Usually, I kind of split it up where I'm getting either 2 and 2 of DHA and EPA or 3 and 3 of each depending on whether or not I'm taking 4 or 6. grams, but I do an unusually high dose. And part of the reason for that is because I just think it's immensely beneficial, particularly for ApoE4, even though the data is— again, you'll get data showing that supplementation with ApoE4 does not have, you know, have benefits on cognition, but the doses were too low. And a new study came out, like, not too long ago.

that showed that people with ApoE4 who supplemented with more than 2 grams of DHA did increase phospholipid DHA in their brain. So, and that was something I kind of speculated in my Alzheimer's disease phospholipid DHA ApoE4 review article I published a few years ago. And so, I'm going to be covering— I am going to have the author of that study on the podcast. We've already been in touch. with each other. And so that'll be something that I am interested in covering as well. The other thing that is interesting is the risk for elevated homocysteine as a risk factor for Alzheimer's disease. And it particularly with— it positively associates with ApoE4 status. So people with an ApoE4 allele that have higher homocysteine have a much higher risk for Alzheimer's disease.

There was a study, it was called the VitaCog study. It was a randomized controlled trial. It included like a quarter of the participants, so about 25-26% of the participants in the trial, it was a very large trial, had an ApoE4 allele. And basically, they were given both a B complex vitamin and they were given omega-3. And it slowed brain atrophy by 70% in people that had high baseline homocysteine, but only if they took both the vitamin D— if they took the vitamin D-B complex and had high omega-3. So the vitamin B complex didn't do anything for cognition in people that took it but had, you know, basically had low omega-3 or were given the placebo, didn't have the omega-3. So I thought, you know, there's some kind— there's— B vitamins are cofactors for a lot of enzymes, a lot of enzymes.

And some of those enzymes are involved in phospholipid metabolism and, you know, DHA in phospholipid form. Is required for transport. A lot of the DHA transported across the blood-brain barrier is in phospholipid form. I mean, I could speculate all day about why there would be an interaction between omega-3 and B vitamins, but at the end of the day, it's something that's going to come down to probably cofactors and homocysteine as well. So the other thing to keep in mind is that you can find like B complexes, you know, that they can have exceedingly high levels of B vitamins. And the vitamins that were specifically used in the VitaCog study were vitamin B2, so riboflavin, B3, so niacin, B6, and then B12.

And the B6 that they used was It was pyridoxal-5-phosphate or PLP, which is— I don't know if that's the most common one or not. But it is. So I don't take a B complex. I take a multivitamin which has pretty decent amounts without going over the top because there could potentially be a concern with going over the top with some B6, for example, vitamins. So it might, you know, just having a good multivitamin, I think, even is something that might be beneficial for ApoE4 carriers. And that's, again, along with the omega-3 and making sure your homocysteine levels are not high.

So in some cases, again, having the methylfolate, which also, you know, to some degree, I would say it's not like, you know, a statement I would say, oh yeah, if you take methylfolate, you're going to have low homocysteine. It's just not that clear-cut. There's lots of things at play here. So, but it doesn't— it can help. It can help to some degree. And, you know, so there you go. I think it's not necessarily a B complex, but perhaps just getting your B vitamins in your multivitamin. would be beneficial. And also meat, right? I mean, meat is high in B vitamins and also greens, you know, getting your folate. So, you know, dark leafy greens are high in folate. So good to eat that stuff. Education is another thing that is associated with Alzheimer's disease with ApoE4.

This was very interesting. So ApoE4 carriers who have at least completed college, basically. So old age cognitive decline in ApoE4 carriers who complete college was completely rescued if, you know, they completed college, essentially, meaning independent of their socioeconomic status. So it didn't matter if you had, let's say you were, you know, an entrepreneur and You made a lot of money, but you didn't finish college. Like, that wasn't rescuing the cognitive decline in ApoE4. It was specifically finishing college, which sort of leads me to this. I, you know, it goes back to a lot of these studies that have shown, you know, just keeping the mind active. And, and that's not to say, you know, entrepreneurs keep their mind active too. So I guess that's a bad example.

But what I'm saying is it wasn't necessarily just wealth. that took away— sometimes education is used as a biomarker for socioeconomic status. And in this case, socioeconomic status was not what necessarily negated the increased risk of cognitive decline in ApoE4 carriers. It was specifically education. So, You know, there's something maybe there with challenging your brain, you know, learn the learning process, you know, just having having that sort of enriched environment and you know making those neuronal connections and stuff. I mean, school is challenging, college is challenging those sort of things as well. So I thought that was interesting. Also, there was some functional neuroimaging biomarkers they did. They as in researchers in the study I'm talking about.

There was— glucose metabolism was looked at, amyloid burden was looked at, and again, higher education protected against cognitive impairment in individuals carrying an APOE4 allele. And it really strengthens that hypothesis that for whatever reason, higher education seems to help protect against cognitive decline in APOE4 carriers. We're getting to the ones everyone's interested in. I told you this is a major deep dive that my team and I did. Sleep, another really important one. I would say that that's probably a pretty straightforward one. The data is kind of just really clear. It's not like, you know, basically not getting enough slow-wave deep sleep.

is really, really, really bad for people with APOE4 because again, the glymphatic system is activated during slow-wave sleep and that sort of takes out all the trash and gets rid of all the things. By the way, the amyloid beta, so this is the 42-amino acid peptide that aggregates outside of neurons, builds up in In between synapses and stuff. And it absolutely plays a pathological role in Alzheimer's disease. There's been people that have been asking, oh, there was a study that came out saying that that whole amyloid burden, like there was a bunch of fraud and, you know, that it doesn't matter, doesn't play any role. Okay, 2 things to note. One, you know, you'll hear there's a guy, what's his name? Max Lugavere.

I don't find him very evidence-based, and he's actually, you know, I'm not going to get into it, but he was saying that amyloid has nothing to do with Alzheimer's, and there was new data that came out, showed it had nothing to do with it. In fact, scientists that actually reading the studies and can follow what was actually shown is there was this whole hypothesis out there that soluble amyloid, like soluble A-beta, which is not the A-beta 42 amino acid, you know, aggregate that is what most, you know, plaques and everything that everyone associates with plaques in the brain. This was some other hypothesis that, you know, had been put out in the literature that there's these— it's not an aggregate of amyloid beta, it's a soluble protein That is what was shown to be bogus.

Completely different, completely different. Not at all the amyloid beta plaques that like 99.99999% of all people that hear the word amyloid plaque, or even plaque, because it's amyloid, soluble amyloid is not a plaque. That is what was shown to be fraudulent and not— doesn't play a role in Alzheimer's disease. So if you've heard that, In the echo chamber, it's wrong. And not to mention, huge, huge, huge buzz. A big, big, huge clinical study just came out where a new drug— I mean, this is all the rage. You're going to start hearing about it in like the next few months. A new drug came out targeting amyloid beta plaques. Okay, this is the protein aggregates that it actually slowed the progression of Alzheimer's disease and improved cognition in people with Alzheimer's disease.

It's the first drug to have ever been shown to do that, ever. It's kind of hard to believe. And I'm, you know, I've never been one to be, you know, like, oh, yay for drugs. But it's impressive. It's impressive. So what their data was very robust. So you'll probably be hearing a lot about that. So again, amyloid beta plaques play a role in Alzheimer's disease. If you've heard this, you know, buzz about amyloid having nothing to do with Alzheimer's, you're probably hearing it from sources that don't understand the science and are trying to get clickbait. Soluble amyloid has nothing to do with amyloid plaques. Sleep clears out amyloid plaques. Very important for people with APOE4.

Sorry for the tangent, but it was kind of a pet peeve since I had heard some people sort of talking about that very inaccurately. And the next thing is caffeine, coffee. So there's a lot of studies, I mean, just study after study after study showing coffee, caffeine consumption through coffee, through green tea, through black tea, reduces the risk of cognitive impairment, dementia, ameliorates cognitive decline in already cognitively impaired people. Lots of, you know, mechanisms at play there. I would say that there's not, like, there's no evidence that ApoE4 affects that relationship. In other words, it seems as though coffee is beneficial for both people without ApoE4 and for with people. people with ApoE4.

So coffee is one of those things that I think could— is beneficial for people with ApoE4 with respect to cognition, brain aging. All right. Finally, the one everyone wants to know about. Alcohol probably is one that everyone's been waiting for. I did a deep dive on alcohol. Gosh, it's probably been about a year now. You guys can look back at the Crowdcast Q&A questions I've covered. We have the PDF. On our on your dashboard, so again, if you go to foundmyfitness.com/dashboard, you'll find you can search it. You can find you can go ahead and search alcohol. It'll pull up all my crowdcasts where I've covered it. But I went into detail on alcohol risk. Sorry, not alcohol risk. Alcohol consumption and cancer risk.

Alcohol consumption and You know, brain aging, alcohol consumption, and longevity. And so I'm not going to go into all that right now. But there was, you know, there was data basically, there is data showing that light alcohol consumption is associated with a decreased risk of Alzheimer's disease in general. However, This relationship does not appear to hold or be true for APOE4 carriers, unfortunately. During later life, higher alcohol consumption has been correlated with a reduced risk of cognition or cognitive impairment for APOE4 non-carriers, whereas carriers of either 1 or 2 APOE4 alleles have the opposite trend. So Later life, higher alcohol consumption basically greatly increases the risk of dementia and Alzheimer's disease in people with an APOE4 allele.

There's really an additive effect as well. So heavy alcohol consumption, which probably most of us here are not, but heavy alcohol consumption in the background of having an APOE4 allele is like I would say, recipe for early onset Alzheimer's disease. Light and moderate alcohol consumption during late life, again, is associated with greater cognitive impairment only in APOE4 carriers. And this is, again, I think, one of the reasons you'll find conflicting data in the literature with respect to how alcohol affects the brain. And I've heard influencers making strong conclusions that I just don't feel comfortable making the same conclusions because I don't think it's all alcohol for all people is bad and bad for the brain. You can find whatever data you want.

And I think that when you start to really dive deep it becomes clear it's really— it comes down to ApoE4. Alcohol, light and even moderate alcohol consumption, can be neuroprotective in the brain for people without ApoE4. Completely opposite for people with ApoE4. Heavy alcohol consumption, I mean, that's pretty clear. It's a disaster. So moderate alcohol consumption has been correlated with increased levels of LDL in APOE4 carriers. And so that could also be mediating the risk because higher LDL in APOE4 carriers is one of the strongest predictors of Alzheimer's disease later in life with people with APOE4 is actually higher LDL. And another one of the reasons is I was talking about traumatic brain injury, TBI, in people with APOE4 and how detrimental it is.

Alcohol does that in people with ApoE4. It is— it's an insult. And people without the ApoE4, there's almost like a hormetic response where the ApoE3 allele is like repairing things, you know, and the repair sort of out— The net, you know, effect is you're getting more repair. in the brain, but APOE4 carriers don't have strong repair mechanisms, and they don't have that net repair effect. In fact, they're having a net damage effect from the alcohol. So it's a little bit of coming down to the basically dysfunctional neuronal repair mechanisms in APOE4 carriers. So unfortunately, it's probably best to not— you know, it's obviously okay. You're not— you're going to have You know, you got to live life. But I certainly wouldn't have a glass of wine a day if I was ApoE4.

And then I have a few other ones. I don't know that I'm going to— I think those were the main ones. Air pollution, bad for ApoE4 carriers. You know, HEPA filters or even like medical-grade quality ones, if you're living close to a busy road or something, might be a good investment as well. I think that's it for my ApoE4. It was a really big deep dive. Lori Miller is asking in the chat if caffeine or decaf coffee also is good for the brain. And there's been studies showing that decaffeinated coffee has benefits as well, probably because of the polyphenols and other compounds that are beneficial in and coffee, but also caffeine has been shown. So it's kind of like maybe you're getting, you know, perhaps 2 additive, you know, or even perhaps even synergistic, we don't really know, effects.

But both have been shown to be beneficial, both coffee and caffeine. Decaf. Sorry, decaf and caffeinated. So, oh, in the chat, someone's asking about the new encouraging results from the clinical trial for patients with Alzheimer's disease. It's a monoclonal antibody. It's lecanemab. I don't know how to exactly pronounce it, but it reduced cognitive decline in people with Alzheimer's disease by 27%. They had early-stage Alzheimer's disease, but that is Compared— this was compared to placebo. That is freaking huge. Almost 30% reduced. These are people with Alzheimer's disease. You know how hard it is? I mean, like, that's been the one thing.

It's like trying, trying to like reduce cognitive decline in people that already have Alzheimer's disease has been just fail after fail after fail after fail. And so this monoclonal antibody targets amyloid beta 42. Amyloid beta, the amyloid beta 42 peptide that aggregates with other amyloid beta-2 peptides to form plaques outside of neurons in the synaptic regions, which prevents, you know, synapses from communicating with each other. And essentially, when that happens, one, you can't remember anything, and two, your neurons start to die because synapses aren't forming between them, which is essential to not— to have your neurons stay alive. And so this is a big, big deal. And it really, like, again, I said, you know, there's this sort of influencer guy that is out there.

I think he went on Joe Rogan's podcast and stated with certainty that amyloid beta has nothing to do with Alzheimer's disease. And he talked about the new study, but he completely got it wrong. I mean, he was— the soluble amyloid beta is completely different. Completely. It's not what's forming the plaques. It's not aggregating and forming plaques in the brain. In fact, among the scientists, I mean, I remember, you know, years and years and years, like, I don't know, 10 years ago or more, scientists talking, oh, this new soluble amyloid. There have been skeptics about that soluble amyloid for like ever. I mean, like, there's a lot of scientists that were never on board with it at all. So it actually wasn't that big of a shock to me to hear about it.

But anyway, so that is the new Alzheimer's disease drug. Here, I'm going to post it in the chat for you guys so you can look it up. I'm following it. You know, I've always— I was considering doing a podcast on it, but I felt like, you know, it was just one study. I was worried. That it was a little too premature, but it's very robust. And, um, I mean, it's, it's, it's about— it's going to get FDA approval and it's going to be starting— it's going to be used as a treatment like soon. And what we're going to have again, kind of like with, you know, with COVID and as we started to, you know, people started to get vaccinated and all that, like we started to get, you know, just like the largest clinical trial you could ever have, right? I mean, with people just real-world data.

That's what's going to happen. We're going to start to have people with Alzheimer's disease using this drug, this monoclonal antibody. And so we're going to start to really have like large, large data samples. And it's really exciting. I mean, so I'm pretty excited about it. So I've got a bunch of other deep dives that I didn't get to, but I think because I did such a big deep dive, I am— I'm gonna scroll down to my rapid-fire questions and see if I can answer a few of those since we have to end soon. And then next time— so let me tell you what I didn't cover that I have already on my list here, which is the best ways to lower ApoB and how to check if you have soft plaque in the arteries. I'll cover next week.

And I will cover— you know what, let me do— let me get to the ubiquinol question because I did mention I was going to cover that in the— that was from last month. So this question was submitted by Chad, and Chad asks, any reason to take CoQ10 or ubiquinone, ubiquinol, if you're not on a statin? Or— and should everyone on a statin take CoQ10? Okay. CoQ10, it's an antioxidant. It's also part of the electron transport chain. It's really essential for healthy mitochondria. It's ubiquinone in its oxidized state or ubiquinol in its reduced state. And you can find supplements for both. Ubiquinol, the reduced form, is more bioavailable, and you'll also find it to be much more expensive because you need a lower dose of it.

Ubiquinone is oxidized, it's less bioavailable, so you actually have to take a little bit of a higher dose. So I mean, the cost kind of evens out in a way. Statins, let's start, let's answer the second part of the question first, which is should everyone on a statin take CoQ10? I think, you know, obviously this is not medical advice, I'm not a medical physician, but I think the data is pretty clear that people that take statins absolutely 100% positively should take a CoQ10 supplement. There's— it's absolutely got a wonderful safety profile. There's no, like, no real bad side effects with CoQ10 supplementation. Statins, basically, they reduce your liver's ability to produce CoQ10. They target specifically mitochondria.

I mean, they're inhibiting the same pathway that they're inhibiting to reduce cholesterol synthesis, the mevalonate pathway. Is the same pathway you need to make CoQ10. So it's a direct effect. This isn't like an off-target thing. This is direct. It's affecting your production of CoQ10. It's plummeting it, period. No question. And there's been some studies looking at people on statins that were supplementing with, perhaps, for example, 300 milligrams a day of CoQ10. By the way, this is the oxidized form. Which you need a higher dose of. It led to 5 times higher blood levels of CoQ10 than people that didn't supplement. And also, people that are taking statins, statin medications, start to experience muscle aches and weakness and stuff. And it's most likely because of the CoQ10 depletion.

So there's been Some other studies that have found that CoQ10 supplementation can help alleviate statin-associated muscle symptoms. And this was a meta-analysis of randomized controlled trials. So essentially, it's a way to manage statin-induced myopathy. And I think that it absolutely should be administered along with statins. And unfortunately, it's still not. Like, it's still not something that doctors immediately— it should be like, okay, I'm going to get you on a statin, but you absolutely have to take, you know, a ubiquinone or ubiquinol supplement while you're taking this statin. I feel like that would be the best way to approach it. That way patients realize, look, this is going to target your muscle and it's going to make you weak, your muscles weak.

But if you take a CoQ10 supplement, that's not going to happen. And I think that, you know, it would be clear if that was stated that way, but unfortunately it's not. Do all people need to be taking CoQ10, like people that don't take statins? I don't think we know. There's just not been enough data. I take CoQ10. There's— I mean, again, there's been studies up to 1 to 3 grams per day. I take 200 milligrams of ubiquinol, which is pretty high dose. I mean, even 100 milligrams is— it's been shown to increase blood levels of CoQ10. And there's been some evidence that it does positively affect— so it reduces triglycerides.

There's been, you know, meta-analysis of randomized controlled trials showing that, particularly in people with you know, dysregulated triglycerides or people with higher triglycerides. It also lowers it in people with not so— not incredibly high triglycerides as well. It also has been shown to reduce Lp. That, you know, this was a meta-analysis of 6 randomized controlled trials, and, you know, Lp was modestly reduced as well. And so, you know, I think there's— I don't know that everyone needs to supplement with it, but I do think it could be beneficial. There's been some studies also just showing that a lower risk for cardiovascular disease with supplementation as well. And like I said, it's pretty safe.

So I don't see any reason to say, oh, it's not okay to supplement with, but I don't know that it's necessary. You know, I don't know if it's one of those you absolutely have to take. So next month, I'm going to cover some of these other— there was another study on digestive enzymes. And I kind of got to like go through my answer here because it's quite long and I think I need to sort of triage it to the most important things. Let's do a couple rapid-fire questions. After listening to all your podcast interviews, I recall several instances when guests recommended plant-based diets for longevity. That, along with Dr. Stuart Phillips' acknowledgement that plant protein is effective, leads me to think that there are more plant-based— the more plant-based diet, the better off I will be.

Are there any remaining concerns you would have with a plant-based diet? I think that if you are doing— if you are carefully doing a plant-based diet, you're supplementing with all the proper things you need to supplement with, and You know, getting enough of the protein, which you're going to need to supplement with protein powders as well to really to reach that 1.6 grams per kilogram body weight. I think you know my my my biggest concerns would really just be the nutritional deficiencies we've talked about in the past. So you know, just being careful about it is the is the is the is the really you know main thing. It's a lot of work, and if you're willing to put in that work, then I think. You know, go for it. There was a question about baby food.

And Lisa asked, you know, when I started introducing solids to my son, if I used the baby-led weaning method or I mashed food or a combination, or did I ever use jars or pouched foods, or which brands did I use, or do I have any that I like? So I would You know, I'm remembering way back. My son's 5 now, but I did not do the baby-led weaning method, although that, you know, I don't— I'm not opposed to that. I think I introduced solid foods around 5 or 6 months, probably like closer to 5 months. And the concern about doing it too early is it could kind of lead to a little bit of You know, autoimmune. Like you want to make sure that it's at the right time, right?

I made all my own baby food, so I would you know was trying to get all the the the meat sources, particularly for the iron and stuff. I would cook the chicken, ground it up in a little baby bullet. Those are great. Get a baby bullet, and then I would cook you know the cherries or the blueberries and ground that up and mix them together so that it made the chicken. Taste better. I made all my own baby food. I did not buy— I never did pouches. I never bought any baby food jarred things. I know that it can be extremely overwhelming, especially if you, you know, have more than one. Timewise, I really look to my friend Darya Rose. She's kind of a super mommy, and particularly when it comes to feeding her kids, her kids eat a very diverse, very well-balanced diet.

And I remember her recommending back in the day when her kids were eating, you know, when they were on the mashed foods when they were young, she recommended— she had used a baby food company called Yumi, Y-U-M-I. And they basically do the same thing that I was doing where they're like, cooking all the food and mashing it up and making these good options. So that might be a good option because I really do trust her. And she's also a scientist, a PhD, and she's very, you know, careful and, you know, reads the science and stuff. And she's also just great with food and particularly with children's food and stuff. So that might be an option as well, the Yumi food. It seems there are 2 contradictory paths.

Ketogenic-ish for greater brain health versus more protein for greater muscle strength and less fragility. Would a compromise serve both, or does one— do you need to choose a path? And I kind of was like hinting at this earlier. I think you could do a modified keto-ish diet and still get your protein. And again, it just takes some experimenting with your home-based ketone monitoring. But I don't think you have to compromise. And also, to some degree, you know, there's some of the ketone bodies are also muscle sparing, right? So they're like preventing muscle wasting as well, which is interesting. David asked about a recent study. It was the COSMOS study. This is the COSMOS Mind study. So there's been 2. There's been a COSMOS Heart and a COSMOS Mind study.

And it was using CocoVia, which is obviously very— it's gotten even more expensive. I mean, it's never been really cheap. It's really gotten more expensive. So the new COSMOS— let's start with the older study. The COSMOS Heart Study, it was a 5-year study. It showed that 500 milligrams of the cocoa flavanols there was a 27% benefit on heart-related outcomes compared to placebo. And, you know, so there was improved blood flow, and that was sort of thought to be part of the mechanisms responsible for the improved heart, 27% heart benefit, right? This was a randomized controlled trial, placebo or the 500 milligrams of CoQ10. Then the new study was also the COSMOS study. This was called COSMOs-MIND.

It was the same dose, but they didn't show— there was no statistically significant benefit for improving cognition. And so my thoughts on that are previous studies have shown cognition improvements at higher doses, so 700 to 900 milligrams. So it could have just been that the dose While that dose of 500 milligrams was good for the cardiovascular effects, it was too low for the cognitive and brain effects, particularly because other studies showed that at a dose of 700 and 900 milligrams, almost— the 900 milligram dose is almost twice the 500, right? That there was improved cognition. So That's all I got. I mean, that's kind of what I'm speculating, that maybe it has to do with the dose.

There's a question here about kefir and what I use in my smoothie, what brand, where do I buy it, is it pasteurized, are pasteurized kefirs like any good? So pretty much all the studies, you know, in the scientific literature on the benefits of yogurt, on the benefits of kefir, are pasteurized. So clearly pasteurization isn't killing off the benefits. So I'm really like, I know there's this whole like group, you know, that likes to go for unpasteurized because you're, you know, you want to get all the bacteria, but of course you're raising the risk of bad, right? Bad bacteria and getting sick. But just keep in mind that like 99.999% of the research out there, they're all using pasteurized. Yogurt and kefir. So, you know, like, don't worry. They're obviously beneficial.

I do not worry about getting unpasteurized, you know, dairy. The goat kefir that I use is Redwood Hill goat kefir. Owen says, Dave Asprey opposes use of raw kale in smoothies based upon the presence of oxalic acid or oxalates, an alleged anti-nutrient compound. He advises steaming kale before consumption. Is there any validity to this opinion? On a technical basis, no, because kale is not very high in oxalates. Spinach is. Perhaps Dave, the all-knowing Dave, got his vegetable wrong. That would be my assumption. So spinach is high in oxalates, and if you consume tons and tons and tons, like if you're just juicing Pounds and pounds and pounds of raw spinach a day, every day, every day. That would be a concern.

There's been a set— there's been one case report of a woman doing that, like where she was eating 5 pounds of raw spinach, juicing it every day, and it caused a problem. Most people, not an issue. Don't worry about eating spinach salad. Don't like— You know, it is it is it is so it's like one of those things where you're creating a problem to make people think that you got this inside intel that you're like know about this secret that no one else knows about. And I'll tell you what, I don't think you should consume you know juicing spinach every single day because you are going to be getting too many oxalic oxalates. But like you know. Even if you were just eating a spinach salad every day, like that's still like raw spinach.

Like, you know, it's like not— it's hard to eat a lot of it because, you know, it's just— you just can't. You can't eat that much of it. So it's really not that big of a concern. Now, if you are juicing it every day, probably not a great idea to juice raw spinach every day. When you cook spinach, you are you're basically, um, many of the oxalates are leaching into the, into the, like, the water and stuff. So, um, then it is sort of quote unquote inactivating them. How young can you directly give fish oil to babies? What dose? Giving, giving it to the mother for breast milk is expensive and less efficient. I mean, um, once they start, once they start eating you know, solid food, you can pop open a fish oil pill and, you know, put 500 milligrams in the food. I did that.

I didn't do it on a daily basis just because efficiency and time, and I was still, you know, I breastfed for quite a while. But yeah, you can just add it to your baby food that you're making. Dr. Rhonda, did you bank your son's cord or placenta blood and tissue? If yes, which bank? If If not, why not? Yes, I banked placenta and cord blood tissue from— and I use the— there's not very many companies doing placenta, but I used LifeBank USA. I think they're a pretty solid company. So that's who I used. Kathy in the chat is saying that Dave was probably thinking of goitrogens from kale. I assure you, Kathy, he's been saying that same thing for years. He's not thinking of goitrogens. He just has it wrong and he hasn't modified for years.

He's called— he's always been thinking, he's always said that kale is high in oxalates. And you'd think by now, I mean, he's been saying this since like 2015. So he's had quite a bit of time to reflect and figure out that he's not saying it right. And yet he still keeps saying it. So go ahead and take it as you will. I mean, interpret that as you would like, basically. I'm just seeing if I can answer a couple more questions here from the chat. Is asking if you sweat just as effectively in a jacuzzi versus a sauna. You do. It's just hard to tell because you're already wet in a jacuzzi. It all—I think it also comes down to if you're sitting in a jacuzzi, are you putting your arms out? Are you, you know, are your arms—are you submerged from your shoulders down?

I mean, like there are things that will make you hotter, right? When you're in the sauna, your whole body is in it. Your whole body is in it, and so it's hard to stick things out and to kind of cool down. Whereas in a jacuzzi, I—I tend to stick my arms out, and you know. When I'm in the whole sauna, I tend to— it's just easier for me to not cheat. I really do prefer the sauna. I do both though. I switch. So, a lot of nights, I do a jacuzzi as well. And, I think it's every bit as effective. It just really depends on what you have access to, what you're more likely to do on a daily basis, right? Or a weekly basis, I guess I should say. So whatever is working for you. All right. Shelby asks, is there a ketone monitor that you recommend? So again, Dom D'Agostino, he really likes the Keto Mojo.

I still use Precision Xtra, and it's just, it's worked well for me, and I just haven't gotten around to, you know, it just takes mental energy for me to like think about the Keto Mojo when I already have this thing that works for me, and I have all the equipment and ketone strips and everything. So I think both are good, both Keto Mojo and Precision Xtra, but a lot of people do have come out and they like Keto Mojo. So that, if you're going to go ahead and get a new one, you might go ahead and try the Keto Mojo. And there was one last rapid-fire question about sort of, you know, feeding kids. Any tips for like feeding toddlers or even like, you know, young preschoolers in terms of like snack examples of what to feed them.

Like, can you give them bread or what kind or any— like all that stuff. So, you know, it's really, as any parent will tell you, you know, there's— it's a balance. And I think the most important thing, especially early on, is avoiding giving the refined sugars. As much as you can. I mean, once they like go to their first birthday party and they get their cupcake, like you can't— like, you know, there's a certain point where like, you know, they're kids and you can't just like take all the joy out of life, right? But like as long as you can, getting them used to the sweetness of fruits and how tasty fruits are, and that's a great, you know, it's nutritional and it's sort of it sort of feeds that craving for the sweetness. Hold on to that as long as you can.

And with respect to bread and stuff, I give my son sprouted whole grain bread. And sprouting the bread lowers— it dramatically decreases a protein in gluten called gliadin that's responsible for opening up tight junctions in the gut. And so I do think bread is a— and particularly, you want to make sure that the children— there's a lot of good nutrients in bread, in whole grain breads that can be beneficial for young kids. Oats as well. Oats are a great snack, like giving them oats and raisins or oatmeal, making the oatmeal. There's also a lot of nutrition, a lot of magnesium in those, especially because You're not going to get your kids eating a lot of dark leafy greens. Now, you sneak them in the smoothies like I do.

I mean, you can sneak them in the smoothies, but like it's hard to get them eating like a serving of dark leafy greens every meal or every day. And so, getting some of the micronutrients from other sources like oats is good. Pasta suggestions? I usually— kids love pasta and I usually do like— The chickpea pasta or the lentil pasta. Those are those are some of the things I do for dips or sauces and stuff. Really, the only sauces I do are hummus and tzatziki. But it's it's it's it's a it's a it's a struggle. You know, you really have to give them a lot of options and little little portions of many many many many options. And then eventually they start to eat or nibble on just a little bit of one thing, and then at least.

Getting exposed to it more and more, and then they start to eat more and more of it. That's what I've learned. So, um, as it is more work, but it does, it does really pay off to just do lots and lots of little, uh, options for them because they're— if they have a bunch of things on their plate, they're a lot more likely to try out some of those things and, um, and then eventually, you know, eat, eat more and more of it. So with that said, I am going to end this Crowdcast. And thank you guys so much for all your wonderful questions. Thank you for all your support. We have a new podcast coming out soon. I recorded a couple of weeks ago with Dr. Brad Schoenfeld. You guys are going to love it.

It's all about resistance training and the types of resistance training to do, like your load, how much, how much, you know, the load, you know, frequency, going to failure, like all those little like mechanic mechanics of it. Like it's really, really, really a good, I think, practical podcast. I mean, everything he said had a take-home. Everything he said, you know, was evidence-based, but had that take-home where you can go, how do I implement this? Oh, he's telling me how to implement this. This is great. So, um, it was a really good podcast and that'll be coming out soon. We again, we just released an aliquot. I hope you guys are listening to the aliquots, um, because you guys, you're members.

And so you guys, one of the benefits you guys get are these, these almost weekly aliquot podcasts that we put out. So check that out on your dashboard, foundmyfitness.com/dashboard. Next week We will cover the digestive enzymes since we didn't get to that. And please submit your question, not next week, next month. Sorry, I got home like at, like, I literally got home almost midnight California time, which was like 3:00 AM Florida time, which I had already adjusted to. So I've had a late night here. Anyways, I look forward to your questions. Submit them in the submit a question section for the next Crowdcast. And so I'll be talking to you guys next month. I look forward to it. Lots of good stuff coming out, and I'll talk to you guys soon. Thank you so much. Have a great rest of your Saturday. Bye.