Q&A #45: Can Melatonin Help Older Adults Sleep—and Should You Supplement With Nicotinamide Riboside?

Hello everyone, welcome to Crowdcast number 45. 45 episodes, amazing. Welcome to those of you who, uh, this is your first time attending the live event. They're really fun. You guys get to chat with me and others in the, in the live chat feed. And so the way this works is I will go through and answer a variety of the submitted questions. And I've been trying to answer questions that are obviously top voted, but also ones that are new areas that we haven't explored too in depth. So, you know, things like grounding, for example, which Lisa submitted today, we'll be addressing that question. I also do a variety of rapid-fire answers. So these are questions that can be answered in a sentence or two or you know, a few. So I usually hit those up at the end of this live Q&A.

I also, throughout the Q&A, particularly after I'm done addressing a question, I'll look in the chat and look for some of the questions that are submitted live as well. So that's a benefit of attending these events. I do, I do quite a few deep dives, particularly on topics that are unfamiliar or sort of new territory for me or something that I've perhaps been skeptical of. And so my team and I will do a deep dive to see if there's any updated scientific literature since I've last done my, you know, my deep dive on that topic. So those are kind of the, I would say, the important things to know about these Q&As. With that said, I did see a couple of questions submitted in the chat about our recent episode we released last week on Alzheimer's disease with Dr. Axel Montagne.

And so, you know, I just wanted to say, so the first question had to do with HEPA filters or air, high-quality air filters. So we talked in this episode about air pollution being a major environmental factor that can increase the risk for Alzheimer's disease, particularly in people with an APOE4 allele who are genetically predisposed to later onset Alzheimer's disease. And a lot of that has to do honestly with increased inflammatory response in the body, so in circulation, but also in the brain. So there's been a couple of studies that have come out showing that particulate matter from air pollution does increase inflammatory molecules and inflammatory processes throughout circulation, but also directly in the brain.

So things that are inhaled through the nasal passages can sort of have a direct route across the blood-brain barrier, which is used pharmacologically. There are some drugs that are administered intranasally that are you know, trying to get into the brain, for example, oxytocin being one that doesn't readily cross the blood-brain barrier. If you're just taking an oxytocin supplement, for example, and it gets into circulation, that's not going to cross the blood-brain barrier. So the way to do it would be to inhale it. So anyways, with respect to answering that question, so right now in my home, so I no longer live next to a busy road or I'm sort of like more in a nature type of environment. Yeah. Took me a while to get there though.

But I've, you know, since I've lived in very metropolitan areas for most of my life actually, I've had a— I wouldn't say it's a medical-grade HEPA filter. It's one of those Honeywell HEPA filters that you, you know, you can have in each room. And so, we have them in the bedrooms in our house. And we've considered and probably will go ahead and get a higher quality medical-grade HEPA filter. And the one that we are looking into getting is from IQAir. IQAir. It's pretty easy to remember. The other question submitted about the recent episode on Allergy and Emergency Disease with Dr. Axel Montagne. By the way, if you haven't watched or listened to that episode yet, I highly recommend it.

It does— there are moments of technical, you know, it can get a bit technical, although Dr. Montaigne is great at defining terms that he speaks about. So he likes to, you know, it's, it's a very educational type of podcast. But also, in my opinion, it's a new lens to look at Alzheimer's disease. And honestly, the way I see it is, for, for, you know, decades, the, the focus of Alzheimer's disease prevention, certainly treatment, has been on some of the major pathologies of Alzheimer's disease, including amyloid beta plaques in the brain and tau tangles. And there's been a lot of disappointing results, although some newer studies— one newer study has been a little bit more promising, just a little.

And, um, so, you know, the, the idea here is, look, we gotta go, we gotta go further upstream to the root cause. of these amyloid plaques and tau tangles and what is causing them to occur. And is there a common underlying theme that we can connect some of these major root, you know, major causes of Alzheimer's disease and dementia? So we know, for example, that having an APOE4 allele is one of the biggest genetic risk factors for late-onset Alzheimer's disease. So what I mean by that is, you know, You're not getting Alzheimer's disease in your 50s. So there are some genes that are rare that actually do have to do with the amyloid pathway and can cause people to get Alzheimer's disease very early in life. That is separate.

So APOE4 is something that increases the risk of Alzheimer's disease, you know, later. You're talking 70s, 80s. Perhaps late 60s even. So ApoE4 is a major risk factor, but we also know type 2 diabetes is a major risk factor. You know, brain glucose metabolism is disrupted decades before any cognitive decline. And so, and people with type 2 diabetes are also quite predisposed to getting Alzheimer's disease. There's also other things like periodontal disease is another big one that's linked to it. And what these, what these all have in common is basically they cause vascular dysfunction at the, the capillaries and blood vessels lining the blood-brain barrier, and they disrupt the blood-brain barrier.

ApoE4 disrupts blood-brain barrier, type 2 diabetes disrupts blood-brain barrier, periodontitis, even IBD as well. There's an increased risk for Alzheimer's. Anything that has bacteria getting into circulation causes an inflammatory response, and inflammation is one of the main drivers of blood-brain barrier breakdown. So it's a really good podcast. I highly recommend you guys listen to it. We talk about mechanisms, but we also talk about biomarkers. We talk about lifestyle factors that play a major role in modifying disease risk in a beneficial way, those being vigorous exercise, omega-3 intake, and blood pressure regulation, very important. Those are 3 really, I think, of the main ones that I can think of off the top of my head.

So this other person in the chat asked about metabolic activators that may— that have been shown in a phase 2 randomized controlled trial to help improve cognition in people with mild Alzheimer's disease. I have seen this study, and the metabolic activators used were Things like carnitine, L-carnitine, which is involved in mitochondrial function. So L-carnitine is essential for mitochondria to use fatty acids. This is important because, again, in Alzheimer's disease, glucose brain metabolism is disrupted. When the blood-brain barrier starts to break down, the transporters that transport glucose into the brain dysfunction. And so you're not getting glucose into the brain.

This is like the type 3 diabetes, and it all comes down again to blood-brain barrier dysfunction because those transporters are are inside those vessels. And so when those vessels break down and and start to basically disappear, your your glucose transporters disappear, and so you're not getting as much glucose into the brain. And so it's one of the reasons why ketones, for example, so people doing a ketogenic diet or supplementing with supplemental ketones that have Alzheimer's disease, there's been quite a few. Early trials showing this, it can improve cognition because, well, I think because they're basically bypassing, you know, it's an alternative metabolic pathway. You know, glucose isn't getting in the brain. And so they need another source of energy.

And that source of energy is ketones. Ketones don't need the glucose transporters. So, so the carnitine does basically activate the pathway to use fatty acids basically to make ketones and whatnot as well. Also was used— N-acetylcysteine was used, which can also be a precursor to glutathione. People with Alzheimer's disease, we talked about this last Crowdcast when we talked about supplemental antioxidants, particularly liposomal glutathione and N-acetylcysteine. And we talked about it really being probably more important in the context of brain pathology. So that would be Alzheimer's disease, any form of dementia, it would be Parkinson's disease, it would be TBI, traumatic brain injury, it would be neurodevelopmental diseases like autism, for example.

So in this, in these situations, there is an imbalance, there is a high amount of oxidative stress going on. And so glutathione, or things that make glutathione like N-acetylcysteine, can help aid in and basically homeo— what's called homeostasis, basically helping get, you know, rid of some of that oxidative stress and countering it so that you're basically not having as high of levels of oxidative stress in the brain. So that was used as well. And nicotinamide riboside was used. And interestingly, a new study just came out very recently.

It was a clinical trial, a small trial that showed people that were given, and that it was a dose-response study, people that were given increasing doses of nicotinamide riboside, as we've talked about in many Crowdcasts, is a precursor for NAD, very important for mitochondria as well, and also important for repairing DNA damage because it's, you know, it's used by a DNA repair enzyme called PARP. So, what the clinical trial showed, much to my surprise, because animal studies had shown that nicotinamide riboside was basically not getting into the brain. And so, we don't know exactly how, but the study used MRI techniques, more sensitive MRI techniques that could measure NAD in the brain.

And what was found was that at higher doses of nicotinamide riboside, there was an increase in NAD in the brain. I find this interesting. It's definitely piqued my interest and has me rethinking certainly that perhaps nicotinamide riboside could be beneficial in, again, people with a pathological disorder. But also, I'm rethinking whether or not I myself would like to supplement with nicotinamide riboside. As you guys know, I often do this where I'm following the literature and I try to keep up with it. And So, so when I find that there might be some evidence that it might be beneficial and has a good safety profile, then I kind of rethink and might start supplementing with that. I would like to see a repeat of this study. So that's kind of what I'm waiting for. All right.

So that was sort of a long-winded answer to some of those questions. I see some rapid-fire questions. And Beck was asking about my nail polish. I do use a clean brand. And for some reason, like, I use it so rarely, like, it was like a Valentine's thing, you know. So I don't remember off the top of my head what it is. But if you ask this next time in the chat, I will make a note of it and write it down so that I can remember to share that. So, Alan's asking, if NR helps the brain, would NMN also work? Not necessarily. Not necessarily, but possible. So, so yeah, and, you know, the big concern I have had mostly with NR and certainly NMN is that there have been some studies with cancer, right? You know, cancer loves NAD as well. And it's always that, it's always that balance.

It's like, okay, well, I don't want to just start dosing up with 1,000 milligrams of NR every day, and potentially allow any precancerous cells to sort of you know, overcome any other mechanisms that would make them die. So, you know, it's one of those areas where I still am cautious and I think there's still reason to be cautious and not overenthusiastic about it. However, it does excite me. Adriana is asking about niacin itself. Does it increase NAD? Yeah, there's some evidence that niacin You know niacin itself does; it can cause flushing. We've covered niacin in a previous crowdcast.

By the way, those of you who are unfamiliar or new, we have a back catalog of all of our crowdcast episodes, not only for viewing and listening, but also we have bulleted timeline summaries, and that you can find on your dashboard if you log into your. FoundMyFitness dashboard, so that's at foundmyfitness.com/dashboard. You will be able to then view a PDF, and it's searchable, so you can just search niacin, and it'll take you to the different crowdcasts and points that we've discussed niacin and gone more into detail about that. The same goes for NAD, nicotinamide riboside. We've done a lot of— we've covered that many, many different crowdcasts, as well as NMN. So please go back and look at those. That way I am not being redundant.

So I'm going to go ahead and start with the first question. This is sort of new, a new area I've, I've been skeptical of. And as you will see, I'm still skeptical of. But Lisa submitted this question about grounding. Lisa says, hi, Rhonda, I'm interested in the efficacy of grounding or earthing products like mats, shoes, pillowcases, sleep mats, etc. Ben Greenfield calls it his number one health hack and claims it reduces inflammation, improves sleep, among a host of other things. The benefits sound awesome on paper. if they are legitimate. I feel like this could be an overlooked, relatively simple way to enhance one's health. What does the science say? What is your opinion?

So, the idea of earthing and grounding is to basically reconnect the conductive human body to the Earth's natural and subtle surface electric charge. So, it's claimed that basically humans lost contact with the Earth by not walking barefoot outside or not sleeping on the ground, et cetera. And, that may contribute to electrical imbalances and a buildup of disruptive static electricity. So basically, there's a— the claim is there's a buildup of positive charges in humans, and that this is basically an unrecognized electron deficiency in the body. So with it becomes vulnerability to dysfunction, you know, disorders, disease, those sorts of things. And the solution would be walking barefoot or using grounding devices like a sleep mat, connecting to the ground, Yeah.

You know, via the house's wiring. And, it's thought to basically replace these lost electrons with electrons from the Earth. Okay, that's the theory. There's critics of this hypothesis, on the other hand. They say that basically electrons are to a very high degree identical whether they come from the Earth or synthetic materials. And thus, you don't get a particular health benefit from electrons when you're getting them being in direct contact with the earth. Also, the hypothesis that you build up an unhealthy positive charge when you're not in contact with the earth is kind of rejected by the fact that it's not possible to build up and maintain a significant voltage imbalance because everything you're in contact with has electrons and they're moving back and forth between objects at all the time, at all times.

So, for example, you know, if you rub your feet on a carpet and then you touch a person or you touch a metal or something, you know, there's a shock. So the built-up voltage is immediately eliminated, right? So like, it's not like it's just sticking around in your body all the time. Nevertheless, you'll find studies and review papers claiming reduced inflammation, pain, stress, improved blood flow, improved sleep, every vitality, improved vitality, whatever that means. However, when you look deeper, most of these studies and review papers were either sponsored by the company that sells the grounding or earthing products, or they're written by authors who are independent contractors for a company that owns shares in a grounding company, or they're somehow employed by an institute like a healing wellness center that uses grounding for treatment.

So there's, there's a pretty significant potential conflict of interest in every single publication, every single one. So something to keep in mind. You know, there's definitely— conflict of interest isn't necessarily something that, you know, is a make-or-break deal with respect to science. But when it's the only thing and there's no other, there's no unbiased or independent, you know, institutes looking into this, it does, it does, it is a little concerning. Also, most of the studies that show positive results, they're not randomized controlled trials. There's only a few study participants. And they're not controlled for confounding factors. And they also have very soft study outcomes.

So, overall, I would say I did not find a single study that did not have a questionable conflict of interest from the author or that had a convincing study design, not a single study was a good study at all. I mean, they're very, very, very low-quality studies. So, I would say that in order to really make a scientific, a solid scientific claim from this research, we need higher-quality studies that need to be done. And, the problem is I don't think anyone wants to do them because there's so many arguments against it. Like I said, the whole theory behind it, it doesn't make sense. In that regard, so I don't know that we're going to get the high-quality studies, unfortunately. With that said, if it makes you feel better and you are—I mean, placebo effects are also a very real thing.

And you know, I don't—you know, maybe maybe walking around barefoot and getting a mat is a is a sort of cheap way of you know basically helping you feel better. So, um, I'm certainly not against it, but, um, I'm not going to be up there saying that the science is solid, that it's a beneficial thing. Okay, the next question was submitted by Linda, and I was very interested in this question because it has to do with the skin. Linda says, does infrared sauna use cause damage to skin collagen? If so, are there any steps to mitigate the potential damage? This topic came up in a conversation with a dermatologist recently, And it caused me concern because I'm an infrared sauna user. So infrared sauna, infrared sauna, okay. So the infrared heaters emit either near or far infrared wavelengths.

And near infrared heaters use incandescent bulbs to produce thermal radiation of varying wavelengths ranging from near infrared wavelengths to mid infrared wavelengths to a lesser degree. Far infrared heaters use a ceramic or metallic heating element and they emit energy in the far infrared range. Which is actually more similar to energy produced by the sun. The effects of visible and near-infrared wavelengths are dose-dependent. So visible and near-infrared comprise approximately 45 to 50% of the sun's emission spectrum. So when you compare it though to UVR, which is 2 to 3% of the sun spectrum, their relative potency for ionizing radiation is relatively low. So it's UVR that's, that's more potent in ionizing radiation.

Several studies have showed that near-infrared radiation may damage skin collagen content via an increase in matrix metalloproteinase 1, MMP-1, activity. It happens in the same manner that is known to occur by UV radiation. But compared to infrared saunas, there's a higher irradiance used in the studies that have shown this. So, it's really not comparing apples to apples. So, for example, far-infrared, so the IRC far-infrared skin irradiance in a conventional wet sauna is around 11 to 20 milliwatts per centimeter squared. And, the infrared radiance at the skin of an infrared sauna is about 20 to 40 milliwatts per centimeter squared. The studies that have looked at, you know, skin damage from infrared radiation are using a much higher dose.

So they're looking more at a skin irradiance of, you know, 105 milliwatts per centimeter squared. You know, so it's greater than 100 milliwatts per centimeter squared. And I think that, you know, if you think about Yeah. In order to get that kind of dose, 105 milliwatts per centimeter squared, you'd have to be in the sun from 6:00 AM to 6:00 PM in the summertime, south, like in the further south of the tropics. So, that's a lot of sun exposure. I don't think you're going to be getting that in an infrared sauna for 30 minutes, 45 minutes, whatever.

I don't really again, so the you know yes it can definitely damage the skin and again you can look at check with the manufacturer to see what irradiance you're being exposed to in your infrared sauna and that and it's actually not a bad thing to reach out and find that out. I mean I think that's good information, but I think what you're going to find is not even comparable. It's not even comparable to what it would require to actually cause damage to collagen in the skin, which is. again, 6 AM to 6 PM in the summer in the tropics, like that's, that's, that's incredible, right? I mean, like that, that's a lot of irradiance that's hitting your skin. So I see a couple of questions here. Alex Themis is asking a little bit off topic about supplements, supplements safe to use during pregnancy.

I would check out my, the first aliquot that I did on pregnancy, and it covers supplements Honestly, you know, when it comes to pregnancy, erring on the side of caution and cutting out things like resveratrol and all that is, it's a good idea and sticking with a prenatal vitamin D and omega-3. So those are things that you can talk about with your OB-GYN. And that is something that I did myself. Troy is asking about my thoughts on the supplement Juvenon, which was created by my mentor, Bruce Ames. And it's a combination of alpha-lipoic acid and L-carnitine. So I think we talked about this a couple of Crowdcasts ago. And, um, you know, Bruce, Bruce, who just turned 95, takes Juvederm every day. He's been taking it every day for over a decade. Um, I don't think it's a bad idea.

So the alpha-lipoic acid, again, we also covered that either last Crowdcast or the Crowdcast before that. Um, so you can go back and search your, your dashboard for the, for that to see. But, um, I do— we did, we did cover those, and, um, it's not a bad idea actually, to be honest. Um, Christy's asking about Lovaza, if it should be refrigerated. Yes, Lovaza should be refrigerated. I think all omega-3 supplements are better off in the cold. It slows the oxidation process. Okay, so the next question also has to do with infrared radiation, and it was submitted by David. David says, Hi Rhonda, for the prevention of Alzheimer's and other brain disorders, Near-infrared light on the skull has many supporting studies and now devices.

What does the evidence say about this as far as efficacy and specific protocols? So, low-level laser or LED, light-emitting diode therapy, also called photobiomodulation, Okay. So, the wavelengths that are typically used in these are about 600 to 1,070 nanometers. This is different from the wavelengths that you'll be getting if you are bathing in an infrared sauna. They're not— the photobiomodulation, sometimes also called red light therapy, These are different wavelengths. There is a lot of emerging evidence using these types of lasers. Again, oftentimes they're applied directly to the skull, either through like a hat-like device or some kind of handheld device that's like put on, on the skull as well. There's FDA approval for some of these devices for peripheral pain management.

And it's applied to acupuncture points. It's intranasal. Transcranial is a big one that's done in a lot of studies. And the finding is that basically these near-infrared light wavelengths that I mentioned, they pass through the bone. And it's like it spurred a lot of interest in basically potentially treating disorders in the brain. There's been a lot of animal models looking at this stuff. And it's you know, shown beneficial effects. But as you guys know, many things don't translate from animal rodents to humans.

And so, looking specifically at clinical evidence in humans, near-infrared therapy or photobiomodulation has been reported to improve executive function, emotional functions, and also There's a variety of clinical pathological, you know, benefits that have been shown to be for ischemic strokes, brain trauma, also depression, and age-related macular degeneration. So there, again, there's a lot of these, you know, small trials that have been done. And I think that there's definitely a lot of promising data. One of the major mechanisms is targeting It's targeting proteins in the body that are responsive to the electrons, and they have, like, for example, copper in them. So cytochrome c oxidase is one big one that's basically a photoacceptor molecule.

Myoglobin is another photoacceptor molecule, as well as hemoglobin, which is in our blood. So I would say, looking at some of the studies, there's been a few that have been in healthy participants. And there was a placebo control group looking at this, this basically putting it on the forehead, and it was like a minute treatment. And the placebo group got 55 seconds of the actual treatment and then 55 seconds of just like fake laser, whereas the control group got like the complete 60 seconds of laser treatment. Again, it was put on their forehead. And it, it's called transcranial laser stimulation. It did improve cognitive and emotional functions. Reaction time in vigilance tasks and psychomotor vigilance tasks were improved. There was improvement in a memory task as well.

So there was also 2 weeks of sustained positive emotional states. And I know There are now a few places, like I know there's a place in San Diego where you can— people with depression can go and get treated with these transcranial laser treatments. So it is, again, it's something that is being implemented. It is available to consumers. It's quite costly, however, but it is something that is now increasingly becoming available. This transcranial laser therapy has also been shown to be relevant for traumatic brain injury. So it improved neuromuscular function and performance. It increased brain-derived neurotrophic factor. It reduced brain lesion volume. It enhanced learning and memory and improved cognition, anxiety, headaches in people with chronic TBI.

So Again, you know, not a, like, large— there's not overwhelming evidence in this, in the sense where there's just a few studies. Like, people are— this is emerging. People are starting to look at this, but I think it's gaining some momentum. The same goes for Parkinson's. A lot of animal studies there. So, uh, waiting. There was one non-controlled, non-randomized study that suggested improvement in speech, cognition, and some of the gait problems. in people with Parkinson's disease. But it was, again, it was a non-controlled study. So that needs to be repeated in a controlled manner.

Depression is probably one of the big ones that's been a lot of— there's been a lot of research on depression, several different randomized placebo-controlled trials showing that, again, when you take this transcranial device and put it on the forehead, this low-level laser therapy can improve depression, depressive symptoms, and a variety of different ways that it's measured. With respect to Alzheimer's disease, again, a lot of animal model studies. So showing what benefits, I'm not going to go into depth on those. But there was a randomized controlled trial in 2022. So there were 60 people with Alzheimer's disease. And the, I think the differentiating factor here were these These Alzheimer's disease patients were also anemic.

Remember I mentioned that the laser therapy is affecting hemoglobin, it's affecting cytochrome c oxidase and energy production. So the low-level laser therapy in these people with Alzheimer's disease was done for about 6 months. Oh, no, 6 to 24 months. So it was a range. So some people got 6 months and some people continued on for 2 years. And basically, people that were in the placebo group or in the actual treatment group also carried out moderate-intensity aerobic exercise. So they were using a treadmill for 3 days. I mean, this is the main thing. I mean, like the low laser therapy doesn't compare to what this exercise is going to do. Yeah.

And so, again, both groups had improvements because of the exercise, although there was a slight— a slightly better improvement in the experimental group that also did, in addition to moderate-intensity aerobic exercise, they also did the transcranial laser. So they also basically had a little bit better on some of these measured outcomes of cognition And so perhaps there's a nice— now whether or not you would have gotten any benefits from the laser itself without the exercise, I don't know. We'll see. You know, like that's a tall order. But in conjunction with exercise, it seems to be a little bit more. But I would say honestly, like the extra— like, I don't— looking at the data, like it's such a modest increase.

It's almost not even really It's the exercise that's really driving it there with the Alzheimer's disease. So in conclusion, I would say this: there's a lot of consumer products available for red light therapy, photobiomodulation. And, you know, I don't know that going and standing in front of a juve, you know, red light therapy is going to give you everything that I just talked about in, in these studies because most of the studies specifically for the brain is what the question was about. They were, they were basically using devices that were put on the head and penetrating through the skull. Um, so, and, and I know those are being used. Again, there's treatment centers that people can go to. They can pay out of pocket and go to and receive these treatments. I'm aware of them.

They're quite costly. I don't— I'm not aware of, you know, buying any of these sort of things, you know, just for an individual person yet. But I'm sure perhaps I missed something or that is something that is already in the works in terms of an efficacious, you know, medical product that is something that can be used and is derived from the science, not just marketing. 2 questions in the chat. One from SC on AMLA, A-M-L-A, A-M-L-A. Never heard of it. Asking about blood sugar and ApoB. So I'll have to look into that. That's interesting. I've never heard of that. All right. The next question has to do with how many meal frequency and how many times to eat during the day. So Elias asked, how many times Should one eat throughout the day?

Can you please do a deep dive on the risks and benefits of eating two large meals a day versus eating multiple small meals a day? And I had previously mentioned, you know, that larger meals do can increase gut permeability. And you know, so the question is, but then you know smaller meals you're. You know, the question then is also like larger meals can induce a larger blood glucose response depending on the macronutrient content of the meal. There's I mean there's arguments for either way, and I'm going to tell you guys the literature is so unclear. So you'll have randomized controlled trials. There's a few, and. If you look at these randomized controlled trials, you know they're most of them are doing isocaloric comparison.

So they're trying to look at the amount of energy intake that is exchanged with an equal amount of energy intake for the different meal frequency between the interventions, right? And you know so that that's a big thing. I you know I don't I don't know that all the macronutrients and they're they're doing energy balance. It's caloric balance, but not necessarily. Necessarily, you know, the macronutrients can be different. So that's, that's also, I think, I think macronutrients are an important factor that are not considered in these studies and can potentially be sort of giving inconsistent results. But a lot of the randomized controlled trials are looking at body weight. Okay, really no, no big difference in whether or not you eat 1 or 2 meals a day versus literally 8 meals a day.

Perhaps 2 meals a day slightly reduces body weight compared to 3 meals. There was no effects observed for body weight when comparing, looking at 3, 4, or 6. So if you ate 3 or 4 or 6, it was all the same body weight. But if you ate 2, it's a little bit less body weight than if you ate 3. Waist circumference, basically there was a little, little bit of an effect if you ate, you know, 1 or 2 meals versus— 2 meals versus, you know, 6. So, but 3 versus 6, no difference. Fat mass, Absolutely no difference between 1, 2, 3, 4, or 6 meals. I would say there was a— I mean, there was actually a little bit of uncertainty. Maybe 1 meal a day was more effective at reducing fat mass than the others compared to like 3, but it was, it was so little.

So honestly, in conclusion of the randomized controlled trials, and there's— this was a meta-analysis of several. It's really like not clear that there's, there's a big benefit with respect to looking at body weight, waist circumference, or body fat. And, but you know, that's not like, like, that's not just the endpoints that everyone's looking at, right? I mean, so that's one thing. And I'm gonna say it like, you know, even at that, it's like, well, okay, if you're talking about a morbidly obese person, I think, you know, one meal a day, they're probably going to lose more fat than if they're eating 6 meals a day, right? You know, so we got to think about the population, who's the target population here, right?

We're talking about normal, healthy people looking to optimize, like, and dial in everything that they can. I don't— with respect to those randomized controlled trials, I don't know that it's clear. But again, they didn't control for macronutrient intake, micronutrient intake. I mean, these are— and they're short-term studies. They're short-term studies. They're not looking at repair processes. Or autophagy or anything like that, right? They're looking at waist circumference, body weight, and body fat, and there's just such minor differences. The epi studies, so these are observational data, it's even more unclear. So I think there's some evidence between epidemiological studies indicating there's an association between higher meal frequencies and lower disease risk.

The experimental trials have shown conflicting results, and so for example, you'll have a study looking like a prospective research study that showed there's a decrease in disease risk with high meal frequencies, like six meals a day versus low meal frequency. In other words, people that ate two meals a day were less likely to get certain diseases than people that were eating six meals a day. Right. And honestly, when I start looking at all this evidence, I could go through it, but it's just so— it's so confusing. And it's like, you'll— you can just find anything you want. So my— here's what I do and what I've sort of boiled down from this very confusing literature. Honestly, I typically On most days, we'll do like 2.5 meals. So like I do, I do a larger breakfast.

Well, my breakfast is a very high protein. And so it's a lot of eggs. And sometimes like I'll have a frittata with, you know, some kale and broccoli. Or I'll have the eggs with, you know, either, you know, a little bit of fruit, or my, my smoothie, which we're going to talk about smoothies as well. Today, and then the the half a meal that you know the the the the quote unquote third meal would be my lunch, which is mostly protein. So it's like I'll have a turkey burger or I'll have a little piece of chicken or a little piece of salmon. It's like it's like protein, and then I have dinner. I think I think two to three meals again, and it the the macronutrient content's important. Because that's not something that's really controlled for in a lot of these studies.

So I think it's really hard to say, okay, you know, you could have someone that's eating one meal a day or two meals a day, and they're like totally becoming deficient in protein because they're like not eating enough protein. That's also very possible, right? And then, you know, then that can increase disease risk. On the flip side of that, you know, you can have people that are eating 6 meals a day and they're like vegan, and the reason they're eating 6 meals a day is because they're not satiated, and so they're eating like a lot of little small meals, but maybe they're not going to have as much of a cancer incidence because, you know, of the fact that they're vegan.

And, you know, so there's too many confounding factors, to be honest, to really definitively say— to say that the science is absolutely clear. I don't think it is. I think the randomized controlled trials are too short-term, and they're only focused on a couple of endpoints. And ultimately, what we're interested in looking at is, you know, what about disease risk? And I think some of the studies that have looked at disease risk, it's not clear. There's always reverse causation as well. I mean, people then that get sick start eating one meal a day, and that, you know, so There's there's too many things going on, I think, to to know for sure. But I do. I think at the end of the day, you know, like obviously anytime you eat food, you know, there's gonna be a little bit of an insulin response.

It's gonna your blood glucose will go up maybe for ninety minutes, maybe for a couple of hours. I don't know. But you know, it that anabolic hormone is going up. And so, in that way, the body is getting into this fat storing mode every time we eat. And so, with that in mind, maybe a smaller number of meals might be better than, you know, within an 8 or 9 or 10-hour window might be better than eating, you know, every hour or every 2 hours. But we don't have a lot of hard data on that. Again, I did mention a couple of studies looking at the body fat and waist circumference and stuff.

But, you know, I think, I think basically what I, what it boils down to me is I do think that eating, eating, not eating, you know, so many meals throughout, you know, the time window, and really what you're wanting is a fasting period. So that, that is not controlled for in 100% of these epidemiological observational data studies. Some of them look at confounding factors like energy intake or physical activity. They do look at those, but they don't look at when people are eating their food. Are they eating 15 hours within a 15-hour time window? Are they eating within an 8-hour time window? Are they eating within a 20-hour time window? None of that is— the time window is never looked at ever. And I think it's a big confounding factor with those studies.

And typically, you know, you could have someone that's eating 5 meals in an 8-hour window, but typically the person that's eating 5 meals is they're extending their eating window quite long, right? I think the main— the bigger thing is to— you do want to have a period of rest. And that period of rest is important for repair processes. It's important because we need to be in a fasted state to repair DNA, to repair proteins, to repair lipids, to clear away, you know, gunk within a cell through autophagy like that. That happens in a fasted state. And if you are digesting, food, which, you know, that process takes a while, that repair process is not going to happen. I mean, it's like 5 hours after your last meal, then you're, you know, you're starting the repair process after that.

So I do think that's probably the most important thing. Again, I eat about most days, I would say, you know, 3. I'm saying 2.5 because the lunch meal isn't like a huge meal. So that's typically what I do. The next question was submitted by Debbie, and Debbie was asking about melatonin supplementation for older people. Melatonin production dramatically goes down with age, and it's, you know, the question is, is it, you know, good to supplement with it, or what's the deal? So background information, there's a tenfold decrease in the secretion of melatonin from the pineal gland in people that are, for example, 80 years old compared to teenagers. A tenfold decrease is quite significant. There's a big difference in age between an 80-year-old and a teenager, though.

Melatonin does start to go down. Melatonin production does start to go down starting at age 40. You get to age 60, 70, goes down even more, and then again, even more as you get to 80. Because melatonin is a hormone, it is regulating about 500 different genes. Many of those genes are in the brain, and many of those genes are antioxidant-related genes. So melatonin can act to some degree as a brain antioxidant. And when people's melatonin production goes down with age, so does their brain antioxidant capacity. Again, as we discussed in the last Crowdcast, number 44, we talked a little bit about reductive stress. This is sort of like the opposite of oxidative stress. Reductive stress is when you have a buildup of the antioxidant, the reducing equivalents, for example.

And so That is always a concern with over-supplementation of antioxidants. That's not been directly shown to occur with melatonin. However, it is something, of course, to consider. It has to still be shown. There's been a number of studies that indicate melatonin basically could slow, like chronic administration of, and these are mostly animal studies, basically showing chronic administration of melatonin slows some aspects of aging. So it reduces oxidative stress, it increases a lot of the cytoprotective, you know, again, a lot of these antioxidant genes and their anti-inflammatory genes. So, you know, those things have also been shown. Again, these are animal studies, finding the optimal dose for humans, that, that still needs to be defined. There's a systematic review and meta-analysis.

So this is 21 different studies. 16 of these are randomized controlled trials. And people on the average were age 55 years or older. And they went up to the age of about 82 or 83 years old. And the most important finding of this study was that melatonin, and also it's a melatonin receptor agonist, It's called ramelteon. Ramelteon. That produced a higher benefit over placebo for increasing total sleep time. And so on average, they slept 21 minutes longer. And these were based off of objective measurements, though. And so on average, those people taking melatonin, a variety of doses, they basically slept on average, they fell asleep about almost 14 minutes earlier than those receiving placebo. They slept 21 minutes longer.

And so their sleep latency was reduced about 8 minutes with both melatonin and that melatonin receptor agonist I was talking about compared to placebo. Sleep efficiency was not really Very different between the melatonin and the melatonin receptor agonist. I think overall, with limited safe treatment options for insomnia for older adults, there's potential evidence in older adults that melatonin may, or even a melatonin receptor agonist, may help improve total sleep time and reduce sleep latency. So Especially since a lot of concerns— I mean, people are taking benzodiazepines, and they're taking benzodiazepine receptor agonists. Melatonin would be a safer option compared to those, those options, for sure.

And of course, there's other, there's other options that people also, you know, can, can, can follow up on as well, a variety of behavior changes, of course. But another— then there was another review, this was in 2022, that also found melatonin appears to be a safe medication in older adults relative to other commonly prescribed medications such as benzodiazepines, antidepressants, antiplatelets, and antipsychotics. But there's also a lot of safety data that's from younger populations. And this is important because Melatonin can react with other other drugs that are prescribed to older people. So one of the things that I found surprising is that basically it it reduces the effect. So so melatonin can basically interact with any type of SSRI, so serotonin reuptake inhibitors.

They somehow substantially increase serum melatonin concentrations. They're somehow, you know, so basically serotonin, the melatonin is a metabolite of serotonin. So you can make melatonin from serotonin. And so these people that are taking SSRIs are already getting melatonin. And so that so people that are taking in combination melatonin and SSRI can have really high levels of melatonin, and like like some people have been known to just like fall asleep like like immediately. So it can have adverse effects, and so people you know also people taking oxycodone as well these things are contraindicated. It also melatonin can reduce the Efficacy of calcium channel blocker drugs, so this is an antihypertensive medication, and melatonin also can lower blood pressure itself.

So people that are already taking you know antihypertensive medication and then melatonin and perhaps I mean so there's some potential interaction there. Blood pressure monitoring is important. There are case reports of people taking melatonin and warfarin as well that somehow, and, you know, it's increasing the— it's basically lowering blood coagulation. So I think older adults on polypharmacy, it needs to be considered the panel of drugs that they're being prescribed and whether or not melatonin is going to interact with those. With those drugs. Because a lot of, again, a lot of the safety trials on melatonin have been done in younger adults and not on people, you know, basically on polypharmacy.

With respect to dose, you know, a lot of studies, you know, have done, I would say, a relatively smaller dose, like 2 milligrams of melatonin. There are cases where people have sleep disorders like night terrors, for example, where a much higher dose of melatonin seems to be required to help counter some of the whatever is going on, you know, in the brain for causing the night terrors. And so I think those things are things to consider. But generally speaking, a person, you know, in their 60s taking 2 or 3 milligrams of melatonin, it appears to be a safe, you know, safe dose. Again, considering not being on polypharmacy. So people in the chat are asking about children with sleep problems and melatonin. And that would definitely be something to speak with your child's pediatrician about.

Probably in, in the cases where there are sleep disorders, the pediatrician may, you know, refer you to a sleep physician or a sleep doctor to help define whether a melatonin gummy is appropriate or not for a child. But that is something, again, to potentially speak with the pediatrician about because, um, it's sort of not something that I've really looked into. And by the way, we have— Mike is asking in the chat about whether or not we've talked about melatonin and cancer prevention or cancer treatment in previous Crowdcasts, and we have. So go back to your dashboard and look up the backlog of Crowdcasts which have summarized timestamps on them. You will, and if you search melatonin, you will see we have covered, there have been a few interesting case reports.

And I don't want to speak incorrectly because it's been, it's been a couple of years since we addressed them in the Crowdcast. But we did talk about, there were some studies that were very high dose melatonin, particularly with brain cancers like glioblastoma. Again, antioxidant in the brain. So, so there were some interesting studies also with breast cancer and high-dose melatonin, you know, treatment. But again, this isn't something that's, you know, translatable to an everyday person looking to take it to help with their sleep latency problems. You know, so that, you know, that's something to consider. So, you know, some people like I don't have any problem with sleep latency, I can fall asleep quite easy. Now I do take melatonin, but I take it for night terrors. And it really helps.

My husband, on the other hand, takes melatonin because he's got a sleep latency issue. And it really, it really helps that and combined actually with heat therapy. So he does either a sauna or a hot tub a couple of hours before he goes to bed. And it's got to be enough time for him to cool his body temperature down after the heat treatment. But it really helps with his, his It helps with his sleep latency and also his efficiency. So, um, I think the heat probably is what's doing the efficiency because I don't— I haven't seen a lot of evidence that melatonin helps with sleep efficiency. And Justin's asking whether or not melatonin makes your body stop producing melatonin naturally. We also have covered this more in detail in a Crowdcast.

Again, go back to your dashboard and search the backlog of Crowdcast, the PDF that you have, search melatonin. I can't remember off the top of my head all the details, but I do remember coming to the conclusion that so far I am not convinced that there's evidence suggesting that supplemental melatonin is stopping you from making it. But, you know, again, we could, we could do a deep dive of the literature. Maybe there's been some new evidence since we covered that last. If you guys want to submit that question, we can we can certainly look into that. All right, the next question submitted was submitted from Christina, and Christina asked: Is there a reduction in the benefits from fiber when blending in smoothies? And I'll tell you, we did a really really really really really really.

Really deep dive into what evidence was out there. I am not going to go through every clinical study with you because that would have taken all like hour and a half of this Crowdcast to talk about. And I'm going to give you a summary. So the results from the various clinical studies that we looked at, well, I think first and foremost, let me say one mechanism that has been identified for how you know, dietary fiber reduces postprandial glucose and insulin response is that soluble fiber increases the viscosity of ingested food. Increased viscosity in food in the stomach then reduces the rate of gastric emptying and subsequently the absorption rate of glucose from the small intestine into circulation. Okay.

So that's That's that's one of the reasons why you know let's say you're comparing and other studies that that we we dove into and looked at when we were doing background research for this comparing like juicing to blending a smoothie. I mean, so juicing you're getting rid of all the fiber, right? And you are getting some of that glucose you know from the fruit and fructose from the fruit in in the juice. Whereas the the smoothie is is is blending up the fiber. Okay, so let's talk about whether you know blending the food is basically you're not getting some benefits compared to like you know just eating eating the fruit for example. Results really varied depending on the type of fruit that was used in the study.

So so vegetables vegetables aside not a big deal, but if we're talking about fruits, it really seemed to depend on the seed content of fruits and better extraction of nutrients from the seeds by blending them compared to chewing and eating the whole fruit. So adding fruits rich in seeds, so seeds that can be, you know, safely consumed in a blended state, to a smoothie actually improved the glycemic response compared to eating the fruit, just like regular eating a normal fruit. Glycemic response to blended fruits that were rich in seeds really again were better than just eating the same whole fruit, the same quantity of amount. So like just like absolutely comparing one apple to one apple, eating the apple versus blending it, right?

Like it— the glycemic response was actually improved when, when blending the fruit. When eating fruits without seeds, the blood sugar response seems to not be significantly different between eating a whole fruit and drinking the smoothie. But eating the whole fruit might prevent blood sugar levels from dropping below fasting levels in a couple of hours. So in addition, one study showed a higher feeling of satiety after eating the whole fruit compared to blending it. And this is both without seeds. There were no seeds in this, in this. And so I would say the biggest benefit from actually like chewing the food would potentially be a satiety effect that would occur a couple of hours after. So you would feel more full.

And that has a lot to do with the chewing process and the— and of course, some of the satiety hormones that are released from the actual act of chewing itself, which does not occur when you're eating— when you're drinking the smoothie. But with respect to the glycemic response, really no difference unless you were using those seeds in the smoothie that you really aren't, you know, eating when you're eating the fruit, then the glycemic response was actually improved from the smoothie, because for whatever reason, there's something happening with the seeds that are beneficial to glycemic response. This was a surprise to me, by the way. This was interesting. It was not something I was familiar with.

And so I would say the biggest take-home for me was that if you are hugely concerned about a little bit of a difference in satiety, than eating, eating the food. So like in my smoothies, I do kale, you know, kale, blueberries, avocado, and, um, you know, some collagen powder, you know, then, then you'd be better off making a kale salad with some avocado, throwing some blueberries in there, uh, eating, eating, eating the salad, you know, instead of blending it. So that would, so that would, that would be another way to get to get that. Now for me, it's easier to make a smoothie and get it, you know, and drink it along with my protein. But I am, I am not someone so concerned with satiety. Like I don't, because I eat my smoothie, I drink my smoothie with protein.

Like I'm, it's not just, it's not most of the time I'm not just doing the smoothie by itself as a meal. If you are a person doing that, then it would be something to consider that a couple of hours, one or two hours later, you may be more hungry than you would be if you had the same amount of food as a salad or eating that fruit whole than you would blending it. So I hope that's clear to you guys. Sri is asking in the chat about L-tryptophan, and they're saying whether it's a Serotonin or melatonin inhibitor. Actually, quite the opposite. So L-tryptophan gets metabolized into serotonin and subsequently then melatonin. So L-tryptophan is a precursor for both serotonin and for melatonin.

However, when you are eating dietary tryptophan from either meat, you know, poultry, whatever source, food source, or supplemental source, the, the, the tryptophan can be converted into serotonin into— in the gut. And often that's— it is converted to serotonin in the gut. Too much serotonin in the gut can cause inflammation. Now you'd have to really supplement with a lot to, to, to get that effect. But, um, In order for the production of serotonin in the brain, which is where you want it, the tryptophan has to be transported into the brain before it's metabolized into serotonin in the gut. And again, the way to do that would be exercise. So exercise really boosts the transport of tryptophan into the brain.

So there's another question in the chat from Yolanda about my Google Excel sheet that I made. About a year ago now. I would say it's close to a year almost on the fish oil brands from the International Fish Oil Standards site. And I haven't posted it. I like— I was gonna make a video on it, but I'm not, you know, I have to go back and now look at the product to see, like, because there's different product batches and, you know, like when I think many of them were like 2027, so they went out to 2027, but I'm not sure. So that would be something on my list to do, to post for you guys. I just haven't gotten around to it yet. Again, we've talked in this crowdcast about some of the top brands that I've sort of looked looked into with respect to the, the IFOS data.

And I really think some of the— one of the good brands, which is no longer being measured on IFOS for whatever reason, is Metagenics. I like their liquid form, which has a really high dose of omega-3. So Metagenics is one that I really like. Some of the other ones that I like So if you're looking for a high EPA, uh, NutraGold is one that had a good, good, uh, concentration and a low oxidation profile. OmegaVia was another one, um, and Norwegian Gold also was a good one. Viva Naturals, Sports Research, AquaMega, uh, was also a good one. And then if you're in Canada, Genuine Health, and in Europe, Bare Biology, those were all high EPA. Uh-huh. For high DHA, some of the some of the good ones that I had found were Clicious or A and B Well Incorporated, CytoMatrix.

Again, Aqua Omega was another one. So Aqua Omega has a high EPA and a high DHA. For people in Europe, San Omega GmbH was a was a good high DHA one, and. Canada, it was called C-A-N-P-R-E-V, CanPrev. Those were high DHA supplements. But again, the Metagenics, they have a Metagenics Omagenics 1000, which is a good— it's got a high EPA and a pretty, pretty decent DHA. But my favorite from Metagenics is the liquid one. I forgot what it was called, but it's a liquid and it's really, really highly concentrated. So you really like, you take a tablespoon or 2 of that and it's, it's like pretty good. So those are some of the brands that I really, I looked into.

Terry's asking about Vascepa, which is a prescription omega-3 purified pure EPA in ethylester form, which means anything in ethylester form, by the way, you need to look at some of those brands. And if they are ethyl ester form, has to be taken with food or it will not be absorbed. So Vascepa is prescribed for high triglycerides, hypertriglyceridemia, and obviously it's it's been shown in clinical studies to to have beneficial effects on cardiovascular disease. My only my only concern with that is I think DHA has a lot of beneficial metabolites. um, like the SPMs, Resolvins, that I wouldn't avoid. Um, so, and also DHA is extremely important.

If you listen to our last podcast with Dr. Axel Montagne, there is a specific DHA transporter, and it's specific for the phospholipid form of DHA, and it's called MFSD2A. If you disrupt that transporter, the blood-brain barrier breaks down. DHA appears to be very important for maintaining blood-brain barrier integrity, and particularly in people with APOE4. So I think that getting a supplement that has either a good ratio of both, like the Metagenics, or getting, you know, independently taking a high EPA. So what I do is I take a high EPA supplement in the morning, And then I take a high DHA, higher DHA supplement in the evening. Now when I say high EPA supplement, the one I take still has DHA in it. It just has a much higher dose of EPA. Same goes for the DHA.

It still has EPA in it, but it just has a much higher DHA dose. So that's kind of, you know, my, my way of supplementing. I take, I take a higher EPA in the morning and a higher DHA in the evening. That's again, I take very, I take experimentally high doses of omega-3. So I'm, you know, taking anywhere between 4 to 6 grams daily and combined. So it's mostly, it's either, you know, 2 grams, around approximately 2 grams of EPA, 2 grams of DHA a day, or I'll do 3 grams of EPA and 3 grams of DHA a day. So it's approximately what I do. I think on most days I'm getting more like 4 grams compared to 6. But Sometimes, some days I do actually get 6, but most, most, most days it's actually 4, 2 and 2.

And SC is asking about the best way to measure omega-3 levels and is OmegaQuant— in my opinion, yes, the best indicator of omega-3 status would be the omega-3 index, which is measuring it in blood cell membranes. And there was a question submitted. There was actually a couple of questions submitted regarding the omega-3 index data from OmegaQuant with respect to the complete test that they offer, which has also the ratios of omega-6 to omega-3. I'm going to go in more detail on that next crowdcast because I've been talking with Bill Harris about it. So Dr. Bill Harris is, uh, one of the co-inventors of the Omega-3 Index, and, um, he's got some thoughts on that.

And, um, so, so I'm gonna— I'm putting something together, and I will, I will talk a little more in detail about, uh, that next time because that was a top-voted question as well. And Barbara's asking in the chat whether or not I also supplement with— um, I'm sorry, if I eat, if I eat seafood in addition to my supplementation, and I do. I actually eat wild Alaskan salmon. I would say I eat it probably 3 times a week right now. And it's one of the lower mercury, higher omega-3 content fishes out there. That's why I choose to eat that one. Yolanda is asking why I split up my omega-3. So My rationale behind splitting up the omega-3 dose between morning and evening is sort of twofold, and it's it's my rationale.

In other words, based on connecting dots in the scientific literature, I personally have decided to do it this way. It doesn't mean it's necessarily the right way to do it. I could be making it harder on myself. I you know so um. Take this with a grain of salt. Reason number one is because it's been shown in both clinical studies and mechanistically in animal studies that omega-3 supplementation blunts the endotoxin or LPS lipopolysaccharide release from the gut with with food intake, and that is something that occurs when eating food. Certainly occurs when you're eating, you know, foods that are very, very high in fat or foods that contain gluten. And, and so, so it blunts that response, not the whole inflammatory response, kind of does because it's, you know, resolves inflammation.

But it does, it does blunt the LPS being released. So, so I like to take it, you know, in the morning with my breakfast and in the evening, I take it after dinner. But the other reason I take it, I split it up, is because there was a clinical study looking at the release of specialized pro-mediators. So these are SPMs, they're these molecules that are resolving inflammation. There's a wide variety of them ranging from resolvins and maresins, protectins. These are important molecules. They are Yeah. Resolving inflammation in circulation. They're preventing, you know, some of these compounds that are harming the brain, blood-brain barrier, and basically, you know, exacerbating leaks and also, you know, exacerbating, you know, the dementia risk, in my opinion.

And so those things have, you know, basically I'm trying to have a constant release of SPMs in my circulation throughout a 24-hour period. So, that's my rationale. It's quite possible that once is fine and I'm overdoing it. So, you know, there you have it. That's my rationale. Also, I should mention that omega-3 bioavailability, particularly in ethylester form, is significantly improved if it's taken not only with a meal, after a meal, but also in a meal that's higher in fat. So, so basically, you know, you want to basically take a— you want to, you want to have some fat in your meal, and that increases, that improves the absorption of omega-3, particularly in ethyl ester form. All right, I'm going to move on to some rapid-fire questions.

There was a question submitted on osteopenia and vitamin D and calcium supplementation, which we will get into next Crowdcast because I would like to get into some of the rapid-fire questions. Also, we'll get in next time, there was a question submitted about this product called NAD3 that I guess apparently Bren Greenfield and Tony Robbins have talked about. So we'll talk about those in addition to the omega-3 ratio, omega quant, omega-3 to omega-6 ratio. We'll talk about those next time. But some of the rapid-fire questions, so let's talk about those. So Lisa submitted a question about the amino acid complex that I take from Thorne versus the protein powder that I often take from Thorne and whether or not there's a big difference.

You know, which which which why why why do I use both basically? So let me just start by saying that you know most of the big experts in the field, including Dr. Stuart Phillips, Dr. Brad Schoenfeld, both who have been on my podcast and talked about this whole protein is better than. You know, taking an amino acid. So whole protein is better. Whole food protein is the best, right? On days when I am working out, like it is hard for me to, to, you know, to get in 1.6 grams of protein per kilogram body weight. You know, on most— I do work out on most days. So I do most of the time like to do a protein powder, which would be the whole protein And I typically am using Thorn right now is what I use. I get the chocolate right now because my son uses it and protein helps children grow lengthwise.

The reason I have the amino acid complex is because if I, if I'm having a meal that is lower in protein than I would like, And I really just don't have the stomach for a full protein shake, then I can just mix in some of these amino acids which have the leucine, and I can take it with my meal. And I'm like, I'm basically boosting a little bit. I'm just getting a little bit more of the leucine with my meal. So really, it's a convenience thing. And it's mostly when it's, you know, it's like a lower protein meal, and I just am not gonna make a whole, like, protein shake. So that's really it.

So I would say when it comes down to it, you know, the protein powder is, is, you know, the way to go if you are trying to supplement your, your diet to get enough protein, particularly when you're, you know, being doing strength training, resistance training, you know, so that, so that would be, that would be, I think, what the experts, you know, what I've learned from them, basically. Another question also was about supplements and the cost of them and pure encapsulation and thorn products can become very expensive. And I agree. And that, like, what's a good way to basically find more economically reasonable options that are still quality brands?

And so, so typically what I do also, like, there are times when I find I can't there's something I'm looking for that doesn't— that's not, you know, made by some like Thorne or, or Pure Encapsulations. So I think looking at ConsumerLab, looking at labdoor.com is a good one, and looking at ConsumerLab because ConsumerLab does a wide variety of products. I mean, they look at like everything from sardines to your Kirkland variety vitamin D supplement. And I really think that, you know, generally speaking, it's a good way— it's a good— for people, you know, that are really on a budget, it is a good way to find a pretty decent quality supplement brand. ConsumerLab.com has an annual membership fee. Think it's something like $70. I can't quite remember. Um, that would be my, my suggestion.

James is asking about sulforaphane supplements. Um, I would say so. So, um, I think in the US there's 2 quality brands, Broc, B-R-O-Q, or Avmacol. Broc is a much higher dose of sulforaphane. Avmacol is something that, um, that has been shown in clinical studies to be effective. Brock has not. Brock is a rebranded Prostafane. Prostafane changed their, um, their, their, uh, supplement form from a tablet to a capsule. I'm having a bit of a coughing attack, but you know, we're at the end of this, so I'm going to go ahead and wrap this up, unfortunately. Thank you guys so much. I will talk to you next month.