FoundMyFitness

#052 New Omega-3, sulforaphane research, and more! [Kevin Rose Show]

FoundMyFitness with Rhonda Patrick 2020-01-06

Summary

Rhonda Patrick discusses new research on omega-3 fatty acids and sulforaphane. Covers the latest findings on these compounds for inflammation, brain health, and longevity.

Key Points

  • Latest omega-3 research findings
  • Sulforaphane mechanisms and benefits
  • Optimal dosing considerations
  • Food sources versus supplements
  • Synergistic effects of these compounds

Key Moments

Omega 3

Omega 3: Dha

Many of you may already be familiar with Kevin thanks to his history as a notable personality in the technology world, his frequent guest appearances on the Tim Ferriss Show, and the many, many podcasts...

"Many of you may already be familiar with Kevin thanks to his history as a notable personality in the technology world, his frequent guest appearances on the Tim Ferriss Show, and the many, many podcasts he's hosted over the years."
Longevity

Longevity Discussion

Many of you may already be familiar with Kevin thanks to his history as a notable personality in the technology world, his frequent guest appearances on the Tim Ferriss Show, and the many, many podcasts...

"Many of you may already be familiar with Kevin thanks to his history as a notable personality in the technology world, his frequent guest appearances on the Tim Ferriss Show, and the many, many podcasts he's hosted over the years."

Blood Brain Barrier: Benefits

I don't know if you can call it drug hot, but it's a very popular drug, at least in Silicon Valley, for people taking it to extend life and some of the potential pitfalls that...

"Finally, we talk about some of the recent updates on the Found My Fitness website, particularly the new premium membership. For those of you that enjoy this conversation, please make sure to also head over to Kevin's iTunes, which you can find by Googling The Kevin Rose Show. He's had many overlapping guests we've had over here, including Drs. David Sinclair and Walter Longo. Outside of HealthSpan, he also interviews founders, entrepreneurs, and notable personalities from the investment world, which you can also find represented on his recently relaunched podcast called Foundation, also on iTunes. Big thanks to Kevin for having me on. Now, away to the episode. Hey, everybody. Kevin Rose here. Welcome back to another episode of The Kevin Rose Show. Happy 2020. It's a brand new year. And so I'm really excited to have Dr. Rhonda Patrick on the show because what better way and thing to address than health and longevity in January? It's surely a topic that is on a lot of our minds. I, for one, am going to try mostly a mostly pescatarian diet for this first month and get my blood work checked and see what it does to some of my numbers. I'm also going to be cutting out drinking for the most part, because I have a trip planned to Japan at the end of the month. I will be drinking in Japan. I'll be having sake and good Japanese beer, but the first few weeks I will not have any, any drinks, uh, and get my blood tested before all of that. Anyway, Dr. Rhonda Patrick is one of my favorite scientists. She goes in, reads all of the published studies, uh, around health and longevity and really takes that information out of there that is too technical for the average person to understand and then translates it into things that we can incorporate into our everyday lives. This is the best way to get your health advice, people. Like doctors are always, always four, five, 10 years behind, except for some doctors like Peter Tia. But the average doctor is many years behind what the science is actually telling us to do. So if you want to know the latest and greatest, it's best to go to scientists. And thankfully, due to podcasting, Rhonda has a fantastic podcast and also a great website called foundmyfitness.com. She has been able to give us that direct link to scientists. And so she interviews a bunch of great scientists and really help us make better decisions earlier on. So for example, in this episode, we talk about omega threes and why they're not all created equally. And there's various different forms of omega three. And we talk about which ones that she takes, how much she actually takes personally, a lot of great information there, because not only is she understanding the science to relate it to us, also has published her own science around omega-3s. And she's done a bunch of research in regards to omega-3s impact on dementia and Alzheimer's. So great to have her talking about that. We also talk about metformin, which is a very hot drug right now. Hot. I don't know if you can call it drug hot, but it's a very popular drug, at least in Silicon Valley, for people taking it to extend life and some of the potential pitfalls that it has. We also talk about a compound called sulforaphane, which is found in broccoli. She has talked about at length on her own podcast about sulforaphane, but there is some new data out there that we cover. And we also talk about a new brand of sulforaphane that she has imported that she takes. So a lot of interesting stuff there. We cover sauna usage, some new studies have come out there. So a lot of really new things to chat about. And this was a great episode. I really enjoyed it. And I know that you will too. So happy 2020. Cheers to you. I'm really hoping that all of you stay happy and healthy this year, um, introduce some new, uh, healthy habits into your life and, uh, hopefully subscribe to all of Rhonda's stuff as you'll hear her talk about, um, later in the episode when she talks about all the new things that she's building for her website as well. So I hope you enjoy the show. This is Dr. Rhonda Patrick. Rhonda, thanks so much for coming back on the show. You were actually my very first guest. And now I look back and I'm almost like 40 plus episodes deep. So thank you for returning. Totally. Yeah, I totally remember that. The first episode we recorded a few years ago. I was living in New York. I didn't have any babies. You didn't have any babies. Right. Things have changed. Definitely. Things have changed a lot. Becoming a parent is definitely a huge change in the life. Yeah, absolutely. I'm just now returning and getting enough sleep again. So, things are looking up, especially for Daria as well. One of the things I want to cover that has changed since we last talked is you had really gone deep and published a paper around the phospholipid form of omega-3s and its benefits. I was wondering if you could bring us up to speed on that and what your current thinking is on omega-3 supplementation. So when it comes to, if we're talking about phospholipid, DHA, when it comes to DHA in general, DHA is one of the omega-3s. It's predominantly found in marine sources. Really what I care about is, you know, getting it to the brain. That's like my number one interest. And the only type of DHA that crosses the blood-brain barrier is DHA that is bound to albumin, which is a protein found in your bloodstream, transports a variety of goodies in addition to DHA to other tissues, including the brain. But there are two forms of DHA that are bound to albumin. And these two different forms are transported by different mechanisms. So the first is DHA that is not as terrified. It's not bound to anything other than albumin. So it's in a free fatty acid form. And I often refer to that as DHA free. It's free. It's not bound to anything aside from albumin. It gets transported across the blood-brain barrier via this mechanism that's passive diffusion, which just means it's passively crossing the blood-brain barrier. And the blood-brain barrier via this mechanism that's passive diffusion, which just means it's, you know, passively crossing the blood-brain barrier. And the blood-brain barrier, there's a variety of things that, you know, make it up. But one of the things that's important in this discussion is that endothelial cells align the blood-brain barrier and the endothelial cells are attached to each other by tight junctions. So this passive diffusion mechanism where free DHA gets across the brain depends on the integrity of the blood-brain barrier. So unfortunately, as we age, the blood-brain barrier becomes compromised. And this is even more of an issue in people that have an APOE4 allele. APOE4 is just a gene, and allele just means one copy of the gene. You have two copies of every gene, one from your mom, one from your dad, so you have two alleles of every gene. And just to bring people up to speed, if you have one copy of this gene, you are how much more likely to get Alzheimer's disease? People that have one copy of the APOE4 allele are about twofold more likely to get Alzheimer's disease than people that have no copies of it. People that have two copies of it, it's not very common. So about 25% of the population has at least one copy of it. Two copies, much, much less common. I don't know the percentage off the top of my head, but you can figure the math out if, you know, 25% has one copy, what, you know what two copies would be. But that increases the risk for Alzheimer's disease from anywhere between 10 to 15 fold. And what percentage of the population that is diagnosed with Alzheimer's disease has at least one copy? Anywhere between 65 to 85%. Wow. Yeah. So this is a pretty big indicator then. It is. And we could spend hours talking about the reasons why that is. And I do talk a lot about that in my paper that I published last October in FASCIP Journal. But basically, to get back to the whole DHA part of the story, I mentioned that there's two ways it can be transported to the brain. This one form that's free, not bound to anything other than albumin, it goes through passive diffusion. However, APOE4 actually disrupts that because it does compromise the blood-brain barrier and that even gets worse with age. Things like traumatic brain injury also compromise the blood-brain barrier. The good news is there is another form of DHA that is bound to albumin. It's a form that is a specific type of phospholipid form called lysophosphatidylcholine DHA, or DHA lysopc, as I like to call it for short. And that's also transported across the blood-brain barrier through an entirely different mechanism. It uses a transporter called MFSD2A. And basically, when this phospholipid form of DHA binds to the transporter, the transporter flips it across the outer membrane into the inner membrane of the blood-brain barrier. And it potentially bypasses any defects, for example, in tight junctions in the endothelial cells that I was just mentioning, which, by the way, APOE4 does disrupt tight junctions in lining the blood-brain barrier. So I sort of argue in my latest publication that this specific DHA lyso-PC form of DHA may be a nice way to bypass that, you know, defect that APOE4 causes or even just normal brain aging causes where you can get DHA into the brain. Is your hypothesis here that lack of this DHA is a potential cause of dementia? Yes, specifically making people with APOE4 more susceptible to it. So DHA plays a lot of important roles in the brain. It plays a role in preventing and ameliorating a couple of the hallmarks associated with Alzheimer's disease, tau tangles and amyloid beta plaques. And that's been shown in clinical studies. It's been shown that DHA supplementation can lower the amyloid burden and also tau tangle pathology in people that have them. So specifically people with Alzheimer's disease. And it also can improve cognitive function. The other thing that DHA does, it's really important for transporting glucose across the blood-brain barrier. And this is a really major hallmark of Alzheimer's disease, not gating glucose into the brain, basically. That is actually something that can be observed before any other clinical features of Alzheimer's disease, and it's specifically found early in people with APOE4. So DHA is important for increasing levels of the transporters that transport glucose across the blood-brain barrier, the glucose transporters. So I always thought that people for a while were calling dementia or Alzheimer's disease potentially type 3 diabetes. I'm sure you've heard it called that before. I always thought too much glucose in the body would be a bad thing. But here you're saying the brain getting a lack of glucose is a bad thing. What I'm saying here, yeah, is that not having glucose in the brain can be a bad thing. But that's separate from obviously from dysregulated blood glucose levels and insulin insensitivity."

Alzheimer Prevention Discussion

It gets transported across the blood-brain barrier via this mechanism that's passive diffusion, which just means it's passively crossing the blood-brain barrier.

"So like brain glucose levels are important for preventing a lot of the hallmarks associated with Alzheimer's disease."
Omega 3

Omega 3: Epa

It's kind of a different thing that I'm talking about here. That would be a completely separate but sort of parallel mechanism as DHA.

"And this has to do with a lot of very specific molecular mechanisms having to do with forming tau tangles and stuff like that. So not being able to get glucose into the brain can play a causal role in Alzheimer's disease. And perhaps that is also linked to this type 3 diabetes that you're referring to. That would be a completely separate but sort of parallel mechanism as DHA. I think it could play a role in addition, right? So DHA is important for getting glucose in the brain, but also some newer research does indicate that, you know, insulin insensitivity can reduce, you know, glucose getting into the brain as well. So those two things could even possibly synergize, who knows? I mean, it'd be nice to see data on that. But in terms of getting the DHA in the brain and like the question you kind of asked at the beginning, and I'm sure people are wondering as well, like, what are the dietary sources of these, you know, different types of DHA, the free DHA versus this lysopc DHA, the one that's a phospholipid form that's transported across the blood-brain barrier? And the simple answer actually is that all dietary forms can form either of those forms of DHA. That's the simple answer. There's definitely a much more complicated answer that involves even getting down to the chemical level. So DHA, looking at dietary sources like fish, fish roe, krill oil, those are all sources that have DHA in phospholipid form. Predominantly, you find phospholipid form being phosphatidylcholine as the phospholipid. Triglyceride form is found in fish, also in fish roe, and also in higher quality fish oil supplements or DHA supplements. There's also other forms that you could find in supplements, a majority of supplements that are molecularly distilled, which is the process used to purify fish oil, to purify away contaminants like mercury, PCBs, etc. A lot of fish oil supplements are found in ethyl ester form. Some are even in free fatty acid form. Those forms are a little less bioavailable than triglyceride form fish oil supplements. But the main thing here is actually the difference between ingesting it in phospholipid form versus any of those other forms, because those other forms to some degree are metabolized in a very similar manner compared to phospholipid form. And the reason for that is because phospholipid form, again, found in fish, fish roe, a variety of different, you know, eggs, fish eggs, caviar, as people call it, and also krill oil have DHA in this phospholipid form, predominantly phosphorylcholine. And the phospholipid form has this backbone, it's a glycerol backbone. And the thing that differentiates it from the other forms is that there's actually two DHAs attached. There could be a DHA attached at two positions on positions, positions meaning different carbon atoms, one on the SN1 position, as it's called, and one on the SN2 position. And so, the triglyceride, ethyl ester, all those forms have DHA on the SN2 position. And there's a difference between the way DHA is metabolized on the SN2 versus SN1 position. On the SN1 position, where it's found in phospholipid form, you can actually metabolize it and it retains its phospholipid form throughout metabolism. It's then bound up into HDL and it gets cleaved by an enzyme and it forms DHA lyso-PC, that form that bound to albuminin crosses a blood-brain barrier through a transporter. The DHA on the SN2 position, which is found in all forms, is cleaved by an enzyme. It forms a free DHA molecule, which then is bound up in LDL instead of HDL. An enzyme cleaves it out of the LDL, and it can form either free DHA bound albuobin or it can form the DHA lyso PC. So it can form either. But the bottom line here is that for the phospholipid form, the dietary phospholipid form you're consuming, you're going to get more bang for your buck in terms of forming that DHA lyso PC form that you want to cross the blood-brain barrier. That's the bottom line. So the majority of supplements that you see out there are mostly, is it triglyceride form? Is that right? The high quality ones are triglyceride. Most of them are actually ethylester. Oh, really? Yeah. Yeah. Because there's an extra, it's more costly when you're molecularly distilling these fish oil supplements, they're removed from their triglyceride form, which is what they originate in. And they're put on this ethyl ester backbone. And that's how they like run it through this column where they're purifying it and doing all this chemical stuff. And then at the end of the day, a lot of people just leave it in that form because the enzymes in your pancreas and small intestine, things like that, they can recognize that ethanol backbone and cleave DHA off of that. The higher quality fish oil supplements after that whole molecular distillation process, then re-esterify it to a triglyceride form. So it's an extra step. So extra step means more money, right? And so that's why I say higher quality. Higher quality usually also means you have to pay more for them as well. What are your thoughts on, say, eating salmon roe versus getting a krill supplement versus finding a form of omega-3 that is phospholipid? I know Nordic Naturals came out with one not too long ago. What do you recommend there? So I should probably start with this. Fish contain around 1 to 1.5% of their DHA in phospholipid form. The remaining is triglyceride form. Fish roe, and this includes salmon roe, herring roe, pollock roe, flying fish roe, they contain between 38 to 75% of their DHA in phospholipid form. I didn't know this was flying fish roe as well. That's great for sushi fans out there. Yes, it is. Because that's the easiest to put down. Yeah, it's the easiest to down because it's smaller. It doesn't have that very pungent, you know, fish. Yeah, they're just little poppy things. Yeah. Right. Yeah. I know you have a harder time than I do eating salmon roe, for example."

Vo2Max Training Discussion

Metformin prevented the exercise-induced improvements in cardiorespiratory fitness by 50%. Other randomized controlled trials have shown this to be true in people with type 2 diabetes.

"So, that's really concerning. Cardiorespiratory fitness is one of the biggest predictors of disease and mortality. So, that is really not good that metformin prevented it by 50%. It also inhibited improvements in mitochondrial respiration. And that may be something linked to some of we I didn't talk about all the mechanisms of metformin, you know, one of the molecular mechanisms that's thought to play a role in improving, you know, all this glucose regulation and insulin sensitivity is the activation of an important pathway called AMP kinase. That pathway is activated by energy stress. And energy stress can be caused by things like exercise, can be caused by fasting or calorie restriction, or metformin. Another thing that metformin does, and it's actually even thought by some people that this is how AMP kinase is activated is by basically disrupting a certain part of the mitochondria that generates energy called complex one. You've got five complexes inside your mitochondria. They're basically just passing electrons around. And this is how you can make energy in the form of ATP. Well, metformin disrupts one of those complexes, mildly disrupts it, complex one. For the longest time, I wasn't hugely convinced by that because the majority of data was in vitro, meaning you dump metformin on cells in culture and this happened. And it's like, well, that could be a really big dose dependent thing. Most in vitro studies, you can show one thing and completely show an opposite thing if you were talking about what's called in vivo or at the level of the whole organism. But there was a study published a few years, like 2014 or 15 or something like that, showing giving, if you fed rats, actually they were rats that had type 2 diabetes and they were fed various doses of metformin, 30 milligrams per kilogram body weight, 100 or 300 milligrams, right? Showed that at higher doses, 100 or 300 milligrams per kilogram body weight, metformin could decrease the mitochondrial oxidative capacity, specifically linked to complex one activity if they isolated muscle from these rats that were orally given these doses. So I was like, okay, that's evidence that it is obviously doing something that's physiologically relevant. So that could be why it's preventing cardiorespiratory fitness, which has been linked to mitochondrial function. It could be why it's in metformin inhibiting adaptations with mitochondria. Metformin also diminished whole body insulin sensitivity after aerobic exercise, but it wasn't like everything was bad. So metformin didn't diminish other improvements from exercise like the decrease in HbA1c, which is like a long-term marker of blood glucose levels. It didn't affect fasting insulin or blood glucose or fat mass or skeletal muscle cheloma length, which increased with exercise. So that's good. But it is concerning that it had all those negative effects, right? And these are in common people. Do you think this is something where eventually, you know, because we do want this activation of AMPK, right? That's a positive thing. So here's the thing. So activation of AMPK... Can we pulse it? So the activation of... So here's the thing. That's the question, right? Well, what if you time your metformin, right? There's things to consider other than the half-life of metformin or, you know, the important thing is, so for example, exercise activates AMP kinase. The activation is relatively transient, but the effects of exercise last about 48 hours. Metformin activates AMP kinase and the effects of metformin last about 36 hours after the last dose. So is it the AMP kinase activation that's responsible for these effects? We don't even know. Like, it's not even known. Or how long is the complex one inhibition lasting after you take your last dose? Is that also 36 hours after? We don't know. They're open questions, right? Not to mention that there was just, I don't know, a couple of months ago, another randomized double blind controlled trial showing metformin. This was also in healthy adults that were doing resistance training. And they were older adults. Both of these studies were older adults, 65, you know, age 65 years and older. But this study also showed that after 14 weeks of taking about 1,700 milligrams of metformin, which is quite high, that it, and this gets back to your friend's anecdote, the participants that took the placebo gained more lean body mass and also thigh muscle mass compared to those took metformin. So, metformin blunted some of the gains in muscle mass. It also diminished the strength, but those results were not significant, statistically significant. So, it's trending towards your friend's anecdote, what he found with his power and output and stuff. What about brain health? What do we know that metformin does there? Well, because glucose levels, like glucose dysregulation is heavily tied to disrupting brain health. It makes sense that improving blood glucose levels and blood glucose regulation improves brain health. So there have been some clinical studies showing that metformin in people with type 2 diabetes taking metformin can improve cognitive function and things like that, which is almost certainly linked to the improvements in glucoregulatory improvements. I say my thoughts, my concluding thoughts on this is that I think exercise is better than metformin for preventing type 2 diabetes. That's been shown treating type 2 diabetes. But also, I think it's better than metformin in delaying aging. I think that you're better off doing exercise than taking a metformin pill. Now, I don't think the effects are going to be synergistic. So, you know, is there a place for metformin? Absolutely. I mean, there are tons of people that will never exercise, right? So, you sit down, you tell someone you have to exercise 150 minutes a week or you can take this pill. They're going to be like, give me the pill, you know? Right."

Resistance Training: Hypertrophy

Do you think this is something where eventually, you know, because we do want this activation of AMPK, right? That's a positive thing.

"In fact, I think it's actually not beneficial for people that are exercising. And you can do this whole argument, I'll take it on days I don't exercise, but we don't know how long the effects of this metformin."
Sulforaphane

Sulforaphane: Nrf2

There's all these sorts of nuances that I, you know, I just don't know, basically. I'm excited to check out that episode.

"And so that, that to me was kind of interesting, but it sounds like this is a pretty complicated topic. Yeah. And when it comes to cancer, I mean, I would come to the same conclusions as your friend, based on everything, you know, the science that we know, with the exception of, and cancer is always, always the curveball. 110% of the time, 1000% of the time, it's the curveball. Everything that's good for you, when you have cancer, it's good for cancer. Now, it seems unlikely that's with metformin. It seems highly unlikely. But I'm always hesitant with supplements when it comes to cancer. That's what scares the crap out of me about MNM and NR and these NAD boosters. I'm sure you saw that paper about promoting cancer. Yeah. So, I actually did a podcast on this. I sort of did this research roundup where I talked about my thoughts on the whole field and that specific study in general, which was, it's a very specific type of cancer. It's a type of cancer, prostate cancer that depends on these inflammatory molecules that are secreted by what are called senescent cells. Senescent cells accumulate with age. So the older you are, the more of them you have. Again, the older you are, the more likely you're to get cancer. but senescent cells accumulate with age so the older you are the more of them you have again of the older you are the more likely you're to get cancer but senescent cells they are still metabolically active but they're just not like it's the cell's not functioning it's not doing its normal function that's supposed to do so it's almost like the cell's dead but it's not dead in fact it's doing something worse it's it's secreting um these pro-inflammatory cytokines and other inflammatory type of molecules that are promoting inflammation to nearby cells. NAD is absolutely essential for the generation of energy. So, you can imagine that a senescent cell wants NAD because they want to produce more energy to make that, they're making their inflammatory cytokines and stuff like that. Let me ask you a question. When you're fasting, doesn't that kill off those senescent cells? Well, it doesn't kill off senescent cells. It kills off damaged cells. Damaged cells. Yeah, that can become senescent, right? Gotcha. Yeah. So, I mean, the fasting is like, that's a really, I would say that's one of the biggest, it all depends on what your goals are, right? With fasting and stuff, prolonged fasting specifically. Yeah, the reason why I ask is because I know that during fasting, your NAD levels increase, correct? Yeah, they do. Wouldn't it make sense to, if you're going to do supplemental precursors to NAD to do them while you're fasted? Yeah, possibly. I mean, that hasn't been tested. When you're fasting, you're increasing the NAD to NADH ratio. So NADH is what's used to actually harvest an electron. Like I was talking about earlier, electrons are moved around inside the mitochondria and that's how you make energy. So when you're eating food, you're getting more of those, you're increasing your NADH. There's all these sorts of nuances that I, you know, I just don't know, basically. Yeah. I'm excited to check out that episode. I saw that you posted it recently all about, it was a follow-up to the Sinclair episode you did, correct? Yeah. So, I know you've had Dr. David Sinclair on your podcast. I've had him on my podcast. He's definitely an expert in lots of things like resveratrol. And also, he's done some studies with nicotinamide mononucleotide. So, I basically just wanted to... Because sometimes, as you often know, you're having a conversation with people, you don't get to explain everything. And so, sometimes people are like, what the heck is going on? So, I just wanted to give a lay of the land and give some of my concluding thoughts on some things that I thought was important. Very cool. Yeah. Speaking of the lay of the land, I'd love to hear your latest thoughts on sulforaphane. I know that, you know, here, gosh, what, it's been a couple years now when you first started doing videos and posts about the benefits of sprouting broccoli seeds and this miracle compound called sulforaphane. And where are you now with all that? I'm still super excited about it. Sulforaphane is, it's something that is formed from a precursor called glucoraphanin. And glucoraphanin is found in a variety of what are called cruciferous vegetables. Things like broccoli, Brussels sprouts, cabbage, daikon, watercress, all these things, cauliflower, these things are all from a cruciferous family of vegetables. So glucoraphanin is the precursor to it. When the plant tissue is crushed, chewed, torn apart, it activates an enzyme called myrosinase, which turns glucoraphanin into sulforaphane. Sulforaphane has about 70% bioavailability if you orally ingest it. The precursor, glucoraphanin, only has about 10% bioavailability to be converted into sulforaphane. So there's been tons and tons of intervention trials where people are given either a broccoli sprout. Broccoli sprouts, by the way, have about up to 100 times more of the precursor to sulforaphane called glucoraphanin than the mature broccoli plant, which is kind of why I've talked a lot about broccoli sprouts because that's a con. I can't eat anymore, Rhonda. You had me eating so many of them. I was eating like cups of those a day and they don't taste good. And I'm like trying to add stuff to them. I just, I had to go to the supplements. Yeah. Well, so here's the thing, the supplements. So there's only, there's a couple of supplements that have been, you know, scientifically validated to really have what they say they have. Sulfurafrase is not a very stable molecule. It's very unstable and it's difficult to get it, you know, in a supplement form. There's been two supplements that are really, I would say, have been clinically validated and have been used in randomized controlled trials that have been peer-reviewed and published. One is Avmacol. By the way, I have no affiliation with any of these supplements or supplement companies at all. You don't have any... Yeah, I was going to say, you don't have any affiliation with any supplement companies. I don't, but I just have to say that because people don't know that. No, I get it. I don't have affiliates, marketing... And neither do I. Yeah, good to mention."

Thyroid Health Discussion

I mean, these people are being exposed to benzene daily. I mean, it's just tons of studies coming out on air pollution.

"The other supplement is called prostaphanes. Prostaphanes is unfortunately not available in the US. I shouldn't say that. Yeah, it's made in France. And because sulforaphane is so unstable, like the company just didn't want to deal with like, the whole shipping it to another country and all that and dealing with all that. But you can buy it. I buy prostaphan. There's online pharmacies. You can have it shipped to you. Oh, really? Yeah. I'm having another shipment arriving tomorrow. Oh, so even you stopped with the broccoli sprouts. Well, so here's the thing. Okay, let me answer your question. So each prostaphan tablet has around 10 milligrams of sulforaphane in it. There are trade-offs for doing broccoli sprouts versus supplements. I would say, first and foremost, the supplements are expensive. Prostaphanie is really expensive. They're expensive. We're talking like $50 a pack? Something like $90-something for a pack of 60 for prostaphanie. It's quite expensive. But again, it has... How many are you taking a day? One. Oh, so that's not that bad. 60 days supply? We each one has 10 milligrams of sulforaphane. And to get to that dose, maybe I should talk about some of the clinical... I mean, there's been some new clinical studies that have been really exciting in the past couple of years. Cool. Yeah. Please do. But let me just finish with the sprouts. They're cheaper and you get a ton of sulfur. So like for a hundred grams of fresh sprouts, use something around like 40 milligrams of sulfur. Basically you can get something around 40 milligrams of sulfur. And that's a lot, right? For a lot cheaper. Now the trade-off is it's a pain. You have to like work, right? You have to make them, I mean, they're not super, super hard, but there's a risk for contamination. They're very, they can easily be contaminated and I've had them contaminated and it kind of gives you some, you know, it's not fun. So that's the risk. And there's all sorts of, you know, people say you should bleach the seeds first. And then I don't personally feel comfortable bleaching the seeds. And I just don't want to like ingest anything that's, you know, had bleach on it. I've been doing the prostaphanes for one simple reason. I'm a mom now. And I'm also running Found My Fitness and trying to do all this research and stuff. And also trying to like exercise. And there's just, I just, there's too much. You know, there's just too much for me. So I found it easier for me to take the prostitutinant supplement. I would like to get back to the sprouts and I will probably mix that up again. But for now, I'm sort of taken the easy way. That's good. You're too busy. Seriously, my fridge looked like a little mini farm. It was like farm built up my fridge. It was like there were sprouts everywhere and some of them were going bad. Yeah, that was like me and I was freezing some of them. So what does this do for people? People have heard us talk about sulforaphane for a few minutes now, but what are the benefits? There's tons and tons of studies that have been published showing that taking either broccoli sprout know, broccoli sprout extract or broccoli sprout powder or even sulforaphane increases the levels of glutathione in plasma and also in the brain. In fact, the first clinical study to show that in the brain was published last year in 2018. In human brains? Yes, in human. This is a clinical study in humans. How did they even get at that? They did some sort of magnetic resonance spectroscopy thing. Crazy. Yeah. But it was so exciting because the amount that they were taking was actually would be equivalent to prostophanes because it was about almost 18 milligrams a day. They were taking that for a week. And that increased their plasma, glutathione, and brain. And for people who don't know what glutathione is, it's like the major, major antioxidant endogenous system, and particularly in the brain. I mean, it's been shown to have a huge relevance for all sorts of brain aging, traumatic brain injury, other neurological disorders, and including autism. So oxidative stress, which plays a role in brain aging and traumatic brain injury. It also has been shown to play a role in autism. Very interesting, there's been two clinical studies, one in children and one in adolescence, where the children were given, on average, like around 12.4 milligrams of sulfur or phane a day. Was this done with Avmical? This was Avmical, yeah. And this is for children that were between 100 to 200 pounds. So that would be like four Avmicals or something like that. And it improved a variety of autistic behaviors in both the children and adolescents. And these are two separate studies that I'm referring to. So it's clearly not only increasing glutathione in the brain, but it's having an effect on behavior, which is really exciting. And it's thought that is probably linked to this glutathione because, again, I mentioned there's been some evidence that autism is multifactorial. Many, many different things have been shown to play a cause in it and not just one thing. So, you know, of the myriad of things shown to play a role in autism, oxidative stress is one of them. And combating that with glutathione is one of the major ways to improve that. And there's been tons of other interventions, trials, for example, eating like 300 grams of Brussels sprouts a day increases glutathione levels also in the plasma and also decreases oxidative DNA damage by like 30%. So it's like literally decreasing the amount of DNA damage, which is, you know, I should probably mention that there has been like an in vitro study that I've seen where sulforaphane at a very, very high concentration was dumped on cells and it caused DNA damage. It's one of those instances, again, where it's like in vitro studies, when you're dumping things on cells in a Petri dish has very little relevance unless you're looking at the broader literature, right? You've got to look at what happens at the level of the organism, something that's even physiologically relevant. And so it's actually doing the opposite. It's not only increasing the antioxidant systems, it's decreasing DNA damage quite significantly by 30%. And this is in humans, okay? This is not animals, certainly not in petri cells in a dish. It's in humans. Very important. So how are they measuring that with the DNA damage? Are they taking samples at two separate times or what's the deal there? Yeah, they do baseline and then after treatment. What was the duration? In this study, oh darn, I don't know. Usually it's like a month or so. I don't know if this study was a week or not. I just can't remember. But there's been other studies also where people were given broccoli sprout extract, like 10 grams or something, and it lowered oxidized LDL in their, you know, oxidized LDL, which is, you know, thought to play a role in the pathology of cardiovascular disease. It lowered serum triglycerides by like 18 point something, like close to 19%. And this was a month-long trial. And it decreased their atherogenic index by 50%, which is a marker of a measure of cardiovascular disease. So this is, you know, of course, in people, again, there's been other studies showing that sulforaphane can cause immediately after 24 hours can cause you to excrete excrete potential harmful carcinogens like benzene and acrolein by up to like 60%. So this is crazy. I remember that. Now, do you think, so this is like what's found in air pollution, right? Yes. I mean, if you're a smoker, it's found in your cigarettes, but I mean, air pollution is a major source of benzene. Yes. A couple questions there. One, okay, let's say I take the sulforaphane, I'm excreting all this crap out of my body. That we can clearly measure, right? Like, let's say I continue to do this and I keep getting tested day after day. Is there a point where the body is kind of like detoxed and all this crap's out of it? Or is this something that just continues to go on because it's built up so long in the body? Oh, great question. I think that has to do with the exposure. So these studies that were done, there's been more than one study done on the excretion of benzene. Most of them are done in China for the simple reason that there's a huge air pollution problem in China. And so you can imagine, and this is always the case for any sort of clinical trial you're doing. It's always nice. You'll see more robust results if you have a starting population with something that you need to fix, right? So like, yeah, if you're trying to lower triglycerides, you want a population of people that don't already have low triglycerides, you want them to have high and then see if you can lower them, right? So the same goes for like benzene. I mean, these people are being exposed to benzene daily. So it probably really depends on the exposure. And these days, you know, and if you live in an urban area, you're being exposed to it, unfortunately. I mean, it's just tons of studies coming out on air pollution. Yeah, that would be a fun study to do, right? Just to see if it kind of like finally gets out of your system and then how long it takes before it builds back up? Yeah. Well, you know, part of the mechanism by which, you know, I sort of haven't gone into everything and do this, it would take too much time. But part of the mechanism by which this is happening is that sulforaphane activates a very, very important pathway involved in longevity called the NRF2 pathway. And this basically what this master regulator gene does is it um it when it gets active it it goes around and finds all these genes that have a very specific sequence of dna and them called an antioxidant response element binds to it and it like either turns them on or off depending on the gene it's it's kind of elegant that you know basically sulfur does this and that you know it basically is the switch on for this whole system. And clearly it's meant to happen. There's like identifiable sequence of DNA in tons and tons of genes that this master regulator will recognize and bind to. I mean, it's crazy. It's super crazy to think about. Anyways, part of what it's doing is it's like turning, it's increasing the, what are called phase two detoxification enzymes. And those are responsible for detoxifying potential carcinogens and a variety of other harmful compounds. It also turns off what are called phase one biotransformation enzymes, which are enzymes that can actually take a pro carcinogen and convert it into an actual carcinogen. So you actually want those turned down. So it does all sorts of interesting things. There has been some concern about sulforaphane possibly competing with iodine for transport into the thyroid, and hence, you know, a potential what's called goitrogen, which is something that can disrupt the production of thyroid hormones, particularly for people that are iodine deficient, which, or have hypothyroidism. Again, that's a concern. Mostly you find in blogs and stuff. If we actually look at the scientific data, for example, clinical data, healthy people that were, you know, that don't obviously have iodine deficiency or hypothyroidism, but they're healthy and they're given the amount of isothiocyanates. So sulforaphane is a part of a broader family called isothiocyanates. They were given the amount that's roughly equivalent to what you'd find in like 70 grams of broccoli sprouts. They're daily for a week and there was no negative effects on thyroid hormones, no toxicity on liver or anything like that. So, the question is, what about people? What about the context of like iodine deficiency? By the way, that's very rare these days. Yeah. I mean, you just get a sea snack at Whole Foods, right? Yeah. And also just most salt, people are eating things with salt and their salt's iodized mostly if you're getting any type of processed foods and stuff too, right? There was a long-term study published last year in animals where rats that were iodine deficient or had hypothyroidism induced by a drug, they were given large quantities of broccoli sprouts for a long period. This is a long-term study. And there was zero effect on thyroid hormones. There was no change in thyroid stimulating hormone, no change in T3 or T4. None of those hormones were affected in these rats that were iodine deficient or had hypothyroidism. In fact, animals that had hypothyroidism, broccoli sprouts actually exerted a beneficial effect on their thyroid because it increased glutathione. Wow, crazy. So there you have it. You know, should you be concerned if you have hypothyroidism? Potentially, I don't, you know, the thing to do would be to do a baseline thyroid test and then do one after a month or however long of your broccoli sprouts and or supplement, right? Yeah. I mean, always talk to your doctor with this stuff. That's the best advice. But I'm still super excited about it, for sure. Especially after the brain study. And you take it daily? So, yes, I do take it daily. But the effects... So, here's the thing It activates Nrf2, and that's, again, a majority of the effects are mediated by that because it's just hundreds and hundreds of genes are being regulated by that pathway. Those effects can actually last a couple of days, at least in animals. So, it may be something that you could take every couple of days, but then again, translating what a couple of days is in animals to humans. I mean, I don't know. So I think it's possible you could take it every couple of days just because the effects are lasting. One last question on the detox side, when people were peeing this stuff out, does it also come out in the sweat? Benzene? Yes. I believe so. Something, I don't know if it's more in sweat than urine, but... So something is going on'll tell you like a n of one uh thing from me so I take avmacol the sulfurement supplement every day for a month and then I take a month off and then I take it again the next month I don't know why I picked that I just did it so here's the weird thing I do a sauna almost every single day right and when I get out of the sauna I lay on this black bench that I have just to kind of cool off and just lay there. And of course, you know, you're dripping wet, there's sweat, all that good stuff. It's nasty, whatever. When I'm not taking it, it just dries up and the bench looks fine. When I am taking it, it leaves like a cloudy kind of like stuff from the sweat. I know it's disgusting, but like something is coming out of my pores when I'm on sulforaphane. It's really weird. That is so interesting. I am going to put that one in my pocket and take it out and talk to Dr. Jed Fahey, the sulforaphane expert about that, because that's something super interesting. I would love to explore. Yeah, something is coming out because Daria was like, what the hell? There's like a stain of like this like stuff. of this stuff. I'm like, I'm sorry. It's like the only thing I changed was the sulforaphane. Wow. It's really, really crazy. But it makes sense if the body is excreting something and getting rid of it, it might come out in sweat as well. Yeah, it's also excreting acrolein and other things. I do believe those come out in sweat. Crazy. I know back in the day, you were one of the early people to come in and realize that there's a serious magnesium deficiency in the United States. And you were one of the very first to start talking about that online, which is awesome. Not too long ago, maybe a year or so ago, I learned about a new form that was developed at MIT called L-theonate. I think I said that right. Therinate? Therinate. For brain health. I'm curious, are you familiar with this form? And given that you're into all things brain health, what are your thoughts on it? I am familiar with this form. My interest was also piqued when I read some of the earlier animal studies that had shown that this specific form, this magnesium L- and 8, was a specific form of magnesium that could cross the blood-brain barrier better than magnesium, not in that form, and that it improved cognitive function and prevents the loss of synapses and reverses memory deficits and all sorts of amazing stuff. Of course course, it was very high concentrations in animal studies. But my excitement for that is still kind of on hold because there was a clinical study, one clinical study published actually showing a high dose of magnesium 3 and 8, something like 1,500 to 2,000 milligrams a day, depending on the person's body weight for for 12 weeks. The study claimed that it improved cognitive ability relative to placebo. But when you look closer at the data, the first thing that kind of jumps out is that they looked at whether or not this, you know, and this is pretty high dose they were giving people, you know, 1.5 grams or 1,500 milligrams a day is a lot. There was a very meager increase in plasma magnesium levels, very small, no difference in red blood cell magnesium. So like getting inside tissues would be some, and red blood cells are, by the way, usually a marker for brain. Things that get into red blood cells are sometimes used as biomarkers for things that get into the brain, for example, like DHA. And so there was no change in red blood cell magnesium. And there was tons of magnesium being excreted in the urine. So people that were taking this up versus placebo. So people that are taking this magnesium 3 and 8 were essentially peeing out most of it. There was four cognitive tests that were done. And if you look individually at each of those cognitive tests, there was no, like the confidence interval, like there was no real significance. But when you pulled all four together, then you could say that it was improving cognitive performance with all four of them pulled together. A little kind of, a little, you know, I would say, you know, a little manipulation there just to get the p-value you want, the significance you want. So I would say that I absolutely think magnesium is really, really important. And as you said, you know, like they're, you know, half, at least back in 2014, you know, 45% of the U.S. population was not getting adequate amounts of it. What does that mean for people? Like if they're not getting enough, you know, most people be like, okay, I'll have a banana or something. Like what does that mean in terms of symptoms? Like why do we need this much magnesium? Well, for one, it's hard to say that. So because magnesium is stored in muscle tissue and in bones, your body, anytime it's low, it pulls it out of those. So your plasma levels, unless you're like severely deficient, your plasma levels aren't going to really indicate much of a deficiency. So the way that inadequacy or deficiency like I'm talking about has measured is from dietary intake. So people aren't getting what they're supposed to be getting, you know, depending on if they're a man or a woman, it's like between 300 to 400 milligrams a day of magnesium. And most people aren't doing that, meaning they're not eating the right foods. You know, these foods, magnesium is high in dark leafy greens. It's, you know, magnesium is at the center of a chlorophyll molecule. Chlorophyll give plants a green color. So things that are dark and green plants have a lot of magnesium. Of course, it's bound up to some, some of it's bound upytate, which can affect the bioavailability. Nuts also are a great source. But the thing is, is you're probably not going to have a clinical symptom. You're not going to wake up and go, oh, my, you know, like I can see DNA damage happening because magnesium is critical to repair damage of your DNA. But that's not something you can see. That's not even something that's ever clinically measured, right? I mean, it's not like if you had scurvy, right? You were so vitamin C deficient, you had scurvy that your gums started bleeding. You wake up in the morning, you're like, oh, my glums are bleeding. Maybe I should get some vitamin C. But magnesium, I mean, this is one of those things where it's insidious types of damage that over the course of decades builds up and starts to lead to diseases of age, right? You know, defects in DNA repair absolutely play a role in cancer, big time role in cancer. And also just in like cellular dysfunction, when you start to accumulate damage and stuff, cells don't work as well, including in the brain. So magnesium is also critical for the production of ATP and the utilization of it. So you can have low energy. That is one of, you know, potentially maybe, but see, you know, the thing is, is that it's possible that because you need to make energy to survive, that all your magnesium then will be used for things that are critical to prevent death in the short term, right? So this is part of my mentor's theory, triage theory on aging that he's talked about and published on, where some of these little insufficiencies in micronutrients like magnesium, they are resulting in insidious damage that builds up over decades, things that you aren't aware of, but show up later in life and actually as diseases of aging. And so, regulate the aging process itself. So, I don't know that you're really going to know if there is a real clinical symptom unless you're severely magnesium deficient. Now, what do you take for something like this? Are you doing like a slow time release magnesium? Because I know one of the big side effects is stomach upset. In what form? Because there's five or six different forms out there. I actually try to get my magnesium from food because, yeah, because the GI problem where you can really cause like diarrhea and stuff, like if you're taking, especially if you're taking high doses."
Magnesium

Magnesium: Glycinate

Jed Fahey, the sulforaphane expert about that, because that's something super interesting. I would love to explore.

"I've previously in the past supplemented with magnesium glycinate dose."
Cold Exposure

Cold Exposure: Protocol

I think it was like 200 milligrams or something like that. Which is what I typically try to do.

"Okay. So the sauna, the newest stuff that I'm excited about is, you know, there've been so many studies showing that frequent sauna bathing has a positive effect on a variety of different..."
Sauna

Sauna: Protocol

I think it was like 200 milligrams or something like that. Which is what I typically try to do.

"I was able to take in to the really hot saunas in New York, like the old Turkish bathhouses where they get like 200 degrees and, and no issues with that one breaking on me. So those work as well."

Cgm Discussion

Let's say you listen to the audio version and you want to see those visuals to help you with more information, to help you get figures and all that so you get that as well...

"Animal studies have shown that they can prevent and also help reverse some of that pathology. And the good news is that like there's been some human studies that have shown that people that go into the sauna about 163 degrees Fahrenheit and stay in for 30 minutes can activate their heat shock proteins 50% above their baseline. And that, you know, so heat shock proteins can remain activated for about 48 hours. And the cool thing is, is that this happens quicker and better in people that are heat adapted. Oh, really? Yeah. And, and heat shock proteins have been linked to longevity, to human longevity, also longevity. And there's been longevity studies in lower organisms, you know, like flies and stuff and worms. It's also great for sleep too, you know, doing it just before. Yeah, it's phenomenal. It totally helps me. It helps with my sleep. It's repeatable, hands down for sure. And in my mood, it helps mood. And that, you know, it's interesting. There's been a sham controlled study where people with major depressive disorder were treated with, they basically had their core body temperature was elevated similar to what would happen in the sauna. And, um, it improved just one treatment actually to improve depressive symptoms. And this thing lasted the improvement lasted for like six weeks or something crazy like that. Crazy. There's another study that's being done to kind of repeat that and try to generalize it and do it with the sauna. So I'm pretty excited about that, but my mood is a totally effect. Like I do the sauna exercise also is one thing I do for my mood exercise and sauna. Like, yeah, I need it for my brain period. Yeah, same. It really helps my mood. And then I do the Wim Hof method every winter and I'm starting on December 1st this year. And that is another huge, just mood booster for me. It's crazy. That for me, it helps me more with anxiety and focus. When I do a cold shower, if I do a five-minute cold shower, I don't do those. I try to do the sauna four times a week. The last two weeks have been terrible because I've been super busy. But I hardly ever do cold showers. I should get back to that, though. I really should. Because I do like doing them. Especially in the winter. I feel like it's just like that time of year. I'm just like, yeah, when the water's much colder. Yeah, exactly. Cool. Well, before I let you go, the last thing I wanted to, to talk about is your website because you've done a massive revamp. It has changed so much over the last couple of years. And I think that anyone that is a fan of yours or is listening to this podcast and will start listening to your podcast, we want to see more content. How can we help? And what are you working on these days in terms of new features for your website? I'm trying to do exactly what you just said, which is get more content out. I mean, it's been an amazing journey. And one of the bottlenecks has been that I just can't do it all by myself. It's impossible. Not only is it impossible, it's not good for my mental health. There's so much to do, so much information that I'm researching and wanting to communicate. And the way to do that is to really get a team of really good people to help me do that. And so one of the ways that I'm trying to do that is by offering people that want... For once, I don't take any advertising. I don't do any advertising on my podcast or on my YouTube videos or on my website. The way I'm able to do anything is because people are contributing and supporting me. And they're doing it on a monthly basis because they want to me keep getting information out, and they want me to get more of it. And the way that I that, you know, we're trying to kind of grow this thing, so I can basically hire more team members. How many do you have right now? Well, I mean, it depends. I've got a lot of contract, different contractors, you know, but I need some full time scientists, you know, I need PhD level scientists, you know, people that can work with me, and that I'm lacking right now. What we're doing is we're offering what we're calling a premium membership to people that want to support us. And this premium membership is that we're giving them extra added perks in addition to everything that we're doing with Found My Fitness with the goal of increasing our output for Found My Fitness. So these extra perks include, you know, they get a private podcast feed where I have early releases of episodes, but I also have unique content, like I'm doing a monthly ask me anything question and answer session. So once a month, supporters can submit questions. And I, you know, go through those questions and questions, it could be anything like things that come up during podcasts, people hear me on or things that come up on posts I do or, you know, you know, anything related to anything that, you know, I've talked about in the past. And I answer those questions in a live, what's called a video chat, I use Crowdcast. So it's like a live interaction thing. So people can chat with me while I'm doing this and I'll answer some of the questions also live. But I select through them beforehand and answer them as well. Those get put on the podcast feed. They're also in a video you can watch. We have a whole members dashboard where you can get access to all these benefits where you get that, you get these background notes that I put together for every podcast I do. So it's lots of information that I think is relevant to whatever the topic is I'm talking about. People get these podcast slides, which are in some cases, over 150 slides, which are used to all the information that we put on our videos for our podcasts. Tons and tons of work goes into that. It's one of the reasons why it takes me so long to get interview podcast out. Yeah, I feel bad for Dan. Yes. I just think of him doing all those... Because you do so many of those graphic layovers. It's a team and we need help. But people, members get that. So they get all those slides. Let's say you listen to the audio version and you want to see those visuals to help you with more information, to help you get figures and all that so you get that as well um for for all the podcasts you can go on the dashboard and see all that you also we have a a science digest that we release twice a month where it's basically a summary we just released our first one last friday we do it every other friday and you get tons of stories and and um that i think are important interesting i gotta see i'm a member see that. Oh, you didn't see it? Yeah, it was sent to your email. It should have been. I got to go check for that. Yeah. So that's another thing. Yeah. And then other things as well. We give you a t-shirt and you get free updates on our genetic report. We just actually released a new version. I haven't talked about it yet. I'm getting ready to talk about the new version. a bunch of new cool jeans and stuff. So there's lots of little perks that you get. And the premium subscription is $15 a month. And it's really people that want to help support me doing what I'm doing. They get extra perks. But the whole goal is for me to be able to do more of it by bringing a team in. So I'm pretty excited about that. That's our premium membership. Yeah. yeah foundmyfitness.com foundmyfitness.com you can hit this the little green button that says become a member i will tell you that the genetic reporting stuff that you guys do is just so awesome like i i'm a firm believer that this is the future of personalized medicine you know just being able to peer into your genes and and figure out what going on. Hopefully compare it then to blood work and then, you know, kind of make tweaks and go back and rinse and repeat until you dial things in. And I go to your website and run my report every time you come up with a new update. That alone is worth subscribing just for that. Because I know there's a lot of other, or not a lot, but there's a few other sites out there that offer, you know, the same type service where you upload your 23andMe data, and then they spit out a report, but none of them are as well researched and as comprehensive as yours. So yeah, I recommend it to everyone. It's awesome. Oh, thank you. Thank you so much. Yeah, I agree with you. There's so many conflicting studies in nutrition that I think can be explained to some degree by gene diet interactions. Like, you know, there are certain genes that are, that are interacting with the food that we eat and regulating the way we're metabolizing saturated fat or complex carbohydrates. And like, I have found so much information. Like you said, you have to do other tests in, in combination, but I think the SNPs give me the why. Like I also wear continuous glucose monitor like you do. And one of the things that I've noticed is that I absolutely need exercise in order to have a good glucose regulation. And after about three days, if I don't exercise for three days, boom, it's like I will wake up with significantly higher fasting blood glucose levels. Crazy. Like how high? Like higher, like higher 90s. Oh, that's pretty decent. Well, compared to like a low 80, like a mid 80s. Well, you know, sometimes it depends on sleep too. Like I can get up to like 101, 105 or something. So my point is that what I have noticed is that I really need exercise. And it also depends on when I like my time restricted eating schedule, how late I eat dinner. Sometimes with a kid, it's like, I got to do all his stuff first, and then he doesn't want this to eat. And I'm making this and that. And it's like, five meals later, I get to eat. And I'm like, oh, no, I missed my TRE. So it happens. And I absolutely notice it with my glucose monitor, continuous glucose monitor. And I found I have this interesting snip in a gene that's like, it's thought to, like, it's like the ancestral gene where before, you know, made like this whole major agricultural, you know, industrialization happened. There's a gene that basically, because, you know, humans went through periods of fasting, right? They had to be able to like make glucose. And, you know, when you're fasting, you want to still make glucose because you need glucose. You absolutely need it. Your red blood cells can't use anything else. They have no mitochondria, right? And so, I have this snip in that gene that kicks in, man, you're going to keep on the way you're like regulating your blood glucose and disposing of it. So, if I do a fasted exercise, which I've actually been doing probably with, I would say the last two months is when I really started being hardcore about it. It has really changed my fasting blood glucose, my postprandial, where it's really like improving it to like I was saying saying, mid-80s. So this is the first time I've really been able to achieve really, really good levels like that. It's crazy what the data will tell you. I have similar issues. I take a glucose tolerance test and I have glucose disposal issues. So I keep a higher elevated glucose for longer than I should. Right. I do too. And there's a just, our new update just released one of the snips on that. It's funny because I find, I gather all this data from my continuous glucose monitor and from the foods I eat and things like that. And then I see the snips I have and I'm like, oh, that explains it potentially, right? You know, or so being the nerd that I am, I enjoy that aspect of it where it's like, what's causing this? And then you kind of like look into it and you kind of find a potential thing. Have you also noticed that like eating a high amount of protein before eating carbohydrates will regulate the postprandial glucose response? It'll be lower. Oh, that's interesting. No, I haven't. Well, I've noticed that. And lo and behold, there's randomized controlled trials showing that a very thing does exist. It happens. So protein before carbs. Yeah. So let's say you had your quinoa salad with beans or whatever or something. You want to eat your chicken before you eat that. That's great to know. Test it out, Kevin. Yeah, absolutely. Because there's always those times when you're like, okay, tonight's going to be somewhat of a carb night, right? For some reason. I try not to do processed carbs, but you're going to get your carbs somehow. Or maybe I do do a pizza. Maybe I should have a little bit of protein first. Yeah, try that out. Yeah. I've been able to get my glucose down in the 70s now, which is crazy through fasting. Yeah. See, that's the thing that, you know, I am, I did an extended breastfeeding protocol, which was a lot of work. So I hadn't done really any prolonged fast, but I really would like to, at the very least, start with some 48 hour fast. Because, you know, for me, it was like, I got super interested in this stuff a few years ago, and I got pregnant, and then I was breastfeeding for a while. And, you know, so it's just like, you know, three years go by and I'm like, dang, I got to do this now, you know? Yeah. So, but anyways, this is sort of, I could go on and on about it. But yeah, I'm excited to try that. Well, try the monk's fast. I think you'll like that. It's a 36 hour. Oh, interesting. Interesting. I would like to work my way up to a five day but that's a whole other story and well i did one five day and it almost killed me so okay i mean didn't almost kill me but it was like it was so i'm your sleep goes to hell mine did i get you get cold like day two you start getting really cold like all your extremities are just like really just like the blood flow is not there and got to take some magnesium too, because I was getting some muscle twitches and heart palpitations and stuff. Your body is in full-on dying mode. You're dying, basically. You're trying to stay alive. It's pretty intense. You know, Walter Longo, I know you've had him on your podcast, Dr. Walter Longo. Some of his research animals has shown that like the prolonged fast, that's what it does. It's literally organs shrink during that stage. And then they regrow during the refeeding phase. And like one of his studies was like a two-day water fast. It's like 28% of the white blood cells like literally were gone, like killed off. And that's activated stem cells and caused the stem cells to grow. I know. And it's like, so that's one of the reasons why I want to try. Because I think a five-day fast for humans is more equivalent to a two-day fast in mice based off of just the IGF-1 level. So the whole shrinking and then regrowing of the organs was dependent on IGF-1 going down. And there's been animal studies showing that IGF-1 after two days in mice will go down more than 50%. And glucose will go down like 30%. But in humans, it takes five days for that to happen. So anyways, I'm digressing. You know what you should do? You should do for members only, like a five-day fast. I think Xero will help sponsor it. We'll do a five-day fast just for your members and then do a private video at the end of every day that you do live. Everyone gets to like... Because I think a big part of it is you want to be doing it with someone else. You want a buddy to do it with. That could be really cool when you're ready. I got to start with the 48-hour fast because I think that's also where a lot of benefits kick in right there. So I'll start with that. Actually, that's a way better idea. All right, Rhonda. Well, thank you so much for doing this. I really appreciate it. And everyone should go check out foundmyfitness.com. And I'll put a bunch of links in the show notes. So thanks so much. Thanks, Kevin. All right. That's it. Thank you so much for listening. If you would do me a favor in this new year and head on over to the iTunes store, find the Kevin Rose show and give me a five-star review. I would really appreciate it. That helps us get more listeners and I in turn have better guests in the show. Thanks so much and take care."

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