Anti-Aging Secrets Of The World's Longest-Lived Woman, The Top Longevity "Drugs", Fat Loss & Muscle Gain Tips & Much More! Q&A 494

In this episode of the Boundless Life Podcast, anti-aging secrets of the world's longest-lived woman, the top longevity drugs, fat loss and muscle gain tips, and a whole lot more. Welcome to the Boundless Life with me, your host, Ben Greenfield. I'm a personal trainer, exercise physiologist, and nutritionist, and I'm passionate about helping you discover unparalleled levels of health, fitness, longevity, and beyond. Welcome to today's show, a solo show Q&A. Been a little while since I've done one of those. I'm Ben Greenfield. Hello. Good to meet you. Thank you very much for listening. What's new in my life? I got the new iPhone 17. Pretty excited about that. It turns out I had a free upgrade, so I figured what the heck, why not do the annual, what do you call it, planned obsolescence replacement of my technology. Which apparently as an iPhone 15 was very unpopular and unfashionable for me to even be seen around. But, when I was setting up the iPhone 17, I actually wanted to mention this on today's show. They actually have a new setting that allows you to disable what's called pulse width modulation. And, this actually means that the screen of the new iPhone 17 or 17 Pro or 17 Pro Max or whatever can be engineered to be a little bit healthier for your eyes and potentially a little bit less irritating to your brain. Okay. So, what is pulse width modulation? Basically, it is designed to quickly switch between LED or OLED pixels to control the brightness that you perceive when you're looking at the screen. Now, if you go into your accessibility settings, I realize nobody who owns an iPhone 17 is remotely interested in this, but I'm going to say it anyways and I'll be quick. If you go into your settings and you turn off pulse width modulation, what that does is it allows your screen to produce less flicker. Now, you might see subpar screen performance at low bright settings, but you shouldn't be on your phone that much at night anyways, people, right? You know that. So, people who get eye strain, headaches, brain fog, irritability, things like that from staring at a screen all day, a lot of times it is due to the flicker. For example, on all my computer monitors, I have a piece of software called Iris and it reduces the flicker on the screen. The light bulbs in my home are all made by a company called Block Blue Light. They're flicker-free bulbs. And now, I can make my iPhone screen flicker-free by simply going into accessibility settings and turning off pulse width modulation. So, isn't that cool? Isn't it cool that my life is so boring and uneventful that the latest greatest thing that I have to talk to you about is the fact that I can disable pulse width modulation on my phone? But, I mean, this is a podcast about health, so I figured Why not? The shownotes, by the way, that I keep track of for everything that I'm about to share with you, including this crazy story of this gal who lived to be 117 years old and the secrets they found about her genes and her lifestyle, you can find all the shownotes at BenGreenfieldLife.com/494. So, this recent study hit the journal Nature and it's been making a lot of headlines lately because they were able to study before she died, the world's oldest person. And it turns out that the University that was studying her, it was located pretty close to where she lived near Barcelona, Spain. So it made it easy for them to do things like collect samples from her blood, from her saliva, from her urine, from her stool. Not when she was dead, which would be gross. I don't know if they did that, but when she was actually alive. And they were comparing it to a bunch of other local women to see what it is that this 107-year-old woman had in her body or in her cells or in her genes that seemed to allow her not to just have pretty good lifespan, but from what I understand, she was actually very vibrant and talkative and communicative as this so-called supercentenarian. So, it was both healthspan and lifespan. So, here's a few things that are really going to disappoint you guys possibly. She never smoked. She never drank alcohol. I'm not saying that drinking alcohol is going to shorten lifespan. I think there's some epidemiological data showing that small amounts of alcohol could increase lifespan or at least not affect it, but she didn't drink alcohol. She loved to work. She lived in the countryside. She exercised for at least an hour a day, right? A lot of the things that we would know from the blue zone. Her diet had olive oil, right? It was very Mediterranean style. No surprises there. She lived in freaking Spain. She also had 3 servings of yogurt a day. And this is interesting because if you look at some of the data in the full paper, her gut microbiome had specific metabolites in it that helped her to maintain very low levels of inflammation. And some of the researchers are hypothesizing that that's due to the active bacteria that you find in fermented food products like yogurt. Could you get some of that through, I don't know, going through the Silicon Valley billionaire tech entrepreneur biohacker route and just using probiotic capsules a few times a day? Probably you could. But the idea here is that it appears that the gut microbiome is pretty linked to to overall longevity. It's also interesting because her telomeres were not necessarily like super duper long, they were actually somewhat short. And, that kind of potentially could tell us the fact that measuring telomere length is not as important as measuring the rate at which telomeres shorten, these so-called new aging clocks. I actually have an interview coming up on a new epigenetic age clock measurement I just did yesterday in my kitchen. I'm going to put that one on hold until I actually get the results back and I'm able to get a doctor to talk more about this idea of using aging clocks, which can now be matched up to big pools of data from a whole bunch of people. And by doing just one blood spot test, you can get thousands of blood biomarker pro— they're called proxies. It's like, here's where your levels are at and what your risks are just based on epigenetic data alone because we have so much big data that we've collected from blood tests. So she did have super short telomeres. It could also be the fact that they were comparing her telomeres at 17 years old to younger women's telomeres. So, she was told that her telomeres actually were— they were slower or lower or shorter. She had more age-related B cells in her system and more mutations in blood cells. So, this was probably not a reason that she aged so well, but what happened because she'd been around so long, meaning her body was showing signs of extreme age, but she was handling it very well. And I'm certain that her active lifestyle and her gut helped with that. She also had somewhat high LDL cholesterol, definitely above 100. I don't have the exact number in front of me, but I remember I was going through the paper. I'm like, huh, her cholesterol would technically flag as being high on an average blood test. But cholesterol does have some anti-inflammatory properties, some cell membrane protective properties, some endocrine properties that in the absence of other risk markers like inflammation, high blood glucose, which she didn't have, high triglycerides, poor sleep, stress, and other things that would stress the heart or cause atherosclerosis from high cholesterol. High cholesterol, particularly high LDL cholesterol, in and of itself is not necessarily a risk factor. So the LDL cholesterol, I would guess, and again, this is just like throwing darts at the wall, that it was probably in her case somewhat protective because she didn't have other risk factors present. And again, her microbiome was conducive to a very low inflammation diet. Olive oil, fish, the 3 servings of yogurt daily, no smoking, no alcohol, et cetera. And again, back to the alcohol thing, I think that by drinking no alcohol, it makes it pretty hard to get drunk, right? I think about this the same way that I think about calorie restriction. There's not a ton of— or about intermittent fasting, rather. There's not a ton of magic to a compressed feeding window, like a 12 to 16-hour intermittent feeding window compared to just restricting calories. But By shortening the period of time in which you're having your meals, you're lessening the likelihood that you'll overeat calories. And by saying, I'm not going to drink any alcohol at all versus I'm going to drink small amounts of alcohol and it's not a total no-no for me, you do decrease the chances that you are going to go on a bender sometime and get drunk. My protocol is I have the equivalent of about 5 servings of alcohol a week, and people come over to my house and they are relatively surprised when I give them a glass of wine and it's a measly little 4 ounces and I make them a cocktail and there's literally like half an ounce of alcohol in the cocktail. So, I do microdose with alcohol. And, I think if you have alcohol around and you can show self-control with it, then that's fine. And, I will admit if I really want to spin a few dials or kind of shift myself into a socially lubricated mode, I would much rather microdose with psilocybin or THC than I would have the socially lubricating equivalent of 2 or 3 drinks. And I know that's becoming more and more popular if people use botanicals, small amounts of psychedelics and entheogens, small amounts of THC, et cetera, as an alternative to higher amounts of alcohol. So, I am not a doctor. This is not medical advice. This is not lifestyle advice. Proceed at your own risk. And for heaven's sakes, please don't eat a bunch of mushrooms and take a few edibles after hearing this podcast. That's not something I'm endorsing. But the whole paper is interesting. I will link to it in the shownotes. And again, it appeared, I think I said published in Nature. It was actually, it was reported on in Nature, but it was published in the journal Cell Reports Medicine. And she died last August, August of 2024. So as I was going through her article, I, or the article about her, I came across another paper that I thought was really interesting and also related to anti-aging. I'll link to this paper again at bengreenfieldlife.com/494. But in this paper, they studied all the different anti-aging drugs/supplements that are out there. I mean, this was like a meta-analysis of long durations of trials and large sample sizes, many of them in like models that don't seem very much like humans, but at least give us clues like yeast and fruit flies. But many of the studies in actual mammalian species that more closely replicate human beings. And so the paper is, is kind of clunky and hard to get through and lists all the different like Drosophila and Canis Lupus familiaris and Adenita vega and all the different species that they studied, over 720 experiments that they analyze in terms of what actually results in meaningful increases in lifespan. And particularly relevant to you if you're listening in and you're a mammal, which I think there's a high likelihood of, um, what actually has meaningful data in mammals. Now, all the different compounds that they studied, uh, 36 in total were tested in at least one mammal. And of those, 22% showed a significant increase in lifespan. And of those, only 8 showed a significant increase— I'm sorry, 22 showed a significant increase in non-mammals, but only 8 showed a significant increase in mammals. Those 8 were— I'll go through them one by one here and explain to you why. But those 8 were, first, curcumin. Okay, curcumin is called a polyphenol. You get it from turmeric. It's well known, as you probably know, for its anti-inflammatory and antioxidant properties, not just in the gut, but if it's delivered in like a liposomal format or a turmerosaccharide format like we do with joint product Kion Flex or in a— let's see, liposomal would be something like Ro Nutrition's curcumin, RHO. Turmerosaccharide would be something like Kion Flex or combined with bioperine, black pepper extract. You can get better absorption of the curcumin compounds. And what it's been shown to do in longevity research is enhance mitochondrial function. By increasing your ATP levels, reducing oxidative stress because the anti-inflammatory component, reducing reactive oxygen species, inhibiting mTOR signaling, which actually makes a case for not taking a bunch of curcumin right after you work out, by the way, because you want mTOR signaling after you work out. It may shorten the rate at which telomeres or decrease the rate at which telomeres shorten and has been shown to extend lifespan in mammalian models. And it was near the top of the list. The next one is spermidine. I used to kind of snicker when I'd hear about spermidine and make somewhat off-color jokes about where it's harvested and how you could take it. But spermidine, all joking aside, is a naturally occurring polyamine. We find it in foods like wheat germ. We find it in soybeans. Yes, we find it in sperm also, even though that's— it could be a sustainable source, I suppose. I could see sperm banks popping up or men are donating for the purposes of both male and female longevity, but I'm not sure where the oral consumption of said sperm actually becomes safe. But anyways, we'll leave that there. Spermidine assists with DNA stabilization and protein synthesis and has multiple longevity-enhancing mechanisms. It induces autophagy, it clears damaged cellular components, it reduces inflammation, And do I take spermidine? I do. So spermidine, I take this little morning powdered packet called IM8, and that has some spermidine in it. And then I also take, if I've had a hard workout, Kion Flex at night on an empty stomach, and that has curcumin in it. And I also use this stuff called RHO. RHO, it's like liposomal curcumin. And at some point during the day, not right after my workout because of its inhibition of mTOR signaling, but at some point during the day, I'll have about a heaping tablespoon. Of that curcumin.

Okay.

The next one is actually a peptide, super popular peptide for anti-aging and longevity right now. It's called epithalamin, also known as epitalon or epithelon. It is a synthetic peptide that is derived from pineal gland extract, and it promotes longevity by activating telomerase to elongate your telomeres. It delays cellular senescence or the buildup of zombie cells. And a lot of research on it has come out of Russia. Some people think that epitalon can only be injected. There are oral forms of epitalon. It is a short enough amino acid that you can use it orally. And the protocol with epitalon is pretty simple, and I do this protocol. You inject— gosh, I don't have the number in front of me. You would have to double-check on this. It's either a gram or a milligram. You can easily look this up. I've done a whole podcast on epitalon, and I'm just going off the top of my head, not off of notes here. It's a milligram or a gram twice a year for 10 days. And that's it. So it's not something you take every day, but epitalon is pretty high up there in terms of its extension of mammalian lifespan. Definitely wanted to add into the protocol here. D-glucosamine, that is actually an amino— it's called amino sugar. D-glucosamine is, it's often sold as a dietary supplement for joint health. It's derived from shellfish in some cases. In other cases, it's synthesized and it mimics calorie restriction. By impairing glucose metabolism, inducing autophagy, and altering amino acid transport and protein metabolism. So it's kind of like a fasting mimetic. D-glucosamine is not something I personally take. I do take amino acids, but I don't take that particular amino sugar. However, after seeing this data, it is one I'm going to look into as far as dosage, sourcing, et cetera. The next one is interesting, especially for all you guys who are on aromatase inhibitors to lower estrogen levels, because estradiol, a steroid hormone and the main form of estrogen in humans involved in brain health, reproductive regulation, metabolic regulation. In longevity context, it acts on your estrogen receptors to activate signaling, what's called NF-kappa-B, which reduces the buildup of senescence, these so-called zombie cells. And in particular, in females, it can increase lifespan. But there are some studies in male mammal models that it can increase lifespan in males as well. Some males are under the impression that any Oestrogen hanging around whatsoever is going to make you weepy at shit flicks and help you— chick flicks, did I say shit flicks? There's those two. The low score on Rotten Tomatoes, those are the shit flicks. Chick flicks, high levels of estrogen can make you weepy while you're watching chick flicks and moody and might make you grow some man boobs. But, that's not true. Yes, you don't want just through-the-roof levels of estrogen, but if you're a guy just trying via aromatase inhibitors or other drugs to lower estrogen willy-nilly, body. It's instead better to have it in healthier reference ranges. I think one of the better tests to look at whether you are in healthy reference ranges, whether you're a male or a female, is a Dutch test, a D-U-C-T-C-H. It's a dried urine test that gives you kind of a daily snapshot of your hormone levels. And take a look at estrogen, make sure it's not excessively suppressed, whether you're a man or a woman. The last few, the 3 more, simvastatin, That's a statin, and that's interesting. So statins inhibit something called HMG-CoA reductase to lower cholesterol levels. The proposed longevity mechanisms for statin is that they have what are called pleiotropic effects, system-wide effects like improving nitric oxide availability, reducing inflammation, and enhancing cardiac health. The reason I don't take a statin, including a simvastatin, is because it can also impair mitochondrial function in some cases. Cause some gut issues in some people and may cause some muscle wasting. Some of those things can be skirted through exercise, through supplementation with coenzyme Q10 or ubiquinol for the muscle wasting component. But I think if you look at the side effects of a statin, you know, I took a statin for a couple of years. I took a statin and a PCSK9 inhibitor to reverse some plaque accumulation that I think largely built up during my years of racing Ironman really hard. And I successfully reduced my plaque using that combo and then a product called Heart Health from a company called Vitaboom. I still take Heart Health daily, but I stopped the statin for the side effect reasons, and I stopped the PCSK9, frankly, because it's an expensive drug and I no longer needed it. It's a twice-a-month injection. And yes, you could make a case that especially if you are a male with preexisting cardiovascular disease or family cardiovascular disease and you have plaque accumulation, that the use of a low-dose statin combo like ezetimibe and rosuvastatin, for example, and a PCSK9 inhibitor could be beneficial for slowing plaque accumulation or even reversing plaque in some cases or regressing plaque. But I don't think that just because simvastatin increases lifespan in some mammalian models that you should drop everything and go get on a statin. If we look at the pathways via which it works, right, increasing nitric oxide. Well, you can do that with other nitric oxide precursors. The Vitaboom Heart Health stuff that I take has nitric oxide precursors in it. Reducing inflammation, you can do that with, say, curcumin or tumor saccharides. And enhancing cardiac health, well, you can do it with exercise. I'm not going to include simvastatin as one I'm personally going to throw into the mix. Our last two, SKQ. That is a mitochondrial antioxidant. It's basically what's called a plastoquinone that's attached to to a cation. And the way that it works because of that structure is it scavenges reactive oxygen species and prevents oxidative damage. And it does have lifespan extension capabilities. There is a product, um, I have it in my pantry, I sometimes remember to take it. It acts very similar to SKQ, it's called MitoQ. Um, I've been kind of looking into it recently after going through this paper. I'm probably going to take it more regularly. Like many people's pantries, I and probably especially many health podcasters' pantries. I have all sorts of supplements that I just don't use but that are there. And after seeing the evidence on SKQ, I'll probably throw this MitoQ into the mix because of its mitochondrial-targeted antioxidant capabilities. Although there are other mitochondrial-based antioxidants as well out there, probably methylene blue being the most popular one right now. But SKQ, I'm talking about things that have actually been studied. So, that's an interesting one. The last one is taurine. Taurine is an amino acid. Tons of research on taurine. I think it's climbing up in the ranks as far as very beneficial amino acid kind of like creatine abundant in your muscle, in your brain. You get it from your diet. You can synthesize it endogenously if you're getting a proper balance of and enough amino acids, but it reduces DNA damage. It reduces mitochondrial dysfunction. It lowers inflammation. It protects against telomerase deficiency, thus increasing or decreasing the rate at which telomeres shorten. I will get that right by the end of this podcast. So I take an essential amino acid complex. I take the Kion Aminos. And so, you know, I take about 10 grams pre-workout and another 10 grams later on in the afternoon. It's just such a great supplement and has even been shown to preserve muscle when you're not exercising. I don't see a need for me to take taurine. I'd rather just take the whole complex of amino acids, especially since I'm getting those. I can synthesize taurine endogenously. But that's another one to keep your eye on. So that's the list. Curcumin, spermidine, epitalon, D-glucosamine, estradiol, simvastatin, SKQ, and taurine are like the top 8 anti-aging drugs based on robust research. Now, I should also throw this in there. I'm not going to spend too much time on this, but another kind of nail in the coffin of statins, for me at least, that I noticed recently is that There was a pretty recent article in the journal Cell Metabolism showing that statins can actually worsen insulin resistance and cause hyperglycemia by affecting your gut microbiome, what's called bile acid metabolism. Here's what's crazy. I'm no conspiracy theorist, but I'm just saying this is very interesting. The way that statins dysregulate your gut microbiota specifically reduced the levels of glucagon-like peptide 1. Does that glucagon-like peptide 1 sound familiar? Well, it might because that stands for GLP-1, meaning that many of the pharmaceutical companies, several of whom also sell GLP-1 drugs, they produce statins that lower GLP, meaning if you are on a statin, then you might be kind of creating a polypharmacy need by reducing hunger mechanisms, increasing risk for diabetic or diabetic-like complications, and potentially causing you to make a purchase of GLP-1 from said pharmacy. I'm not saying this is like the fox guarding the henhouse. I just thought it was interesting that statins can lower GLP-1, thus impairing insulin sensitivity and glucose uptake, aggravating insulin resistance and hyperglycemia. And I know that some of you might say, well, I'm on a statin, I can just start injecting a GLP-1. Well, yes, but again, creating a clunky polypharmacy scenario might not be the easiest, most efficient, or healthiest way to go. I am not opposed to microdosing GLP. I personally do it. I take about a very, very small dose of retatrutide, about 0.25 milligrams, 3 times a week. It quiets food noise for me. It helps me work through lunch. I don't use it to lose weight. If anything, I eat like a horse. I eat like 4,000 calories a day. It doesn't suppress appetite that much for me. It doesn't make me nauseous around food. But I like some of the system-wide effects of what I've seen from retatrutide, including lowering neural inflammation. However, I would never just, like, get on a statin and then start taking a GLP-1 because the GLP-1 reduce— is reduced by the statin. Now, if you wanted to, let's say— and again, I'm not a doctor, don't take any of this as medical advice— but let's say you're a person with preexisting plaque and you want to start on a low-dose statin and talk with your doctor about it, and maybe a PCSK9 inhibitor to help out with your cardiovascular risk factors and because you know a statin is going to reduce GLP-1, maybe you are going to get on a GLP-1. I would consider that kind of like a short-term thing because if you're on a statin and a PCSK9, you can do like I've been doing and just track your plaque via a carotid intima-media thickness score, which is a simple ultrasound scan. I'll link in the podcast show notes to a few companies that do that. Vasolabs.com is a great way to search for one. And the reason that's so convenient is that if I were to get a CT angiography on a regular basis, that's a huge dose of radiation. But I can get a couple of times a year a CIMT, a carotid intima-media thickness score, which is just ultrasound without radiation, to kind of keep my finger on the pulse, pun intended I suppose, of whether or not I'm doing a good job with plaque regression. And again, took me about 2 years, and my plaque's looking good, and all my cholesterol numbers and triglycerides and everything are looking good. So I no longer use those drugs, although I'm not completely opposed to them like a statin and a PCSK9. But I thought that was interesting, the effects of a statin on GLP-1s. Alright, another piece on aging here. I get a lot of questions about this and it does have to do with aging because these things have been shown to affect aging parameters via several different pathways. Hyperbaric chambers. I love my hyperbaric chamber. I feel incredible. I feel like a three-lunged mutant when I climb out of that thing. I nap in there. I'm getting massive amounts of oxygen delivered to my tissue, but it's a soft shell. I get it from a company called HBOT USA. It's almost like this sleeping pod or this pod that I climb into and zip myself up into. I don't even need help getting into it now. I figured out how to zip myself up into it. It's called the Vitaris 320. V-I-T-A-R-I-S 320. RIS 320. I'll link to the one I use in the shownotes. But, it only goes up to 1.3 atmospheres. Actually, I take that, 1.4 atmospheres. And then, I breathe oxygen while I'm in there. And, a lot of people ask me, "Well, is the soft shell really any good compared to these big hard shell chambers my local biohacking facility or wellness club or hospital or whatever have?" And, Jason Sonners who I've learned a lot about HBOT from, he's been on the podcast before and I'll link to our episode. He's He's done quite a bit of research on soft shell versus hard shell hyperbaric chambers, and he just released a pretty groundbreaking study comparing the two. And, there were some pretty surprising findings that he discovered that make me kind of glad that I didn't have to go out and buy a super expensive hard shell unit and then talk my wife into what giant room of the house that was going to take up, and I just had a little soft shell next to the lounge in my office. Or in the lounge next to my office. So, both— here's what Jason found. Here are the key takeaways. Both soft shell and hard shell hyperbaric chambers reduce systemic inflammation, but they affect different types of inflammation. So, the soft shell lower pressure chambers affect inflammatory markers called cytokines like TNF-alpha and interleukin-6 more strongly. Those are things you would see elevated from chronic inflammation, overtraining, stress, or autoimmune disorders, which is great that soft-shell hyperbaric can have an impact on those. While the high-pressure chambers, the hard shells, those have stronger effects on the inflammatory marker myeloperoxidase. That means that if you are using a hyperbaric for something like cardiovascular inflammation, heart disease, and even Long COVID, in which we see higher levels of myeloperoxidase, you might be better off using the hard shell. Right? So, it kind of depends on what you want. Both low pressure and high pressure resulted in statistically significant improvements in memory, which is one reason why people with TBI and concussion use these things. And, um, the higher pressure was a little bit better for the cognitive effects, but the lower pressure still gave pretty good effects. Um, both of the pressure types affected biological aging clocks. The low pressure affected what are called generation 1 clocks while the high-pressure affected generation 2 clocks. So, what's an aging clock? Well, a Gen 1 aging clock, that is an estimation of biological age that looks at DNA methylation patterns. And then, a Gen 2 clock would be more like blood and biomarker data like traditional clinical and lifestyle data. So, both of the chambers, the hard shell and the soft shell, seem to reverse biological age. But the low-pressure clocks or the low-pressure chambers had a higher acute effect on these aging clocks and the high-pressure chambers had a better effect over time if I understand Jason's research properly. Meaning, you can see an anti-aging effect from both the low pressure and the high pressure. And the high pressure seems to affect the clocks better over long-term use. I think with both forms of hyperbaric from the research that I've seen, the results do accumulate. In many cases, don't even kick in until you've done 30 or 40 sessions. I'm in my hyperbaric when I'm at home 3 times a week. And, when I travel, I'm often popping into one of these clinics like Next Health, for example, to do a hyperbaric session. You feel so good, especially for jet lag, for inflammation. So, if I want to take a nap, I'm making phone calls and looking for a local hyperbaric chamber I can I'm into when I'm traveling. So, if you stack a hyperbaric as Jason and also another guy named Scott Sherer discussed on my podcast with either calorie restriction and fasting, anything to boost nitric oxide or methylene blue, those can all enhance the results. But then, if you use high-dose antioxidants like glutathione and vitamin C in combination with hyperbaric oxygen, because remember part of what hyperbaric oxygen does is it increases reactive oxygen species you could impair some of those effects. Same reason you would want to take curcumin, vitamin C, vitamin E right after workout because you want some of that inflammation to kick in so it produces the hormetic effect that you want from the exercise. Same thing with hyperbaric. Nitric oxide, yes. Methylene blue because it's a selective antioxidant, yes. Hydrogen water because it's a selective antioxidant, yes. Calorie restriction, yes, but— meaning going into the hyperbaric without a super full stomach. But taking glutathione, vitamin C, or any powerful antioxidant directly before or after a hyperbaric session is not a great idea. So, those are a few of the key takeaways from Jason's studies. And, I'll link to Jason's website in the shownotes. You can go see some of his research a little bit more. But, I thought that was interesting. Okay. Ben Greenfield: And then, I've got one more for you today just because if we're talking all about aging, we should definitely mention the idea of muscle and aging. Because muscle, as you probably know unless you've been hiding under a rock, is a great way to reverse the effects of aging and grip strength, muscle mass, power. They're all correlated with longevity. Well, there was a study, and this study isn't super new. It was in 2019, but I came across it again in, in some of my reading. And it's a study that looked into whether you need an energy surplus to maximize your skeletal muscle hypertrophy, your skeletal muscle mass. So specifically, what they were examining was whether eating more calories than you burn is necessary to achieve ideal muscle growth when combining the eating more calories than you burn with weight training. So, what they did in this paper was they synthesized a bunch of existing research to actually challenge the longstanding assumption that bulking or creating a surplus is necessary for muscle gain. And, it wasn't a new experiment, but this was just a review of a bunch of other papers. Now, this is important because if you read traditional sports nutrition advice, the same stuff I was taught in college, you're often recommended a surplus. Of 350 to 500 calories per day to be able to maintain muscle in a hard-charging athlete and up to 1,000-calorie surplus per day to fuel muscle growth. And that stems from the idea that building muscle requires extra energy and amino acids for protein synthesis, for tissue repair, for metabolic processes. But the, the, these guidelines are somewhat simplistic, right? Just saying randomly, hey, eat an extra 1,000 calories per day doesn't take into account the metabolic cost of the resistance training itself, like post-exercise oxygen consumption and the metabolic increasing effect of resistance exercise, the energy needed for tissue synthesis, the increased resting metabolic rate as one trains. And so what the paper was looking for was, was a little bit better research, or to sift through the research to see what the true energy cost of muscle gain is. So they looked at like training variables, volume, intensity, frequency, training status, like a novice versus an advanced weightlifter, genetics, sex, age, body fat percentage, even protein intake. And so, what they found was that there are some studies that show that a calorie surplus can lead to a greater increase in fat-free mass or muscle versus just pure calorie maintenance. But, here's the first interesting thing they found. You can maintain strength just fine on a calorie deficit or eating as many calories as you're burning. There were other studies that have shown that if you're lifting weights even on as little as 800 calories per day, given adequate protein, you can also maintain and in some cases build muscle, meaning muscle growth can occur in energy deficit if your protein intake is high and you're continuing to resistance train, which is interesting. I mean, you can potentially lose fat and gain muscle at the same time if you're eating enough protein and lifting weights. And muscle hypertrophy is possible without a surplus. Now, that seems to be more true in untrained individuals, meaning athletes who have experienced lifting and are pushing themselves pretty hard. They don't do as good of a job maintaining or building muscle at a calorie deficit. Deficit. But untrained people, let's say the average, let's say overweight person wants to lose weight and build muscle at the same time, they can get away with not eating as many calories as they're burning and assuming they're getting enough protein. And that ranges, but my recommendation is 0.8 to 1 gram of protein per pound of body weight. You can actually maintain or even build muscle at a calorie deficit. So basically, this paper debunked the mandatory surplus for hypertrophy. And I think that it's more important for a trained, experienced lifter or exerciser to eat as many calories as you're burning or be at a slight surplus to build muscle. But especially if you're just like new to the fitness game and you want to build muscle and lose fat, you can do it if you're lifting weights and eating adequate protein, even if you're at a calorie maintenance or calorie deficit. So good stuff to know. Basically, long story short is you don't have to eat extra calories to build muscle. Especially if you're new to the lifting game. Alright. Well, I'm going to stop there. I know I've thrown a lot at you. I fed you through the fire hose. All the shownotes are at BenGreenfieldLife.com/494. If you like these little Q&A solo shows where I go through some research for you and give you some updates, you can leave a comment over at the shownotes or wherever you're listening to this podcast. Leave me a review, leave us a review, leave the show a review. I really appreciate it. It helps the show to grow. I've been doing this for 18 years now, this podcast, twice a week without skipping a beat. And, I'll keep on doing it as long as you guys enjoy it and you get good information out of it. And, all the shownotes where I'll be in the world, what events I'll be at, where you can attend, different retreats I'm throwing, all of that, just check out BenGreenfieldLife.com/494. It's there. And, until next time, I'm Ben Greenfield with The Boundless Life. Thanks for listening. To discover even more tips, tips, tricks, hacks, and content to become the most complete boundless version of you, visit BenGreenfieldLife.com.

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