Why the Seed Oil Debate Is More Complicated Than You Think

In this episode of the Boundless Life Podcast, the latest seed oil controversy, the most important body part, CBN for sleep, and a whole lot more. Welcome to today's show. It's little old me just by myself, flavored and fueled by LMNT Orange Salt. I drink so many of these. I don't have high blood pressure yet, and I don't think I'm going to get it because it actually is a pretty good mineral balance. I could probably overdo it on this stuff, but no sugar, no caffeine, 500 milligrams sodium, 100 potassium, 30 of magnesium. The sparkling flavor is great. There you have it. But it is what I use to stay hydrated. I had a killer sauna session this morning. Once a week, Actually, twice a week now, now that I'm getting old and I need 2 recovery days. Instead of lifting weights, I do a Vasper session. And the Vasper is this fancy exercise machine that combines blood flow restriction and cold and grounding and full-body exercise. And I have an oxygen breathing unit next to it. I realize this is advanced and nerdy stuff. So, I do a 21-minute exercise session on that Vasper and then I do some flow for addressing body parts that tend leg or that tend to not get addressed in the full-body lifting I do the rest of the week, like the glute medius. And I'll do some deep tissue work on the piriformis and the psoas, do some balance work, some big toe flexor work, which we may learn more about today. And so, I do that for about 20 minutes and then I finish with 20 minutes as hot as I can go stretching in the sauna, kind of my own bastardized version of Yoga Flow. And I had this company, shout-out to Western Soul, S-O-L, fly up from Boise and build a sauna on my property. The sauna is grounded. They use like a thermal-pressed aspen wood that's low VOC, no chemicals treated in the process. It's beautiful sauna, but man, oh man, it gets hot. The heater in it when you put it on takes the water, the steam from the water that you put on the rocks, and then kind of recirculates it up to the top of the sauna. But that means all the heat hits the lower part of the sauna, and then goes up to the top. So, you can't hide from the heat even when you're down on the ground. So, I was in there this morning doing yoga flow and some push-ups, and it's a big sauna. I can fit 20 people in there. I think I'm going to do a podcast with those guys at some point just so you can learn more about some of their prefab and custom saunas and the difference between dry, infrared, and steam. Anyways though, cool build. So, shout out to the guys from Western Soul. Anyways, so that's why I'm rehydrating. Long story short. But today is not about the sauna. Today is about all of the interesting things that I have found on the internets and in the research that I pour through every morning, mostly in exercise, sports science, health, fitness, biohacking, longevity to make your life better. So, here we go. New, brand new, hot off the presses, 2026 BMJ, British Medical Journal of Medicine study of over 100,000 thousand people. And what they wanted to look at was how exercise, and more specifically exercise variety, impacts your mortality, your risk of dying from just about anything, with the idea that exercise should protect you unless you, I don't know, fall off the aerodyne or something. Anyways though, so very few prior studies have specifically looked at how exercise variety impacts mortality. So what they did was they used health and lifestyle data for more than 111,000 adult men and women, followed them over the course of more than 30 years. And what they looked at was how much time per week these folks spent walking, jogging, running, bicycling, including stationary bike, lap swimming, rowing, doing calisthenics, playing tennis, squash, racquetball, lifting weights, doing lower body stuff like yoga, And also passive stuff like lower-intensity stuff, again, yoga, stretching, toning, outdoor work, digging, chopping, climbing stairs. I know how much all of you love to just dig for exercise. Anyways though, they then scored each participant according to the activity variety and the intensity levels, and then examined those scores looking at primarily risk of premature death and some other chronic diseases. And what they found was that intensity of the exercise aside, the people who engaged in the highest variety of exercises had a 19% lower risk of premature death compared to the people who engaged in the lowest variety of exercising. Now, the takeaway here I think is pretty obvious. To illustrate this for you, I used to do triathlon, I used to swim, bike, and run all the time. Those were my 3 primary modes of exercise besides the occasional core workout and a little bit of weight training. I was in good shape and arguably had more exercise variety than if I'd just been a pure runner, a pure cyclist, or a pure swimmer. And so, triathlon is an example of the introduction of cardiovascular exercise variety. But still, when I started obstacle course racing, Spartan racing, after seeing one on TV and getting super interested in it, I couldn't carry a bucket. I didn't have the mobility to crawl under barbed wire. I couldn't climb a rope to save my life. I couldn't haul sandbags up hills. My strength was low, and the variety of movements that I'd been throwing at my body over the past 15 years of swimming and cycling and running was also low. I got in the best shape of my life doing Spartan Racing because I probably went from 3 exercise varieties, maybe 4 if you include core and weightlifting, to like 20 exercise varieties. Today, I walk, I play pickleball, I play tennis, I play frisbee golf and regular golf occasionally, I lift weights, I do kettlebells, I use a wide variety of exercise modalities, and I'm constantly looking for new sports and new activities to learn. If you get stuck in a rut, well, let me put it this way, the best form of exercise is the one that you enjoy and that you're actually going to do. Okay. So, If you're just like, "Hey, Ben, listen, I don't need complexity. I'm going to run and I'm going to do the same Nautilus strength training workout at the gym for the rest of my life," great. You're going to be better off than somebody who's sedentary. But if you're able to switch it up, to constantly learn new sports, to constantly learn new exercises, new skills, to go from Nautilus machines to barbell training to maybe landmine training to kettlebell training to elastic band training to vibration platform training, across a wide variety of exercise modalities, rinse, wash, and repeat that with the type of cardio that you do, you will have a lower risk of death because science, the latest science says so. The other important thing I think to realize, and this was a big aha moment for me when I recently interviewed neuroscientist Tommy Wood, is that by stimulating the mind, you keep the brain young. And Tommy kind of bashed the myth that our brains get old and, and dumb as we age. More typically, as we age, we get comfortable, we get set in our ways, we get less resistant to public embarrassment or discomfort from learning new activities, whether mental or physical. And that's what causes more of the loss of neural health compared to just brain degradation. So that means if you're introducing a wide variety of exercises and sports over the course of your life, you're not just lowering your risk of premature death, but you're also going to be ideally or predictably one smarter cookie the whole time that you're doing it. So, great information there. Switch up your exercises. Don't get stuck in a rut. Yes, again, the best form of movement is the one you're actually going to do, but the more you can vary it up, vary it up. So now, you have no excuse to not go learn the sport of pickleball. Okay. Next up, I did just briefly mention the barefoot exercises that I do in the sauna. This was pretty cool. Comparison of the effects of barefoot and shod training on foot structure, muscle strength, and sensory function. This was in the Journal of Strength and Conditioning Research last month. And the word shod, should any of you be unfamiliar with that term, is the fancy scientific word for wearing shoes. So now, you have a new word in your vocabulary. When you're wearing shoes, you can tell people, "I am shodding. I'm shod." So, what they looked at was 3 different groups of healthy adults, a group that did barefoot training and a group that did shod training, and then a control group that basically didn't train. So, the barefoot and the shod groups both experienced increases in what's called relative toe flexor strength, which sounds super boring and pretty useless, Not a lot of us go to the beach to flex our toes, but I'll get into why this is important momentarily. Now, the barefoot group had the highest amount of an increase in toe flexor strength, even though the people wearing shoes also saw an increase in toe flexor strength. Arguably, if you're wearing shoes with a narrow toe box, which most shoes are made to be unless you're wearing, I don't know, Vivo Barefoot or something like that, The toes are going to be compressed, your risk of bunions goes up, your proprioceptive feel for the ground might decrease, but you're still going to get some toe strengthening compared to not doing any exercise at all, whether you're barefoot or shod. So, what this study showed was that when you're exercising barefoot or we could extrapolate this to something like Vibram FiveFingers, or my favorites, shout out to my friend Mark Sisson in Miami, Peluva 5-toe shoes, you get a big increase in what's called standing toe strength. And standing toe strength is what allows you to use the big toe muscle for postural control, for getting greater ground reaction force whether you're walking or jogging or sprinting, and better weight-bearing balance, which trickles up to your knee health, to your hip health, to your low back health, to your shoulder health, and to your overall posture. For example, toe strength is the single best predictor of falling in older adults. The single best predictor. Okay. Six-pack abs, glutes of steel, a neck like a freaking elephant. Nothing beats big toe strength when it comes to your risk of falling when you're older which is pretty important considering that falling when you're older is one of the primary reasons people wind up injured and becoming more frail over time. Poor postural balance, which is also drastically affected by big toe strength, is also one of the most common reasons, actually is the most common reason for lower limb injuries in younger populations like athletes. So, the technical name, the scientific name for the big toe is the flexor hallucis longus. The flexor hallucis longus, that's a muscle that kind of feeds into the big No, that's essential for maintaining what's called the medial longitudinal arch of your foot and ensuring proper force distribution across your foot. So, when that muscle, the flexor hallucis longus, the FHL, is weak, you lose push-off power while you're walking or jogging or running. You lose the ability to recover from what are called perturbations, which would be stumbling and catching yourself or say walking on an uneven surface. And importantly for people who deal with plantar fasciitis and pain in the heel or the bottom of the foot, the muscle that has to pick up the slack when the big toe or the flexor hallucis longus is weak is the plantar fascia. So, the plantar fascia takes on more repetitive loading, and that's why plantar fasciitis is so widespread in populations that don't train toe strength or say just don't do what they would normally do in the weight room but do so barefoot or wearing minimalist shoes or wearing like five-toe shoes. So, if you're an athlete or someone who trains hard, this means that if you do have good big toe muscles, that translates directly to sprint push-off, to single leg stability, to deceleration, to the dynamic balance you want on the tennis court or the pickleball court or the basketball court. Like I mentioned, one way to do this is just to do the training that you normally do, but to do so, if your gym will let you get away with it or if you're lucky enough to have a home gym, barefoot, wearing minimalist shoes, or wearing 5-toe shoes like Vibram FiveFingers or Peluva shoes. There are also actual exercises that you can do to strengthen your big toe. A few of the more common ones, and they sound kind of dumb, but you could literally do these while you're watching TV, while you're reading a book, while you're sitting and staring at the sunset, sipping your glass of wine, you can pick up stones or marbles with your toes. That's simple. Pick up a marble, put it in a little plastic cup next to you, pick up another marble or stone, and you're doing this with your toes, not your hands, with your big toes specifically. Curling your big toes, picking something up, setting it down. Another example would be what's called an isometric big toe press against resistance. For this, you get a strap like a yoga strap, you wrap it around your big toe, you try to resist your big toe holding onto that strap, and then you press your big toe into the ground as hard as you can for anywhere from 3 to 5 seconds, and you do that several times per side for each big toe. Probably only have 2 of them if you're a normal person, so this shouldn't take too long. Another example, this one's great. I talked with this, I think, Blinda, Belisa Vranic, I believe, was my podcast guest who I'll put the link in the shownotes at BenGreenfieldLife.com/501. BenGreenfieldLife.com/501 is where the shownotes are. I'll link to a podcast that I did with her where she just talked about, hey, when you're standing, waiting for the airplane to board, waiting at the doctor's office, which hopefully you aren't doing too much of, waiting in line at the grocery store, just simply grip the ground through your shoes or using your minimalist shoes, grip the ground with your toes, just hold with all the toes and then release. And then, hold with all the toes. This is called foot doming and then release. You're basically pulling the ball of your foot towards the heel of your foot. If you can imagine doing that, pulling the ball of your foot towards the heel of your foot, that would be another example of a great toe-strengthening exercise. Another easy one you can do if you're walking up a set of stairs or have a set of stairs in your house is eccentric toe flexion. So, you put the balls of your feet on the edge of the step with your toes hanging off, and then you lower the toes into extension. You drop the toes down and then you curl them back up. So, it's like a heel drop. So, your toes— let me make sure I explain this correctly to you. Your toes are basically hanging off the edge and you're lowering them into extension and then curling them back up. So, you're essentially doing what would be specifically called eccentric toe flexion. And this is also great, by the way, for the Achilles. If you really want to go to town, you could wear a weighted vest while you're doing these. And then, another one is just towel scrunches. Lay out a towel, Use your toes to scrunch that towel up, right? So, you're repeatedly curling and extending your toes, and then reach down with your hands, pull the towel back out to flat, and scrunch it up again. And you could literally do that during the course of your favorite 30-minute TV show and strengthen your toes that way. My own strategy is that I just do the training that I normally do since a lot of my exercises in the gym are standing exercises anyways, barefoot or wearing my Peluva shoes. And since I wear And since I'm barefoot or wearing Peluvas 80% of the time, I get a lot of big toe strengthening just naturally doing what I would do anyways. And I should note that when I say naturally doing what I do anyways, a lot of the activities that I do in the gym, I try to do occasionally standing on one leg. So, when you're standing on one leg, just try this right now if you're not driving, I guess. Stand on one leg and you'll immediately feel that to maintain your balance, your big toe has to contract. So now, imagine doing dumbbell curls or overhead dumbbell presses or side-to-side rotations or anything else in that single-leg standing position. Well, as you can imagine, you're automatically going to get some pretty good isometric big toe strengthening and that so-called foot doming effect. So, train the big toes and train with a variety of exercises. Alright, let's turn now to everybody's favorite topic, Seed oils. Hooray. I tweeted a study that recently came out that evaluated the effects of seed oils on lipid profile, on inflammatory and oxidative markers, on blood sugar control. And this was primarily a systematic review of 11 clinical studies in diabetic and what are called dyslipidemic patients, people with cholesterol that is out of control or off or imbalanced. Long story short is that this review concluded that seed oils primarily from canola oil, flaxseed oil, and sesame seed oil can positively, yes, I said positively, influence lipid profiles doing things like lowering LDL cholesterol and allow for better glycemic control while potentially modulating or controlling oxidative stress markers. Now, if you're deep in the, I don't know, the health podcasting or health sciences realm, you have probably heard many people say, "Well, avoid seed oils like the plague." I've kind of been more adamant lately about avoiding fried and excessively heated seed oils more than just avoiding seed oils in general, right? Like, I eat from the Whole Foods salad bar, which uses like a cold expeller-pressed canola oil. I don't eat any of the fried foods that are on the hot salad bar section, but I'm more concerned about seed oils that have been heated, repetitively heated, foods that have been fried in seed oils, etc. When I tweeted about this study and I said, hey, look, I think more of the damaging effects of seed oils come from when they're fried or heated, like I just said. And you could actually make a case that seed oils compared to saturated fat, when we hold calories equal, have a good effect on cholesterol and a good effect on glycemic control and a good effect on inflammation. A few intelligent people on the exosphere, they came back to me with a little bit of data that made me think a bit more deeply about this. So, for example, one person responded, I think this might have been, I think this wasn't James DiNicolantonio. He was one of the doctors who replied to me. This was somebody else. I don't have the thread in front of me, but basically they sent over a table that was published in The Lancet medical journal. And this was a randomized controlled trial of 188 patients, and they were randomized to take fish oil, which is rich in omega-3 fatty acids, sunflower oil, right, which would be a traditional polyunsaturated fat seed oil, uh, richer in omega-6 fatty acids, or a control oil, which is kind of like a blend of palm oil and soybean oil. And then, uh, they did surgery on these people. They were doing surgical removal of plaque from their carotid artery. So obviously a pretty intensive study here. The surgeons cut the plaques out and then examined them under a microscope. And this is a big deal because they were looking at the actual plaque tissue, not at the blood draw. So, there's a difference between the cholesterol that you find in the blood and looking at the actual plaque to see what's manifested in terms of, say, like fatty streaks in the plaque or issues that would actually contribute to atherosclerosis. Now, what they found was that, first of all, the fibrous plaque with a thick protective cap over the lipid core, the type of fibrous plaque that you would actually want because it indicates that plaque is more stable and it holds plaque together and it prevents rupture. Well, that was at 66% in the fish oil group and it was at 53% in the sunflower oil group, meaning that when you actually look at the plaque of the people who have cholesterol that— or LDL that's more comprised of fat from seed oils, you actually see a 13% increased risk of, or decreased protection, I should more accurately say, of the thick caps that protect plaque. Now, when we look at thin fibrous plaque, which is the plaque that is more likely to rupture, the fish oil group, right, the omega-3 group, non-seed oil group, had 15% of the thin fibrous caps, the bad ones, right? Basically, that's a thin cap over a lipid core is like a bomb waiting to go off. Right? Sunflower oil folks, they had 29%, nearly double the bad thin caps compared to fish oil. And once again, that, that's a little bit of, of a blow against seed oils. When we look at plaque rupture, right, the, the actual rupture of the plaque, which is what you really don't want to happen, fish oil group had 3.8%, sunflower oil group had 5.6%. So, and then finally, if we look at what's called fibrocalcific plaque, fibrocalcific plaque, fish oil had 5.7% of that and sunflower oil had 1.9% of that. And that's important because the calcified fibrocalcific plaque is the more stable form of plaque. It's hardened, it's unlikely to rupture, and the sunflower oil group, the seed oil group, had the least of that type of stable plaque. So long story short is that in people who have a higher amount of seed oil consumption, we see fewer thick protective caps, more thin vulnerable caps, more rupture, and less stable calcification. Now, James DiNicolantonio, who's a cardiovascular research scientist and, uh, PhD, he also replied when I posted this study, and he pointed out a chain of events that we need to think about when we're comparing seed oil with other oils. So, when you eat a lot of omega-6 fat, which is primarily linoleic acid, the dominant fatty acid in like the sunflower oil I was just talking about, soybean oil, corn oil, canola oil, most seed oils, it gets incorporated into your LDL particles. Your LDL particles, in other words, become composed of whatever fats that you eat. Now, linoleic acid, the acid, the fatty acid we find in seed oils, the polyunsaturated fat that means it has two double bonds, polyunsaturated. So two double bonds, those double bonds are more chemically vulnerable to oxidation. The more omega-6 your LDL carries, the more easily it oxidizes. And that oxidation mostly happens inside the arterial wall, inside what's called the subendothelium, and not in the bloodstream. So when we look at a study on seed oils and it's showing measurement of oxidized LDL, being lower, that's looking at a blood draw and not telling you much about what's happening at the site where atherosclerosis actually develops. Incidentally, that's why there's no studies I know of that show that antioxidants help for heart disease, because antioxidants aren't operating in the subendothelial space, right? They're operating in the bloodstream, and so they're not going to have an effect on oxidized LDL because they can't get at it. It's in— it's inside the, the subendothelium or inside the arterial wall. So, when omega-6 fatty acid-laden LDL oxidizes in your arterial wall, that's what generates a large quantity of what are called oxidation byproducts, things like lipid peroxides, what are called aldehydes, which can be harmful like 4-HNE and MDA, oxidized phospholipids, and then macrophages or what are called immune cells. Those would rush in to try to clean up those oxidized LDL particles, by engulfing them, and the macrophages get overwhelmed and they can't process the load fast enough. And that's when the macrophages become something you've probably heard of, foam cells, these bloated lipid-filled immune cells that can't leave the arterial wall and that are the building blocks of atherosclerotic plaque. So more foam cells means more plaque means a narrower artery means a higher risk of a cardiovascular event. So what this means is that the study that says that seed oils are better for you than, let's say, saturated fat, are looking at blood markers like lipid panels, inflammatory markers, fasting glucose, and those markers could look fine or even improve, but the actual plaque composition could get more dangerous. And that's, that's the core argument here. Seed oils would improve your cholesterol numbers on a lab report while simultaneously making the plaque inside your arteries more fragile and more likely to rupture. Now, I should note that the study that I just talked about had a relatively small population. Obviously, the study population was already severe enough to need surgery. So these were people with advanced disease, and there was only 162 of them. The supplementation period, right, of fish oil versus sunflower oil was only 42 days. But in my opinion, that makes the, the plaque composition changes even more striking. Then if you look at the systematic review that was the newer one that said that, that seed oils can improve things like lipid markers and glycemic control, They use canola, they use flaxseed, they use sesame oil. And technically, flaxseed is high in ALA, which is omega-3 fatty acid. Sesame oil is a unique lignan with antioxidant properties. So, lumping all seed oils together kind of obscures the fact that the real concern is specifically the seed oils high in linoleic acid. What are the seed oils high in linoleic acid that you may want to think twice about, especially if you're heating or frying with them? It would be sunflower oil, soybean oil, corn oil, safflower oil, cottonseed oil, and grapeseed oil. And those would be the ones that, because even though I would say all the studies on seed oils still produce a little bit of an incomplete picture, those would be the ones if you want to play things safe, you should actually avoid. Now, the last thing I should note is that if we look at big epidemiological studies No matter which way you slice things up, if you have high LDL, that can track pretty well with risk for heart disease. Okay, so there are some camps that say, oh, the higher the better LDL, you don't even have to pay attention to it at all. Well, uh, certain polyunsaturated fats do result in lower LDL, and lower LDL period makes less LDL available for oxidation. What I'm not making a case here for is letting your lipids get out of control, not caring about them, and only looking at what's going on with plaque in the subendothelial space. What I'm instead saying is pay attention to LDL and pay attention to ApoB and pay attention to Lp and make dietary modifications that based on you as an n 1 allows those numbers to improve. But if you want to play things safe, my advice to you is to avoid heated oxidized, like stored in plastic, long shelf time, or fried, sunflower oil, soybean oil, corn oil, safflower oil, cottonseed oil, and grapeseed oil. That would be the most important takeaway for me when it comes to what you should do in terms of all of this chatter about seed oils. So, no, I don't carry an "I'm allergic to seed oils" card to a restaurant. I often don't even ask at a restaurant because occasionally I'm fine just eating whatever's on the menu. But as a rule, I avoid those oils I just listed, and I will list them again in the show notes. At BenGreenfieldLife.com/501 if you just want a shortlist of the ones that you need to be most careful about. Let's move on. Done with that TED Talk. Cannabinol, cannabinol, CBN for acute treatment of insomnia. This was a new study that looked at CBN, cannabinol, not necessarily the stuff that gets you high. So, let's talk about this and how it relates to sleep. Cannabinol or CBN, it's a minor cannabinoid. It is a product of THC oxidation. So, when THC in cannabis is exposed to heat or light or oxygen over time, it degrades into CBN. Old weed basically. This is actually where the idea that aged cannabis, like skunky cannabis, has been sitting around for too long makes you sleepy. It's probably because it's higher in CBN. Well, How is CBN different than THC and CBD besides that? Well, THC is what's called an agonist, a strong agonist at the CB1 receptor. CB1 receptors are concentrated in your brain and your central nervous system, and that's why it gets you high. It alters cognition, it stimulates appetite, it has strong sedative properties at higher dosages, not as high as CBN, but that's how THC works. And then, we have CBD, also a really popular one. All right, that's the one that has very low binding affinity for CB1 receptors and CB2 receptors, two of the primary endocannabinoid receptors in your body. It does not really get you high unless you have a ton of it because just about any CBD that you get has trace amounts of THC. As a lot of people know, if you do enough CBD oil, you can get high off of it, but you're not getting high off the CBD, you're getting high off the trace amounts of THC that are in the CBD. And CBD acts as what's called an inverse agonist at CB1. It lowers THC psychoactivity, which is good to know. Like, if you smoke weed, If you take an edible, if you get high, if you didn't mean to get high, whatever, and then you take CBD, it does take some of the edge off because it does the opposite of what THC does at the CB1 receptor. And, it acts on a lot of other receptors, especially those related to lowering inflammation, which is why it's common in the health industry right now. And then, CBN, the one that we want to talk about right now, that sits in the middle. It kind of weakly agonizes CB1, like about 10% of what THC could do, but it's a strong agonist of what's called CB2, meaning that because of the low CB1 affinity, it has a weak effect on the central nervous system. It's non-psychoactive, but because it acts strongly on the CB2 receptors, it's mildly sedating and seems to help with sleep. And this new study is actually one of the better studies on CBN for sleep to date. They took 20 adults with doctor-diagnosed insomnia disorder and they got a 30-milligram dose of CBN or a 300-milligram dose of CBN or a placebo, meaning something without CBN at all. And what they found was that although the 30-milligram dose didn't do much at all, the 300-milligram dose increased non-REM stage 2 sleep, it improved subjective sleep quality, and it reduced sleep onset latency. Meaning how long it actually took to fall asleep. Now, there have been some previous studies that have suggested this to also be the case. Probably the strongest one study back in 2023, which I actually talked about a long time ago on the podcast, which found that a group that took CBN, in this case a lower dose like only 20 milligrams, actually had reduced nighttime awakenings and reduced overall sleep disturbances, meaning people just slept more soundly. On it, which obviously affects insomnia. CBD didn't do that, but CBN did. So, we've got everything from 20 milligrams getting some results up to 300 milligrams in this latest study seeming to get pretty good results. And some people compare this to the results that they get from diazepam anecdotally. Again, this is anecdotally, I'm not a doctor, don't take this as medical advice. I know some people who have used CBN to wean themselves off of Valium. Okay, again, not a doctor, uh, speak with your doctor before getting off any type of pharmaceutical. But it's interesting to know that something that would have less of a deleterious impact on sleep architecture and improve sleep quality, CBN, at doses as high as 300 milligrams, could be a safer and more reasonable alternative to taking a pharmaceutical like diazepam, AKA Valium. Now, where do you get CBN? There's one company, Element Health. I've had their guy on the podcast before, Adam Wengaur. He sells a THC gummy, right, which will get you high, but he puts CBN in and primarily markets it for sleep. I take it sometimes if I'm traveling. I don't like the feeling of being high as I'm falling asleep, and I'm not a fan of what THC can do long-term to the brain. I think it causes some mitochondrial free radical leakage in the brain, and I think it can impact memory long-term. And of course, I'm Very careful with that around teenagers. I have 18-year-old teenage sons. I don't want much THC around the house. There's one company that I found that does a maximum strength, just pure CBN. They're called Selah Organics, S-E-L-A-H Organics. They have an organic CBN derivative. I haven't personally used it. I actually ordered some after reading this research study to experiment with it a little bit. Remains to be seen for me personally, but CBN and trying that if you have sleep issues could be a good idea. And, by the way, I follow all normal sleep hygiene parameters, cold room, dark room, no hefty light usage in bed, using noise blockers, et cetera. But particularly when I travel, I'm just a light sleeper. In ancient times, I probably would have been the guy up protecting the village or whatever. So, that just is what it is. So, next, let's talk about muscle loss with GLP-1 drugs. Here's what you need to know based on the most recent study, which turned a lot of heads in the GLP-1 peptide realm. So, GLP-1 drugs like semaglutide, tirzepatide, retatrutide, et cetera, it's been suggested that those cause alarming lean body mass loss. Sometimes reports of up to 40% of total weight loss coming from lean body mass. So, social media and personal trainers and supplement companies would run with this as like, these drugs are eating your muscles, with the fear being that people were losing contractile skeletal muscle tissue at a dangerous rate. New study comes out that looks at weight loss with GLP medicines. This was in Cell Reports Medicine Journal. So here's what they found. The lean mass loss that shows up on what are called DEXA scans, right, which is kind of like considered to be one of the gold standards for measuring body fat percentage, it's mostly not skeletal muscle. It's mostly not skeletal muscle that people are losing on these GLP-1 drugs. It's predominantly liver mass, glycogen or storage carbohydrate, what's called intrahepatic fat and what's called intramuscular substrate, which are basically triglycerides that are stored inside your muscle tissue. So this is mouse data, right, which we're translating to human data. But basically what they're finding is that a lot of the lean body mass loss is not skeletal muscle loss, which we wouldn't want to happen, but the loss of some things that could actually be good. Now, DEXA scans, these dual— see if I can spit this out— they're called dual X-ray absorptiometry. I think that's the acronym. These DEXA scans, they can't distinguish between lean body mass or soft lean tissue and fat that resides within that lean tissue. So, if you're losing triglycerides from your muscle or you're losing glycogen or storage carbohydrate from your liver, a DEXA scan can't differentiate between that and muscle loss. So when you take a GLP-1 drug and it clears out fatty liver and it shrinks a bloated glycogen-loaded liver back to normal size and it pulls triglycerides out of muscle tissue, a DEXA reads all of that as you lost muscle, bro, right? Lean mass loss. And in people with obesity or people with, with, you know, non-alcoholic fatty liver disease, The liver can carry more than a kilogram, right? More than a couple pounds of excess glycogen and, and triglycerides and, and structural proteins that are above its lean baseline. And GLP-1 drugs can clear that out. Now, furthermore, this study looked at what actually happens to muscle function. They did see that absolute muscle mass and strength decreased, but relative muscle mass and strength improved. The mice got lighter,, but proportionally they got stronger. What's interesting is, is if we want to really get nerdy, the muscle proteome, which is the actual protein composition of the muscle, it also changed differently than simple calorie restriction caused, uh, meaning the drug wasn't just starving muscle tissue the way that a crash diet does. So when I say absolute versus relative, what I mean by that is let's say you weigh, uh, 250 pounds. And you've got 100 pounds of muscle, and then you go on a GLP-1 drug and you lose 50 pounds of mostly fat and liver glycogen. So now if you were at 250, you'd weigh 200 pounds, but you'd still have 95 pounds of muscle. So yeah, your absolute muscle mass went down, you lost 5 pounds of muscle, but your relative muscle mass went up because that muscle now represents 47.5% of your body weight versus 40% of your body weight, right? So 100 pounds of muscle at 250 pounds versus 95 pounds of muscle at 200 pounds, your relative muscle mass actually went up while your liver got healthier, you know, and you lost intrahepatic fat and some of the things that you'd actually want to get rid of. So that means also that the load your muscles have to move all day drops dramatically. So your joints and your heart and your postural muscles aren't lugging around an extra 50 pounds. And so your relative strength actually goes up, your functionality improves. And again, that's what they found with these mice. So the, so the bottom line here is the whole GLP-1s destroy muscle narrative was built on a measurement problem. Uh, DEXA can't tell the difference between your liver shrinking, which is good, glycogen going down, which is like neutral to good, intramuscular fat clearing, which is good, and actual contractile muscle protein disappearing, which would be bad. It turns out that most of what's being lost is visceral fat and organ fat. And for people who are obese, that means these drugs could be a pretty handy thing to have around. Now, people who do need to pay attention, again, because this isn't all just like rosy farts, is that older adults, people who are sarcopenic, who have lost muscle, people who aren't training, people who aren't eating enough protein, people who are prone to anorexia or eating disorders, these drugs need to be very, very carefully monitored and used in a very controlled fashion. For people like that. They got to eat enough protein, they got to lift weights. I'm telling you stuff that is all over the internet now. And if they're just doing it to look better in the mirror, they're probably prone to anorexia or some sort of other eating disorder or body dysmorphic disorder where they wind up with like the swollen cheeks and the starving poster kid image, uh, because they thought they were too fat when they really weren't. Now they're super skinny because they were on Ozempic. You know the type of people I'm talking about. Do I use the GLP-1 drug? I do. I take a baby dose of retatrutide. I stocked up on it back when you used to be able to get it. I've got bottles and bottles of retatrutide in my freezer. Somebody's going to come rob my house now because good versions of that stuff can be hard to get, good clean versions. But anyways, I take 0.25 milligrams on travel days when I'm getting on an airplane and I don't want to think about eating during a day of travel. Because my gut is more sensitive, food sucks more, I'm more sedentary. And to contextualize that for you, most of the studies on retatrutide are using 6 milligrams, 8 milligrams, 10 milligrams, or up to 12 milligrams, and I'm using 0.25 milligrams about twice a month. So yes, I use it, but very sparingly. All right. Well, that is everything I've got for you today. Hopefully, I didn't raise more questions than I answered. But if you like these solosos, if you'd like me to fill you in on this type of stuff, if you love it when I put on the propeller hat just feed you through the fire hose. Subscribe to the show, share with others, like it wherever you're listening to it, and visit the shownotes, which are always super helpful at BenGreenfieldLife.com/501. That's BenGreenfieldLife.com/501. And, thanks for tuning in. 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