Latest Seed Oil Controversy, Most Important Body Part?, CBN For Sleep & More! Solosode #501

Ben Greenfield: My name is Ben Greenfield, and on 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 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.

You might be familiar with my book, Boundless: Upgrade Your Brain, Optimize Your Body, and Defy Aging. It got a little out of control writing it. The original manuscript was over 1500 pages. I got it down to about 700 pages and released it about a year ago. The fully updated version of Boundless is kind of like the Bible of biohacking, a cookbook for everything you'd ever want: hormones, gut, digestion, and more. And I realize it's a little bit intimidating to pick up and read. So here's why I'm telling you all of this. If you would like the audiobook version of Boundless on Audible or elsewhere, to download and listen to at your convenience, in the gym, on your commute, on your hike, while you're cleaning your kitchen, in the bathtub, whenever you listen to an audiobook, and you want me to make that happen so you can have it in your ears wherever you go, go to BenGreenfieldLife.com/BoundlessAudio. Your opinion matters.

Welcome to today's show. Solo 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 of potassium, 30 of magnesium. The sparkling flavor is great, and I guess now they're getting free advertising on the show, so 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 two recovery days instead of lifting weights — I do a VASPER session. The VASPER is this fancy exercise machine that combines blood flow restriction, cold, 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 to lag or that tend not to 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. 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 a yoga flow.

I had this company — shout out to Western Soul — fly up from Boise and build a sauna on my property. The sauna is grounded. They use a thermally pressed aspen wood that's low-VOC, no chemicals treated in the process. It's a beautiful sauna, but man, oh man, it gets hot. The heater in it, when you turn it on, takes the steam from the water that you put on the rocks and 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 like 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, cool builds — shout out to the guys from Western Soul.

Anyways, 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 internet and in the research that I pour through every morning — mostly in exercise, sports science, health, fitness, biohacking, and longevity — to make your life better. So here we go.

New — brand new, hot off the presses — 2026 BMJ (British Medical Journal) study of over 100,000 people. 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, very few prior studies have specifically looked at how exercise variety impacts mortality.

So what they did was use health and lifestyle data for more than 111,000 adult men and women, followed them over the course of more than 30 years, and looked at 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 work like yoga, and also passive or 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, they then scored each participant according to activity variety and intensity levels, and examined those scores looking primarily at risk of premature death and some other chronic diseases. What they found was that, intensity 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 exercise.

Now, the takeaway here, I think, is pretty obvious. To illustrate this for you: I used to do triathlon, right? I used to swim, bike, and run all the time. Those were my three 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. 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, cycling, and running was also low. I got in the best shape of my life doing Spartan racing, because I probably went from three exercise varieties — maybe four if you include core and weightlifting — to like 20 exercise varieties.

Today, I walk, I play pickleball, I play tennis, I play disc 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 — 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 and new skills — going 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 and repeat, and also vary 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. Tommy kind of debunked the myth that our brains get old and dumb as we age. More typically, as we age, we get comfortable, we get set in our ways, we become 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 simple 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 and predictably — one smarter cookie the whole time you're doing it. 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, the better. So now you have no excuse not to 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 a pretty cool study: a 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. You can tell people, "I am shod."

So what they looked at was three different groups of healthy adults: a group that did barefoot training, a group that did shod training, and a control group that basically didn't train. Both the barefoot and the shod groups 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 greatest increase in toe flexor strength, even though the people wearing shoes also saw an increase. Arguably, if you're wearing shoes with a narrow toe box — which most shoes are made to have, unless you're wearing, say, Vivobarefoot 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, 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 five-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, jogging, or sprinting, and for better weight-bearing balance, which trickles up to your knee health, your hip health, your low back health, your shoulder health, and 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 — 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 the most common reason for lower-limb injuries in younger populations, like athletes.

So the technical, scientific name for the muscle associated with the big toe is the flexor hallucis longus. The flexor hallucis longus — that's a muscle that kind of feeds into the big toe and is 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, jogging, or running. You lose the ability to recover from what are called perturbations — stumbling and then catching yourself, or 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 FHL 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 their regular training barefoot or in minimalist or five-toe shoes.

So if you're an athlete or someone who trains hard, this means that good big toe muscles translate directly to sprint push-off, single-leg stability, deceleration, and the dynamic balance you want on the tennis court, the pickleball court, or the basketball court. As I mentioned, one way to do this is just to do the training you normally do, but barefoot — if your gym will let you get away with it, or if you're lucky enough to have a home gym — or in minimalist shoes or five-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 simple. Pick up a marble, put it in whatever little plastic cup is next to you, pick up another marble or stone — and you're doing this with your 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 on to that strap, and then you press your big toe into the ground as hard as you can for anywhere from three to five seconds. You do that several times per side for each big toe. You probably only have two of them if you're a normal person, so this shouldn't take too long.

Another example — this one's great. I talked with, I think, Belinda Melissa Vranic about this. She was a podcast guest, and I'll put the link in the show notes at BenGreenfieldLife.com/501. She talked about how when you're standing waiting for the airplane to board, waiting at the doctor's office, standing at the grocery store — just simply grip the ground through your shoes, or if you're using minimalist shoes, grip the ground with your toes. Hold with all the toes, and then release. Hold with all the toes, and then release. It's called foot doming. 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's 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 stairs in your house, is eccentric toe flexion. 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, but for the toes. Your toes are hanging off the edge, you're lowering them into extension, and then curling them back up — specifically, eccentric toe flexion. 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. You're repeatedly curling and extending your toes. Then reach down with your hands, pull the towel back out flat, and scrunch it up again. 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 anyway, I do them barefoot or wearing my Peluva shoes. Since I'm barefoot or wearing Peluvas like 80% of the time, I get a lot of big toe strengthening just naturally. And I should note that a lot of the activities I do in the gym I try to do occasionally standing on one leg. Just try this right now — if you're not driving, I guess — stand on one leg. You'll immediately feel that to maintain your balance, your big toe has to contract. Now imagine doing dumbbell curls, overhead dumbbell presses, side-to-side rotations, or anything else in that single-leg standing position. 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.

All right, 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, and on blood sugar control. 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, off, or imbalanced. Long story short, 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 allowing for better glycemic control while potentially modulating or controlling oxidative stress markers.

Now, if you're deep in the health podcasting or health sciences realm, you've probably heard many people say, "Avoid seed oils like the plague." I've been more adamant lately about specifically avoiding fried and excessively heated seed oils, more than just avoiding seed oils in general. Like, I eat from the Whole Foods salad bar, which uses a cold expeller-pressed canola oil. I don't eat any of the fried foods from the hot salad bar section. I'm more concerned about seed oils that have been heated — or foods that have been fried in seed oils — than I am about cold-use seed oils across the board.

When I tweeted about this study and said, "Hey, look, I think more of the damaging effects of seed oils come from when they're fried or heated, 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, a good effect on glycemic control, and a good effect on inflammation" — a few intelligent people on the exosphere came back to me with a little bit of data that made me think more deeply about this.

For example, one person — I think this was James DiNicolantonio; he was one of the doctors who replied to me; actually it may have been someone else, I don't have the thread in front of me — sent over a table that was published in The Lancet. This was a randomized controlled trial of 188 patients who were randomized to take fish oil (rich in omega-3 fatty acids), sunflower oil (a traditional polyunsaturated seed oil richer in omega-6 fatty acids), or a control oil (a blend of palm oil and soybean oil). Then they did surgery on these people — specifically, surgical removal of plaque from their carotid artery. So obviously a pretty intensive study. 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 a blood draw. There's a difference between the cholesterol you find in the blood and looking at the actual plaque to see what's manifested in terms of, say, fatty streaks or issues that would contribute to atherosclerosis.

What they found: the fibrous plaque with a thick protective cap over the lipid core — the type of plaque you'd actually want, because it indicates that the plaque is more stable and prevents rupture — was present in 66% of the fish oil group and 53% of the sunflower oil group. That means when you actually look at the plaque of people whose LDL is more comprised of fat from seed oils, you see a 13% decreased protection from the thick caps that stabilize plaque.

When we look at thin fibrous plaque — the kind that is more likely to rupture — the fish oil group had 15% of the thin fibrous caps (the bad ones). A thin cap over a lipid core is like a bomb waiting to go off. The sunflower oil group had 29% — nearly double the rate of those bad thin caps compared to fish oil. That's another blow against seed oils.

When we look at plaque rupture — the actual rupture of the plaque, which is what you really don't want to happen — the fish oil group had 3.8% and the sunflower oil group had 5.6%. And then finally, when we look at what's called fibrocalcific plaque: the fish oil group had 5.7% and the sunflower oil group had 1.9%. That's important because fibrocalcific plaque is the more stable form of plaque — it's hardened, it's unlikely to rupture — and the sunflower oil group had the least of that stable plaque type.

So, long story short: in people who have higher seed oil consumption, we see fewer thick protective caps, more thin vulnerable caps, more rupture, and less stable calcification.

Now, James DiNicolantonio, a cardiovascular research scientist and PhD, also replied when I posted this study. He pointed out a chain of events we need to think about when comparing seed oil with other oils. When you eat a lot of omega-6 fat — which is primarily linoleic acid, the dominant fatty acid in sunflower oil, soybean oil, corn oil, canola oil, and most seed oils — it gets incorporated into your LDL particles. Your LDL particles, in other words, become composed of whatever fats you eat. Now, linoleic acid is a polyunsaturated fat, meaning it has 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, not in the bloodstream.

So when we look at a study on seed oils showing that oxidized LDL is lower in blood draws, that's not telling you much about what's happening at the site where atherosclerosis actually develops. Incidentally, that's why there are no studies I know of that show antioxidants help with heart disease — because antioxidants operate in the bloodstream, not in the subendothelial space, so they're not going to have an effect on the oxidized LDL that's inside the arterial wall.

So when omega-6-laden LDL oxidizes in your arterial wall, it generates a large quantity of what are called oxidation byproducts — things like lipid peroxides and what are called aldehydes, which can be harmful, like 4-HNE and MDA, and oxidized phospholipids. Then macrophages — immune cells — rush in to try to clean up those oxidized LDL particles by engulfing them. The macrophages get overwhelmed and can't process the load fast enough, and that's when they become something you've probably heard of: foam cells. These are bloated, lipid-filled immune cells that can't leave the arterial wall and are the building blocks of atherosclerotic plaque. 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 studies saying seed oils are better for you than, say, saturated fat are looking at blood markers like lipid panels, inflammatory markers, and fasting glucose — and those markers could look fine or even improve, while the actual plaque composition gets more dangerous. That's the core argument here: seed oils can 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 I just talked about had a relatively small population. The study subjects were already severe enough to need surgery, so these were people with advanced disease, and there were only 162 of them. The supplementation period — fish oil versus sunflower oil — was only 42 days. But in my opinion that makes the plaque composition changes even more striking.

Then, if you look at the systematic review (the newer one that said seed oils can improve things like lipid markers and glycemic control), it used canola, flaxseed, and sesame oil. Technically, flaxseed is high in ALA, which is an omega-3 fatty acid. Sesame oil has unique lignans with antioxidant properties. So lumping all seed oils together 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? Sunflower oil, soybean oil, corn oil, safflower oil, cottonseed oil, and grape seed oil. And those would be the ones — even though all the studies on seed oils still produce a somewhat incomplete picture — that, if you want to play it 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 tracks pretty well with risk for heart disease. Some camps say, "Oh, the higher the LDL the better, don't pay attention to it at all." Well, certain polyunsaturated fats do result in lower LDL, and lower LDL means less LDL available for oxidation. I'm not making a case here for letting your lipids get out of control and only looking at what's going on with plaque in the subendothelial space. What I'm saying is: pay attention to LDL, pay attention to ApoB, pay attention to Lp(a), and make dietary modifications that, based on you as an N=1, allow those numbers to improve.

But if you want to play things safe, my advice 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 grape seed oil. That would be my most important takeaway when it comes to all 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, because I'm generally fine eating whatever's on the menu.

But as a rule, I avoid the oils I just listed, and I will list them again in the show notes at BenGreenfieldLife.com/501 if you just want a short reference.

Let's move on. Done with that TED talk.

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. Let's talk about this and how it relates to sleep.

Cannabinol, or CBN, is a minor cannabinoid. It is a product of THC oxidation. So when THC in cannabis is exposed to heat, light, or oxygen over time, it degrades into CBN — old weed, basically. This is actually where the idea that aged, skunky cannabis that's been sitting around too long makes you sleepy probably comes from. It's probably because it's higher in CBN.

How is CBN different from THC and CBD? Well, THC is what's called a strong agonist at the CB1 receptor. CB1 receptors are concentrated in your brain and central nervous system, and that's why it gets you high — it alters cognition, stimulates appetite, and has strong sedative properties at higher doses. That's how THC works.

Then we have CBD, also a really popular one. That's the one that has very low binding affinity for CB1 and CB2 receptors — 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 you get has trace amounts of THC, a lot of people know that if you do enough CBD oil, you can get high off it — but you're getting high off the trace amounts of THC, not the CBD itself. And CBD acts as what's called an inverse agonist at CB1. It lowers THC psychoactivity, which is good to know. Like, if you take an edible, if you get high and you didn't mean to, 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. It also 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 we want to talk about right now — 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 CB2. Because of its low CB1 affinity, it has a weak effect on the central nervous system and is non-psychoactive. But because it acts strongly on the CB2 receptors, it's mildly sedating and seems to help with sleep.

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 received either a 30-milligram dose of CBN, a 300-milligram dose of CBN, or a placebo. 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, improved subjective sleep quality, and reduced sleep onset latency — meaning how long it actually took to fall asleep.

There have been some previous studies that have suggested this as well. Probably the strongest one was a study back in 2023, which I talked about on the podcast a while back, which found that a group that took CBN — in that 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. 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 getting pretty good results. And some people compare this to the results they get from diazepam. Anecdotally — again, this is anecdotal, not a doctor, don't take this as medical advice — I know some people who have used CBN to wean themselves off Valium. Again, not a doctor; speak with your doctor before stopping any pharmaceutical. But it's interesting to know that something with less of a deleterious impact on sleep architecture, and that actually improves sleep quality — CBN at doses as high as 300 milligrams — could be a safer and more reasonable alternative to a pharmaceutical like diazepam (a.k.a. Valium).

Now, where do you get CBN? There's one company, Elément Health. I've had their guy on the podcast before — Adam Wengower. He sells a THC gummy which will get you high, but he puts CBN in it and primarily markets it for sleep. I take it sometimes when 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 twin sons. I don't want much THC around the house.

There's one company I found that does like 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 yet. I actually ordered some after reading this research study, to experiment with. Remains to be seen for me personally. But CBN — 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 heavy light usage in bed, using noise blockers, etc. 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 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: GLP-1 drugs like semaglutide, tirzepatide, retatrutide, et cetera — it's been suggested that these cause alarming lean body mass loss, with some reports of up to 40% of total weight loss coming from lean body mass. Social media, personal trainers, and supplement companies ran with this: "These drugs are eating your muscles," with the fear being that people were losing contractile skeletal muscle tissue at a dangerous rate.

A new study in Cell Reports Medicine changes the picture. Here's what they found: the lean mass loss that shows up on DEXA scans — which is considered one of the gold standards for measuring body fat percentage — is mostly not skeletal muscle. It's predominantly liver mass, glycogen (storage carbohydrate), what's called intrahepatic fat, and what's called intramuscular substrate, which are basically triglycerides stored inside your muscle tissue. This is mouse data that we're translating to human context, 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 — but loss of some things that could actually be good.

Now, DEXA scans — dual-energy X-ray absorptiometry, I think that's the acronym — 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 losing glycogen from your liver, a DEXA scan can't differentiate that from muscle loss.

So when you take a GLP-1 drug and it clears out fatty liver and 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" — lean mass loss. And in people with obesity or non-alcoholic fatty liver disease, the liver can carry more than a kilogram — more than a couple of pounds — of excess glycogen, triglycerides, and structural proteins above its lean baseline. GLP-1 drugs can clear that out.

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 — if we really want to get nerdy — is that the muscle proteome, the actual protein composition of the muscle, also changed differently than simple calorie restriction, meaning the drug wasn't just starving muscle tissue the way a crash diet does.

So when I say absolute versus relative: let's say you weigh 250 pounds and you've got 100 pounds of muscle. Then you go on a GLP drug and you lose 50 pounds — mostly fat and liver glycogen — so now you weigh 200 pounds, but you still have 95 pounds of muscle. Yeah, your absolute muscle mass went down — you lost five pounds of muscle — but your relative muscle mass went up, because that muscle now represents 47.5% of your body weight versus 40% before. 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 lost intrahepatic fat, and you got rid of some of the things you'd actually want to be rid of. That also means the load your muscles have to move all day drops dramatically — your joints, your heart, and your postural muscles aren't lugging around an extra 50 pounds. So your relative strength actually goes up, your functionality improves, and again, that's what they found with these mice.

So the bottom line: the whole "GLP-1s destroy muscle" narrative was built on a measurement problem. DEXA can't tell the difference between your liver shrinking (which is good), glycogen going down (which is 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. For people who are obese, these drugs could be a pretty handy thing to have around.

Now, people who do need to pay attention — because this isn't all just rosy: older adults, people who are sarcopenic, people who aren't training, people who aren't eating enough protein, and people who are prone to anorexia or eating disorders. These drugs need to be used very carefully and in a very controlled fashion for those populations. They've got to eat enough protein, they've got to lift weights. I'm telling you stuff that's all over the internet now. And if someone is just doing it to look better in the mirror but is already prone to anorexia, some sort of eating disorder, or body dysmorphic disorder, they can wind up with that hollow-cheeked, starving-poster-child look — because they thought they were too fat when they really weren't, and now they're super skinny because they were on Ozempic. You know the type of people I'm talking about.

Do I use a 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, clean versions of that stuff can be hard to get. But anyways, I take 0.25 milligrams on travel days when I'm getting on an airplane. I don't want to think about eating during a day of travel, because my gut is more sensitive, food sucks more, and I'm more sedentary. To contextualize that: 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 solosodes, 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 and just feed you through the fire hose — subscribe to the show, share with others, like it wherever you're listening, and visit the show notes, which are always super helpful, at BenGreenfieldLife.com/501. Thanks for tuning in.

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