Health Hacks Big Pharma Doesn’t Want You To Know - Biohacking Roundtable

People of the UK and Ireland, if you are coming to see me on tour this October, I want to hear from you. Tell me what problems you're dealing with, your worst first date, and any questions you've got for me — I'll be bringing some of you up on stage to talk about it. Go to chriswilliamson.live/stories to submit your stories, and I might see you with a mic in front of your face very soon.

Everyone, tell me what peptide you're on. That's all I care about.

Woohoo. Let's go. Which day of the week?

Which time of day? I view peptides more as a condiment in your refrigerator that you use for a specific reason, rather than following an exact protocol every day. For example, when I travel, I use thymosin and alpha-1 — which I'm on right now, as you can tell — for the immune system. I keep BPC-157 and TB-500 around for injuries. A couple of times a year I run a tesamorelin–ipamorelin cycle with CJC-1295 for growth hormone. Those are the biggies. Oh, and Dihexa and Semax intranasal. Dihexa is more of a cognition, brain-drive neurotrophic factor booster, and Semax is more of an anxiolytic — so kind of an upper or a downer.

It's like my version of Valium and caffeine. What he said.

I agree with that protocol, and I tell everyone: the answer is not at the bottom of a peptide bottle. It's diet, lifestyle, nutrition — living by the principles first. These are additives that can help optimize your health, especially given how stripped our food sources are of nutrients. The only compound I take that you didn't discuss is IGF-LR3 — insulin growth factor LR3. A lot of people have historically taken growth hormone, but the reason was to get the therapeutic benefits that growth hormone provides when it converts to IGF. If you use the IGF peptide directly, you get all the benefits of growth hormone with a much better safety profile, and it won't impact your natural growth hormone levels. That's why I'm a huge fan.

Does it have similar issues to pure HGH? You get almost a glucocorticoid response — a surge in cortisol, higher resting glucose, a lot of people don't sleep as well because of the downstream pathway. Do you skip a lot of that?

You do skip a lot of that, but bigger than that, you're not impacting your natural growth levels. I'm in my 40s — 46 — so I want to be cognizant of that. I'll go on for four to six weeks, and when I come off I'll cycle onto CJC and some of the other things you discussed, just to boost my natural growth hormone levels.

I have the simplest protocol here. I microdose GLP-1 once in a while for inflammation. I think there's going to be new emerging research. I was actually at the Protein Working Group Summit 3.0 — the Oscars for nerds and protein scientists. Invitation only, a hundred of the finest scientists doing protein research. There were topics like the challenges we face, but more importantly, I sat with Arne Astrup, who discovered GLP-1's impact on appetite. He was essentially responsible for what we now have as this obesity — now not called obesity, the sarcopenic epidemic — GLP-1 use. And again, I'm totally for GLP-1s.

You're microdosing it for inflammation?

Yes, and there's going to be new emerging research that it will have an impact on cancer, they believe.

We don't totally know. He believes it's through inflammation — and this was the guy who discovered GLP-1's effect on appetite.

How do you know it's not just a reduction in the turnover of food?

Right — we don't. So all of this could just be eating less cancer-causing food?

Could be, but that remains to be seen. The second leading cause of cancer is obesity. If you were able to address aging and obesity, you're naturally going to reduce the risk of cancer.

There's definitely going to be a correlation to the weight loss. Obesity is one of the biggest risk factors for cancer.

Inflammation and smoking — inflammation independent of obesity as well. How many bros do you know who are relatively lean but turning over tons of sugar? They're just training it out of them, or they're still young and their metabolism is still kicking.

Right. That's one of the possible benefits of intermittent fasting — autophagy, and giving that reactive oxygen species production a break. Yes. I have microdosed GLP-1s before on flight days. There's something about it that just quiets food noise. You don't really have access to great food anyways, and I don't want to be distracted by food or think about it.

I'm sedentary for most of the day anyway, so even if I could eat, it's probably not the best scenario for me to be eating. When I say microdose, I'm talking about 0.25 — and to contextualize that, a normal dose would be what, 8, 10, 12 milligrams, something like 100 units?

It's crazy, because what you're saying matches what we've seen anecdotally. We're at over 70,000 patients now in the patient population as a whole at Waste to Well, and a lot of patients are now doing microdosed GLP-1s. They say they see a big difference in their inflammation, and I think that's what we're going to find more and more. The bigger point we have to make is that these medications are here to stay — there's never been anything nearly as revolutionary. And in the 90s, we had the food guide pyramid, and then all of a sudden obesity hit.

We are at the precipice of trading obesity for sarcopenia. We're going from people who are too big to people who are too frail — a decrease in muscle mass and strength. And we've seen it, right? Your parents all of a sudden get frail, your grandparents get frail. If we're not careful, we're going to miss the early warning signs, which I think we're already seeing with people out in Hollywood — we're just seeing a transformation. I read your book, and you talked about how we're under-muscled. It's not just that we're obese; we are also under-muscled.

If we can maintain lean muscle mass and bone mineral density as we age, it is one of the leading indicators of health span and longevity.

Asked which biohacks or interventions they believe in without any supporting data, the guests shared their personal favorites.

The BioCharger

One guest kicked things off with "bro science": the BioCharger. He explained that he once saved a patient's life, and she told him to pick any piece of equipment he wanted. She kept raving about the BioCharger, saying her sex drive was up and it was the best thing ever. Since he already had a sauna and a cold plunge, he decided to try it too.

The device works via radio frequencies based on a Tesla coil surrounded by 12 noble gases in tubes — and there is zero clinical data for it. Another guest borrowed one from Tony Robbins, who reportedly keeps one in every room of his house, and used it semi-consistently for about a month. He noticed no difference, though he noted that putting a phone near it makes the phone glitch out.

The Raisin Bran Remedy

A simpler recommendation: the raisin bran recipe. If you're constipated — say, from traveling — sitting in front of a bowl of raisin bran for 12 minutes produces immediate results.

Tehart Therapy

Another guest described being lent a "Windback" machine using something called Tehart therapy. It's not quite EMS, but involves high radio frequency muscle stimulation through patches, with a controller. He had been using it for his hamstring and it seemed to promote tissue healing. He hadn't seen good US data on it, but felt that feeling better means it has to work somehow — and it's not a stim device. He admitted he didn't know exactly what frequency it operates on.

The Roxiva Lamp

The final recommendation was the Roxiva lamp: a sound lounge that vibrates like a vibroacoustic bed you lie on, paired with a lamp connected to headphones. It offers around 100 different sessions ranging from 5 to 60 minutes — described as psychedelic "blast off to the moon" experiences like a full-on mushroom or LSD trip, depending on what you choose — with zero biological payback, meaning no need to swallow a substance or put anything under your tongue. You just lie there, put on the headphones, flip it on, close your eyes, and it whisks you off to another state.

The proposed neural benefit is based on what's called light-sound entrainment: shifting you into different brain waves using the light and sound.

There's a session on there, like a Shiftwave, but imagine if the Shiftwave didn't just have sound—it vibrates. Not just vibrates; it shakes the roof with nodes. I've got one at the house. The cool part is that it guides you through breathwork sessions, specifically the breath holds. You can go about 25% longer just based on the distraction of the vibrating chair, and you're wearing a fingertip monitor for HRV, and your HRV climbs through the roof while you're doing it. Imagine that plus flickering light designed to whisk you off into a completely different state.

There's a session called Rebirth where they actually recorded whooshing sounds in a mother's womb and the fetal heartbeat. You put on the headphones, close your eyes, lay under this thing, and it feels like you're being primally whisked back into a fetal state. You lay there for 45 minutes, sometimes falling asleep, in and out of consciousness. Then in the last 5 minutes you get "birthed": the music crescendos, everything starts beating, the lights get brighter, your heart rate speeds up, and you get this dump of adrenaline—then everything goes dark. You sit up and feel like you could go conquer the world at 2 p.m. in the afternoon.

Wow, that's cool. Does it work if you use—

I've used the Shiftwave. The Shiftwave is not as comprehensive as that. There was an interesting thing around the sounds from the mother's womb: I had Stephen Porges on—the polyvagal theory guy. He came up with the Safe and Sound Protocol (SSP). Are you familiar with that? It's a mode of nervous system re-entrainment, a combination of meditation with a facilitator—somewhere between mantra meditation, psychotherapy, soundwave work, and breathwork. One thing he taught me, which is fascinating: the soft, gentle, reassuring sounds that mothers give their kids are the same frequency at which the Safe and Sound Protocol works.

You mean the same sound frequency, like the tone?

Yes. It's the same for dogs and the same for horses, and that's the reason equine therapy works and that humans and horses, and humans and dogs, are able to connect as well—because the sound frequency that mothers and kids have in all of those species falls within the same band. Isn't that cool?

What if your mom has a really low voice?

She's probably jacked. Doesn't matter at all. What else have I been using that's been interesting? Hyperbaric oxygen therapy. I know it's not super experimental—

Not sexy at all.

But that hard shell at about 2.2 ATA is so good. I don't know what's happening to make me feel the way I do after coming out of a hyperbaric session, but it's 20 minutes on, 5 minutes off, 100% oxygen on the mask, normal oxygen outside of that, in a 90-minute session down at depth 2.2—

Better than any coffee, better than any cold plunge, better than anything.

There's a little bit of parasympathetic activation too, just from the whole sensory depth nature of it. I did one at Big Bams yesterday and my tongue was lolling out of the corner of my mouth. But it's just a standard hyperbaric chamber that they've been using in operators forever.

Yeah, Michael Jackson was using one back in the '90s. Have you guys used the hydrogen bath stuff?

Yeah, I used one in my garage. I haven't looked up whether there's evidence—I just have one.

It's transdermal absorption of hydrogen, with inhalation studies behind it. I just use it, and I like getting hundreds of times more hydrogen than a pill.

Hydrogen Baths, Inhalation, and Selective Antioxidants

The hydrogen bath is relaxing because it's a hot tub with hydrogen in it. Ideally you'd run a placebo-controlled trial where you're actually in the hot tub and nobody tells you whether hydrogen was added. The idea is that there's some transdermal absorption of hydrogen in a hydrogen-rich environment—either the air or the water—that's greater than what you'd get from a pill dropped in water. Since hydrogen is a selective antioxidant, for inflammation and soreness you do feel pretty good afterwards. I record books for my podcast, and my bookshelf of books to read is in the garage—that's where my wife helped me put the bathtub, a hydrogen bath with red light. I lay out there and read books.

"How long do you stay in?" About 40 minutes.

Chris uses one almost every day now, though the hydrogen bath he used previously—only at Lumati in San Diego, where he got his hydrogen concentrator—he used really intermittently.

Inhalation machines

Alex Tonava's inhalation machine is the only hydrogen inhalation machine that can reach that high a percentage without using a nasal cannula, so you get a pretty high concentration without risk of explosion. You don't want to mess around with hydrogen. Alex has been working on it for a decade, and it's not even clear whether it's for sale. What pushed things over the edge is Tyler LeBaron, a very trustworthy figure in the hydrogen research sector who founded what I think is called the Hydrogen Research Foundation. He put his name behind it because he was so impressed compared to other machines, many coming out of Asia, that have low concentration, no adjustable percentage, or use a nasal cannula instead of a mask. When I asked him about it, he said, "Thumbs up. This is the best one on the market."

Comparing delivery methods

With hydrogen tablets, infusion flasks, inhalation, and now baths all available: I've used a test kit on the bottle and the tablet. The bottle produces a higher concentration—about 8 to 10 ppm—but the bottles poop out after around 300 uses, so you'll be buying one frequently. The pills are slightly lower. There's not a lot of research on transdermal absorption. Inhalation is the highest concentration you can infuse into your body, as far as what's actually been measured for hydrogen concentration.

Mechanism: selective antioxidants

The proposed benefit of breathing hydrogen is that it's an antioxidant, so it would quell inflammation. Because it's a selective antioxidant, it can accept or donate electrons—unlike, say, high-dose synthetic vitamin C or vitamin E, or an NSAID. That means it wouldn't quell the hormetic response to exercise. After a hard exercise session, you're not supposed to take high-dose antioxidants.

On cold plunges: you have to drop muscle temperature by about 1°C, which takes at least 10 minutes at a pretty cold temperature. A quick cold plunge or cold shower after a workout isn't the thing that's been overblown—the concern is overblown because I don't know many people who have time to sit in a cold plunge for 10 to 20 minutes after a workout, which is where the research showing you blunt the anabolic response actually comes from. So if you're going to do a long cold plunge, wait a few hours; a 10-minute plunge is fine.

So hydrogen and methylene blue are two examples of selective antioxidants that can accept or donate an electron, making them acceptable for post-exercise inflammation without blunting the anabolic response.

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What about muscle temperature being a mediating factor? I saw that Brian had swallowed a pill thermometer and was looking at the temperature you need to reach for heat shock proteins in the sauna. He'd been doing maybe 20 or 25 minutes at 200 degrees, but he actually needed 30 minutes at 200 to get there. What was your read on that data?

He did. He's also very lean, right? That's going to be a factor—he probably needs higher temperatures to be efficient with heat.

Exactly, efficient with heat, less insulation. I think it also depends on your activity level in the sauna. I move a lot in the sauna—push-ups, squats, hot yoga, all the things one does in a sauna—so if you're moving around a lot, you can get pretty hot. But he does make a good...

He makes a good point, though: if you want the actual heat shock protein benefit of a sauna—the main mechanism that kicks in at higher temperatures, not just the detox from sweating—you need a hotter temperature than most people are probably using. There's a paradox here: sauna decreases the risk of dementia and Alzheimer's, but when your cranium gets hot—above about 200 degrees without a sauna hat—you actually increase that risk. So you probably need to go hotter than you're going, or move more in the sauna, or both—and invest in a wool cap to do so.

That's the protection. Interesting.

How important are ice balls?

I bought my sons—I forget the brand—the ice nut. I have 18-year-old sons and I want grandkids, so we do something.

That is the thing: if you're trying to reproduce, hot temperatures can decrease fertility.

The crazy thing is, when I went to freeze my sperm and asked what I needed to avoid, one thing the guy came back with was that there are so many guys who go away for a bachelor party and just hang out in a jacuzzi with their friends for ages. He said that will do far more damage to your sperm count than a ton of saunas, because you've got direct heat from the water absolutely infusing your testicles—

—and chlorine, parabens, phthalates and everything else getting through.

Do we really need the heat shock proteins, or can you get a lot of the benefits without getting into that?

You can. A couple of months ago, a study compared sauna versus weight training, and the weight training protocol produced heat shock protein elevation similar to what people get from a sauna session—I don't remember the time or temperature used. Exercising in the heat in general would be one way. Paradoxically, cold plunging can also increase heat shock protein, because it's a thermoregulatory mechanism. So there are other ways to stress the body—kind of like fasting triggers autophagy—that activate a similar pathway. It doesn't just have to be sauna.

I've been loving resonance breathing lamps. There's one called M. Health with an FDA-registered heart rate sensor built into the top — imagine a big glass lamp with a stone on top containing a 100 hertz sensor. You just hold the stone, and since the lamp connects to your Wi-Fi and runs the algorithm, it detects your HRV while you breathe. The stone vibrates, so you breathe up and down with it, which maximizes your resonance — that respiratory sinus arrhythmia. It even makes an ocean sound. I got targeted on Instagram for it two weeks ago.

Funny story: Jay Wilds, the HRV expert who developed that lamp, was my podcast sidekick for about four years back when I didn't want to do a podcast without a co-host. He was the witty banter guy and he's super smart — whenever anyone asked a question about HRV, Jay would jump in. Then he developed this lamp, and it really is cool.

The best thing about it is you can use it while watching TV. If you're lying in bed or on the couch with the lamp nearby, you can crank out 45-minute resonance breathwork sessions without even thinking about it, because you don't need the light cue — just the vibration, which doesn't interrupt anything. If you keep it next to your bed and can't sleep at night, you can roll over and grab it without disturbing whoever you're in bed with.

So is it the vibration or the breath that makes the difference? The idea behind resonance breathing is fascinating: nearly every human being on the planet achieves peak HRV at a breath rate of about five and a half seconds in and five and a half seconds out. That's where you see really good vagal tone. The lamp is essentially an entrainment tool that uses visual or vibratory cues — via the stone — to make you breathe at that rate.

There's a book called Coherence, one of the first I ever read on resonance breathing. In the later pages there's a link or QR code to a downloadable MP3 called "the clock and bell" — literally tick tock, tick tock, ding. I played it while working or checking email, anything normally stressful. It prevents email apnea because you know you're resonance breathing, and it trains you to breathe that way subconsciously. It's a far more stripped-down solution than what Jay developed, but the lamp is super cool.

The real goal is trait rather than state — that's what everybody is trying to get to. You want the practice to carry beyond the end of your session. One interesting thing I discussed with Jay: below 10 minutes, you only get a state change. Between 10 and 20 minutes, you start moving into trait changes as well. You only need maybe three or four sessions a week — an hour a week or so — and it's so easy. That's on my list.

It doesn't do fetal heartbeat and woo-whooshing sounds, though — which is a shame. They've got to build that.

Asked about other interventions or supplements he's been experimenting with, the speaker points to MUSE stem cells as the other big one he's seen results from, noting Ben has experienced them too.

A scientist named Mari Dawa out of Japan discovered a subset phenotype of stem cell called MUSE. It's fascinating because everything researchers outside the United States have been doing—stressing stem cells to get them to adapt and change—has been an effort to create a cell with a phenotype optimal for healing, recovery, and treating an array of chronic diseases, but that would not become tumoric. One challenge with a cell that can differentiate, meaning it can become anything, is that it could in theory become a cancer cell, or take on a cancer phenotype after contact with a cancer cell and worsen it—especially once you put trillions of these cells in the body.

Dawa, one of the leading scientists in stem cell research, discovered this cell in 2014. MUSE stands for multi-lineage stress-enduring. Traditional stem cells must be cryofrozen at −80°C or colder, and the moment you thaw them they begin to die, so they have to get into the body quickly. MUSE cells can stay alive for days at room temperature. Less than 2% of stem cells are MUSE, but they're the super soldiers.

The research is now coming together. Dominic Deutscher, a German scientist and former Stanford professor, couldn't understand why diabetic patients weren't responding in certain ways like other patients. He realized that even though they had stem cells, they were missing this tagged subset cell—which turned out to be MUSE.

In layman's terms, a MUSE cell can become anything—like a kindergartener who could grow up to be a scientist, doctor, or attorney because they haven't set their identity yet. In America, most people who say stem cells don't work are getting bone marrow aspirate or cells from fat tissue, and the problem is that those cells have already developed a phenotype. The fraction of MUSE cells in such harvests is very large, so a lot gets stuck. If patients are diabetic or elderly, they have no MUSE cells at all—just traditional MSCs.

What makes these cells special:

• They will take on any phenotype.
• They can pierce the blood-brain barrier; traditional MSCs mostly get caught in the lungs.
• Traditional MSCs have a 3% engraftment rate; MUSE cells have a 30% engraftment rate.
• Traditional stem cells take multiple days to engraft; MUSE cells engraft within 48 hours.
• They have high histocompatibility with almost no immune system response—they're immunomodulators.

Asked whether this was what Matt Cook had him atomized with, the answer is that it was probably MUSE-derived exosomes—you can nebulize them now. You can place them on a fulcrum plate intranasally, and they will pierce the blood-brain barrier. This was demonstrated on stroke victims in Japan, whose brains lit up like a Christmas tree with the tagged cells. Through phagocytosis, they consume the damaged cell and take on the personality of that cell: if you have a damaged neuron, they become a baby neuron that's young, healthy, and vibrant.

This is proven quantifiably in babies born with encephalitis. In a Japanese randomized controlled trial, untreated children almost all end up brain damaged, but in the treated subset, 90% had totally normal brain function out to two years from one intravenous treatment.

They had a patient on a heart transplant list. Because the patient couldn't get a heart, they treated them intravenously. By the time a heart became available and the doctors reran all the patient's data, the doctor took them off the transplant list—and there is crazy data on the heart.

They use Dawa MUSE cells, because the actual fraction percentage of MUSE cells widely varies between sources. Mari Dawa is the woman in Japan who discovered these cells.

This is the most game-changing thing I have seen, and I don't own into the company — I wish I did. Because Texas has right-to-try laws, this is what Brett has seen the most impact with for his Parkinson's. I'm not saying it's going to cure Parkinson's; it's more, can we slow things down? Can we give your body the best chance? There are so many different benefits, whether it's tendons, joints, or orthopedic-related injuries. The data is really compelling when you go back and look at everything this woman has accrued over the last decade, and now it's a culmination of work by the scientist in Germany, Dominic Deutscher, who has been trying to understand these subset phenotypes. It's all come together where he's like, "I've wasted 20 years of research."

A joke followed about the cells being harvested from a rare breed of cattle in the Middle East — a callback, not a real claim.

The actual source is a healthy birth, a planned C-section: they take the discarded afterbirth and from that can extrapolate out these supercells — "super soldier cells," basically afterbirth super soldiers.

These will be game changers as they become more readily accepted. Florida has passed a law allowing access; Tennessee just passed a law that I lobbied for; I also lobbied in Arizona, where it got through the House and the Senate but the governor shot it down. I think Texas is going to pass more accessible laws around this, and then Utah. So you can get it in certain states, other states regulate it, and it's obviously not an FDA-approved modality for anything — any use of these cells would be off-label. There is no label.

Why are GLP-1s a concern for sarcopenia, and are you more worried about sarcopenia than osteoporosis?

I'm worried about both, and that's a great question. Outside of bariatric surgery, we've never had the ability to lose this much weight this fast. We're at the intersection of something we've never seen before, which is very unusual in medicine — to be in a place we've never been. We now have the capacity to reduce weight by magnitudes we've never had before, which means that if these drugs are utilized — and the expectation is somewhere between 40 to 60 million people on these medications —

It's like 20% of Americans.

Plus all the people using gray-market stuff and not even telling anyone. Hopefully things will evolve there. But here's what's going to happen: obesity has been our focus for the last 50 years and we haven't gotten very far. All of a sudden GLP-1s are now available, and obesity will become less of a problem. But the fact that people are sedentary means sarcopenia — the loss of muscle mass and strength — is going to become a primary problem. And we know how bone is formed. By the way, osteoporosis is a pediatric disease with geriatric outcomes.

Explain that for the idiot in the room, please.

It means that what you do when you're younger to protect bone and muscle plays a role in the rest of your life.

So you're saying it's predictive of your osteoporotic status late in life?

Exactly. Athletes who lose their menstrual cycle are very underweight; people who have struggled with anorexia end up with very low bone mineral density and are then at risk for osteoporosis.

It's strange to hear three people in a room who are quite forward-thinking, experimental, and open to new evidence being skeptical about GLP-1s. I understand obesity was a problem for a long time, and we've got this intervention which appears to fix it — but now there are all these potential consequences. And they're not even side effects; they're more like second-order consequences. That's probably a better way to look at them. So how do you feel about the potential for tens of millions of people taking GLP-1s over the next decade?

One of the big challenges — and this is what you just touched on — is that traditional medicine runs on an insurance model. In that model, you're based off an indication, and that indication is tied to a specific dosage. These trials were based on chronically sick, morbidly obese people; this was originally going to be a diabetes medication. So all of the initial data — which is where the lion's share of human clinical data comes from — comes from those populations. The problem is taking that and rolling it out to the general population, over the 33 BMI threshold — and now every housewife in Malibu is using it to lose 10 pounds for vacation.

Guess what else it does? And this isn't really talked about: it has different sexual side effects depending on whether you're a man or a woman.

Is that like the anhedonia thing, where it reduces pleasure but it's more pronounced in one sex?

Yes — in women. The data is still emerging because we haven't been using it that long. For men, it can increase testosterone, decrease body fat, decrease estrogen, and increase sex drive. But what we're starting to see for women is that while it again decreases body fat, it also seems to decrease sex drive.

So just give them some PT-141 nasal spray and we're back off to the races, right?

Or we study women more — and perhaps we get to your point about specialized dosing. The problem with that model is real: right before we walked in here, I got a text from someone saying his wife's tirzepatide is no longer covered by insurance, and they're trying to move her to a dosage that would be covered — meaning moving her up to a higher dose, even though she was getting efficacy from the lower one.

Insurance companies are a big challenge here. I've broken this down on your podcast before: roughly 30% of an insurance company's revenue comes from monetizing drugs, so they change dosages based on rebates — whichever rebate pays them the most. You may be on an efficacious dosage that's working great for you, but they'll say, "We're not covering that one anymore. You've got to bump up."

Which is great, because we were just talking about 0.25 — a microdose that suppresses food noise. For a lot of people, that's enough. It's nowhere near enough to get covered by insurance. But at the larger doses you run into the sarcopenia issue: you're told to go to the gym and lift weights, and the only way to do that without feeling flat is to eat a good meal — but you sit in front of your favorite smoothie or pre-workout and get nauseous trying it, so then you're flat in the gym. This is the whole grey-man hypothesis: the road we're going down is getting really smart, getting big like AI, potentially hardware-infused brains, while our bodies waste away into little stick figures. The grey men are us from the future — GLP-1s and AI.

Thank goodness we have testosterone.

Is the dosage issue because it's a pre-click pen? When I think "dosage," I picture a vial and an insulin syringe, where you'd just draw more or less.

Those companies are launching other dosages to give patients more mobility and options. The commercially available manufacturers — and compounders — have been doing that for the last five years. But it still comes back to what was in the clinical trials and which dosages showed efficacy there — and that was an obese patient population. If you want insurance to cover it, insurance follows the literature.

We're in a space where we don't really understand microdosing yet. What we do know is that GLP-1s affect muscle positively, despite what the literature shows about reduced muscle mass — the majority of the mass lost is fat. I actually think GLP-1s are really good because they have the potential to improve muscle quality by reducing intramuscular triglycerides.

Imagine you have a Wagyu steak. You go on a GLP-1, inject it, and your Wagyu steak becomes like a filet. The texture and composition can improve. We need this, because we haven't been effective before — and again, I don't think body fat is the major problem. I think it's intramuscular.

That's true — a lot of the studies showing muscle loss, primarily with retatrutide, were done via DEXA evaluations, which couldn't differentiate between lean mass loss coming from muscle and lean mass loss coming from things like intrahepatic tissue or intramuscular triglycerides — losses that would actually be a positive benefit.

But if you're not eating enough food, muscle loss is still a pretty big risk.

Let me try to recap, because that was mind-blowing. The studies that have been done are mostly on morbidly obese people, who are given quite high dosages. When it comes to prescriber-approved dosages, because they need to follow the science, even people looking to lose a little weight who might get efficacious effects from microdosing need to be given the big-boy dosages — because those are the only ones currently studied in the literature. Is that right? It's an attempt to thread the needle and get insurance coverage. And the initial prescriptions for the first few years were pre-loaded syringes, right?

That autonomy to shift dosing matters. When we were seeing muscle wasting, it was because a lot of these people were taking far higher dosages than they should have been, and their doctors were just trying to give them a solution — nosediving their weight when they didn't need to. They could have gotten away with 0.25 and titrating up from there.

As Gabriel was saying, the muscle loss isn't necessarily a direct mechanistic effect of the GLP itself, and some of the actual loss from that might even be favorable. It's the loss that occurs simply from not being able to get into the gym, or from not eating adequate protein — because you have such low energy from not eating, and such low food volume.

Asked what the mechanism is for the sex drive changes in women, the answer is dopamine — the brain reward pathways. Those pathways are very similar to the ones involved in addiction, which is why GLP-1s are being studied for alcohol and drug addiction. It's not just anything hedonic, and it's not solely related to body fat and appetite. GLP-1 isn't only found in the gut, making you feel full and slowing gastric emptying; it's also present in the brain, where it impacts your dopamine response and desire generally.

One speaker raised the broader question with Joe Rogan: what happens when our entire economy is driven by consumerism and you pharmacologically suppress desire? Most people buy things they don't need, just things they want — a repeat habituation of trying to satisfy themselves, whether it's sex, video games, porn, social media, or weed.

From clinical practice at Strong Medical, patients on GLP-1s are getting a little depressed and don't get the same enjoyment from sex, eating, or spending. The point was made carefully: this isn't anti-GLP-1 — they prescribe them. But as trials were run in sick people with type 2 diabetes, we don't really know all the secondary outcomes. Some are positive, but decreased sex drive, enjoyment, and mood are a problem.

One speaker joked it's a great aid for stoicism, then cited research on bariatric surgery outcomes: there's an increased suicide risk after bariatric surgery, but not just because the procedure is highly traumatic or because complications occur. Typically, people overweight enough to use bariatric surgery are eating to deal with something happening in their life. The surgery takes away that pathway of reward and sedation, but the underlying problem still exists. The same applies to GLP-1s: the weight loss has been achieved, but the reason someone was overweight still exists.

This is why the model of care matters. At a practice like Dr. Lyon's, you get a full workup — blood work and a holistic assessment. In an insurance-model primary care practice, a doctor has about 6 minutes with a patient on average and wants to put a win on the board. The patient asks for a GLP-1, is probably pre-diabetic or diabetic, and probably does have weight to lose — but those are symptoms, not the root cause of the illness. The prescription gets written without asking whether the patient has a hormonal inadequacy or a family history of mental health issues, depression, or anxiety. In a cash model, you have the ability to do all of that.

The counterpoint: someone may genuinely need to lose weight, and medicine has been very unsuccessful at helping — now we have a tool that makes us successful. But consider the analogy. If you're hypothyroid and I give you thyroid replacement to normalize your levels, you wouldn't think twice. If your eyes have aged and I give you glasses, that wouldn't be an issue either. But if someone comes in with low testosterone — as a woman or a man — they are now seen as juicing, as being on steroids. That's the problem: not that your testosterone is low and I'm giving you testosterone to bring you up to a normal level. We're not talking about optimization or enhancement. We're talking about someone on a GLP-1 who now has low testosterone, man or woman, or low sex hormones — partly because of the stigma around these treatments in general.

Everyone at this table is very interested in health, but for the average person, if you say, "Hey, I'm on testosterone," they react as if you're juicing or on steroids.

There's a stigma around testosterone even in primary care. A real-world example—and he covered this on Joe Rogan—is Jelly Roll. We've helped him lose 250 pounds. Everyone immediately assumes we put him on a GLP-1. No. We ran his blood work: he had low testosterone, he was chronically inflamed, and he had all sorts of other biometric issues unrelated to discipline. All we did was fix those root causes. He never took a GLP-1, and to this day everyone assumes he did—and I sell GLP-1s, so I would tell you if he took one. He did it with blood, sweat, and tears: diet, lifestyle, gut health, hormones. But in general medicine, testosterone is viewed as the boogeyman.

It's a misunderstanding between hypogonadism and supraphysiological dosing of testosterone, and not understanding the sweet spot in between. I was watching Pete Hegseth's recent video about putting war fighters on testosterone—

He wasn't putting war fighters on testosterone; he was screening for it.

Right. I'd still like to see that conversation couched in a discussion of lifting weights with your legs, where there's a high concentration of androgen receptors, and covering the bases with creatine, zinc, boron, omegas, magnesium, and some of the upstream precursors—looking into sleep and recovery, and then making the decision. I know you guys aren't saying to throw testosterone around willy-nilly; you did blood work with Jelly Roll. The problem is that the number of people—men in particular—who are hypogonadal is massive. I don't think testosterone replacement therapy is the first solution, but sometimes it's the most effective one, especially in a scenario like a war fighter who can't live the optimal lifestyle.

What you're saying is absolutely correct. We're seeing testosterone decrease year after year: obesity goes up, healthy behaviors go down, people aren't eating well or sleeping. There's a medical risk when someone has low testosterone—for heart disease, osteoporosis, cognition, depression. If I had one dream for this room of strong, powerful men, it would be to clear up the idea of a testosterone revolution, and to clear up the idea that testosterone equals steroids—that somehow I can give medication to make someone less fat, but giving medication to build muscle is a problem.

Why has testosterone become so demonised?

The popular claim is that it makes your blood super thick and gives you a heart attack.

Testosterone was discovered in the 1930s as a medical intervention, and at first there was no stigma attached to it. People were interested in it because we saw an increase in sports performance — we know testosterone increases muscle mass, and combined with training you get better outcomes — plus motivation for forward motion and all of these things.

Then a study came out by Huggins showing that testosterone caused prostate cancer. For decades, men were castrated because of the fear that testosterone would cause or worsen prostate cancer, and as a treatment for prostate cancer itself.

But the study was wrong. There were only three patients in it. And they didn't give men testosterone — they suppressed androgens, actually tying rubber bands around their testicles. The logic was: if too much testosterone might cause prostate cancer, we'll cut it off — or if you already have prostate cancer, we'll do the same. It was hard to survive that, but it was wrong.

It was dogma that got adopted by the medical establishment. Dr. Morganthaler, who was on my podcast, debunked it in the 1990s. How did it take 60 years? And now we're seeing the opposite: testosterone doesn't cause prostate cancer, and it doesn't make cardiovascular disease worse. The real risk is having low testosterone. These myths matter, because we got it wrong.

Some of the fears aren't true — like hair loss. What Dr. Morganthaler uncovered comes down to saturation levels. Think of receptor sites like watering a plant: if a plant gets no water, it dies; if it gets too much, it dies. Receptor sites are the same. When men were chemically castrated and had no testosterone, their risk of prostate cancer was statistically lower — but they had a higher risk of every other form of cancer, of metabolic disease, of diabetes, and they lost bone mass.

Most of the actual risks of testosterone are not what we thought. They're things like excess aromatisation and conversion to estrogen if it's improperly managed, which can cause emotional issues or gynecomastia, or increased conversion to DHT, which can cause male pattern baldness. But these are not life-or-death issues, and most of them occur with misuse.

There's a difference between enhancement and replacement of something the body already makes. For military operators: Tim Parlor, the attorney who submitted a memo on this (not yet released), argued that if you have low testosterone, you're at a disadvantage. If we send guys to war, we're not talking about enhancement — we're talking about men who are symptomatic with hypogonadism, with low testosterone. Right now they're not even screening. If we don't screen, we're sending soldiers to war with a massive disadvantage.

Suboptimal.

I want every single soldier to have 2,000 nanograms of testosterone. Yes, I do — though we don't want two monsters who can't control their rage. Bald, rage-infused, thick-skinned soldiers everywhere.

Well, we don't want that. Listen—

Screening, Controversy, and the Testosterone Stigma

As a military family, a Navy family with high testosterone — my husband does have high testosterone — we would never want war fighters going in uncontrolled. And I want to address the question people keep asking: what about the women? Considering only about ten people have read the memo, women will also be screened. They are also complicated — it is more complicated — but if we can get screening done initially to protect our soldiers, then we have a way to do something about it: to fix, identify, and acknowledge that there's a problem. The fact that it is so controversial, that it has gotten people so upset, is outrageous.

You do see a political agenda here. I'm sorry to get conspiratorial, but I've watched this play out — I've been behind the scenes, I've been all the way to DC, I've sat at the FDA and testified there. The same thing that happened with men and testosterone happened with women's hormones in the Women's Health Initiative. I was a drug rep when that study was released, and the first thing the company did was hand me osteoporosis drugs. Suddenly all of us were carrying them, and our job was to go into doctors' offices and scare the hell out of them: never put a woman on estrogen again — put her on an osteoporosis drug to preserve bone mineral density. But that osteoporosis drug exacerbated hot flashes, so now they needed a hot flash drug. You end up selling four drugs to fix what one natural hormone — one that had existed since the dawn of time — would have fixed. The whole study was flawed to begin with and got debunked, but it took twenty-some years to bring estrogen back to women.

I don't know how much of the cultural pushback around testosterone comes from people misunderstanding a study of three people from 1930. I think it's much more cultural — about what testosterone represents generally.

I think it also gets the same treatment GLP-1 does in terms of being perceived as a shortcut: you're not going to lift weights or address lifestyle factors, you're just throwing a band-aid on it.

But no one cares about taking GLP-1. Nobody accuses someone who lost a ton of weight on GLP-1s of being non-natty. But if you ever do a six-week course of enanthate, your natty status is gone forever.

So what's the difference? It's a good split test: two drugs with similar delivery mechanisms — one IM, one subq — and actually testosterone can be subq too, so you can use them in similar ways. They achieve similar things, like a leaner, more built physique. Why does testosterone carry this stigma? Is it the masculinizing side, the aggression?

I think it's the performance-enhancing benefits in sports that created the dogma. But it goes beyond sports — there's simply a perception that someone on testosterone is taking a shortcut when it comes to muscle mass and recovery.

If they're hypogonadal, they're not taking a shortcut — they're addressing a deficiency. But the perception that you're not doing the work persists, and I think the unfairness of the sports performance angle feeds into that.

Do you not think the indication is wrong today — the clinically low threshold?

I have to be careful here, because you're way too well read. Basically, the indication is 300 nanograms per deciliter, though it varies by country — in Italy it might be 350. That number defines what counts as hypogonadal. The lower range of normal for an adult male in the US right now is 300 nanograms per deciliter, and in my opinion that's too low.

You think the lower range should be raised?

I want to couch this very carefully as a practicing physician—

This is not medical advice. This is a bio.

Right — which lets me say it.

Testosterone: Numbers Aren't the Whole Story

"I'm not a doctor," the physician jokes, before couching his point carefully. It's not just the number—other factors come into play. He recalls a patient from Homeland Security whose testosterone was 600 yet who had all the signs and symptoms of low T. His advice was simply to get more sleep, but it turned out the man had a CAG repeat: the testosterone he had wasn't effective because of issues with his receptors. Everyone's receptors differ—a testosterone of 900 for one person might equal 300 for someone else.

Another speaker clarifies that the CAG repeat is not a matter of SHBG or free available testosterone; it's an actual receptor issue, and whether the hormone converts to free testosterone is a separate question. These receptor markers aren't tested routinely—it's primarily done in research, and the data on the impact is still being gathered.

The core clinical problem: the idea that testosterone causes harm within physiologic ranges. If someone measures 300 or 500 but feels terrible and looks like they need testosterone, guidelines say physicians essentially shouldn't treat them. A lot of that is insurance-driven, which feeds back into the "sick care" model—the challenge being that medicine should be personalized, since each individual's physiological response is different. As one puts it: "Insurance will cover 299 but not 301."

Is TRT an Artificial Solution?

One speaker asks whether TRT creates the same problem as Ozempic—people pharmacologically solving a problem that lifestyle should have partially fixed, an artificial solution to an artificial problem. The physician agrees this applies to some people, pointing back to lifting weights, micronutrient replenishment, relationships, sunlight, de-stressing, recovery, and sleep. But even with all those parameters in place—which many people today do have—environmental factors can still influence testosterone availability: endocrine disruptors, plastics in packaging and personal care products, industrial and air pollution, even light pollution affecting stress and sleep. Add to that the fact that few men today chop wood, build fences, or haul rocks outdoors. It's a cluster of modern-lifestyle factors putting people at higher risk of hypogonadism.

Society definitely has higher levels of low T than ever before. His friend Cali Means breaks down the food system and ultra-processed foods: the big changes started in the 1980s, when the government began regulating big tobacco and companies like Philip Morris went out and acquired most major food production companies, which pivoted from hearty, healthy meals to ultra-processed foods. Ultra-processed foods carry a 30-plus percent profit margin; a banana has about 8 to 10 percent. So it's the food systems, the glyphosate rules around crops—all controlled by much bigger dynamics. Another speaker quips: "All I hear right now is that cigarette companies have made us less yolked."

When Lifestyle Fixes Aren't an Option

But here's the problem: take the war fighter. Everything named so far is a luxury—sunning your perineum, going to bed early, sleeping in, reducing light pollution. A war fighter, a new mom, and a lot of people simply don't have those luxuries. So if we restrict treatment by requiring lifestyle factors to be solved first, there is enough evidence that low testosterone contributes to disease risk. Certain people don't have the degrees of freedom within their lifestyle—constraints on their sleep, on their ability to eat, and so on.

Asked where testosterone ranks among performance interventions compared with sleep, resistance training, light, diet and stress, Ben said the answer depends primarily on age. He has been on testosterone for four years, starting at 40, and the main benefit he noticed was faster recovery. His morning gym routine keeps him sane, active, productive and clear-headed, and he can keep doing it day after day, whereas he had been seeing a significant increase in recovery time between workouts — measurable in both HRV and soreness. So he ranks testosterone higher and higher in priority the older a man gets, though he notes women are part of this discussion too and haven't been studied nearly as much. He'd put the threshold somewhere around 35 to 40 years old for most men, after which it becomes pretty important.

Another speaker raised the fertility question: the younger you are, the more this matters, and he criticised the "looksmaxxing" community of 16-year-olds screwing themselves over in terms of legacy and future children. A 30-year-old who may be hypogonadal — partly because of the uphill battle of a modern, post-industrial lifestyle — needs to know that testosterone replacement therapy affects fertility, and his practitioner needs to know methods for maintaining sperm quality.

One participant said he froze his sperm last year as an insurance policy in case he ever wanted to go on TRT — he isn't on it — and noted how cheap it is for men compared with egg freezing for women. Another speaker added that going on testosterone doesn't mean infertility: there are interventions like HCG, though you have to work with a knowledgeable provider. About 10% of men have low fertility at baseline, and 2% have no sperm at all.

The clinical recommendation: if a younger man is hypogonadal, he should still be treated — bank his sperm, have the appropriate discussion, give him HCG — but you wouldn't want to withhold a medical treatment; that's a mistake. Part of the problem is the stigma, wrapped up in a moral panic that testosterone is going to ruin the world.

He finds it fascinating to compare the moral reaction to GLP-1 drugs on one side and testosterone on the other. Morally there shouldn't be much difference: one helps you eat less, the other helps you build muscle and improve your hormonal profile. His sense is that much of the difference comes from coding — testosterone is male-coded, associated with aggression, dominance, pursuit and forward motion, while GLP-1s are more female-coded, helping you lose weight and be more slender. One looks like health; the other looks like luxury or unnecessary enhancement. And weight loss is visible — everybody can see a fat person who lost weight — whereas you can't see someone's low testosterone in the same way.

But what happens when a woman goes on a GLP-1 and her testosterone is low? She tells her sister, "I have low testosterone, I'm going to start testosterone," and the sister reacts, "Oh my god, you're going to start steroids" — and then she's shamed.

We know that a person will typically go on a GLP-1 for two years and then come off. Essentially there's weight cycling: it becomes a skinny-fat situation where they've lost lean tissue and put on fat. And let's say, in a profile of a decreasing milieu, her estrogen goes down, her testosterone goes down, all her hormones go down. But then, because of this stigma, she's ridiculed or shamed because now she's "on steroids." So in a moment where we have the ability to shift her life and her trajectory, she doesn't take it because of all the noise that she's now juicing.

And that's a problem.

I didn't even realize the stigma was that significant for women.

It is. And testosterone for a man is the number one biomarker. There is no other biomarker that reflects the risk of type 2 diabetes, that reflects the risk of potential depression.

When you say biomarker, is that the whole hormone picture — total T, free T, everything?

Yeah. Well, I would say total testosterone, because again, it's really free T — which is a really good point. But if I had to pick one biomarker, it would be testosterone. So let's take that back to soldiers: if we don't routinely screen them, that one biomarker will give us more information about their future than any other biomarker.

I want to know what's happening with peptide access right now, because you were part of this big hearing that recently happened.

What happened inside the FDA hearing? What's going on?

That's a good question. I've been trying to ring the bell on this since it started. During the Biden administration, the FDA, kind of in a vacuum, blindsided the public by putting peptides on the naughty list — it declared that 17 peptides are now considered dangerous to compound. Overnight, the regulatory landscape shifted, and compounding pharmacies like mine legally could not make a safe product that had often been on the market for more than five or six years. And there was no heads-up: we weren't seeing any adverse safety data, nothing.

One way I've tried to prove this is that I submitted multiple FOIA requests to the FDA over the last three years, and they had not responded to a single one. So when Secretary Kennedy was put into his position and given the opportunity to drive change, this was one of the first things I discussed with him: we've submitted these FOIA requests and haven't gotten answers. The industry is just asking for guidance. We're not making this up — the ban created a gray and black market overnight.

Just two weeks ago, they federally indicted a gray-market peptide manufacturer out of Florida who was buying all of his API from China, tainted with testosterone. And so women were injecting—

And API is the...?

The pharmaceutical ingredients — the base product you use to compound the medication.

After a lot of lobbying, begging, pleading, and flights to DC — and thank God for guys like Joe Rogan, who's been a voice on this, asking why we're banning peptides and forcing people onto the gray and black market — we got a hearing. And that's a crazy story in itself; we could write a book on it. The group built out the case: we submitted over 800 studies, 5,000 pages of documents, and did a retrospective analysis of 16 million patients who were on BPC-157. Out of that, we found three adverse events. Three.

Yeah, somebody sent me that paper — by the hundreds of thousands of uses of multiple peptides, including BPC, the number of adverse events was close to zero.

Correct, almost zero. This is one of the largest retrospective analyses ever done of a medication. And I want to be clear, because another famous influencer-clinician just took to the internet and tried to debunk this hearing: the hearing wasn't about efficacy. That's the confusion for people.

It's all about safety, because what people fail to realize—going back to the process and the legal structure—is this: if you file for a new drug indication, what you're asking for is Medicare and Medicaid dollars. You're asking to force employers to cover a treatment for their employees, since 90% of Americans get their coverage through employers. That's why insurance plans go up every year—they're monetizing all of this.

This is not that world. This is a cash-pay product, where a patient uses their hard-earned money to decide, under the supervision of a clinician, to fill this prescription through a board-certified pharmacy inspected by both state and federal government. We had a safe pathway, and that pathway was removed in a vacuum with no evidence. Then we argued with evidence—we submitted over 5,000 pages of studies—and the FDA gave these clinicians literally about a week to review everything. These poor doctors were trying to cram for the test before coming in, even though we had submitted everything a month in advance. Then the FDA released a statement to the public with a black-market peptide API data set, saying they would stand against this most likely even if the clinicians voted yes. And by the way, they presented a certificate of analysis supposedly from a compounding pharmacy—it wasn't a compounding pharmacy at all. It was a black-market manufacturer that had already been shut down.

So it was very misleading.

That's a difficult question to answer. When we sat in there, the clinicians got so frustrated that at one point one of the FDA individuals said, "Hey, look, I just want to be clear—we're not intentionally hiding or misrepresenting data." And the clinician was basically saying, "Well, yeah, it really feels like that. It doesn't feel like you were giving us a shot at this." They ended up overturning six out of the seven peptides. What was disappointing is that the FDA voted straight-line one way, while the clinicians—people who actually use these products as end users in the medical space—all voted straight-line yes.

This raises a good question that practicing physicians often ask: why are there no randomized controlled trials? Why is this mechanistic data, why rodent and animal models? If you can prove it mechanistically, we should be able to see it in some kind of randomized controlled trial.

On BPC, we submitted at least four human studies—I think it was four to six, but let's say four to be safe. The issue with a peptide is that you cannot patent something that is readily available in nature; that's patent law in the United States. Look at what's happening with the GLP-1s: a 503A patient-specific pharmacy can compound a GLP-1 weight-loss drug, and it is infuriating the big pharmaceutical companies. They say, "Wait a second—we spent billions of dollars to make these drugs." So a lot of the pressure on peptides as a class has come because big pharma is now monetizing them at a new level. In one breath, these big pharmaceutical companies tell the FDA, "These are dangerous, these are this, these are that." In the next breath, Eli Lilly spends $7 billion to acquire a peptide manufacturer out of China, and Merck is attempting to patent over 200 potential future peptide compounds.

A lot of the physicians who are or were prescribing peptides have a pathway via an IRB to start gathering data—to actually show what's working. The general gist of the FDA's stance, from what I can gather having testified there and given my two cents on where we are and how we got here, is: "We have an IND process, so go get a new drug indication." My rebuttal is: apothecaries predate big pharma—the founder of Pfizer was a compounder. Compounding has existed for over a hundred years. In 1997, Congress passed a bill to protect compounders, saying patients and clinicians would be allowed to prescribe unique medications to a patient and provide accessibility.

The problem is, if we hand the keys to the castle over to industry—I said this in my speech to the Senate—everyone talks about Eisenhower's speech and the military-industrial complex, but the second half of that speech was about the scientific-industrial complex: what would happen if we hand science over to industry, if we allow industry to control our scientific processes and protocols. And that is—

where we are headed, and that is terrifying, because what you will have is everyone getting the same dose of GLP-1 — everyone getting the same thing, because that is what we have a double-blind placebo-controlled trial on. And this is where academia drives me mad. When Rogan posted his pictures of plasmapheresis, some doctor claimed it wrecks the immune system. No — it's a 24-hour decrease in your immune response. He called it pseudoscience, but plasmapheresis does have a double-blind, placebo-controlled randomized trial, and that trial showed it actually took 18 months off your biological age in people over 50. Yet people want to split hairs and decide when they want to use double-blind placebo-controlled randomized trials and when they don't.

Well, here's what I've seen in medicine. What's so relevant here is that there's a need for improved care, and because there's a need, that's why people are reaching for peptides. That's why people are looking for plasmapheresis. Typically the consumer, the patient, will drive forward plasmapheresis for something different than, say, myasthenia gravis or another approved indication — but this is how we start to grow. Before, no one thought mold was a thing. I moved to New York, got really sick, and no one was talking about mold 15 years ago. All my blood work was great, and I was living in Stachybotrys. Now environmental testing is more of a thing. There is the patient, and then there's the need we have to fulfill, and hopefully the science catches up. Randomized controlled trials are valuable — we still need them for peptides. Maybe not within your sphere, but the general medical community needs them.

My argument is that this is about medical access, accessibility, and medical freedom. If a patient, under the supervision of a clinician and the guidance of a subject matter expert, wants to utilize a compound that is safe, who is the federal government to obstruct a safe pathway and force them onto a dangerous one? And if people love randomized controlled trials, let's look at the products that have hit the market. What happened with OxyContin? What happened with all the anti-inflammatories? What happened with antidepressants? In the second-largest retrospective analysis of a drug that went through randomized controlled trials, what did we see 25 years later? We saw that antidepressants don't work. They work for a small subset of the population and barely differentiate from placebo, yet they increased suicidal ideation, suicidal tendencies, and violent thoughts — most of the school shooters were on antidepressants. We have created a colossal disaster for a product that, developed from a Pfizer consultant's work, barely differentiates by one point from placebo. And yet we spent trillions of dollars on these medications.

Service announcement brought to you by Saffron. Who gets to decide how much

Who gets to decide how much risk people should be able to take with their bodies? Should the FDA protect people from making bad medical decisions, and how much evidence should be required before adults can access experimental treatment?

That's a difficult one. I think it comes down to risk–reward, which I say about everything. Peptides are not a silver bullet; they're a tool in the tool belt. A real-world example is Brett Favre. He's diagnosed with Parkinson's, which is terminal and progressive, and the doctors basically say we've got nothing. But there are things that have a shot at helping, and a lot of those trials are in other countries and not accepted here. He's getting benefits from modalities that are being obstructed. I believe in a patient's right to choose. One thing we're working on in Texas: Congresswoman Lacy Hull is going to submit a bill called the Right to Try Act, which will try to provide patients in Texas with medical freedom, and we're trying to do the same thing at the federal level. The belief is that through citizens' petitions, if you're a chronically ill patient, you have a terminal disease, or you have some catastrophic debilitating issue, why is the government stopping you from using a stem cell product? This is the end of your runway.

So beyond a threshold of severity in terms of your health, you're allowed to throw anything you want at the wall, within reason?

I think you should.

A lot of that would still be out of pocket, though, right?

All of it's out of pocket. None of this would be covered by insurance, which goes back to the main crux of the issue: if somebody wants to spend their own cash, who are you to tell them no? If I want to fly to Thailand for a treatment, I can do it — I just have to pay for myself. When people are leaving the country to get treatments, those treatments should be available here. We don't need big brother impacting every decision. And I get protecting the consumer, but where was that protection with glyphosates, with the antidepressants, with OxyContin, with the level of corruption we've seen from regulatory bodies that are supposed to be here to protect us? Those people are swapping spit with industry at a level that's nauseating.

But it's challenging, because you might be doing something ethically, but if there's another compounding pharmacy, like in Florida, putting all this crap in — how do we protect the people? I do believe in medical agency, that people should have the freedom to do whatever they want. If they want to use a medication because they have five pounds to lose, they should get to choose. We as physicians should never dictate what an individual wants to do. There has to be agency. But then the question is, how do we protect the people who don't know and think they're getting one thing?

I think we have to assess it as a different model — that's where I keep going with this. There's the insurance model and then there's the cash pay model. In the cash pay model, we don't need a new drug indication that costs $300 million to a billion dollars, because that stifles and limits innovation. That entire model was built around a framework built by industry, which has a reason to build a moat around accessibility of care because they are monetizing chronic disease at an astronomical level. That's why the average American in the 80s was on one prescription drug and now the average American is on four or more — and we're the sickest developed nation in the world.

So in a perfect world for you, in a cash pay model, there would be right to try in every state?

I think right to try, under the supervision of a clinician — that's an important caveat.

I personally believe in a doctor holding me back.

I believe in the sacred relationship of a patient and clinician. I believe that most clinicians, when given the opportunity, want to do what is right for their patient, and often their hands are tied. You were even wary to say it: "I have a patient who's sick, but I don't want to prescribe off-label because it puts your license at risk." That's a travesty, because that patient needs help, and we shouldn't have to look over our shoulder.

I remember during COVID I had written a prescription for ivermectin for an indicated use. This was before it all went crazy, and I got a letter saying that if I ever did that again, it would affect my license.

But this was a legitimate case—we test for parasites all the time, and there was an actual indication. They didn't care what indication I put on the prescription.

They shut us down as a pharmacy. We got a letter saying they would revoke our pharmacy license in the state of Texas if we shipped one more ivermectin prescription. I can ship ketamine, but I'm not allowed to ship ivermectin.

Can you imagine being a provider and being told you can't write a prescription for something that could help someone? They don't even know what I'm treating—we treat parasites all the time. It's terrifying, because providers and clinicians spend their lives dedicated to caring for their patients.

The conversation turns to experimental, forward-thinking interventions. Asked what he's been playing around with recently, the guest points to plasmapheresis, which he finds interesting because of the variety of blood and plasma filtration protocols people are turning to—for microplastics, lipid management, and mold.

Asked to explain it literally, he describes pulling blood out, filtering the plasma, and replacing it—typically with albumin, in some cases actual human plasma, or a "soup" of stem cells and exosomes that Bergman's clinic offers. The idea is like an oil change for the body. Some places, in Mexico and Europe, will filter whole blood, not just plasma, using different filtration mediums for different purposes: a heparin-based filter designed to trap spike protein—like a sticky fly trap—for something like long COVID, and another called the marker filter specifically for microplastics. A lot of people are electively doing these out of pocket, often internationally; you can do a basic plasmapheresis at Bergman's clinic, sitting in a chair for two to five hours squeezing a rubber ball.

The other speaker notes the problem: when someone like Joe Rogan posts about it, clinicians immediately tag the video to debunk it and coast off the momentum he created. He finds this contradictory: "You're an academic. You're now trying to debunk a placebo-controlled randomized trial. At what point do we pick a side? Do you believe in randomized control or do you not?"

The first speaker presumes the critics claim to have contrary data to the trial. The debunker's main argument is that only one major study demonstrated the effect and the rest is anecdotal—but plasmapheresis has been used in hospital systems for decades. The theory is that antibodies, the reactive agents in many diseases, exist within the plasma, and so do toxins and other substances that can't be excreted naturally through urine, feces, or sweat. Hospitals still use it for extreme cases like burn victims or anyone exposed to high levels of mold and toxins.

A real-world example is Jelly Roll: after losing so much weight, he was chronically inflamed, and despite many interventions to bring down inflammation, all that weight loss put a major load on the kidneys—you can only sweat and excrete so much. It started impacting his sleep, and as soon as they ran him through plasmapheresis, he called saying he hadn't slept that well in years.

On the natural alternative of sweating it out in a sauna: microplastics are measured in Daltons, ranging from slightly under 100 up to a thousand Daltons, while a sweat gland can only pass about 100 Daltons. So arguably only a tenth of your microplastic exposure can be sweated out—and most microplastics from food packaging or plastic cups are far larger than 100 Daltons. It's an inconvenient truth: once it's in your body, it's difficult to remove. There are some gut binders, though—probably ten different supplement companies making them.

Over the past few months, people have been mailing me sulforaphane-based compounds for microplastic removal, or other binding stacks that supposedly remove microplastics from the gut and possibly, via some osmotic gradient, from the tissue as well. But none of those are that proven. So at some point you just have to filter it out. The problem is that it's a long and expensive protocol that not everybody is going to do.

But eventually maybe there will be a way to democratize it. We've seen that with a lot of medicine.

That's the goal with all of this: to make it affordable for the masses.

How long does it take your body to replace the plasma? Because I think that's one of the concerns—you've gotten rid of all this plasma, and then what?

What we do is add back albumin, so you immediately have that replenishment. The big critique people have tried to make is that there's a drop in your immune system, but the truth is that drop lasts only 24 hours. We were just talking to one of your buddies who did it and then got on a flight, and I thought, "I would not have done that."

What happened—did he get sick?

He felt run down, but nothing more than that. There's also the risk of the catheter, depending on where it's placed—a rupture or some issue. But you do have a compromised immune system for 24 hours, and that is a legitimate risk. As with anything in medicine, you have that discussion and make sure you tell the patient that for the next 24 hours their immune system will be compromised. After that, the immune response is boosted, and all the inflammation that was in the plasma is removed—along with the shock proteins and other things causing so many issues. We're basically taking out the trash, replacing years and years of inflammation and gunk with young, clean albumin.

What's albumin?

It's just a protein. Think about egg white—egg white has a ton of albumin in it. It's basically like putting egg white back in.

Very, very similar, yeah.

Asked which longevity interventions are cost-free, since much of this stuff sounds difficult to access or available only outside the country, the answer names three.

Grip strength, VO2 max, and walking speed

Epidemiologically, grip strength is often identified as a metric — but not because people with big meaty hands live longer. It's because people who lift heavy objects, whether manual labor or training in a gym, tend to have high grip strength as a byproduct. You won't live longer by keeping a handgrip dynamometer in your car and squeezing it all the time; it'll make a little bit of a difference, but physical activity that exhausts the grip is what counts.

VO2 max is another. The misperception is that you need fancy Norwegian 4x4 protocols to significantly increase it — four minutes at maximum sustainable pace, all-out, four-minute recovery, repeated four times. But just yesterday a study came out showing that small bursts of 10 to 20 seconds, done 3 to 5 times a week, had an impact on VO2 max. These are tiny bursts — quick, on a dime.

Muscle mass vs. VO2 max

Asked which matters more for longevity training if he could pick only one, he chose muscle mass — and not just because Gabriel is sitting next to him. Low muscle mass means a higher risk of frailty, and frailty is a bigger killer than not being able to outrun a lion; stepping off a curb while frail is the real danger. Joking aside, VO2 max does significantly affect cardiovascular health, but you can get pretty good cardiovascular health, including blood pressure management, from strength training. Since picking one is unrealistic anyway — VO2 max work is easy to do — you do both.

Walking speed

The third free intervention, setting aside Harvard's longest-running longevity study on happiness, relationships, and love, is walking speed. Yes, 7,000 to 8,000 steps a day is advisable, but the actual pace — the cadence of the walking — is important. He doesn't remember the exact pace, but it's quicker than you might think: walk slightly faster than what your brain wants to do.

There was a device, if it's still available, called Counterpace — a heart rate strap worn with ear pods that tracks your heart rate and helps you maintain a cadence matching it, so your foot strike occurs during the diastolic phase of the heart's pumping. You're essentially teaching your heart to pump with each step. That's very similar to counterpulsation therapy done in hospitals after a heart attack. As one speaker put it, it's like resonance breathing but resonance walking — instead of rising and falling with the breath, you step in step with the heartbeat.

Where to prioritize

Asked where to stop if someone is a five out of ten on both VO2 max and muscle mass — given that muscle mass is largely about protection in later life, frailty, falls, hip replacements, and metabolic health — he admits he doesn't know. Coming from a "bro" background, VO2 max was never something anyone considered, and it seems to have had the ascendancy recently.

And it gets chased a lot as a number, but VO2 max is largely reflective of cardiovascular health. If you're competing as an Ironman, marathon runner, or swimmer, it's important as a performance metric. But the reason it tracks with longevity is not necessarily because maximum oxygen utilization is going to help you live longer—at least I don't think so. I think it's because it reflects overall cardiovascular health. It's the same with grip strength: being able to hold on to something for a long time isn't going to make you live longer.

This is exactly where our approach differs from traditional medicine. When somebody comes in, the first thing we do is comprehensive blood work—one assessment tool. We also run them through a DEXA scan and a walking VO2 max test to assess their cardiovascular condition. Give me those three things, I put them into an AI algorithm, cross-reference everything, and we begin to model all-cause mortality and project whether you're headed toward chronic disease. In traditional medicine, somebody shows up sick, you write them a pill, and you mask the symptom. Why aren't we practicing proactive, predictive medicine? You can prevent it—1.7 million Americans die every year of chronic disease. That's more than every war we've ever fought in the history of America, in a single year. And it's all preventable.

But it's not longevity. I wish there was another name for it, because the reality is—

I think it's health span.

I think it's muscle span, but yes, health span. As a geriatrician—which means I've taken care of a lot of dying people—there's one harsh reality: nobody gets out alive. No one. So is this increase in longevity just a distraction from the end result, which is that we will all die? At some point we have to recognize that it's going to happen, and it's how we live within that time frame. Maybe there's a genetic push past 85—we don't know. Genetics play a role; we all know people who smoke and eat tacos and live to be 105. So yes: being strong, being capable, not restricting protein. I know you had a guest talking about protein restriction—that's not where I would go.

Not a lot of people need to hear that right now.

My argument is always: if we can buy you time—if we can buy your health span time and keep you healthy longer—there are folks like David Sinclair, and my buddy Dr. Ian White, who spent 22 years at the bench doing stem cell research at Harvard. Those are interesting. What he'll break down is pretty crazy, and it's why I have dinosaurs and jellyfish at our clinic.

He literally breaks down that we share a common ancestor with every species on Earth—we share DNA with the immortal jellyfish. Within us is a black-box code. There are companies in Texas right now doing gene activation: we can literally inject you with a virus that will go turn on a gene that has been turned off. We can tell your body to put on more muscle, or turn on a gene that can increase bone mineral density eightfold. These things exist today. So my only question, getting into the biohacking woo-woo futuristic stuff, is: can we buy you time? Not the woo-woo—through good old bread-and-butter smart medicine, can we buy you health span until one of these brilliant people cracks the code of how to turn on that gene, how to turn on the jellyfish gene?

Where we all live for 150 years floating in water in the dark?

Aging is not abnormal—aging is normal. But the chronic disease is not normal. That's not a normal part of aging, and we've come to normalize all of it, and that's a problem. So if we stop stigmatizing testosterone and allow ourselves to replace the things that we need—

Well, perhaps there's a through line here: if you downregulate fertility enough and don't have children, that might be a viable life extension strategy. You're sending a message to your lizard brain that you'd better stick around as long as possible because you have no progeny—once you're gone, that's it.

Yeah, basically. I would say the most potentially impactful life extension strategy is not having kids. Don't have kids.

Don't jerk off, don't have kids. Okay.

Asked about the criticism that current protein recommendations are overblown — Dr. Daniel Lieberman, when asked on the show about the 1 gram per kilo to 1 gram per pound of body weight advice, said he thinks it's overblown, that people don't need that much, and that from a longevity standpoint there doesn't seem to be much evidence for it. He said he'd looked at every big diet on the planet.

That's interesting — he wasn't invited to the protein working group, which brought together around a hundred of the finest protein scientists. They disagreed on some things and agreed on others. I don't know this gentleman, so it's not a knock on him, but that room contained the finest protein researchers from all over.

Would that not mean that they're kind of biased?

They don't all get along — some are low-protein researchers. Yes, they're all protein experts, but they're all over the place: some agree on 1.1, others on different figures. What they do is present all the evidence to the best of their ability, and what they came up with is that there is no evidence that going below the minimum requirement has any benefit at all. Going down to 0.55 g per pound was argued. Could you go from 1.1 to 1.4, or is anything better than 1.6 grams? No — no one agreed on that. So that's not one gram per pound.

What about protein cycling — the idea, from an autophagy standpoint, of a fasting-mimicking diet on a quarterly basis, or a period of protein restriction to stimulate autophagy, while eating 0.8 to 1.2 g per kg most of the time? To be clear, I wasn't there as a guest researcher; I was interviewing these guys. One interesting finding: in terms of human trials, the sweet spot for aging and optimal health seems to be closer to 1.2 to 1.6 grams per kg. So it's not one gram per pound, which is what I recommend — it's slightly below that.

On protein cycling: the body turns over 250 to 300 grams of protein a day, and as we age we become less efficient at that — liver turnover and so on. If we then begin to restrict protein as we age, that's not moving in a positive direction. There's no aging data in humans suggesting that would be beneficial.

His argument, then, is epidemiological — observational, association-based. If this is the Lieberman being discussed, you don't come across many long-lived cultures feeding at the levels currently recommended.

I like to keep it simple, because my brain isn't smart enough to figure all this out. The Forever Strong playbook — which I'll plug, since it took me two years to write — has pictures to make it simple and digestible.

My main takeaway from it: I've learned in my life that if I prioritize protein, it's a calorie-dense, nutrient-rich part of my diet, and I end up eating less of the ultra-processed and other bad things. Just anecdotally — I'm not saying there's no science behind it — protein fills my appetite, and it's hard to overeat. If I eat a steak, I'm done. So do you not see value in prioritizing protein first as part of the diet?

You're arguing for the benefits of protein intake as a calorie restriction mechanism. I imagine Lieberman would agree with that too. I think my question to him was something like, what do you think about one gram per pound of body weight? He said that's on the higher end — more than is necessary. I would agree with that statement: that is more than is necessary.

It depends on the population, though. I have 18-year-old sons who are probably hitting 1.4 to 1.5 grams per pound right now, based on my grocery bill — but they're highly anabolic, they're growing, and we're lifting every day. So it's pretty population-specific. That is exactly what they came to at the summit.

The host asks about fiber, framing it as the next health trend after protein and creatine. He predicts air quality topics like mold will be huge next, followed by light quality and light pollution, and sees fiber as sitting at its "hockey stick" moment. He also suspects protein and fiber will be somewhat antagonistic when designing a diet, and asks the guests about optimizing gut health, bloating, digestion, and leaky gut.

The first guest agrees fiber flies under the radar and doesn't think high protein intake rules it out. Fiber benefits everything from glycemic variability to bowel movements to the microbiome, often serving as food for probiotics and leading to postbiotic production. The problem is the large portion of the population with issues like small intestinal bacterial overgrowth (SIBO), diverticulitis, or some form of IBS—people who hear that giant kale salads are a great idea and that they should load spinach into their smoothies, only for it to wreck their digestion.

So it depends on what the gut biome looks like—especially the gas production by specific bacteria—before deciding what kind of fiber someone should eat. Highly fermentable fibers like inulin and chicory root completely wreck some people with gas and bloating, while for others they're great gut food. Fiber is much more individually variable than protein: you could tell most people that one gram per kilo of body weight of protein would probably be fine, whereas throwing uncooked oxalates from spinach at one person produces a very different response than in someone without that gut flora.

The host agrees this is a frontier we don't know enough about, and offers his own prediction: the food matrix conversation is next. The bodybuilding sphere—himself included—knows the macros of boiled chicken, egg whites, and rice, but not how the compounds within a food matrix interact. He cites a recent study on high-fat dairy: we don't actually understand how the fat compounds in dairy work with its protein and carbohydrates. It's not repeatable through supplementation; it exists within the dynamic of, say, a steak, which has protein and B vitamins but also its own compounds you'd normally associate with phytonutrients in plants. We don't really know how foods' components work together.

He then asks whether general advice on fiber for gut health is even possible, given that each person's flora is a fingerprint. With protein you can say one gram per kilo is a good baseline—what's the equivalent baseline for fiber for people who just want a good diet?

The doctor's answer: "We test. We don't guess." They run stool tests and breath tests, and if someone has SIBO, they treat it and put them on essentially a low-FODMAP diet. You can experiment, but also test, so you're guessing less.

The other guest adds that low-FODMAP isn't synonymous with low fiber—you're limiting fermentable oligosaccharides, disaccharides, monosaccharides, and polyols. These are specific compounds (searchable as "high FODMAP diet") that are fiber sources causing gas and bloating. But that doesn't mean you can't eat fiber at all: on a low-FODMAP diet you can have a chia seed slurry—chia seeds soaked in water as a pudding—and often seeds and nuts, whose fiber and skins are also acceptable.

But then apples, pears, garlic, and onions would all be out. Mixed greens, romaine lettuce, and a lot of things you have in salad are fine. Kale kind of depends, because there's the whole issue you brought up: is oxalate sensitivity a problem?

Gabriel makes a great point—we now live in an era where you can get a GOVA diagnostic stool test or a Trio Smart SIBO breath test and see whether you're reactive to certain fiber-based foods. Those tests aren't trivial—you can't just have everyone breathe into a tube every 20 minutes for a couple of hours.

What you could say is: have 40 grams of fiber a day or more, and if you get gas or bloating when you start doing that, go get tested to figure out what's causing it.

Yes, that's a good rule of thumb, but there are always outliers. Everybody's different. Personalized medicine should take a personalized touch—it requires the analytics and data to know you specifically as a unique individual, and then tailor a unique program to you.

This is why people feel overwhelmed by health in the modern world: "I've got to get this special fingerprint thing done, I don't know where to go, maybe I'm in a country that can't provide it, maybe I'll have to pay out of pocket and can't afford it, and then I've got to adjust everything." But there are workarounds and there are levels. For the FODMAP and SIBO issue, there's an at-home breath testing device called FoodMarble that gets a pretty decent correlation. It's not as good as a more expensive lab-based test, but it can help you track the fiber-based foods that cause bloating.

The other option is simple food elimination—the old-school tactic. Cut everything out, start from scratch with steak, chicken, fish, and maybe some sweet potato mash, something like a paleo-esque approach. Then start adding in some grains, some dairy, some different forms of fiber. Within about four weeks, you can identify the culprits.

You can use an app for that, too. You can easily use a Claude or GPT model now to literally say, "Here's everything I ate, here are my gas and bloating symptoms," and within four weeks you'll get a pretty good map of what's causing problems. It doesn't have to be complicated to be effective. We live in information overload, and that's the disease—the disease is distraction.

We can fully simplify. People know what works well for them; if they don't, they can track it. Eliminate, keep it simple, and add things in slowly. We overcomplicate.

That's where I was going with the protein point: don't let perfection get in the way of progress. It's baby steps. You don't have to be perfect—just be better. Make slightly better choices and test things out. You're not going to die if you try a fiber and it doesn't work out and you're bloated with stomach upset for a while.

There was a case report of a pear bezoar—someone ate something like 300 pears and actually got one, a kind of hairball, which caused a small bowel obstruction.

Who eats 300 pears? There's one case. I think 300 of anything is going to cause a small bowel obstruction.

I could easily eat 300 blueberries. I'll take on the small bowel obstruction challenge—I could make it happen.

Do you guys follow a specific diet?

It's called the Forever Strong playbook. It's a higher-protein diet, and I don't eat a ton of processed food at all. Prioritize protein—we keep it very simple, because I have two crazy kids.

What about grains and dairy? We're starting to see that they have protective effects. We do high-fat dairy and fermented foods. The one thing we don't eat is a ton of packaged processed foods—aside from beef sticks. We'll eat sweet potato and rice; I'm not a low-carb person.

It sounds very Weston A. Price-ish, where grains aren't eliminated but need to be fermented, soaked, or sprouted, dairy is the full-fat variety, good meats, and fermented vegetables.

Asked where his diet has landed after all his experimenting, Ben says he's pretty close to a paleo diet with a lot of fermented vegetables. Most of his carbohydrates come from underground storage organs like sweet potato, yam, and purple potato, plus berries and honey. His vegetables are mostly kimchi and sauerkraut, and he eats a lot of hunted wild game meat. His fish is farmed rather than wild caught, so he knows the exact sourcing and what the fish has been fed. He also eats steak, chicken, and pastured pork. For dessert he typically has coconut yogurt—Coco June—with blueberries and dark chocolate; he's eaten that twice today as a meal. He rounds it out with macadamia nuts and Brazil nuts.

Sourcing clean fish

He gets his fish from a company called Ctopia, which runs 30-plus farms around the world and tightly controls what the fish are fed. The fish are tested for microplastics and parasites, then flash-frozen and shipped to your house. The selection includes king salmon, halibut, and some shellfish like scallops, and it's the cleanest fish he could find.

A Middle Eastern cattle breed

The steak comes from a breed of cattle originating in the Middle East. These animals carry the myostatin knockout gene, giving them unparalleled muscle growth—"big Arnold Schwarzenegger-esque cows." As a result, the muscle fiber thickness is about 1/16th the diameter of a normal Angus cow, making the meat super digestible: a medium-rare cooks at around 95 degrees, that's how fast it cooks.

The breed also developed sweat glands, which is uncommon in cattle. Cortisol is one of the key contributors to off-flavored or tough meat, whether hunted or farmed: cortisol upregulation causes calcium influx—essentially the effect of chronic rigor mortis. A cow that can manage thermal stress eliminates one of the most common sources of cortisol in cattle, namely being subjected to extremes of heat or cold and unable to deal with it.

The cows wound up in Canada, where a farmer up north on the west side had one bull and three cows. About 30 years ago, a horse farmer in Washington state connected with these folks in Canada and shipped some across the border.

A year and a half ago, Ben got an Instagram message from a farm near Spokane saying they had the only 100% pure Piedmontese beef in all of North America—otherwise it can only be found in Italy and the Middle East. Much Piedmontese beef is crossbred with Angus, at 75/25 or 50/50, so he talked to these guys and then actually went to the farm. When he asked whether it was grass-fed and grass-finished, they said no: it's grass-fed, acorn-fed, fed pressed wine grape skins and carrots—a customized diet from birth.

He ended up buying a whole steer, and these animals are massive. The farm stores it and ships to him as needed, so he's still ordering off a spreadsheet. He, his wife, and his 18-year-old sons still haven't eaten the whole cow, nearly two years later.

Because the meat is so lean, when he asked the butcher for tallow to cook his potatoes with, they told him there is none—no drippings, no fat whatsoever. When cooking it, he adds plenty of olive oil or tallow, because he thinks the flavor profile without the fat is still a little too lean. The company is called Monzo.

Fiber, Bloating, and the Supplement Boom

The listener or watcher is thinking, "I'm never going to get that cow. I tried to get some of this meat and couldn't get it." I talked to the founder and asked how many cows they have — it's VIP, it goes to the NHL and NFL.

They do. But for everyone else, there are meal delivery services. I use one that's only in Texas, Oregon, and Denver. There's a company — not Piedmont, what is it, Grazing? There's another one. Well, anyway, there is a company called My Fit Foods, available in Texas, and they use grass-fed, grass-finished beef — for those of us who can't get the crazy stuff.

What about beans? I haven't heard you say anything about beans.

They have beans in it.

Beans do not agree with me, so I don't want to talk about those.

It's insoluble fiber. The whole blue zones data — which is rife with birth record issues and falsified data — but I think you could make a case that legumes and beans in general do provide good fermentable substrate for the microbiome. It's just that in many people, including myself, those bacteria produce massive amounts of gas. I'm not a chili guy. I don't know about you guys.

I love chili. I don't know whether it loves me, but I absolutely love it.

Why the interest in fiber?

Why the fiber? Why are you interested in fiber right now?

I just have this prediction. Seeing what's happening with probiotic fiber at the moment — Lollipop, Poppy, Bloom Pop, that whole world — and looking at what happened with AG1, with companies like Seed, with David Beckham's new thing, IM8: if you want to sell to women, put bloating on the front of the packaging. Every woman's worried about bloating. How much of this is just an artificial solution to an artificial problem? Tons of high-calorie, highly processed foods, sugar, fermented foods — maybe some EPG or something else in there. Whatever it is that's happening, it's causing people to feel digestively off, and now they're looking for the solution.

We've already been through the protein revolution; the creatine revolution is happening now. I think people are now buying more fiber supplements than protein supplements. That's a problem. Paradoxically, fiber contributes to a lot of the issues just described. And the elephant in the room is that one of the primary causes of all that gas and bloating is lack of digestive enzyme production and slowed gastric emptying — most of what happens when you eat quickly or in a stressed-out state, which basically defines a lot of our culture's eating habits. Slow eating and eating in a parasympathetic state would be way better for people's gas and bloating than sucking down a bottle of inulin.

"Did you see that recent study on eating speed and endogenous GLP-1 release? Can you explain it?"

The body releases GLP-1 naturally, typically in response to protein—once you get a protein bolus, it should release GLP-1. The response should be very short-lived and then done; this is how protein increases satiety. Some fat is likely involved as well. The faster you eat, the faster nutrients arrive, so I'd assume the GLP-1 response would be smaller.

Eating more slowly produced a higher GLP-1 release, meaning people felt satisfied more quickly.

Satisfied, yes—but the question is how long that lasts. It would not be comparable to the long half-life of a GLP-1 drug.

All I know is that if you look at digestive enzyme production, vasoconstriction and reduced blood flow to the gut, and slowed gastric emptying, it's better not to suck down your superfood smoothie while driving 60 miles an hour down the highway on your way to work. I'd rather see someone fast, or wait until they can actually eat in a parasympathetic state.

Asked what the current data around fasting says—given how often it's been debunked and re-debunked, whether autophagy really works, and whether it's just calorie restriction or an easier route to it, or whether there's something special about 16:8—the answer is that head-to-head studies of intermittent fasting versus overall calorie restriction show no big winner. There's nothing magic about fasting that beats simply eating fewer calories. The advantage of a compressed feeding window is that it becomes more difficult to eat excess calories—and that holds mostly up to about the 18-hour mark of fasting.

Past 18 hours, cellular autophagy and other longevity mechanisms start to kick in, which could make the case for an occasional longer fast, depending on your activity level and what anabolic phase of life you're in. For most men, the recommendation is a 12 to 16 hour overnight intermittent fast, with an occasional fast longer than 18 hours—say a 24-hour dinner-to-dinner fast once a month. On top of that, tied to the earlier discussion of protein cycling and protein restriction, is a quarterly fasting-mimicking diet: a few days of slightly underfeeding protein and calories to simulate a famine-type scenario.

The reason this is framed "for men" is that for premenopausal women, regularly fasting longer than 12 hours may affect kisspeptin, which is upstream of LH and FSH—fertility-related hormones. So women should stay closer to the 12-hour mark, men closer to 12 to 16 hours, and postmenopausal women closer to the 12 to 16 hour mark. In short: a daily 12 to 16 hour intermittent fast, a quarterly fasting-mimicking diet, and about once a month a 24-hour dinner-to-dinner fast.

Asked whether this means there is something special about autophagy and cell clearance in intermittent fasting versus grazing with restriction: yes, once you get past 18 hours—but in most cases the definition of intermittent fasting isn't these long one-to-three-day fasts. It's typically a daily compressed feeding window, usually topping out around 16 hours.

On whether a 24-hour fast has some special benefit: occasionally, but you have to balance the anabolic-catabolic tradeoff, and there are other ways to trigger those mechanisms, such as through training stress. If you're somebody at risk of frailty—or just trying to get yoked—(a joke follows about whether people at risk of frailty actually listen to this podcast).

Asked where people waste the most money or effort on longevity diagnostics or interventions, the guest points first to tests that add little beyond what you can learn yourself. The MTHFR test, for example, only gives you more knowledge — you could reach the same conclusion through process of elimination, cutting and adapting which supplements you take and trying methylated versions, and save the money.

The problem with relying on lipid panels

His contrarian stance is that too much emphasis is currently placed on cardiovascular risk based on a risk score — high blood pressure, smoking history, family history of cardiovascular disease — plus a lipid panel: LDL, HDL, triglycerides, Lp(a), ApoB. That can be a clue, but it is definitely not a telltale sign of actual plaque deposition in the heart.

He is increasingly convinced of this after seeing many people return from CCTAs — a CT angiography of the heart, usually with AI-based diagnostic imaging — that clearly show where hard, stable plaque (typically seen in athletic populations who have scarred up their hearts a bit) or unstable, more likely-to-break-loose plaque that can cause a stroke or heart attack lies. The reason this matters is that many people, including himself, have a pretty good lipid panel, yet the CT angiography reveals plaque deposition that, if not monitored and addressed — either allopathically with a statin or a PCSK9 inhibitor, or more non-traditionally with enzymes like lumbrokinase or nattokinase, or a new cyclodextrin currently in trial to actually break down plaque — means you could be at risk and not even know it. Conversely, you could be on a statin or Repatha due to high cholesterol and not even need it, because you have no plaque deposition.

So myopically focusing on a lipid panel either causes people to be prescribed a medication they might not need, or tells them they're okay when significant plaque is actually at play.

Who should get a CT angiography

When asked whether people should just get a scan instead of obsessing over lipids, he says anybody with a history of hard exercise or a family history of cardiovascular disease — adding that he's not a doctor and this shouldn't be taken as medical advice — and even perimenopausal women, whose risk goes up significantly, should get a CT angiography.

He notes that after men leave the pediatrician, there's traditionally no reason for them to see a doctor, whereas women continue going to an OB/GYN for gynecological exams. That's a mistake. Getting a baseline testosterone and baseline cardiovascular testing is valuable, but not necessarily treating with medication. He recommends a baseline heart scan by age 40, covering both hard and soft plaque. The gold standard is a Cleerly scan, which quantifies plaque in cubic millimeters.

The gap in muscle imaging

On measuring muscle, he thinks the future lies beyond DEXA. DEXA compartmentalizes bone and body fat percentage and extrapolates lean body mass, but doesn't assess muscle quality. We don't routinely image muscle quality — he believes they do in Japan, via ultrasound or MRI. You can occasionally glimpse muscle quality if you get a treatment like a stem cell injection done under ultrasound, but it isn't done routinely.

That's a significant omission, because fat within the muscle is a greater driver of insulin resistance than body fat percentage — and we don't image it.

So you'd be looking at a whole body MRI rather than a DEXA. Yes — you sit still for an hour, and there aren't that many of them available.

There's a new alternative, though: a water-based scan where you step into what's basically a hot tub, and it uses frequency-based mechanisms to produce a digital signal similar to a full body MRI. An AI-based company is developing it, though I don't know quantifiably how well it works. That's the future of medicine — but you still need a DEXA for bone density. Looking at tissue quality this way, I think, will turn out to correlate with insulin resistance and disease outcomes.

What surprises me is that Cleerly scans aren't more widely used, given that heart disease is the number one killer.

They're more expensive, and depending on the speed of the machine, they subject you to a somewhat significant amount of radiation. There are also still holes in the process: if you got a CT angiography in 2024, the software algorithm has changed something like six times since then. Running the same data through updated 2026 software means the results aren't necessarily comparable — you have to request your raw data and run it back through the old dataset. So there are issues, but even if this falls into the "concierge-based medicine" category, I think more people should be considering a scan like that.

Do you have any idea how much Cleerly costs out of pocket? A grand, maybe? Yeah, I think it's around that. That's not cheap, but you don't need to get it done often — get a baseline at 40 as a guy. It's controversial. I've seen claims of up to 97% accuracy correlating carotid intima-media thickness scores with a CCTA — using actual ultrasound to look at carotid plaque deposition and, based on datasets, correlating that to what you'd get from a CT angiography. That's a five-minute scan on both sides of your neck. It's difficult to estimate how powerful that prediction really is, but unfortunately a lot of companies in this space claim it's really close to CT angiography.

Full body MRI is also very controversial, but we recommend them. These are early detection screening tools. You'll hear physicians say, "Why would you screen for something? What are you going to do about it?" Well, that's like saying, "I don't want to look under the covers — I'm just going to hide and put my head in the sand." If there's an issue, you want to find it early.

It can freak you out, though. I have full arthritis, literally from my cervical spine down. But a lot of what shows up doesn't necessarily mean you need surgery — or that you need your spine operated on. In my case, I do Stuart McGill's big three, I hang from a table, I do a lot of plank training, I take care of my spine, and I always have a giant water bottle behind me on an airplane, which helps a ton. So I go relatively pain-free, but the full body MRI shows I'm super messed up — my entire spine. It can be scary for a lot of people. Have someone else read the scan for you.

A lot of it comes down to good clinicians having good conversations. Same thing with cancer screening: we can screen for 200 types of cancer at stage zero, and tell you seven years in advance — we use the Galleri test. But then it's important to have the nuanced conversation, and to have the time for it. Traditional medicine will say you don't need that; we will.

I helped implement this with special operators, because they're exposed to so much — they have threefold the risk. Burn pits, you name it. Where does that come from? Exposure to random particulates. Also shooting guns — all that gun powder gets absorbed through your skin, and people don't think about it. We've saved guys' lives because we caught things early enough in detection.

Back to microplastics — here's a crazy example I didn't realize until a meeting with Ken Paxton, where a woman advocate was banging on the desk about it: girls now start putting on lip gloss between ages six and eight. The average American girl starts between six and eight, and it's flavored lip gloss.

Moms and dads are buying it, but it's loaded with microplastics, so the kids are absorbing plastic. The reason your lips are pink is that they have more blood vessels, which means a higher absorption rate — so little girls are absorbing crazy levels of microplastics through lip gloss.

The immediate advice: avoid lip gloss, and don't eat right after loading your mag.

Surely someone will come along and make a kid-friendly, microplastic-free version. At minimum, they need to change the labeling of what's called "all natural" and mandate disclosure of a risk profile. Texas is looking at potentially forcing companies to do this, but what we've learned with food is that if you can get two or three big states to act, it's so painful for the big corporations that they'll just change the label everywhere — because they don't have to split their labeling by state.

The conversation turned to whether warning labels might spread the way they have in the UK, where cigarette packets devote nearly 90% of their surface to graphic health warnings. Could the same happen for microplastics or other harmful elements — even a photo on a lip gloss bottle? The joke about tiny testicles landed on a real concern: microplastics are one suspected contributor to rising infertility, with studies finding that 97–99% of men have microplastics in their testicles.

But there's a catch in that research: much of the contamination may have come from the gloves worn during the study itself. Nitral gloves bend because tiny bits of plastic break off them, so the plastic gloves used in the experiment contaminated the very samples meant to detect microplastics. A March 29th University of Michigan study confirmed it: common nitrile and latex gloves release tiny particles called sterates, which closely resemble microplastics and can contaminate samples during testing — in some cases producing wildly exaggerated results before researchers tracked down the unexpected culprit.

There's a lot of confusion and misperception around microplastics. The sweat scare is one example; chewing gum is another. The microplastics in chewing gum are actually too large to be absorbed in the gut in significant amounts in most cases, so gum is less of an issue than headlines suggest.

What actually matters: oral exposure from food

A major study a few weeks ago compared how much microplastic exposure you can actually reduce through lifestyle changes — clothing, food packaging, and personal care products like shampoo and conditioner stored in plastic bottles. The number one contributor, bar none, was oral exposure via plastics in your food — what you store food in, or food you buy wrapped in plastic. If you're going to change anything, start there.

That's hard to act on, though: almost everything at the grocery store comes in plastic, and we live in a society currently engineered for you to get your food in plastic, even when the food itself is healthy. One guest admitted that ten years ago he heated his pre-prepped meals in their plastic containers in the microwave — something he now avoids by transferring food to a plate.

He asked the meal company for their data and confirmed there was no BPA in the containers or covers; they use an expensive supplier specifically to avoid microplastics.

The same issue applies to canned drinks: every can contains a plastic liner to prevent contamination from the metal. The alternative is a biodegradable, natural plant-compound liner, and they're currently costing out what it would take to switch. The reaction was half supportive, half wary — who knows what the replacement turns out to be ten years from now, some phytoestrogen slowly taking over your brain.

Asked where attention will go in the future, the speaker predicts air quality is going to be huge — it's just coming online — along with internal light pollution: flicker, LED, and similar issues. Other guests add social media and anabolics as trends that will keep growing.

Social media and child development

On social media, the point is that we have awareness but don't yet really understand how detrimental it is to children and development — the level of technology kids are exposed to will have some major impact that we'll look back on and ask, "Was that the tobacco of our time?" The smoking of teenagers in 2026, in other words.

Anabolics beyond testosterone

On anabolics: these are the anabolic agents used in HIV and wasting conditions, FDA-approved — things beyond testosterone, like nandrolone. The question is whether anabolic agents will become an increasingly popular treatment strategy for sarcopenia. There's an amazing study on nandrolone and bone mineral density, and there are chondrocyte receptors for growth hormone, suggesting a possible use for actual cartilage repair.

There's also the issue of free versus total testosterone in men: total testosterone can be at an optimal level while free testosterone suffers, often because of sex hormone-binding globulin (SHBG). Adding a micro dose of an Anavar-type compound will, like Pac-Man, gobble up the SHBG, spiking free testosterone.

But the elephant in the room with SHBG is that it also increases when the body senses famine, starvation, stress, or any scenario in which it would be unwise to bring more humans into the world. People on a strict ketogenic diet have high SHBG, as do people under heavy cortisol load and stress. So in many cases the fix can be as simple as eating more carbs with dinner, sleeping a little more, and lowering stress.

Nandrolone in older men

Asked about nandrolone in older male populations — keeping them on testosterone cypionate or enanthate but adding a micro or low dose of nandrolone — the speaker thinks that's going to be the way of the future, and we have to address it.

He cites a mutual friend, Dr. Larry Lipshultz, the godfather of male fertility, whom he's known for some 30 years. Lipshultz has been using peptides for literally 20 years, used to write for GQ magazine, is heavily accredited at Baylor College of Medicine in Houston, Texas, and literally wrote the book on urology. He's the one who originally taught and helped the speaker: at 25% body fat, doing CrossFit daily, eating right but feeling run ragged, the speaker was optimized from 25% to 7% body fat without testosterone. Lipshultz used HCG and clomiphene and was one of the first to do so.

But that's the future—we have to address it. Whatever happened to GHRP-2 and GHRP-6 and mod GRF? I was messing around with that 15 years ago, and I'm surprised that when we're talking about growth hormone, the approach is to go exogenous rather than trying to create some endogenous feedback loop.

You mean like growth hormone secretagogues?

I think better options came out, and there was such a hunger surge too—there was a lot of—

Did you ever use it? Try it?

No. GHRP-6 was an early growth hormone releasing hexapeptide and bipapeptide.

You know who prescribed it to me? Larry Lipshultz, and again, this was like 15 years ago.

I think the other peptides you were talking about, like tesamorelin and ipamorelin and CJC-1295, have replaced a lot of those—they're what people are using now.

Do they mimic the same sort of effect?

Yeah, same pathway, but with a lower side effect profile.

We used to shoot it when I was in university. The only way you could use it was if you hit yourself with it as you were cooking, because by the time you finished the meal you were beyond ravenous—it's just dumping ghrelin into you over and over. It was overwhelming. It was great if you're trying to put on weight.

So what happened? Is it still used?

No, it's transitioned out. Nobody really uses it. Everything would be stacked secretagogues now.

By the way, you mentioned light pollution and you said air pollution, right?

Yes. I think air quality and light quality are going to be—

I think water and electricity are three and four.

I think water's already been done. Electricity would mean non-native EMF, such as Wi-Fi routers, 5G, square waveform signals at a higher intensity—things that may cause either actual thermal heating if very close to the body, like cell phone radio frequency, or low-level upregulation of channels in cells. How crazy do you go at the adenosine level? Are you that aggressive with it?

My house is pretty aggressive. Everything is hardwired with metal-shielded Ethernet cables. There is no Wi-Fi. Every floor is grounded. At my house we pulled out all the stops in terms of circadian-friendly lighting to address light pollution.

You don't understand—air filter, air scrubber. Ben showed me the guy who came in to help. Who was it, the bio-home guy?

Brian Hoyer.

Right. This guy comes in looking like a dude out of Ghostbusters, with more meters than you've ever seen in your life—like Dr. Octopus, magnetic and everything attached to his arms, going around like he's spraying for poltergeists. He's like, "I can see there's some 5G in the corner. We've got to get rid of the 5G in the corner."

"There was a murder here 20 years ago."

So do you feel a difference?

Oh, you absolutely feel a difference. A lot of this stuff has the big fat woo bat signal on it, because it is an inconvenient truth that there may be an effect on everything from the neurochemical balance in cells based on low-level exposure to radiation, radio frequencies, or EMF, to the effect it might have on something like negative ion load in the body—which is why I'm a huge fan of grounded floors, earthing, grounding, going outside barefoot. But I don't think there is a biological free cost to having a radio frequency device in your pocket, as some bone scan data suggests might be an issue, and sperm data, or just sitting next to a Wi-Fi router.

Somebody broke this down—isn't there, in the iPhone itself, a disclaimer that literally tells you you're supposed to keep it a certain distance from your body?

A great disclaimer. I think the best metric, though, is if you eliminate that stuff. The single most important place to do it is your bedroom, where your nervous system has a chance to arguably repair and recover for like 8 hours of a 24-hour cycle. But as many places in the home as you can downregulate exposure to that stuff, I think is a good idea. It fits right into the category with light, water, and air.

Are you worried about Eight Sleep, then?

I do not use an Eight Sleep for those reasons. I use a different one that still cools my bed but tests lower with an EMF meter.

Although I prefer my Ghostbuster, too.

Talking to a bunch of friends, they Faraday-caged the cooling tower of their Eight Sleep. If you do the actual test, there's much less EMF on the pad than on the controlling device itself. So they just Faraday-caged it totally.

Asked for a layman's explanation of the most defensible science on EMF exposure—ionizing versus non-ionizing radiation, Bluetooth, wireless headphones—the guest started with Class 3 Bluetooth signals, which cover most of what people use on their heads and ears. There is very little data showing any deleterious effect, so using wired headphones is less a proven necessity than a "not sure, so I'll play it safe" strategy—a technological Pascal's wager, as the host put it.

For Wi-Fi, 4G, and 5G, the biggest factor from a cellular electrochemical standpoint is proximity to the source. The farther you are from a Wi-Fi router in your home or office, the better. A neighbor's Wi-Fi isn't much of an issue even if your home isn't fully lined with Faraday paint and cages, because the distance is large. The real problem is sleeping with your head one to two feet on the other side of the wall from the router.

Other common concerns include electric cars. Teslas are actually designed to be fairly low EMF, but there is one signal that exceeds the safety limit in the back seat right next to the battery—relevant if you put a child there. The rest of the car tested safe; the guest has a video online where everything in the Tesla was measured. If you were going to shield anything, it would be the back seat.

The other major household sources are appliances—dryer, washer, and the microwave while it's running—so keep them away from the bedroom or anywhere you spend extended time. In short, don't put your laptop on the washer and work there all day.

With phones, two things matter: proximity to the body and the signal strength. The lower the bar signal, the higher the radio-frequency output as the phone searches for a connection. When a plane is about to land and a hundred people all switch their phones on at maybe 2,000 feet with one bar of signal, that's a genuinely high-exposure moment—a hundred devices pushing out a lot of radio frequency while all searching for a signal at once. That's the moment to put on your tinfoil hat, or an EMF-blocking one; both speakers mentioned owning EMF-blocking headwear for long-haul flights.

The host said the Tesla back-seat finding blew him away. The guest noted that where there's a problem, a solution will follow—presumably someone will make a shielded child seat. He has called four body shops and found none willing to install shielding material, and the Tesla dealership won't do it for warranty reasons. For now, a large piece of shielding fabric from Brian at Shielded Healing just sits in the back of the car, because he hasn't found anyone to pull the seat out and install it properly between the back seat and the battery—a business opportunity, he suggested, for "biologically safe EMF shielding for the back seat of a Tesla."

Asked whether shielding makes a meaningful difference, he said yes: when the material is in place, the meter reading drops. The problem is purely aesthetic—a giant piece of shielding fabric propped in the back seat—so it needs to be installed under the upholstery.

The host then mentioned watching the guest's new documentary and offered his congratulations, which the guest accepted.

I was watching your documentary last night and looking at you.

By the way, he was disappointed they didn't actually show the penis injection scene.

I was only there for the penis. I only arrive at events for that—me and Zac Efron at the back of the cinema, just waiting: show me the penis.

One thing I noticed was the most Ben Greenfield thing in the world: designing the perfect house to ensure there are no EMFs, with everything locally networked and copper wiring and all the rest of it—while the living room is full of tons of boxes of new stuff he had sent to his house. Tons and tons of cardboard boxes. That's a man who gets lots of packages, and I have a soft spot in my heart for a man that receives a lot of packages.

It's the worst when you try to deal with them. I literally have an assistant who sits at home, opens packages, and sends me photos to an ASA project while I'm traveling, so everything can be unboxed and put away by the time I get home. One of my greatest sources of stress when I travel is coming home to all the boxes, so I've outsourced that.

I enjoyed seeing the boxes—lots of cool free things.

On the air quality front, CO2 is something people are going to pay a lot of attention to, but that's further down the line. Before that, it's going to be humidity and mold — huge. If we had small travel mold detectors you could put on your backpack, that would be amazing. Air quality detectors generally would be amazing. Or like a canary you could train for mold.

One of the problems — I only found this out from speaking to Mike from Jasper — is that you can't have the sensor inside the scrubber itself, because the turnover of air is too high. It's basically pulling air through the sensor, so you always have to have two separate units: the detector and the scrubber.

If you could have the perfect setup at home and weren't renting, you'd put in your own HEPA filtration system. That means three things. First, a filter — the MERV rating is the particulate rating, the actual filter catching stuff that you pull out and change every six months or so. Then a scrubber, which keeps mold from building up in the ducts themselves, usually using UV or ozone. And then a recirculator pulling in fresh air from outdoors, so you're not just filtering stale air. Scrubbing, recirculating, and filtering — all three together is the best setup.

So it's three different technologies, typically used in something like a central HEPA filter. And I think this is where Mike from Jasper is going to end up: all of this can be fixed if you just build it into the AC. If you go after the AC unit, you don't need any of the additional standalone units. The reason Jasper exists right now is that there isn't enough cleaning going on through the AC. If you're in an apartment block or a house trying to retrofit that, you'd have to bodge it together like some Ben Greenfield or Tesla car — it's too much to do. So you end up scrubbing inside a room, because the air coming in from the AC, even with a dehumidifier, is tough at best right now.

What did you do for your AC? Did you have to bodge it together, or did you find something ready-made? We went with a local company called Laser, and they do scrubbing, filtering, and recirculation at the particulate level needed to get rid of mold. They use a MERV filter that will basically catch anything at PM2.5 — I think PM2.5 to PM10 are the main sizes to be concerned about.

But I still use standalone units because of wildfire season, and also the kitchen: the hood over the stove is mounted too high to actually catch everything released when you're cooking. So even with a filter in the kitchen, you get a massive amount of PM2.5 every time you cook. I have a standalone HEPA air filter in the kitchen, and a bunch in other rooms that I pull out during wildfire season or when there's smoke. There are eight Jasper filters back in our Airbnb here in Austin right now, running in every room.

To me, it's worth it. As much as I travel, I'd rather filter than get exposed in an Airbnb or hotel room and be dealing with mold for the next two years. And what you said is important: when you're exposed, you're exposed over a period of time, and it takes a long time to get rid of it. So you might as well prevent it.

You work a lot with mold, obviously. It's been a huge part of my life over the last couple of years.

Mold Exposure, Genetics, and Emerging Solutions

How brief an exposure do you need to cause an effect? Is one night worth six months of detox? Is there any equation for this? Part of it comes down to genetics—some people are affected and some aren't, so there's no simple formula like "you had low-level exposure for six months, here are your subsequent effects." But an exposure of even a week can matter.

Have you gotten sick from mold yourself? I've been pretty lucky—I haven't. I do have somewhat impaired glutathione detoxification pathways and I use some glutathione, but I've never had significant mold exposure, knock on wood.

I lived in the same house as my best friend Zach, and the difference was stark. He was ripping vapes, going to bed at 3 a.m., playing gigs, while I was getting up with sunlight in my eyes, grounding, listening to health podcasts—and it wrecked me. It really is a genetic dice roll, and I hit the inverse jackpot living in that environment. My roommate was completely untouched by it.

I think the mold issue is already picking up speed. Ariana from Mold Co is great, and I think the Shoemaker protocol—teaching people about binders, sauna, exposure, and TGF beta—is going to be massive. Mold Co has systematized everything: testing, solutions, all in one-stop shop.

Really cool—slash possibly the fox guarding the henhouse. If they're testing and then supplying the solutions based on the test results, you're incentivized to get the test. But I've gone through their website and I think they're doing a good service. You'd have to be a real scumbag to falsify people's tests so you could then sell them therapeutics.

What's cool is that all the problems we think are in the future already have solutions or proto-solutions: people thinking about LEDs for mold, Mold Co for blood testing, Function for air quality, AquaTru for reverse osmosis. The beginnings of solutions exist—it's just a matter of telling people about them.

That makes me feel more confident, because fifteen years ago these problems all existed but there wasn't even the nascent version of a company that could maybe fix them.

The best resource I ever found was a book called Prescription for a Healthy Home. It covers everything—carpets, appliances, roofing, painting. I bought it for my architect and building team because I wanted them to read it. It's thorough on building materials from the ground up, or on outfitting an existing condo or apartment you're not building from scratch. I think it was published about two years ago, so it's pretty relevant. I wanted to interview the author on my podcast—hopefully she doesn't hear this, because she was a little boring and didn't explain things well, but the book itself was fantastic.

The final thing I love, and I think it will pick up speed, is proper genetic testing. Intellex DNA is who you guys use — that Lisa put me through. It's a little expensive, and you need a healthcare practitioner or provider to act as an intermediary. I know Function is about to release their own version later this year, which will democratize it, and I'm sure you all have your own versions too. But it's the only test you ever need to do once.

That's true — until CRISPR gene editing really takes off.

Well, you got the follistatin thing when we were in Roatán together. How did that work?

I gained muscle at a more rapid rate than I would have expected without changing my protein or calorie intake or my weight training protocol — around 10 lbs in 3 months. It's not permanent; you'd need to repeat it every one to one and a half years. And unfortunately, at the time I was under the impression it was reversible in case something went wrong. It's not actually reversible.

I thought it was reversible — I thought you just took a...

No, that's the issue: it is not. The company is now readily admitting that, and doctors were supposed to reach out to their patients and tell them, oops, it's not. So the only issue now is that if you're going to get your genes edited, it'd be nice to know you could reverse it if something goes wrong.

Well, I mean, we did go to a small island off the coast of Honduras — specifically a network state that doesn't have oversight from basically any nation — so that you could get this experimental gene therapy. And now you're like, "Well, they didn't."

My understanding, from what I was taught about that technology, is that it's not editing a gene — it's turning on a pre-existing one.

You are correct. It's not a CRISPR gene-editing scissors tool; it's basically upregulating or downregulating a gene. So, joking aside, the only reason you'd ever have to do a genetic test twice in a lifetime is if you were actually using CRISPR gene editing.

That'd be pretty sick. Guys, you all rule.

The guests shared where listeners can find them: Ways2Well at ways2well.com (with the number two), and Dr. Gabriel Lion's website drgabriellion.com, which links to all of her channels and podcast. She mentioned that these two are getting PhDs to come on the show, and also pointed to Strong Medical with Lifespan MD for anyone who wants to become her patient — joking that she doesn't do rectal exams. Ben Greenfield noted there aren't many people with his name, so Googling him works fine.

The host thanked everyone for keeping people alive and signed off, and the guests agreed it had been fun. The episode closed with an outro congratulating listeners on finishing without dying and pointing them to the next episode.