The Dr. Hyman Show - The Unexpected Dolphin Discovery That May Hold the Key to Longevity | Dr. Stephanie Venn-Watson

Episode Date: March 26, 2025

What if the key to aging well had been hiding in plain sight—inside our cells, our food, and even… dolphins? That’s exactly what Stephanie Venn-Watson, DVM, a veterinary epidemiologist, discovered while studying dolphins in the U.S. Navy’s marine mammal program. She found that some dolphins were aging significantly slower than others, leading to the discovery of C15:0—a newly recognized essential fatty acid that supports cellular health, fights inflammation, and may even slow the aging process. In this episode of The Dr. Hyman Show, we dive into: How studying dolphins led to the discovery of C15:0 as the first essential fatty acid found in 90 years. Why a deficiency in this nutrient could be accelerating aging and chronic disease. How C15:0 strengthens cell membranes, reduces inflammation, and promotes longevity. The connection between diet, metabolic health, and optimal aging. What you can do to ensure you’re getting enough of this essential fatty acid. This groundbreaking discovery could change how we think about nutrition and longevity. View Show Notes From This Episode Get Free Weekly Health Tips from Dr. Hyman Sign Up for Dr. Hyman’s Weekly Longevity Journal This episode is brought to you by PaleoValley, Timeline Nutrition, LMNT, BON CHARGE, and Big Bold Health.  Get nutrient-dense, whole foods. Head to paleovalley.com/hyman for 15% off your first purchase. Support essential mitochondrial health and save 10% on Mitopure. Visit timeline.com/drhyman to get 10% off today. Get a free LMNT Sample Pack with any order—just head to drinklmnt.com/hyman. Order BON CHARGE’s Max Red Light Therapy device today and get 15% off. Visit boncharge.com and use code DRMARK for 15% off.  Try Big Bold Health’s HTB Rejuvenate and get 25% off by going to bigboldhealth.com and use code DRMARK25 at checkout.

Coming up on this episode of the Dr. Hyman show. Numerous studies have consistently shown people with higher C15, just like we saw on the dolphins, lower risk of developing type 2 diabetes of heart disease, specifically coronary heart disease, of developing fatty liver disease and certain types of cancers, specifically a lot of work on colorectal cancer. Dr. Nick Schorck, he was at ARDD, which is one of the world's leading anti-aging therapeutics meetings. He said, listen, I've seen every longevity molecule under the sun, and I've not seen a molecule that has more supportive data of being a longevity enhancing molecule than C15. At 65, I'm still pushing my limits, cycling long distances, trekking through

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check out my membership community, the Hymen Hive. And if you're looking for curated and trusted supplements and health products for your health journey, visit my website at drhymen.com for a summary of my favorite and thoroughly tested products. Stephanie, it's great to have you back on the Dr. Heiman show. Yeah.

And your work continues to astound me and discoveries that I think are going to hopefully make us all live a little bit longer, feel a little bit better, prevent some of the disease of aging. And we're talking about today the work you've done as a veterinary epidemiologist, working with the Navy SEALs, I mean, the Navy Dolphins. We're going to help the Navy SEALs too.

I feel like a Navy SEAL right now. I'm like, I'm like trying to not shiver to death and I'm not in freezing cold water, but I'm wearing a thick coat because we're in Austin, Texas. And it is freezing out with the wind chill. It's like minus 12 degrees or something. So I'd love to start by having you sort of describe, uh, the, the sort of this incredible

work you did with the Navy dolphins, which are used for kind of what are they used for? And then, and then what, what did you find as, as sort of, you looked at the natural lifespan of dolphins compared to the dolphins in captivity and how did that start to get you thinking about the sort of longevity aspect of what might be in the dolphins that you could discover and how did you begin

to discover that, so. Yeah, boy, this is gonna be an exciting talk. I love the TF. Dr. Hyman, it's great to be here. It's always good to see you. So yes, as a veterinary epidemiologist, I love the TF. Dr. Hyman, it's great to be here. It's always good to see you. So yes, as a veterinary epidemiologist, I wanted to track diseases. I read Laurie Garrett's The Coming Plague when I was an undergraduate and said, I want

to do that. And I thought it was going to be infectious diseases. And it ends up that thanks to being recruited by the Navy, to help lead their clinical research program with their dolphin population to help improve the lives of their dolphins, it quickly pivoted to chronic diseases and chronic diseases of aging. So it's been a- Dolphins get chronic disease of aging? This doesn't make any sense to me. They're not eating McDonald's and they're not exercising and they're not doing their normal sleep routine and they don't, I mean maybe they have more stress living in captivity.

Right, well that was the key question, right? It really, you hit the nail on the head that moved over to the Navy, ended up spending 20 years there, you know, 10 full years working with the Navy's dolphins with the purine goal of improving Navy dolphin health. So they live, Navy dolphins, they live in San Diego Bay, go out into the open ocean every day. Every day they choose to come back. So it's a pretty nice environment with regard to quality of life. They just are free to go and then they come back? Yeah, it's pretty amazing, right? So they live in the open ocean that's their pod. So they choose to be there and it meant a lot to me as a veterinarian. I didn't know how I'd feel.

I mean, you'll see a listing probably going, whoa, wait a minute, why does the Navy have dolphins? Like they're not... Right. Yeah. So it ends up that they're really good at being able to find underwater objects that we can't see very well. And so they've done humanitarian demining missions in the Mediterranean where they're able to find buried mines, target it. They, you know, mark it and then humans come in. And everything. The things left over from World War II or whatever, right?

Exactly. So they have now made entire areas of the world safe, which is amazing. They can also find underwater swimmers, enemy swimmers, and be able to interdict and put a leg cuff on those swimmers and they get reeled up by their human counterparts. So- Wait, wait, you mean enemy scuba divers? Yeah. Yeah, in case they were in nefarious areas, but Navy dolphins are there to help.

So what made for them, their job is easy peasy, right? They have echolocation, they're able to do these things. And the program has been so successful, being able to deploy the dolphins all over the world and have them stay, right? That that has allowed, you know, this program has been around for 60 years. They've had a sustained population of 100 bottlenose dolphins. Wow. So that has resulted in what we're talking about today with regard to this unprecedented patient population that gets older, like you had mentioned, that in the wild, dolphins live

to about 20. At the Navy, they're living into their 50s and even up to 60 years old. So... They're living like two or three times as long... That's right. ...in captivity as they do in the wild. Is that because there's predators or just it's more tough to get along out there? Great healthcare system.

Great healthcare. Good preventative healthcare system, access to fish, that you watch any kind of wild animal show these days and the world isn't so friendly anymore. Yeah. For animals, it's getting harder and harder for wildlife. Do you think the wild dolphins like a couple hundred years ago lived longer? That's a good question. I do think there are things, there are studies that have shown that there were times that dolphins might have lived slightly longer,

like maybe a few years, but nothing on the average like what we're seeing at the Navy. So there I was, right? So taking care of this older geriatric dolphin population. And what we started seeing, Mark, was an increase in that some of the dolphins were developing aging-associated diseases like chronic inflammation, high cholesterol, fatty liver disease, and even the full suite of changes consistent with Alzheimer's. And what was really important was that some of the dolphins were developing these conditions, which has now culminated in what we now understand as a syndrome, that some dolphins were developing

this and others were not. So we were able to go in, use metabolomics, which is this advanced technology to study thousands of small molecules. In your blood. Yeah, exactly, in the blood. And we had this amazing archived inventory of dolphin serum, look at those molecules in their blood and in their all fish diet to find which small molecules

predicted the healthiest aging dolphins. We expected omega-3s to be at the tip top of the list and instead it was C-15, which none of us even knew what C-15 was, but pentadeadecanoic acid was the top predictor of healthy aging dolphins. So that was 10 years ago and what started the next 10 years of research now over 100 papers on C15. That's incredible.

So basically this is C15 is a, and the number 15 is really about where the carbons and the bonds are on the chain of fatty acids. And it's a saturated fat, which in most people's mind think is bad, but it's actually not. It's actually, it turns out to be very powerful and have many effects on many of the longevity pathways.

And there's a lot of molecules that are being studied for longevity, everything from rapamycin to metformin to NAD, and the list goes on, AX, you know, astaxanthin. I mean, there's a lot of interesting molecules that are being used. How does C15 stack up against some of these? What is the sort of the research that's been done today

to help to look at what it does? How does it actually facilitate longevity? Because it's just a fatty acid, so you wouldn't think, how is it doing all these things, right? Right, right. So the first important discovery that we made, and this was alongside Dr. Ed Dennis, who's a leader in fatty acids.

So he was the editor-in-chief for the Journal for Lipid Research for 15 years. And when we first made the discovery of C15, association, right, because in the dolphins this was just association with better health, we went to Dr. Dennis to Ed and shared our hypothesis. And Ed was like, well, chances are this isn't going to pan out because we've known about C15 since the 1950s and Chances are that stuff, you know, no offense that a dolphin veterinarian didn't discover something new about fatty acids And he's like but it's intriguing about the dolphin

So we spent the next three years doing eight studies to show that C15 not only has direct Benefits and is a beneficial saturated fat like you shared, but that it meets these rare criteria of being an essential fatty acid, the first essential fatty acid to be discovered in over 90 years. One makes something an essential fatty acid because we think of these things as essential for life

and if we don't have them, you're gonna be in trouble. Like there's essential amino acids, fatty acids, by the way everybody, there's no such things as essential for life, and if we don't have them, you're gonna be in trouble. Like, there's essential amino acids, fatty acids, by the way, everybody, there's no such thing as essential carbohydrates. Right, it's a good point, good point, dang it. But, you know, what makes it essential, and how do we have to think differently about it? We do, yeah, so what we've learned is that

our bodies require a certain amount of C15 in our bodies, including in our cell membrane. It's a sturdy saturated fat that is, because it's an odd chain saturated fatty acid, has an odd number of carbons, it has anti-inflammatory properties. We'll talk about all the different mechanisms that C15 has.

So it's really this Goldilocks healthy fatty acid that is essential to maintaining the stability of our cells. If we don't have enough C15 specifically, at least 0.2% of fatty acids are C15 in our cell membrane, our cells become fragile and we develop a nutritional deficiency syndrome, which we published last year in Metabolites called Cellular Fragility Syndrome, the first deficiency syndrome to be discovered in 75 years, which leads to, you know, we can talk about this whole new form of cell death called ferroptosis. So it's been, you know, an accelerated...

If someone has fragile cells, what does that mean? What are the consequences? How do they feel? Right. So if you have fragile cells, your cells basically start falling apart, which is what happens when we age. So a lot of aging-related breakdown that we feel,

our aching knees, our foggy brains, our slower metabolism, increased inflammation, all of those things come with more fragile cells which leads to, if we nerd out a little bit, leads to lipid peroxidation. There's this abnormal iron sitting inside the cell. They combine and they cause this increase like explosion of reactive oxygen species that take out the cell. So when that happens, our whole bodies get affected from our immunity to our metabolism.

So it ends up that while this process, C15 deficiencies, can accelerate our aging, and everything that we feel with aging, we've now been able to work with the Navy and look at how can we optimize C15 to flip the story and how can we actually optimize our longevity through C15. So you talk also, you wrote a book actually just quite good, it's called Longevity Nutrient

and the full title is The Unexpected Fat That Holds the Key to Healthy Aging. So it's kind of a good title, it got my attention. I actually have been measuring fatty acids in my patients for decades and decades. And I'd always see C15, but it didn't really register as something that was important to look at. And now I look at it every time,

and I'm surprised to see how many people are actually quite low in C15, which comes from dairy products, right, and from fatty fish. That's right, that's right. And so now we're seeing that as many as one in three people are C-15 deficient. And then there are some that are extremely C-15 deficient, right, which you'll see on your test.

And it's exactly for that reason. We have taken C-15 out of our diets globally. So our primary source, Mark, like you just shared, is dairy fat by far. And we're not saying go back and eat a bunch of dairy fat. 1% of dairy fats is C-15. Over 40% of the fatty acids in dairy fat are pro-inflammatory saturated fats. So we still need to work our way through that.

But the Navy was interested enough to say, hey, can we find a way to use C-15 and leverage it for longevity? Meanwhile, let's also talk about the need to prevent these deficiency syndrome that's showing up in our kids. And that might just be by helping to get milk fat back into kids' diets, including mom's milk fat.

Yeah, breast milk for sure, although conventional dairy has a lot of problems and is very inflammatory for a lot of people. That's right. I wonder if it's high levels in goat or sheep, is it? It's a good question. So what the studies have learned is that C15 levels are driven by what the ruminant, so

it could be a cow, goat, sheep. Whatever what you're eating. What they eat. Yeah. So if you feed either a cow, goat, or sheep grass, it has twice as much C15 in its dairy fat than fed corn. If you feed it high altitude grass, it has been higher C-15. So, you know, we don't know when you go by your dairy product, what that animal was eating.

And so one thing that we're pushing for is to have the dairy industry report C-15 levels in their, you know, in their foods and to help change industry practices to help maximize C-15 levels. Interesting. Yeah. So it's not, you're not what you eat, you're whichever you're eating eight.

That's right. That's the stuff that you've got that. Yeah. Now let's get into some of the sort of the, I mean, the discovery of it's fascinating. You know, so you've had this like trove of blood from dolphins for decades and they can go back and check like, okay, who are the dolphins that age fast?

Who are the ones that age much more slowly? And then you kind of looked at all of them and then rose to the top where, where we'll see 15, but you mentioned there's like a hundred other molecules you're looking at that may have promising benefits too, that we haven't looked at. And that's the beauty of sort of modern science, where those listening, we really have gotten the ability to look at not just 20 blood tests or function. We do 110 and there's now ways to do metabolomics, which looks at thousands and thousands of molecules that are floating around in your blood that have meaning and that do things,

but that often we've neglected or ignored. This is clearly one of them. In terms of this seven longevity enablers you talk about, FATI-15, which is the sort of brand of the product, C-15, which you can now actually buy, and I personally take it every day, is because the science was so compelling to me that I was like, okay, well, this is, you know, if it doesn't work, you know, okay,

but if I'm missing something, it's gonna be a big deal, so I wanna take it. What are the sort of seven you call it it must haves of a longevity enabler that this molecule meets? Yeah, so there are, we have established these seven must haves. And by way, I mean, you know, the longevity scientific community. This was also put together in part with Dr. Nicholas Shorke, who is the head of NIH's Longevity Consortium. And so Nick was really interested in the dolphin angle, because he's like, wait, you've got a long-lived species that has clean data.

So let's work through that to make these discoveries. And when we get to these longevity must haves, we're now able to, you know, a lot of longevity research is on short lived species of how do we help mice and worms live longer. Right. And it's like. We're good at making worms live to be like a

thousand years old. And it doesn't really translate. Right. And mice, you know, to be like 120. So, you know, Nick really, Nick and I really came in and we're like, oh my gosh, we have this incredible opportunity. Nature's already figured it out, right Mark?

I mean, nature's already figured out how a mammal can live 27, 30 times longer because humans and dolphins and elephants live a lot longer than a mouse. So why? So let's figure out how evolution has already enabled massive longevity enabling, tap into that and then make it even better.

So... Yeah, so the bowhead whales are like 200 years old. Right. So it's just like, let's focus on these species, not to dismiss the... The basic science. The basic science, right, the basic science, but it's an unlock, right? So the seven must-haves of longevity, and this is assuming that longevity, the way we define it is as a geroprotector.

So a molecule that slows our aging rate and therefore slows the onset of the chronic diseases that kill us. You mean that actually live longer, but you'll live healthier. Healthier, and then by default, be able to extend your own longevity, so that you can live longer.

So of those, the seven longevity must-haves are, first, this molecule needs to tap into the longevity regulating pathway. It's this complicated keg. It's called the keg pathway. And it's based upon a hypocaloric diet, so caloric restriction and the whole pathway that's been built out on how caloric restriction extends longevity across multiple species. At the heart of it is activating

AMPK and inhibiting mTOR, which as you had mentioned, Metformin activates AMPK and rapamycin and inhibits mTOR. C15 does both. So that was really exciting to see. It's really hitting at the heart as other longevity molecules. Did you know that staying hydrated isn't just about drinking water?

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amazing product. You can try it now by heading to bigboldhealth.com and use code DRMARK30 again, that's big-bold-health.com. The second is that it needs to target. And just to back up on that for a minute, if you might not understand that. So AMPKs regulates a lot of things, inflammation, your blood sugar control, your mitochondrial function, and it interacts with a lot of other longevity pathways.

I call them longevity switches, like the four longevity switches that I wrote about sort of in my book, Young Forever, which is mTOR, which regulates protein synthesis, and also when you inhibit it causes autophagy, which is cellular cleanup, which is really important to healthy aging, insulin signaling, which we can talk about,

and that causes us to kind of reproduce insulin and leads to obesity and diabetes and Alzheimer's and cancer and pretty much everything else. And then there's the pathway, the, uh, pathway called sirtuins, which is very involved in, in, in, um, regulating DNA repair and oxidative stress and other than that, overlapping redundancies in terms of the key fundamental things of aging, which we talk about in the hallmarks of aging, whether it's mitochondrial dysfunction, whether it's autophagy, cellular cleanup,

whether it's inflammation, oxidative stress, blood sugar regulation, protein synthesis. So all those things are necessary. And they're fundamental to understand because they're the things that underlie all disease. And what people don't realize is now we're discovering these new frameworks for understanding disease that are based on root causes.

And so the hallmarks of aging are really discoveries that have helped us map out what are those things that disease that are based on root causes. And so the hallmarks of aging are really discoveries that have helped us map out what are those things that tend to go wrong as we get older. And now we can think about how do we treat those. And if we treated those, we might extend life by a third, rather than just, if we got rid of cancer and heart disease, we'd extend life by five to seven years.

We completely eradicated from the planet, so that's not much of a life extension compared to 30 years, right? That's right. So, um, they're really important to understand, but there's also causes of dysfunction, which I think doesn't get addressed. Like why do we have these dysfunctions?

But C15 seems to work on some of these key pathways around the hallmarks of aging. That's right. That's right. Thank you for that. And, and your book, by the way, does a great job explaining all of those. So. It's hard to explain, trust me. If, and your book, by the way, does a great job explaining all of those. So.

It's hard to explain, trust me. If anyone wants to dive in more, please, yeah. Young Forever. If you want to read it. Please read, please read, yeah, your book, Young Forever. So, and then, so then the second one exactly feeds into the hallmarks of aging.

There's 12, it keeps getting, the list keeps getting longer. It feels like every couple of years. It was nine, it was 10, it was 13. Yeah. So, um, uh, there's now, uh, multiple studies, uh, showing that that C15 targets six of them. And that includes, um, helping C15 directly repairs mitochondrial function.

It has the skip function where it's able to help restore broken mitochondria, um, by enable, enabling it to make energy when normally it wouldn't be able to Which is exciting. Yeah And important it helps with poor cellular signaling We know that it not only activates AMPK and inhibits mTOR but it also activates P par alpha delta and

AKT and it inhibits JAK stat and H DAK six. So that was a bunch of letters. What she's saying basically in English is that these are, these are other pathways that we all have that regulate inflammation, that regulate blood sugar and that, that when we look at actually the things that drive aging, it's dysregulation of blood sugar and insulin and inflammation that is

a consequence of that. And the downstream effects is it harms our mitochondria, causes more oxidative stress. It has so many awful effects on inhibiting autophagy and causing stem cell exhaustion and shortening telomeres and all the things that I talk about in my book. So, you know, when you kind of get to the kingpin of what's going on for most of us as we age and what's so curious about these long-lived dolphins is that they they had this protective molecule that they seem to accumulate. Now what I don't understand is if all the dolphins were eating the same stuff and all of them had the same environment like why were some actually having high levels of C15 and

others it's some genetic component here that we don't understand or there's some variability and how people keep or utilize it or absorb it? What explains that? Right, so with the dolphins, it was pretty, it ended up being pretty straightforward. So they have an option of five different fish types and or they might be fed different fish types

based upon what their job is at the Navy. So if they're doing a job in which they're going through, you know, training of learning how to find an object, for example, they might get a bunch of low fat fish that they get kind of, you know, given throughout the whole day. It ends up that those low fat fish had no C-15 in them. And what we were able to get to remarkably, it ends up that those low fat fish had no C-15 in them.

And what we were able to get to, remarkably because the Navy's vigilant data collection, we were able to see that some dolphins were getting a higher C-15 diet than other dolphins. And then even better, we did two Navy funded studies in which we gave those dolphins with lower C15 a higher C15 fish diet, and we saw that their aging-related conditions reverse. So then we were like, oh, okay, now we're onto something.

That's how you test the hypothesis, right? You see, oh well, it's associated with, the lung injury, but it's a causal. That's right. When you add the molecule into the diet through fatty fish, it actually reverses the things that you saw as, as consequences of aging. That's right. We saw complete reversal of anemia. If you get the fish, the dolphin herring, that's good. But if you give them like flounder, probably not so good, right?

Yeah, that's right. It was not like a common food that we eat, but it was like capelin and squid. Squid had no C15 in it, but you're right. Herring was a great, and mackerel were great fish. So that's how it led to all of those. So then with the Hallmarks of Aging, targets six of them, it helps with, we now understand from a clinical trial, it helps with gut dysbiosis.

How does it do that? So C15 multiple ways. A lot of exciting research coming out on C15 for gut health, not from us, from other teams around the world. They've shown, multiple studies have shown that in multiple mouse models of colitis of IBD with regard to leaky gut syndrome, that C15 specifically helps improve the gut lining and it stops the leakiness. So it decreases inflammation and it stops the leaking. Is it because it sort of embeds itself

in cell membranes in the gut? That's it. It becomes more stable and less fragile. Is that the kind of hypothesis? That's the hypothesis. We know that it gets in there. We know that it has this effect. And so it helps with that.

In addition, really fascinating work on the microbiome that in a clinical trial that was done in Singapore with C15 supplementation showed that women who had a history of fatty liver disease, when they took C15, they saw an improvement in the growth of bifidobacterium adolescentis, which is like a mama microbe that's really good at helping to regulate our metabolism. It's also been shown to extend longevity in worms. So we already talked about the limitation of that, but with an interesting side point.

Worms have a microbiome. Worm poop. It lowered, in that clinical trial, it also lowered LDL cholesterol, which was great. And then there are other studies showing that we know that fiber can help improve metabolism. And so there was a whole series of studies that was done to figure out how fiber helps. It ends up that there's a molecule in fiber called inulin, not to be confused with insulin, and inulin is being fed to our gut microbes that then

use inulin to make C15. And so it's because of the C15 that's being made by the microbes that helped explain the benefits of fiber. So it's just like- Interesting. Interesting. So basically you don't- Interesting, interesting. It's essential. So basically you don't have to eat any fish or dairy. If you have enough of the right fiber and prebiotics,

you can grow the right bugs in your gut and they'll produce C15 for you. It'll get you to, it's like an additive, it's kind of like how to order all the different tips and things we can do to maximize our C15. So that is one component. None of the single things alone can do it, but additively.

I mean, it's interesting. We've been measuring fatty acids on our patients at the Ultra Wellness Center, my practice in Lenox, Massachusetts, for 20 years. And before that at Kenya Ranch, we also did for another 10 years. And it would be interesting to go back and see, okay, who has low levels of C15?

Because it wasn't something I was really paying that much attention to. Right. And now I pay very close attention to it. And I'm like, oh, wow, this one's low. You're low, you're low, you're low, you're low. And I'm like, it's an important biomarker for actually understanding how people are navigating

the health journey and longevity and aging itself. So really quite amazing. So we were kind of going through the seven longevity must haves. We went through. So we got through the first two, which were the biggest. So in addition to targeting the longevity pathway, human pathway, regulating pathway,

which also targets key hallmarks of aging. It needs to show the thirds, it needs to show evidence of slowing the rate at which we age. And that's usually, we talk about Navy SEALs, right? So if this was a Navy SEAL course, this is where most longevity molecules would be, not make the cut and drop out of the competition. So we did, Nick, Shrock and I, we did a study

showing dolphins that, showing what hadn't yet been proven before, which is if you take individuals within the same population, that there will be some that age at different rates, despite having a relatively controlled environment. And it was crystal clear in the dolphins that we had fast aging and slow aging dolphins. It ends up the aging rate biomarker for that was hemoglobin.

And that had to do with, again, fragile cells in which they were increasingly losing red blood cell health over time, one measurement of that is called red blood cell distribution with our RDW, which has become, see there you go, a really popular way of understanding aging rate is RDW. So we saw that crystal clear in the dolphins.

Yeah, it's interesting actually, RDW is one of the biomarkers that's used to kind of calculate your biological age that we use at function health, which is based on epigenetic testing and correlating that with certain blood biomarkers. And that's how we come up with function health of a biomarker. So it'd be interesting to be able to start to test FATI-15 as part of our functional panel.

But it's really, it seems like such an essential molecule. The fact that it's quote essential, is that something that's been established by the scientific community? Is that something they just sort of figured out or? Right. That's a pretty bold claim. Yeah.

So we put the stake- It's like discovering a new vitamin that's essential for health. Right. It's a big deal. And it hasn't been a new one in like 70 years or something, right? It's been a a new vitamin that's essential for health. Right. It's a big deal. And it hasn't been a new one in like 70 years or something, right? It's been a long time, exactly. So we've hit the stake at the ground back in 2020 and we published that in Nature's

scientific reports. This last year has been really exciting, Mark. There have been now to date three other independent teams that have evaluated C15 as meeting the criteria of essentiality, all using different methods of gold standard methods of looking at pregnant mice and saying, hey, if you make the mom C15 deficient, does her neonate show evidence of a nutritional deficiency? And the answer was yes. And when you give it just C15,

does the nutritional deficiency, is it fixed? And the answer was yes. So the- It's like an infant mice. What are the symptoms of nutritional deficiency? Poor growth and poor neural development. It ends up that epidemiologically, we're seeing the same trend, disturbingly,

in humans. That if mom has lower C15 levels, her baby gets lower C15, and lower C15 now has been associated with poor body growth, poor brain development, even up to cognitive development of kids up to six years old. The upside, right, what's the hope in all of this is that nutritional deficiencies and essential fatty acids, these are fixable. So now we have with regard to essentiality, another study Shad, again with worms, showed that if you deprived a baby worm of all nutrients,

right, it goes into this, it doesn't die, it goes into this like slumber state. And they showed that if you give it just C15, it will regrow as if you were feeding it in a full nutritious diet. So walking through and then another group looked at all the wealth of human data to date. And so all of these papers came out just this last year, again, re-validating that C15 meets the criteria

of essential fatty acid, including the discovery of a nutritional deficiency, like vitamin C and scurvy and vitamin D and rickets. So what has been the human data? I mean, we talked about worms, we talked about dolphins, we talked about mice. Yeah. What's the human data on C15,

and how does it stack up against, for example, other longevity molecules? Because the NIH has a program to study various compounds and looking at rapamycin or metformin or astaxanthin or acribose, which most of these are drugs. or metformin or astaxanthin or acarbose, which most of these are drugs. And there's not a lot that actually show significant benefit.

Rappamycin is probably the most promising, but it has significant side effects, and there's coming up with analogs that are without the side effects, it only affects one of the pathways of mTOR, but that's way too complicated. You don't understand. Tell me, tell me like,

how does this sort of stack up in that, in that line up? Yep. So, so we'll start with human cell systems. Cause it's, you know, it's hard to do the long-term studies to show, hey, if you take this molecule, will you live longer? And to your- Like a randomized control trial for 50 years to see what happens. Right. Yeah, yeah. Yeah, and those are underway, which is good, but they just take time and they get really complicated.

So again, working with Dr. Shorick, one way we looked at that was to say, okay, we use this panel called Biomap and they're human cell systems, 12 different human cell systems that are mimicking various disease states and has a bunch 148 different biomarkers. And what you do is you treat these different cell systems, disease systems, with different doses like ascending doses of C15, of rapamycin, metformin, acarbose. And what we showed was that C15 had the most cellular clinically relevant benefits that are longevity enhancing compared to rapamycin metformin in a carbose. It was really close to, it was most close to rapamycin, which is exciting for the longevity consortium, right?

They really leaned into that. It doesn't have all the side effects. Without the side effects. I mean, this is a molecule that every mammal gets at birth. Yeah. And then when you look, you step back a little bit and you look at the activities, the things we care about. C15 is anti-inflammatory. It has an antioxidant.

It has anti-cancer functions. It has antim antioxidant, it has anti-cancer functions, it has antimicrobial, it even stops the growth of pathogenic bacteria and fungi. And you look at that kind of wonky list of benefits and that's what rapamycin does. So it just means that maybe we didn't have to go to Easter Island to discover rapamycin. To San Diego, to the Navy dolphin program. The dolphins. And it was like, mom's milk.

It's like, thank you, mom. How do you get breast milk though? You can't get that easily. Yeah, we don't want to. And no other mammal continues to eat dairy after the initial growth. So it's again, it's like, how do we leverage this molecule in our later years?

Well, that's a good point. How do other mammals who are not eating fish, like you've got bears who eat fish, you've got certain other mammals that might eat fish, like otters or seals or whatever, but most land living mammals, like elk or deer, don't eat fish. How do they get C15? And they're not eating dairy, no ice cream, no cheese, anything like that. So there are

plant-based forms and there haven't been a lot of studies yet to understand what are the different C15 sources, because now that we understand C15's essentiality really expands to the animal kingdom, as far as we know it, of how different animals get it, but it could be part of micro, like cows make it, right? So they eat grass and their rumen is able to, to produce. To produce, yeah.

So it may be a combination based upon the species, how well their microbes are able to make it from the food versus how much they get from their food, the food directly. So if you like regenerally raised cows, they're going to be eating more variety of wild grasses and plants, they might have more. That's right. If you're eating sheep or goat, they typically don't feed them corn and soy. That's right. So they may have more and it's often better tolerated because they have a different form of casein which is the protein in milk that tends to cause problems and most cows are bred to have A1 casein which is

really problematic and inflammatory for most people. So there are A2 cows like Jersey cows and Guernsey cows and there are A2 cows heirloom cows but you know I think what I'm curious about is how this molecule also can be a therapeutic molecule, not just sort of a preventive molecule that does something as basic mechanism, but how could it affect your treatment of diabetes or heart disease or fatty liver disease? How does that work? Yeah, and that's where it gets to conveniently like longevity molecule must have number what are we on four you know clinically relevant benefits within months. If a molecule says hey we target these mechanisms of longevity but you're not really going to see anything but

you'll live longer that doesn't for for Nick and I that just is not what we were looking for. We're looking for to say can C15 actually have meaningful benefits specifically with people with diseases. So again, caveating that as a supplement, supplements aren't intended to treat diseases, but we're talking about the studies that have been done to date and what we're seeing. That we need C15 and putting C15 back into our system and optimizing those levels, we are seeing disease treating effects. And this is both in people, so let's take for example, clinical trial

with Dr. Jeff Schwimmer, fatty liver disease, right? So that didn't exist non-alcoholic fatty liver disease or now mazzled. They changed the name because you eat to only see this fatty liver issues in alcoholics. And now the most prevalent form is those with metabolic dysfunction, meaning diabetes, pre-diabetes, and they call it metabolic associated fatty liver disease.

Maybe us docs inside should have been involved in branding a disease disease. I, I, maybe us docs inside should have been involved in branding a disease name. So, yeah. Nafl-D, as opposed to Nafl-D. So there you go. So, so I'll call it fatty liver disease, not associated with, with, with, um, alcohol. So, you know, that did, wasn't known until Mayo

Clinic published a paper in 1980 for the first 20 cases. And then, so since then, we move fast forward to today, the latest paper showed 38% of people globally have fatty liver disease. So this has been an alarming rise in people with fatty liver disease, a percentage of which are progressed

to steatohepatitis, inflammation, cirrhosis, becoming one of the leading causes of liver transplants and liver cancer. I mean, this is important. What you said was really important because about one in 10 or less, the one in nine now keeps getting worse in America, have diabetes, type two diabetes. But what you're saying is four in 10,

almost four in 10 have fatty liver disease. Even if you don't have diabetes, it still increases your risk of heart attacks, 10, almost four in 10 have fatty liver disease. Even if you don't have diabetes, it's still increase your risk of heart attacks, cancer, stroke, rapid aging and death. That's right. Now, none of the, we don't want any of those. Even if you don't have diabetes.

That's right. Right. That's right. So it's important and it's often not diagnosed. It's often missed. There are now really great blood tests you can do to find out if you have it, not just your regular liver function tests.

And we, we offer these as part of function health testing. So you can go to function health.com slash Mark and actually get these tests as add on test to the basic function panel that look at fibrosis and liver and are really helpful to kind of pick up people who have this. Cause you don't want to continue to have this.

If you have it, I mean, you can diagnose it through a, uh, you know, an MRI or various kinds of, of, uh, fancy testing, but to a simple blood test, you can also kind of get a pretty good idea. And it's important to understand because this is an silent epidemic and nobody ever heard of. And now it doesn't really have a ton of

symptoms other than, you know, maybe you're overweight and maybe you've got a big belly or maybe you're like, but it just, it's quite important. And so what you're saying is that C15 has the potential to impact fatty liver disease. Exactly. And so when Jeff Schwimmer is a leader in pediatric fatty liver disease,

and he opened the first clinic for fatty liver disease for kids. And so Jeff, back in 2012, I had published a paper on fatty liver disease in dolphins. And he wrote me, he sent me an email and he's like, ah, it's probably not what we're seeing in people. It's probably not the same disease, but send me some liver slides that you have, you know, and let me get back to you. Sorry, Zeno. These were dolphins who died and then you found it. Exactly, dolphins who had it, yeah, exactly. And then afterward we had found.

You're not like sacrificing dolphins to get the tissue specimen. No, no, no. Yeah. They do mice. Thank you for that clarification. Yeah, we're actually able to go back and look at pathophysiology reports

of dolphins that had passed. So we had this, that was another amazing archive, right, of information. So we were able to send those slides to Jeff, and then a couple weeks later, Mark, I got an email, and the title was, We Are, I'll Go. He's like, this is the exact same presentation of fatty liver disease that you're seeing in dolphins

that I'm seeing in my kids. And he's like, you're blowing my mind because dolphins don't eat sugar. They're not eating trans fats, it's not ultra processed foods. That's what I'm wondering. Right, and it's just like what? And so that started our 10 year journey

in which we have worked together, but independently that Jeff then did a study in which he looked at 237 kids and he did, at the time they didn't have your wonderful test which everybody should get the test that Mark just mentioned to assess your liver regardless of who you are and your age. Everybody should get this test. So that Jeff did this study and he looked at these kids

So Jeff did this study and he looked at these kids and he showed that the higher their C15 was correlated with lower liver fat. And this was a linear correlation. So the higher the C15, the lower the fat in the liver. So he's like, okay, well, that's interesting. So then that resulted in him doing a randomized placebo-controlled clinical trial with fatty-15, with C-15 supplementation among young adults

who were graduates of, who had a history of fatty liver disease. And what he found, there were really key important things that happened that he found. The first is he found that two out of three of the people in his study had the definition of a C15 deficiency, two thirds. So if you have fatty liver disease,

yet you had an even higher risk of what we were saying the general population has. One in three, two in three. Yeah, exactly. And then for the people who took a C15 supplementation and got their blood levels above that threshold of deficiency, they had lower liver enzymes, lower ALT, lower AST, and improved red blood cell health within 12 weeks. So now the leading hypothesis and

what we have found in the Dolph, is that nutritional C15 deficiencies may actually be the cause, or at least one cause of a substantial phenotype of fatty liver, because why did it show up, why? Like why did this show up all of a sudden, in fact so many, so that is obviously where it's a surgery. Well I mean, because sugar and starch is a massive part of our diet,

and I think it's probably, in my view, a combination of the increase in sugar and starch plus the C-15 deficiency, right? Yeah. And you know, our, for us, you know, we kept going back to the dolphins and for the dolphins, we call this the dolphin phenotype of fatty liver disease. The only change they had, they had moved to, they were eating a high-fat fish called eulicon, which is called a candlefish. It has so much fat in it that you can stick a wick in it. You can dry it, stick a wick in it, and be a candle. That fishery died

out in the 1990s. And so that's when they moved to this lower fat Kaplan. And so at the same time that humans, we were moving away from whole fat dairy and our C15 sources, the dolphins were moving, going on a low C15 diet and fatty liver disease. You know the Native Americans, you might not know this story, but the Native Americans used to trade in these really I don't know the story, but the Native Americans used to trade in these really highly fatty little, tiny fish as part of their trade. So if you were a Pacific Northwest Native American, and you would trade with inland tribes, and use the fish as your currency.

So instead of dollars, you'd send them fish, and they'd give you beads or whatever else they wanted. So that's fascinating, because it was such a valuable commodity back then. Yeah, and now we understand even more so, like how valuable that was. So that kind of, as far as we also know that... That's a human trial. That's just seemed to be... That's right. Yeah. And so that was published also. And directionally showed what's possible. Like it didn't cure their fatty liver disease,

but it seems to sort of create a downward trend in the effects. And you still have to cut out the sugar and starch. Yeah, we need to look at the whole picture of lifestyles and how we're changing things. What's interesting is it really goes against the whole idea of all saturated fats are bad, and that we have one that's essential, so it's like how do we get it back into our diet?

So there's a lot of, you could feel the urgency around this movement. The reason for the book is really to help increase education and let's have the conversations around it. We can't explain it away anymore. So you know. And what kind of studies have there been in humans around diabetes, type two diabetes and heart disease?

Is there anything? So with regard to, there was a second study in Singapore, and that's the one I had mentioned. That was also fatty liver disease, women with fatty liver disease. And it showed that it lowered LDL cholesterol and then increased the improved gut microbiome. That was an interesting study because what

they did for this clinical trial, and this was also a controlled clinical trial, that they had, the control group was one that went on a hypocaloric diet. So they had between, they had an average. Low calorie diet. Yeah, exactly, like 1,000 calories per day. That'd be tough to sustain.

That was the first group. The second group was a low calorie plus Mediterranean guidelines, which both of those have been shown to help with fatty liver disease metabolism and various things. A low ketogenic diet works best. Even better, even better. You're spot on.

And then the third was low calorie Mediterranean plus C15 supplementation. So it was a big lift to ask of C15. In those groups, not only did the third group, the C15 supplementation result lower LDL cholesterol and improved gut microbiome, but it also had the lowest, it had the greatest loss of liver fat, the greatest loss of body fat, the greatest glucose improvements, but it was trending.

It was not statistically significant. You just kind of saw the stuff. but again, it was 12 weeks. Yeah. And so the question is dosing, timing, things like that. In numerous studies of studies of, so these meta-analyses, studies of studies that prospectively follow thousands of people over decades, numerous studies have consistently shown people with

higher C15, just like we saw in the dolphins, lower risk of developing type 2 diabetes of heart disease, specifically coronary heart disease, of developing fatty liver disease and certain types of cancers, specifically a lot of work on colorectal cancer. This is why with all these different aspects of the data from epidemiological data, clinical trials, mechanisms of action, in vivo efficacy studies, this is why Nick, Dr. Nick said, listen, I've seen every longevity molecule under the sun and I've not seen a molecule that has more supportive data of being a longevity enhancing molecule than C-15. But most people haven't ever heard of it

and don't know about it. Right, and it's like, what? So then, until now. Yeah. Right. That's why you wrote the book and why we're having this podcast so people can understand this sort of emerging science around this, which is kind of cool because it's not very often you come up with a new discovery like this and it's pretty cool.

There's a few questions I have around the foods to help people understand what foods they should be eating. We kind of touched on a little bit, but what are the foods that are highest in C15? So probably not the groups that you're most excited about. Uh, dairy fat, you know, by far is our primary source. But depending on what the cows are eating. Depending upon what the cows are eating. Or what the sheebered goat are eating.

Exactly, exactly. And so C-15, um, you know, for a long time has actually been used as a biomarker of how much dairy fat people ate. They didn't know that it had any meaning. So it was used as a reliable marker of how much, so that's how much dairy fat and again, dependent upon what that animal was eating really drives our C15 levels. It's a big reason why we, you know, the Navy funded, again, our development of the C-15 supplement because it's a pure pre-fatty acid supplement that's bioavailable. Just importantly, it's vegan and it, you know,

it is not having to compete with all of these pro-inflammatory fatty acids. So when the good comes a lot of the bad in dairy and that's what you want to avoid. That's right. Yeah, yeah. Otherwise, we would have just... What's interesting, some of the studies, looking at, and these were epidemiological studies, we were looking at people who eat more dairy seem to have less diabetes, right? So that's interesting. Is it the dairy fat? Is it something else? Is it the saturated fats that protect them? I don't know, but it just sort of makes me wonder. Yeah, it's, you know, it's, the dairy studies are super messy.

And so there are absolutely studies showing this benefit. There was a recent study that looked at this to say, hey, why do some studies show that people who eat more dairy have a lower risk of a given disease and other dairy studies don't show it? And so what they were able to narrow down to and they concluded was that C15, higher levels of C15 were one of the main predictors of having a benefit. Higher levels of C18 was a predictor of having it being harmful. So again, it's not- And that's another fatty acid that's saturated in dairy fat.

That's right. So it's, you know, it's, and that's not gonna be the simplistic answer. But I think it's, the more we can understand how to maximize C15, you know, and maybe having a ratio, like we have omega- to Omega 3 ratios, maybe it's an even chain saturated fats which are these pro-inflammatory fats to C15. Yeah, I mean that's the thing you've learned, people say saturated fats bad,

saturated fats good. I mean there is no such thing as saturated fat, they're saturated fats. Yes. And each one has different properties and different benefits and different risks. And so uniformly they're not the same. Spot on. And they don't affect your lipids the same way, your health the same way. I wrote a lot about this in my book, Eat Fat Get Thin, because people were super confused about it.

I think that, you know, just kind of sort of sum up what I'm hearing is that this is like a newly discovered molecule that is an essential nutrient that one in three of us are missing that has profound effects on many of the longevity pathways that have to do with aging, mitochondrial health, blood sugar health, microbiome health, effect your liver health, cholesterol. It's almost too good to be true, right? Yeah. We hear that. we hear that,

and I think we get down to it's essential. You know, it's just one of those rare molecules where we need it. And what's beautiful about these molecules, they're not needing huge amounts, right? So when you think about a vitamin, like vitamin C and scurvy, you know it only takes like 60 milligrams of vitamin C

to cure scurvy, which is a deadly disease if you don't have enough vitamin C. Uh, and by the way, 10% of Americans don't have enough vitamin C to prevent scurvy. Which is mind blowing, right? Which is cause they're eating ultra processed food and they don't get any green vegetables and they don't get any, no food. And, and so yeah, it's, it's a, it's a big problem. But what I find interesting about vitamins is that they have very, very powerful effects or essential nutrients at very low levels.

And without them, our whole metabolic and biochemical machinery doesn't work the way it was designed to work. And so things go wrong. And the things that go wrong are the things that we don't want to go wrong, like damaging our ability to keep healthy cells, right? The cell fragility syndrome, where your we don't want to go wrong, like damaging our ability to keep healthy cells, right? The cell fragility syndrome where your cells don't function properly and the membranes

aren't right, and fats make up your cell membranes, so they have to be healthy, and this is a key component of that. We have to regulate our mitochondria properly, our immune system properly, free radicals and oxidative stress properly, our microbiome. So it's interesting that it sort of seems to work in so many different ways. And I think there's a word that probably people have heard me talk about that is pleiotropic, meaning it has many different effects. So drugs usually have a single effect.

They might have a few other side effects, but they're designed to be a single drug for a single biochemical targeted with a single receptor or the single outcome working on a single pathway. And what nutrients do, like for example, magnesium activates over 300 different enzymes in the body. So it's, so does zinc or maybe 200 different enzymes. So these are, these are highly, I think vitamin D controls hundreds and hundreds of gene expressions

throughout your genome. And these are multifunctional molecules that go beyond what we would normally think of as a pharmaceutical intervention. So these are the things that create health as opposed to simply treat disease. And I would say when you create health, disease goes away as a side effect.

And that's kind of what you're talking about here. This is a component of our biology that we've neglected, that we haven't known about, that has really discovered thanks to the dolphins in you. Well, thanks to the dolphins. This was truly kept. And just having an observation that, wow, like, geez, these dolphins aren't living very long.

These are living longer. Like, what's up with that? And just asking the right questions, you were able to come up with this discovery. And I think it's really groundbreaking. I think people need to eat fatty fish. I think small fatty fish is key. If you're not gonna eat dairy,

like herring, mackerel, sardines, anchovies, all this stuff that people don't like. Right, you gotta get the head and skin. I'm Jewish, so I like all those things. I grew up on those things. I didn't know at the time. Yeah. You're already like dosing yourself well with C15.

Yeah. Tons of cans of mackerel in my cupboard and sardines. And in terms of the dosing, like what kind of doses do people need of this? To your point, and that was a remarkable summary. Uh, the, we need we need about 100 to 200 milligrams per day. So if you compare that to like omega-3s, right, then you're talking more about grams. A thousand, a thousand, 2,000 milligrams, yeah.

That's right. So this is, to your point, it's a very low dose of C15. It's 100% bioavailable in the free fatty acid form. So we only need a small amount. And again, in order to help fortify our cell membranes and keep them strong, we need greater than 0.2% of that cell membrane needs to be C15. So we don't need a lot. So basically a fifth of a percent of the fats in your cells have to be C15. So we don't need a lot. Basically a fifth of a percent.

Yeah. Of the fats in your cells have to be this fat in order for it not to become fragile and break down. You know, we only need these low amounts to achieve these levels in our cell membranes. We also know it's been remarkable is that all these studies about all these different

mechanisms, like activating AMP AMPK inhibiting mTOR They're all showing the same concentrations It's all the same amount that we need in our blood to have all of these many, you know, pleiotropic Benefits so it's very good that the story just is so consistent on what we're Intended to have to stay healthy now what're seeing is, hey, can we increase it and push it further so it's like 0.4 to 0.6%, can that help us be even healthier and live longer? And there's a big study that was done by a group at Harvard

and a bunch of other teams, and they did a large study and they showed that people who had these higher levels of instead of 0.2%, 0.4 to 0.55 percent, that they were less likely to develop heart disease over time. And then you know the longevity zones are going through you know an evolution but in Sardinia the people there who have they live longer in part because they have a lower risk of developing heart disease and specifically men live longer, longest in Sardinia than anywhere else in the world.

Yeah, I've been there. Right? Oh, I'm jealous. Okay, so they have a mean C15 level of 0.6 and they have, and they've replaced their. That's fascinating. Right, and they've replaced their meat for the most

part with cheese. Yeah. They're using local cheese from local goats and sheep. Yeah, yeah, no, this all makes sense. Eating grass, high altitude. What was really fascinating was when I spent quite a bit of time in Sardinia, I got to meet with a lot of these very old men and old women and I mean, one couple,

I think was a hundred was 210 years old together. Oh my gosh. And they were fit and they were vibrant. This guy Pietro was like 95, was just kind of retired from herding his sheep five miles a day up the rocky terrain. And what was really fascinating was they understood that one of these guys, Olinto said,

you know, we flavor our meat before we kill the animal. And I'm like, what do you mean? He says, well, whatever you feed it determines the quality of the meat and the taste. So whether they feel a carob or acorns or whatever, like the black-footed pigs in Spain from the Iberican ham, very different fatty acid profile because all they do is live in oak forest and eat acorns.

And in Sardinia, they, they, they know that if they take the sheep or the goat and they, they kind of graze them on different plants at different times of the year, it'll taste better. They're not doing it because it has high C-15 levels or looking for better phytochemicals or whatever. They just want it to taste better. The reason it tastes better is that phytochemicals create the taste in food.

So flavor always follows the phytochemical richness or density of the food. And they just kind of knew this intuitively by how they raise these animals. And so these animals were eating all these wild plants all the time. That's what they fed them. And so that makes a lot of sense.

Right. That makes a lot of sense to me, just given sort of being there and seeing what they were eating and what they were eating, what they ate and what the cheese was made from. It was really fascinating. Yeah. That is really cool. Yeah, they, they, they're, one of their cheeses, right, in which you might have seen, there was Pecorino. And Pecorino a particular, has higher C-15 than most other cheeses. So yeah, it kind of feeds into this all kind of neat. It's really fascinating. I mean, I, I,

I think what I would love to sort of know from you is, um, where's all this going? Like what's next? And are we, what are we going to see next in terms of the research just underway, the things that are promising? Yeah, well, this, this is the next step. So we've, you know, we spent, uh, 10 years on credibility. Um, you know, that was really important before we even thought of bringing a supplement, um, and all the research right out is really building the credibility.

Um, you could imagine a dolphin veterinarian saying you need to take a saturated fat, you're better be able to back that up with really good data. So we went above and beyond with regard to the science. And then now the world has picked it up. So again, you can go to discoverc15.com and that's where all the peer reviewed papers, again, over a hundred from people throughout the world. So that's a fun place to go. And it's the letter C in the number 15. Thank you, thank you, yes. Yeah, so discoverc15.com, we'll put in the show notes, but it's a treasure trove of current

and ongoing kind of research. Yeah, and now probably once every two weeks, there's a new paper coming out. So it's really exciting. It's not just you anymore, there's people all around the world who've taken up the research around this. That is right, that is right, which is really exciting. It's not just you anymore. There's people all around the world who've taken up the researcher on this. That is right. That is right. Which is really exciting. You know, now the movement, right?

This, well, I mean, that's how science works, right? Somebody discovers something and then other scientists try to validate it and or discredit it. Right. Yep. That's right. So that's been great to see. So then now we're moving toward exciting new avenues, obviously getting the conversations going. Um, how can we change nutritional guidelines? How can we get C15 for our kids into infants with all the new studies that are coming out around the importance to infant health as well as supporting our aging as we get older. And then we have some exciting new research coming out around brain health.

So stay tuned for that. Cognitive development. Cognitive development. From both spectrums, right? From young cognitive development and also brain aging and all sorts of things. Yeah, so a lot of exciting work coming out around that. And then for us, it's like we really

have really taken a step back and said why? Obviously there's urgency to fix global crisis that's happening and if there is a chance that restoring C15 can help with that. The global crisis of what? Of just metabolic diseases. Metabolic diseases. The increase.

Brain diseases and yeah. Yeah the kids that were born into basically this height of the C15 deficiency world which is the 1990s, they're now in their 30s. And so is this why people in their 30s are developing certain types of cancers? The rise in coronary heart disease, the rise in type T diabetes, it's fatty liver disease showing up. And how much is the C15 deficiency part of that?

So let's stop accelerated aging. There are kids that are developing diseases that their grandparents before their parents. So we gotta fix that. So let's stop accelerated aging. There are kids that are developing diseases that their grandparents before their parents. So we gotta fix that. And then how to then, again, leaning in, how do we optimize C15 through supplementation, through various practices to be able to extend our longevity.

So that's exciting. And then what is it all for? I mean, longevity so we can live healthy for as long as possible and enjoy life. And I have a question for you, which is to give us more time. And so if you were given two extra hours of every day, and those two extra hours, whatever you did was guilt free. You didn't feel guilty about it because you weren't working on something else because

you're so busy. What would you do with those two hours? Two hours a day? That's a great question. I probably would exercise more. Ah, that's great. It's more time to be able to do things because it makes you feel good, right?

And then it makes you healthier and it feeds all those things. And so for us, it's the ability to say, everybody has the right to longevity, to live a long life, to have a meaningful life. The book is about the purpose that fell in my lap through the dolphins, and let's give us all more time to be able to fulfill our purpose. Well, I'm excited to see what's next. This is very exciting. You can read about this in great detail in Stephanie's new book, The Longevity Nutrient,

The Unexpected Fat That Holds the Key to Healthy Aging. It's new book, the longevity nutrient, the unexpected fat that holds the key to healthy aging. It's out now, so you definitely should check it out. Uh, also, if you're interested in learning more, go to discovererofc15.com and you can actually buy C C 15 as a supplement and it's called fatty 15, which I love. And I take, uh, I just to take two capsules a

day and that's it. And it's pretty straightforward. Uh, it's a low friction way to get it. You don't like sardines and herring and mackerel. Hopefully I'm not overdosing because I do eat those. No overdosing. I think we're kind of in this moment where we are discovering a lot about aging and longevity,

but we can't miss the force for the trees, which is the fact that we're eating a diet that's killing us. And the amount of sugar and starch is driving our metabolic crisis, is causing a lot of the things that are going on. I think C15 can be helpful in mitigating that, but without actually also changing your diet,

exercising, getting up to sleep, managing your stress, having connections and relationships, it's not enough, right? That's right, it's part of the solution. But boy, all those things are so, so important. Yeah, exactly. So you don't want to eat your C-15 supplement and. Not exercise and socialize.

Three cans of soda a day. So. Please don't do that. So thanks for coming on the podcast again. This is really great. Everybody can find out more and we'll put it on the show notes for the links that we talked about and keep up the good work and we'll stay tuned for what's next on the horizon. Great.

It was great to be here Dr. Hyman. Thank you. If you love this podcast, please share it with someone else you think would also enjoy it. You can find me on all social media channels at Dr. Mark Hyman. Please reach out. I'd love to hear your comments and questions. Don't forget to rate, review, and subscribe to the Dr. Hyman show wherever you get your podcasts. And don't forget to check out my YouTube channel at Dr. Mark Hyman for video

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