Good Life Project - How Dolphins Unlocked a Hidden Key to Longevity and Health | Dr. Stephanie Venn-Watson

Episode Date: April 14, 2025

Take Our Podcast Listener Survey!Have you ever wondered what the key to healthy aging might be? In this fascinating episode, we explore the groundbreaking discovery of C15:0 - the first new essential nutrient in over 90 years - with Dr. Stephanie Venn-Watson, author of "The Longevity Nutrient: The Unexpected Fat That Holds the Key to Healthy Aging." Discover how this unique saturated fat may help combat inflammation, stabilize cells, prevent iron overload, and even support brain health.You can find Stephanie at: Website | peer-reviewed C15:0 science | LinkedIn | Episode TranscriptIf you LOVED this episode, you’ll also love the conversations we had with Matthew Park, Ph.D. about how aging immune systems affect cancer risk.Check out our offerings & partners: Join My New Writing Project: Awake at the WheelVisit Our Sponsor Page For Great Resources & Discount CodesJoin journalist Danielle Elliot as she explores why ADHD diagnoses are surging among women in the limited-series investigative podcast, "Climbing the Walls." Hosted on Acast. See acast.com/privacy for more information.

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The studies of data to show that we cannot explain it away anymore. We have to be talking about this. It's becoming the number one cause of cancer in kids. Just that alone. Dr. Stephanie Van Watson, author of the Longevity Nutrient, is the world's leading expert on C15, a critical essential fatty acid discovered through groundbreaking research on navy dolphins that just might hold the key to healthier aging in humans. With over 60 patents and 80 plus peer-re peer review publications, her

revolutionary work is redefining our understanding of aging and wellness. The higher the C15 levels in people, the lower their risk of developing type 2 diabetes, heart disease, fatty liver disease. These little secrets that were so simple, Jonathan, that were right in front of us, but we didn't see until we changed our perspective. That's so interesting. If we had done the study three years earlier, C15 wouldn't have been on the panel. We wouldn't have found this. Good Life Project is sponsored by Aveeno Baby. So you know there's something remarkable about how nature protects newborns, that natural moisturizing layer babies have in the womb. It got me thinking about how delicate baby's skin really is. So I've learned it's

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veterinary epidemiologist, over 80 publications, 70 patents. And back in, I guess it was the early 2000s, you find yourself studying aging Navy dolphins and come upon this discovery, which is actually relevant for humans. Now, before we even get there, I've gotta ask you, what exactly is a Navy dolphin? Right? It's a good first question, Jonathan, yeah. So a lot of people don't realize and don't know

that the Navy has cared for the sustained population of about 100 bottled-nosed dolphins for over 60 years. And so they, you know, initially brought dolphins on. They thought they were going to study their structure to help make faster submarines back in the 1960s and just learn, watch dolphins swim and see what we could learn. And instead what they found is they had this program called the Aquanaut Program, Jonathan, where there were aquanauts that were based deep in the ocean and they needed supplies routinely delivered to them.

And they found that these dolphins, while it didn't really help with submarine shapes, that the dolphins willingly were with them in the open water and would actually deliver supply to the aquanauts. And that started the whole program where now the dolphins live in the San Diego Bay, go out into the open ocean every day.

It's a really incredible program where dolphins help to find lost objects, enemy swimmers, and easy peasy for them, and a good life where they live a lot longer. So we're not talking about dolphins in captivity here. We're talking about dolphins that it sounds like live in the bay and sort of like keep returning to the same place voluntarily. It's incredible.

Like I didn't know how I would feel about dolphins in the Navy as a veterinarian, to be, to be honest. And when I went, I quickly saw again, they're living in San Diego Bay, and they choose to be there, which is incredible. And you know, they help reproduce, they do all the things that healthy populations would do. And then the biggest indicator is that with good healthcare and protection from predators

and things like that, you know, they live a long time, which was a big gift for the dolphins, but it ends up also for us too. So I guess this is sort of like where the story really starts to dive into. You looking at these navy dolphins and saying, okay, it seems like they're living longer, I guess, and tell me if I'm getting this right. It seems like you notice that these dolphins are actually living longer than the typical dolphins who were just out in the wild and starting to explore what's going on here.

So dolphins in the wild, just to provide some context, live on average into their 20s. Dolphins at the Navy are now routinely living into the 40s and even 50s. I was brought in as a veterinary epidemiologist as some people might know. I don't even know how to swim. You're unlikely, right, dolphin veterinarian, but I can crunch numbers and see patterns. And so they had this half a century of data on these aging dolphins and so they brought me on to be able to understand aging in

dolphins and that's where we started seeing over a 10-year period of diving into the records of seeing that some dolphins but not all of the older dolphins were developing things like high cholesterol and chronic inflammation and even the full suite of changes consistent with Alzheimer's. So it became fascinating where my job was then to reach out to the human health experts in these areas to say, hey, what have you learned to help people so that we can help dolphins? And that's what kicked off this whole wonderful One Health collaboration. You're sort of like living these two worlds at the time. You're deep into the epidemiology side with aging dolphins trying to figure out what's

happening here and then saying, okay, I'm seeing things that we're also seeing humans as they age. These are some of like many of the classic chronic conditions or quote age-related conditions and humans. So let me actually start to interface with people who are experts on that side of things. Take me deeper. What starts to emerge here? Right, so I had this amazing gift where I could reach out to anyone because we were talking about dolphins, so I was really able to reach out to the

world's experts in these different diseases. And what became rapidly clear is that on the human side, we don't know how to fix this either. So, but wait, are you learning something? Maybe there's something we can learn from dolphins that can help both sides. So at the time, this was back in 2012, 2013, a new technology called metabolomics was emerging and most importantly readily accessible to humble folks like myself. And metabolomics is the method of studying thousands of small molecules that are present in the blood and in our diets to understand what are predictors of health and disease.

So we had this amazing opportunity where we had really clean data from these dolphins, right, who don't smoke, they don't drink, they have the same socioeconomic status, and yet we saw some dolphins developing aging-related diseases and others not. So we used this technology called metabolomics to look at these molecules and see which molecules predicted the healthiest aging dolphins. We thought it would be omega-3s because all they eat are fish. And instead, it was this quirky little molecule, C15 or pentadecanoic acid, that predicted the healthiest aging dolphins. Most surprising, Jonathan, this is a saturated fat in which our primary source is butter. So we were like,

what? What's happening here? So when you discover this, I'm curious also, so you start out with a whole bunch of different things that you're looking at. You think maybe it's the omega-3s because everyone's been talking about how important they are and also, you know, the different, especially in human beings, right? You know, like there's been so much conversation and research around omega-3s as a category and how they affect heart health

and all sorts of other things. So you're thinking maybe they eat tons of fish, we know there's tons of fish in omega, or omega-3s in fish, that's gotta be it, right? And then you realize that that's actually not it. There's just one other thing. Had you heard of this one other molecule before that? I had not.

So it ends up, so then of course this pops up. And then we did a couple of studies. We then gave, this is all funded by Office of Naval Research again to help improve Navy dolphin health. We then did two studies, we repeated it, where we gave dolphins a higher C15 diet. So we found fish, some fish have C15 and some don't. So we gave dolphins a higher amount of C15 through their fish.

And then we saw within 12 weeks, they started getting better. These aging-related diseases started going away. Cholesterol went down, inflammation went down. So that was really encouraging. So then from then, we really said, okay, we need to pay attention to C15. And it ends up it's this odd chain saturated fatty acid that's been known since the 1950s. But you know, because it's a saturated fat, it's in butter, and it's present in really low levels. It just was kind of written off as

not relevant to help until the dolphins helped reveal the secret for us. So when you do this study and you see the first time, like, oh wait, this is actually literally improving all of the symptoms of these conditions that the dolphins are facing, I'm guessing the bells are going off and saying, I wonder if the same thing happens in humans.

Oh, how did you know that? So then, exactly. I'm guessing the bells are going off and saying, I wonder if the same thing happens in humans. Oh, how did you know that? So then, exactly. So then what happened? We started looking into the human literature. And it was there, like breadcrumbs were there, Jonathan, where you go back and you look at some early studies in which they looked at fatty acid panels in people.

And they started showing repeatedly that the higher the C15 levels in people, the lower their risk of developing type 2 diabetes, heart disease, fatty liver disease. But it had just, there wasn't, the studies were done to show that saturated fats were bad for us. And what we've learned is not all saturated fats are created equal, so there are these even-chain saturated fats like C16 and C18 that are present in high levels in dairy fat and bread meat and things like that. And those studies did show higher levels of these even-chain fats, C16, C18, were associated with a higher risk

of type 2 diabetes heart disease. So the studies really leaned in on, aha, we showed yet again saturated fats are bad for you. But then they kind of had a PS in which they said, oh, and by the way, we happen to see that this C15 was associated with better health, but that's not the point of the study. So it ended up being there. And so now since then, this discovery, 10 years ago, we then, well, I guess I should say at that point, we then took C15, pure C15 into the lab,

brought in one of the world's experts on fatty acids, Dr. Ed Dennis, who was the editor of the Journal for Lipid Research for 15 years. And we worked with Ed to then do eight studies over three years to show that not only is C15 a beneficial saturated fat, but that it met these rare criteria of being the first essential fatty acid to be found in over 90 years. So that was yet another big aha moment of how important C15 has been. And now since then, 10 years of research, over 100 peer-reviewed studies from teams throughout the world, all showing this little fat is one we've, you know, we've needed all along. I don't want to leave behind this conversation around saturated fat though, just as a category,

because I've been having recent conversations with researchers who are sort of like exploring often different conditions. I sat down with Ben Bickman, who's been researching insulin resistance, right? And, you know, we had this conversation around saturated fat, how we've become so deeply phobic of it. I'm not the scientist, I'm not a researcher, so I can't make any claims myself, but I get to talk to researchers like you and Ben and so many others. And I remember him describing to me that actually a lot of the original research on saturated fat, there's a huge political angle to why it became adopted

as policy. And also, as what you're saying, there are pieces of the research that seem to have been just conveniently ignored. That's right. And you know, there's a whole fascinating story of, you know, back in 1977 when Congress, right, released dietary recommendations for all Americans to drastically decrease our intake of whole fat milk and butter.

And if we think about it, it's like Congress really released recommendations. And when you dive even further into that fascinating story, it was a group of about five senators who were in this committee. There was an absolute high prevalence, scary high prevalence of heart disease and heart attacks, especially among men in the 1950s and 1960s. In response to

that, you know, it took 10 years, they then developed these guidelines. The problem is that these guidelines were built for all Americans, not just men, older men who are susceptible to heart disease, but for children and for women. When they released the first round of dietary recommendations of decreasing saturated fat, they had thousands of people reach out, experts reach out and say, no, no, no, no, this is wrong. We can't jump the gun. We're not ready for it.

So much so that three out of five of the senators said, we're getting a little nervous about this and we actually don't back these recommendations anymore. And so a second version came out that started with that letter of saying, hey, we actually don't agree with these anymore, but there were two senators who still believed in it, and it went forward. And so we've really gone through this 50-year experiment of removing all saturated fats, good and bad, from our diets.

And now we're seeing the consequences, the promises. We get a chance to fix it. And I guess nearly part of the conversation here is also that it sounds like what happened is we lost nuance too. We just sort of said, okay, there's this one category of fats, we're going to call them saturated fat, and they're all evil. Rather than saying, okay, so there is this one broad category, but within that category, and tell me if I'm getting this right, there are a whole bunch of distinct fats and different types that fall under it. And yes, maybe some we should take a

closer look at because maybe they are inflammatory or cause, maybe they're related to the cause of things that we don't want, but maybe there's another subset here that actually is really beneficial. Is that kind of right? Yeah, that is absolutely right. And what's fascinating is your history tends to repeat itself. And so if you go back to 1929 to 1931, Dr. George Burr and his wife Mildred, they had, Dr. George Burr had just discovered that vitamin E, had just discovered vitamin E, right, as essential. So he was doing studies and he discovered along with his wife that fats had benefits and in fact two of them were essential. That's when the first two essential fatty acids were discovered.

This was heresy at the time because not only were they talking, like today we're talking about saturated fats. Back then it was wholly believed that fats provided no benefit outside of calories and they certainly had no health benefits. So we're just a hundred years later and now we understand there are good and bad fats. We're just at that next evolution and phase exactly like you're saying where we're understanding that even among saturated fats, there are good and bad the nuance exactly what you were talking about. So when you then discover,

there's this other thing called C15, it falls under the umbrella of a saturated fat, but when we increase the amount that dolphins are taking, it's having all these incredible effects on them. And then when we start to run actual, you know, like human trials, we're seeing a similar effect here. I wanna go a lot deeper into that, but I'm also really curious. Does this then make you start to question the claims that have been made around omega-3s? Because it sounds like this kind of comes paired, at least in the early research, with eating

a lot of fish. Eating a lot of fish has a lot of omega-3s in it. So is it the type of thing where like that was the obvious one and that was the kind of quote, okay fat to point to, so let's see if we can attribute the benefits to that, whereas maybe it was actually C-15 that was driving some of the benefits. We're learning, we're stepping carefully, right? If you could imagine, I mean, John,

we've done 10 years of research before, we were really ready to bring this up, because you could imagine, I mean, Jonathan, we've done 10 years of research before we were really ready to bring this up because you could imagine a dolphin veterinarian saying saturated fat is good for you. We better have the science and credibility to back that up. The dolphins did provide a clue to us, which was like exactly like you're saying. So fish are good for us.

There's no question, it is very clear and clean that in general, people who eat more fish are healthier. We still have to be careful about some pregnant women and like high mercury load fish. But aside from that group, eating fish is good for us. So the dolphins helped to tell us which part of fish was the most essential. And when we start looking at humans now, there have been tens of thousands of studies on omega-3s. And we're not saying that omega-3 and omega-6, which are the categories of the other two essential fatty acids, are not essential. It's almost like we discovered vitamin E, we wouldn't say don't take vitamin A, right?

That they all work together. But we're coming more and more to understand that omega-3 fatty acids have limitations once they get outside of the fish. They have this chemical structure that involves having double bonds in it. And every time you have a double bond, it allows it to be flexible, which is why it's an oil at room temperature, but it is also susceptible to attack by oxygen. And so it's this process called lipid peroxidation, what most of us know as rancidity. So it's a fragile molecule that once you take it outside the fish, it's harder for it to do its job in supplements, which is why Omega-3 supplement supplement studies are really next i think it's really more down to the quality of how much that molecules oxidized

and that omega threes absolutely still have a role in our health it's just about how can we. Get it in a way that you know that's most beneficial and balancing it right you know, that's most beneficial and balancing it, right? Omega-3 is well, they help with flexibility. C-15 is the sturdy fat with no double bonds, super resistant to lipid peroxidation and anti-inflammatory. So they serve as like a yin and yang in our cell membrane. You need one for flexibility and the other for resilience and stability. So we're still, you know, watching the research and seeing how it moves along. But Omega 3 is not the only story we're learning and the Dolphins helped with that. And we'll be right back after a word from our sponsors.

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but people just kind of ignored it, which makes me wonder, have we been testing for this for decades or not really? This is a great question because it gets to two important points. The first is a lot of fatty acid panels up until the late 1990s and even the early 2000s used C15 as the ruler for all the other fatty acids.

So by default, C15 wasn't included as a fatty acid to see if it had a benefit or not. It was the dime that's next to let you know the size of everything else. It was the reference fatty acid. So as soon as the reference fatty acid, it automatically got excluded from studies. Then, again, this is just so much of good discoveries and big discoveries include some luck. We were lucky in which the fatty acid panels

had just started, that we used, had just started including C15 as something that you're measuring and assessing. And it was only because of that. If we had done the study three years earlier, C15 wouldn't have been on the panel. We wouldn't have found this, made this discovery in dolphins. So that's the first. And the second is, you know, really being able to understand that C15 has been measured in studies for a long time, but it's been used as a biomarker of how much dairy fat we eat. So the assumption was never that C15 was beneficial.

It was just that it was a biomarker of whether or not dairy fat is beneficial. That's so interesting. So it's almost like we've had the data for a while, but we haven't really understood why it matters. Right, it's just kind of like, missing what was right in front of us when you look back. Right, that's amazing. So C15, is it now sort of like a normal part of testing

or still not really in terms of like giving actual reference numbers? Like if I go to get my physical this year and I get my CBC, my standard blood counts, and I have it, is that generally included or not? Would you have to ask for that? You have to ask for it, but a lot of progress is being made

because of the wealth of studies that have been coming out about C15. So you have to ask for it, and then you ask your doctor, usually it's through a fatty acid panel, and then your doctor your doctor. Usually it's through a fatty acid panel. And then your doctor just needs to make sure that C15 is included in that fatty acid panel.

Because even today, there are a lot of times that C15 is still the reference fatty acid and not being measured. But you can get levels. We now know we need about 0.2% of our cell membrane of fatty acids. 0.2% needs to be C15 to keep it stable. Otherwise, our cells become fragile and it's what we published last year of a nutritional C15 deficiency

syndrome called cellular fragility syndrome that we now think are present in as many as one in three people globally. It's the absolute clear and clean picture we saw in the dolphins that was fixable. So take me more into cellular fragility syndrome and how does it show up? What we found in the dolphins, the good thing is it was a super clean phenotype and what's the process of a disease is called pathophysiology. And it's when you truly understand from the cellular level all

the way up to what doctors see in blood tests and what you feel, it's that whole pathway of explaining it from the beginning to the end. And we were able to do this thanks to the dolphins and then subsequent studies. So what happens is we need a certain amount of C15 in our cells to keep them stable. Aging is driven by cellular instability. As we age, our cells become more unstable, they start falling apart. We start feeling all the aches and pains of aging, joints and all the things, mood like me,

just not being able to think of the right word right now. So all of these things happen as we get older. It's all driven by changes of aging at the cellular level. So we now know that C15 stabilizes our cells as we take and it's completely dependent on how much C15 we get in our diet. So our bodies don't make enough C15, which is why it meets this definition of essentiality.

The dolphins, navy dolphins for a long time have been fed this fish called eulichon. And they're super fatty fish that are so fatty that you could dry them, stick a wick in it, and they were called candlefish. So they were chock full of great C-15. The problem was is that in the 1990s, the fisheries dried up. And so the dolphins stopped getting this rich C-15 source.

And they changed to a variety of different fish types. One of them was called capelin, which has no C-15 in it. So there was an accidental introduction of a C-15 deficient diet in dolphins that concurrently was happening in humans when we were taking C15 away because we were drastically decreasing our intake of dairy fat. So we had dual experiments happening in long-lived large-brain mammals, and what we were able to see in the dolphins is we started to see the emergence of fatty liver disease, which is a condition that showed up in people in the 1980s, non-alcoholic fatty liver disease. It got a rebrand. It's now

called Masold, but I won't go into detail about that. But initially identified in people in 1980, now present in more than one in three people globally. We saw that same phenomenon happening in the dolphins, and the dolphins developed this condition. What we now have come to understand is red blood cells become fragile because they don't have enough C15. Those red blood cells get engulfed by the liver, who helps just try to clean up any messy red blood cells in the system. Excess deposition of red blood cells over time led to iron overload in the liver, which

then led to all the downstream effects of poor liver function and in fact a whole new form of cell death called ferroptosis, which was discovered by a scientist at Columbia University back in 2012, the same year we identified the syndrome in dolphins. And it's an entirely new way that our cells are dying, Jonathan, which is a huge discovery. Ten thousand papers on this new form of cell death that accelerates our aging, accelerates heart disease, type D diabetes, fatty liver disease, cognitive decline, but nobody has known why for apoptosis showed up in the first place. Until the dolphin showed us

very cleanly, C15 deficiencies caused this form of cell death that translates all the way down to all these downstream things. So as humans what we're showing and what we talk about in the book is that as we've decreased our intake of C15 and deficiencies have increased it's explaining the accelerated aging especially among younger people and the rise and type 2 diabetes, heart disease, and now the emergence of entirely new disease called with this non-alcoholic fatty liver disease,

or Masold. Yeah, so this is really wild. It's like we've got these two concurrent experiments being run with dolphins and human beings at the same time. We're effectively We're reducing the c15 intake with humans not intentionally trying to do it This is just you know guidelines come out dietary guidelines come out all of a sudden the primary source of this for people Which is as you describe dairy full fat dairy all sudden people come super phobic of it not realizing we're reducing this thing because nobody really is focusing on it at all. Same time, dolphins are having this like shift

over in their diet, which is reducing it. But what's fascinating to me about this also is that if you study the same types of things that you're talking about in dolphins and humans simultaneously, with humans, it must be so much more confusing to try and figure out what's going on because there are a bazillion confounding variables, lifestyle, smoking, inactivity, stress, all this stuff, right? So it's like, who knows what's actually causing this?

But then you look at dolphins, you're like fundamentally the same lifestyle choices. Yeah. Exactly, exactly, yeah. So it's like you remove all these confounding variables. So it's almost like you can see what's actually going on by looking at dolphins so much more readily and then translate that back to humans.

Am I getting this right? That is 100% correct. I mean, it is when we talk about luck and fortune, it's just the foresight of the Navy to actually want to bring in a veterinary epidemiologist, not to help humans, to help the dolphins. Just for me, it leaves me with excitement and some angst with regard to how many other things we could be learning by helping other species, applying these advanced technologies

we have focused on for humans, especially in the pharmaceutical world, that we could apply to help improving the lives of giraffes and elephants and how we could help their lives. But these little secrets that were so simple, Jonathan, that were right in front of us but we didn't see until we changed our perspective. And now has resulted in a discovery that could truly improve global health. I mean, it's just thank you, Dolphins. Yeah, I mean, it's amazing. You used this phrase earlier in our conversation, One Health. Is this kind of what we're talking about or is that a different context?

It is. And One Health has been used in different ways, but for the most part, the point of it is, is that by caring for one species, we can care for all. And that a dolphin, initially people were saying, well, what you're doing in dolphins is how is that even relevant to people? And that's when we share, well, a lot of studies to understand drug development or diseases are being done in mice and labs. And these are like short-lived small mammals that are being induced to have

these diseases. Certainly, dolphins are going to have better insights because they're just so much more like us. So it's, yeah, it's this idea of One Health is that we have something to learn by taking care of animals. It doesn't have to be binary. We don't have to do research on animals for the benefits of humans or as humans sacrifice lots of things for the sake of preserving, you know, helping animal health. We can have one if we take care of our earth, if we take care of our animals, it comes back so quickly to helping to improve all of us. And how wonderful that is that it happened so quickly. We discovered 200 molecules in this work.

C-15 was just the first. So there's just, I really think this is just the beginning of understanding how veterinarians and physicians and biologists and chemists, we can all be working together, not in our silos, to help solve problems and look at things in new ways. Yeah, that's amazing. And again, by studying animals in a natural environment and a natural habitat without all these other things, you may well get cleaner data

that then you can translate back to human beings or a clearer path to being able to point to like, oh, this is a causal connection that's just so much harder to try and make in humans because there's so much other stuff going on. You mentioned also, so you talked about this phenomena, phareptosis, am I saying that right? You did, yeah.

Okay, okay. So I'm like breaking it down to the root, pharo, iron, right, like, poptosis, death, like, so it's almost like iron-related death. So, but then you also made this jump and you mentioned offhandedly, like, connections to heart disease, potentially type two diabetes, cancer, bridges this gap a little bit more for me. Like, take me from where you are to, like, these other types of conditions where these are all so often age-related, stress-related, lifestyle-related conditions in humans. Iron became a critical part of the picture for us with the dolphin work that we were

seeing dolphins, again, some dolphins getting these aging-related diseases including insulin resistance and then elevations in liver enzymes, which are indicative of angry liver. But they go up and they go back down and go back, you know, so it was kind of a phasic condition. The dolphins didn't look sick, right? It's just we were picking it up on the routine blood samples that the Navy takes to assess their health. So we went into the archives. So we looked at archive tissues and old histopathology reports of pathologists that had looked at dolphins' livers after dolphins have died, they get a full workup and histopath report. And we went back into those and literally

piles of paper, sitting in a room, finding where pathologists had described the livers of, you know, about 125 dolphins. And we started seeing this trend, Jonathan, where as we started getting into the 1990s and beyond, where the pathologists would say, well, interestingly, there was what's called hemocyterosis. There's iron deposition in the liver. And then it became almost normal. It became so that one in three dolphins had hemocyterosis, iron in their liver. And that became a really big clue for us, again, of this pathophysiology.

Once you have iron in your liver overload, plus fragile fatty acids in your cell membrane because you don't have enough C15 that are susceptible to lipid peroxidation. That lipid peroxidation combines with this free iron and it creates massive reactive oxygen species within the cell and it basically kills the cell. It takes out the mitochondria no more and the cell doesn't work anymore. And so that was the definition of theroptosis at the time and still today. What we now know is that iron overload, if you look at peer-reviewed publications on iron overload in humans, it goes from a handful per year and then once the 1990s hit, you just see this dramatic increase in papers on iron overload.

And now the highest number of papers, 1024 peer reviewed papers on iron overload, the highest year ever was last year in 2024. And what they're looking at, Jonathan, is that they are now finding iron overload that's coming with fructose. So once the liver has iron overload, the iron spills over into the blood and that seeds our heart, our brain, our pancreas, you know, our different tissues, and as different silos, because you have people who don't work on the whole body, right? They're working on the brain, the heart, the pancreas, that all of those groups started looking in and they started finding iron overload in all these tissues. And so now there's an understanding that it's all connected. It's called Dysmetabolic Iron Overload Syndrome or DIOS that helps explain how all of these diseases are worsening exponentially and facilitating and speeding up aging.

So consider iron as like a major accelerator of the aging process. And when we roll it all back to the dolphins and then now the studies that have been done since then, we know that putting C15 back into our system stabilizes the cells. The red blood cells don't get eaten up by the liver. The iron stops getting deposited and all the downstream effects slowly heal over time. So it's really fascinating again,

the parallels of what were happening and being discovered in humans and dolphins at the same time. I've heard of it. I think probably a lot of people have heard at some point of iron deficiency. Like you get your testing, you're like, oh, iron is low. And I think that's probably the more common thing that shows up on testing and the more common thing that is, quote, treated often through supplementation or like other means. And it's often what people feel more immediately, like fatigue or things like this. Sometimes it has an effect on your brain function.

So we sort of like say, okay, so like, I can point to this number, it's deficient. I don't think I've ever heard of sort of the flip side of this iron overload. And what you're saying is this is maybe a much bigger issue. Right, and in fact, they're linked. So what we're finding is that as the red blood cells get fragile and they get engulfed by the liver, it actually causes iron deficiency in the blood, iron overload in the tissues. And so you can imagine what happens if a

person... So basically the measurement of iron overload is an indicator biomarker called ferritin. And every doctor I talk to, Jonathan, when I say hyperferritinemia, they all go, what? You have an explanation for the hyperferritinemia? I am seeing everywhere. So I was like, yeah, yeah, yeah. And that's you. And again, just to be super careful with your listeners, this does not mean stop taking iron. This does not mean changing any of your regimen. It just means that we're learning that there is a sub- and iron deficiency anemia

is very real. And like you said, it remains a big problem globally. What we need to ferret out now is, do you have iron deficiency anemia because your red blood cells, because it's part of this whole syndrome. And if that's the case, then you probably wouldn't supplement with iron because it just continues to feed the problem. You've got to fix the problem on the front end, get those red blood cells stable again so that the iron can stay in the blood and

not go into the organs. So we're just right on this cutting edge of it. But yeah, but it ends up being all linked. So you could literally show it with labs that have you deficient in iron as measured in your blood, but also high in ferritin. That's right. I mean, iron is being deposited in your tissue, which kind of makes you like, how can this happen? But maybe this is actually, and maybe this isn't the one and only

explanation, but maybe this is something we've been missing for a while. It's really important. You know, with the dolphins, they had one phenotype, Jonathan, and like you said, and it was one problem that we were able to fix. Humans, there's a subset, we think, a large number of people who fit into this, but it's not the, oh, this is it, this explains all the problems we've had and it's gonna fix it. Like you said, we're very complicated as humans and our lives, and so, but it's the way that we explain

when we go over a hundred different papers and where we're at is you just can't explain it away anymore. And if we have the opportunity to fix something in a relatively simple way like vitamin C deficiency and scurvy and vitamin D deficiency and rickets like if we have a chance to help restore some health especially to what we're seeing in the kids and young adults gosh it's time to have that conversation. Now that makes so much sense. And we'll be right back after a word from our sponsors. So we've drawn a line between potential C15 deficiency, fraptosis, sort of like how the

blood then potentially the levels of iron and cellular fragility potentially affect things like, you know, like all the quote diseases of aging. What I'm curious about now also, this is again something that you write about, is a linkage between this and mental health. You know, like for sure, we have seen over the last few decades, just a stunning and horrifying increase

in the incidence of depression, anxiety. And we can point to a whole bunch of things in modern life that might be a part of it. And in fact, they may well be a real exacerbation. But I'm wondering if you see a role for C15 in this as well. We are. It's the early days, just to be transparent. But there are a couple things that have emerged over the last 10 years that have fed that same question, which is like, oh, this rise that we're seeing in mental health problems. And could C15 deficiencies be playing a role? And so the clues that we have to date, we took pure C15

and we ran it against this. We used a third party who develops what's called a cell-based phenotypic profile. And so what they do is they expose 12 different human cell systems that mimic various disease states. They then treat these disease systems with the agent, in this case, C15, and they measure 148 different biomarkers and see if they go up or down. And so you get this profile and then it's math, fancier math than what I can do. But then they're able to compare the profile of C15 with

all those different measurements with, they compared it with 4,500 other molecules. And what they showed is that at lower concentrations, C15's cell-based phenotypic profile matched that of bupropion, which is one of the leading antidepressant drugs. And it's considered this odd stepchild of antidepressants because it behaves in a very different way than other antidepressant drugs. And so that was an interesting finding. At the same time, as we were getting C-15 out to the world as a supplement, we started getting people reporting to us that they had a calmer mood, they were sleeping deeper, and their joint pain was gone.

And we thought, that's great, but that's called the placebo effect. So, because we're like, this is within two weeks, it's just not what C15 does, restores your cells and your liver and your heart. But then I started experiencing that myself, and then we had a second study come out where we showed, and again, going back to the dolphin data, showing that our body uses C15

to make a second molecule, which is called a metabolite, and it's called PDC. And PDC is the second ever discovered full acting endocannabinoid. So I mean, like make that make sense, but you know, we have these receptors in our bodies and brain that respond to cannabis, which is responsible for its effects of calmer mood, deeper sleep, less pain. But we didn't have these receptors for cannabis. I mean, dogs and pigs have these receptors and they don't have edibles. So that's not what the receptors are there for. They're there for something else. And so now we know that C15 makes the second ever discovered molecule that does

target both CB1 and CB2 receptors, which helped immediately for me explain how people can be getting those benefits so quickly. So it's about half. So then that leads to if we have nutritional deficiencies in C15, not only does that affect our cellular fragility and stability, but now we're not making the second molecule that was meant to activate the receptors that keep us calm and sleep well and have less pain. So it's fitting in the story, but again, we're, you know, we're watching that one carefully. Yeah. Is there ongoing research on this question right now?

We just finished a study and I should mention all of our studies have been funded by the Department of Defense. So it's, Defense. So this is peer reviewed not only in being published, but in the ability to do the study and to come up with the design. So we were funded by the Navy because dolphins can develop histologic changes that are consistent with Alzheimer's to understand C15's potential role with regard to brain health. So we were able to find some really compelling mechanisms that can help explain cognitive health. The paper is close to being published, so we'll be able to talk about that in more detail when it comes out, but just stay tuned on that front. So the research is happening,

and it's not just like affect, but actual cognitive health potentially, sort of like the things that we see in Alzheimer's or dementia. But because we're having this conversation at a time where you can't actually speak in specifics to that research is what I'm reading, what I'm hearing basically.

That is correct. But there are a couple, again, interesting studies. One was published looking at people with major depressive disorder, MDD, and showing that. And major depressive disorder actually has multiple subtypes. And these subtypes are so different. There is an argument that this is not one disease. This is three different diseases caused by three different entities.

And so one of the phenotypes is called anxiety-related depressive disorder within major depressive disorder. And it was that phenotype specifically showed that people with higher C15 levels were less likely to have anxiety, to have this phenotype of MDD. So that is suggestive, but again, it's correlative. And then there was another study showing that people who have higher C15 have better cognitive function as older people. And perhaps most importantly, there's a bunch of studies that have come out in children showing that the more C-15

mom has, the more C-15 baby gets. And the more C-15 baby gets, the better their body growth, their brain development, cognitive development, and even their language skills all the way up until six years old. So there's urgency around the ability to say, like, gosh, if C15 is not in most infant formulas, most moms these days are probably C15 deficient. So again, we need to get this conversation going to help the generations that are coming into this world. Yeah.

I mean, as you're describing that also, it makes me wonder. There's been some really interesting work going on now with ketosis and mental health. Functionally, for a person to be in a ketosis state, there's kind of no way around eating a very high-fat diet and often it's saturated fats that become a part of it. They get reintroduced as part of that diet. It's almost making me wonder if part of the effect might actually be a reintroduction of C15 as part of that just you know without really thinking that's what's happening Like maybe that's a meaningful contributor, but I guess do we learn more of that like in in the upcoming research? That's right. And what's good is that there are so many people paying attention to this and now studying it So probably every two weeks, there's a new paper coming out on C15 from different teams throughout the world. It's a very

exciting time. Yeah, that's amazing. One of the other things that so many people experience and has become I think a lot more prevalent in the last few generations is the broad basket of autoimmune conditions. Is there a tie-in here as well? It's so hard to keep saying yes, Jonathan. It's like, this is too good to be true. So before I get into that, I think what's important is essential fatty acids and vitamins,

things that we must get from our diet to sustain our health. Nature has made all of these to do a lot of heavy lifting, to do a lot of things. So it actually should not be surprising given that C15 is an essential fatty acid, that it's doing a lot of things. So if we go back to that cell-based phenotypic profile, in addition to allowing you to compare with other compounds and drugs, it also tells you what it does in these different disease systems.

And several of these disease systems in a dish, like diseases in a dish, mimicked autoimmune diseases and allergies. And what it showed was that C15 had a remarkable ability at being able to lower multiple pro-inflammatory cytokines across a bunch of these systems. We now understand that a big reason for that is it's called a JAK-STAT inhibitor. So when we talk about targets, it does a bunch of, there's a lot of different targets. It activates AMPK and it inhibits mTOR

and blah, blah, blah, blah. But specific to autoimmune diseases and allergies, it decrease inhibits what's called the Jack Stat pathway, which explains how it lowers these pro-inflammatory cytokines. So a lot of those commercials you see where it's like the person's now able to expose their skin because the autoimmune skin condition is gone and a lot of those are Jack Stat inhibitors. For me, I have been cursed with atopic dermatitis my whole life. It got worse as I got older.

I became allergic to all raw fruits, vegetables, and nuts. So like anything healthy, I can't eat. Like it's terrible. And it got to the point where it was just, it was affecting my face, my hair, my like, it was very severe. And so I have seen for myself that it doesn't fix a disease, it is not a drug, but I think it was more like maybe my lack of C15 that was making me more susceptible and once I was able to

bring it back into my life in a concentrated way, it's been able to just kind of calm things down. But clinical trials are needed in that specific area. There have not been done any autoimmune allergies, but it may help explain why we're seeing an increase in some of these autoimmune diseases. Again, just little pieces and hints of ways that we can take the edge off of this kind of worsening global health problem. So let's talk about the big lingering question that's going to be on anyone's mind after

diving into this conversation with us, which is, okay, assuming that you're not a dolphin, but you're a natural human being. How do we, and maybe, you know, you're kind of curious, am I deficient? I think you sort of shared, okay, we can actually just add this to the panel of testing that we get next time we get bloods done, and that'll start to give us a hint for like our numbers actually where they need to be. Let's say we realize we are deficient, how do we as people like what are the different ways that we can reintroduce more C15 into our diets if it makes sense for us? Yeah, this is the whole movement, right?

Is this how what are different ways that we can introduce C-15 back into our lives? That makes sense. With regard to children, you know, in the 1990s, the rules or the guidance of avoiding whole dairy fat doubled down in the 1990s. And the guidance that's coming out from pediatricians was that if your baby has a family history of type 2 diabetes or fatty liver disease or obesity, it should never get whole fat

milk at all. Our first step is not just dramatically, okay, start giving all children whole fat milk again, but we need these regulatory bodies to look at the data, take a hard look at the data, and be able to revisit about what we believe is that it's likely that getting whole dairy fat back into children's diets fits what all of it again from a comparative one health perspective. All mammals drink milk right at birth and for development. It is nature's perfect food for development. We shouldn't take that away. So for kids who can have whole dairy fat. So that would be step number one. Step number two is our industry changes. That if a cow is fed grass, it has twice as much C-15 in its dairy fat

than a cow that is fed corn. So let's get diets back into the cows that maximize the amount of C-15 in their food. And one thing we're calling for is for dairy food products to share how much C-15 is in their product. Because if I was a consumer and I was looking at different types of butter, different types of milk, I'd pick the one that has the highest C-15 in it. Because you can't predict what it has unless you know what that cow is eating. So that would be number two way to get that when we do eat dairy fat. Cheese can be a good source of C15 sardinians who live to 100 and beyond.

It's where the oldest men in the world live. They're less likely, they live longer because they're less likely to die of heart disease. They have C15 levels that are two to three times higher than the rest of the world. They're at 0.4, 0.6%. They have local sheep and goats that graze on grass and make their cheese, which is Pecorino. Pecorino has twice as much C15 as other cheeses. Those are good ways to get back in. Yeah, and maybe you were just about to address this, but my curiosity is, like, if somebody

is listening to this and saying, like, but dairy doesn't, like, I don't do well with dairy. Yeah, and this, exactly. And the other big elephant in the room is that there have been, just like with omega-3, there have been thousands, tens of thousands of studies on eating dairy. And it's a mess. Like, some are good, some are bad, some are neutral. And it might be because of all of this variation we just talked about.

But in the end, there's a group that actually got together in Denmark in 2017, and they were scratching their heads about this problem and saying, wait, we're seeing remarkable studies coming out about individual ingredients within milk that are really beneficial, but as soon as you put it back into the whole food matrix of dairy fat, you don't see that benefit in the studies. And so what they concluded is, you know, there are over 400 fatty acids in dairy fat. Only 1% is C15. Over 40% are pro-inflammatory saturated fats. So it just doesn't get a chance to win. … Yeah, it's not clean.

… It's not clean. So just like mammals, there are no other mammals that continue to eat dairy beyond infancy. So we should also maybe follow that guidance and be able to be, and which is why the Navy invested 10 years of research so that we could develop a pure C15 ingredient that doesn't have to, that is vegan, you know, that is not an animal product. So people who are lactose intolerant, people who don't want dairy fat or don't want the pro-inflammatory fats, the Navy truly understood the problem for Beyond Children and they invested 10 years to be able to provide a solution, which is such a testament to the military. So basically this is now available in supplement form in just pure C15. And we should also probably disclose that for you,

you're a researcher, you're independent, you're really trying to understand conflict of interest disclosure. Yeah, absolutely. And so that's where it's important to note that we then were funded by the Navy to do all this work. Specifically, even we were funded by the Navy to make the supplement. We then, we being myself, a Navy veterinarian and my husband, a Navy physician, we then left the

Navy to be able to start a small business to be able to use those funds and develop the supplement and commercialize it because that's not what the government does. So for us, it does need to be completely transparent as far as conflict of interest. For us, Jonathan, it's like, this is what the military does, right? I mean, Eric deployed to three wars. You know, it's just like, you find a problem, figure out how to fix it, and then you fix it. You don't do 50 years of research and publish papers and not translate it. You don't do 50 years of research and publish papers and not translate it. So for us, it was a very natural process of saying we found a problem in dolphins, we figured

out how to fix it in dolphins and be able to have a spin out benefit to human health too. And then the Navy said, well, then go do it. Go make this molecule accessible to all. So we started with the supplement, which is fatty 15. But now, it's really the goal and the movement is accessibility. And so we're now advancing it as an ingredient. I can then fortify foods, infant formulas, in addition to all those other things I talked about. How do we change industry practices?

How do we change dietary guidelines, especially for children? So it's part of the solution, which you know, we're really proud of being able to have this ability to have a positive effect. Yeah, so we talked about potential for dairy, we talked about direct supplementation. Are there other fishes that we can eat? Are there other whole foods that we can eat that would there other whole foods that we can eat that would give us any meaningful level or not really? I so wanted there to be.

So for it really, the studies to date support that. Now, like by far, dairy, again, it used to be a biomarker for how much dairy fat we ate. But there are some ways that we can plus up our C-15, right? And two of those are, one is, so fish can have C-15 in it, but in the most part, it's in fatty fish and it's in the skin and the head. Yeah, we don't eat that. Or you can make soup out of it, right? Yeah, exactly. And I'm half Chinese and it used to be that the person of honor at the table, we get the head of the fish. I'm like, ah, they didn't know back then, but they were giving C15.

Two other things we could do, a study showed that pregnant women who exercised had higher C15 levels in their blood. And the hypothesis is that the C15 that you store, if you have enough C15, it gets stored in our tissues and by exercising, you're releasing it into your blood. So that could be a way, right, To kind of re-release C15. So exercising is good for many reasons. I just gave you another. And then the third is there's clear, we now know that microbes in our gut can make some levels of C15, which is why nobody has zero C15 in their blood. It just isn't enough to get up and over

that deficiency level. So, if specifically by eating fiber, fiber has inulin in it, which feeds specific types of bacteria. Those bacteria then use inulin to make C-15. And a really cool study showed, explained that's how fiber is beneficial to liver and metabolic health.

Oh, that's so interesting. So fiber. Right. And how many times have we all heard, have more fiber in your diet? I know. Sorry that sounds boring, but exercise and fiber, good for many reasons, including helping to kind of get those C15 edge up. As we start to, like as we have this conversation and you're sort of like looking forward at

the next maybe five, 10 years, what are you looking at like moving forward? What's the vision in terms of like, where's the research going? Where's accessibility going? Right, exactly. So, you know, we've, when this all started, we've had three goals and the first was credibility, which is why 10 years of studies and the studies continue and now others have taken the torch, which is great. There are three other teams that have critically evaluated that stake we put in the ground of saying it's an essential fatty acid, right? That's a very big claim. So now we have three other independent teams have looked at it on their own and they have all concluded that C15

meets the criteria of essentiality. So those studies need to continue happening. So credibility, one, that continues. Two was the ability to be able to increase awareness. Jonathan, thank you. So we need to get out there. That's why we wrote the book, The Longevity Nutrient. Simon and Schuster approached us, which like that doesn't happen to them. They said, listen, we've been following your story for a year and this is a book and would you be willing to put it out there? And the book is serving as a really helpful form, especially at this time, that there's

this level of research, voluminous research to support it. And so the book goes into much of everything that we talked about but really helping to lay out the studies and data to show that we cannot explain it away anymore. We have to be talking about this so that's the awareness piece which again will continue. The last is accessibility. So we need to increase access to not just just through the fatty 15 supplement, but again through ingredient, through agricultural changes. So that's the next five years, Jonathan, I see the world including ourselves, but more importantly, lots of scientists really leaning into C15 to understand what we need understanding like we talked about its role in as a neuroprotectant and cognitive health and understanding the breadth of how quickly we could fix something if we could cure fatty liver disease, especially showing up at this would this is just it would

mean everything. You know, it just it's becoming the number one cause of cancer in kids and liver transplants globally and just that alone. So the hope is there will be a lot of leaning in on specific, the most important components that C15 can help reverse meaningfully. And so I see that the liver disease component being a big focus area. Yeah. I mean, super powerful and exciting to be in a moment

where it seems like it's just really tipping more into the mainstream. A lot of people are paying attention, a lot of academics and researchers and scientists are paying attention, and hopefully there's more to come in this story. We're in the beginning stages. Feels like a good place for us to come full circle as well.

So I always wrap with the same question, which is in this container of Good Life Project, if I offer up the phrase, to live a good life, what comes up? Oh gosh, fill it with purpose. Allow the moments to happen in your life where a purpose sometimes lands in your lap, and be ready, and you'll know when it happens. And just be ready to, as I talked about in the beginning of Teddy Roosevelt's quote about being in the arena, that, you know, it's about being in there and fighting the good fight. And it is hard and it is difficult,

but if you feel for us in science, you follow the data and the data continues to support what you're trying to achieve, you fight like hell to be able to do something meaningful and impactful to the world. And so for me, it's made it an incredibly good life. Thank you. You're welcome. It's been great being here, Jonathan. If you love this episode, safe bet you'll also love the conversation we had with Matthew Park about how aging immune systems affect cancer risk. You'll find a link to that episode in the show notes.

This episode of Good Life Project was produced by executive producers Lindsay Fox and me, Jonathan Fields. Editing help by Alejandro Ramirez and Troy Young. Christopher Carter crafted our theme music and special thanks to Shelly Del Bliss for her research on this episode. And of course if you haven't already done so please go ahead and follow Good Life Project in your favorite listening app or on YouTube too. If you found this conversation interesting or valuable and inspiring chances are you did because you're still listening here. Do me a personal favor, a second favor, share it with just one person. I mean if you want to share it with more that's awesome too, but just one person even, then invite them to talk with you about what you've both discovered,

to reconnect and explore ideas that really matter, because that's how we all come alive together. Until next time, I'm Jonathan Fields, signing off for Good Life Project. Good Life Project is sponsored by Aveeno Baby. So you know there's something remarkable about how nature protects newborns, that natural moisturizing layer babies have in the womb. It got me thinking about how delicate baby's skin really is. So I've learned it's actually about 30 percent thinner than adult skin.

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