Could This Controversial, Newly Discovered “Dolphin Drug” Be A *Missing Key* To Longevity? The C15:0 Story, With Dr. Stephanie Venn-Watson

Ben Greenfield [00:00:00]: My name is Ben Greenfield and on this episode of the Boundless Life Podcast.

Stephanie Venn-Watson [00:00:04]: When we first made this link in the dolphins, we did eight studies over three years. We showed that C15 is not only a beneficial and active saturated fat, but that it was meeting these rare criteria of being an essential fatty acid. And importantly, this is critical that over the last 24 months, and really 12 months, four independent teams have now looked at the criteria of C15 being an essential fatty acid, including gold standard studies that were used back in 1929 and 1931. Really important follow up from independent teams that have nothing to do with us all concluding that yes, C15 meets the criteria of an essential fatty acid. So lots of exciting work on that frontier.

Ben Greenfield [00:00:53]: Welcome to the Boundless Life with me, your host, Ben Greenfield. I'm a personal trainer, exercise physician, physiologist and nutritionist. And I'm passionate about helping you discover unparalleled levels of health, fitness, longevity and beyond.

Ben Greenfield [00:01:15]: My guest on today's podcast is a veterinary epidemiologist. That might be the longest multi-syllabalic phrase I've used in quite a while on my show, veterinary epidemiologist Dr. Stephanie Venn-Watson. Welcome to the show, Ben.

Stephanie Venn-Watson [00:01:33]: It's great to be here. I'm glad to challenge you right out of the gate.

Ben Greenfield [00:01:36]: Right out of the gate. You wrote this book, the Longevity Nutrient. This thing was intriguing for me because I'm always looking around for things that haven't been talked about yet in the whole nutrition and supplementation world. This definitely fit into that category and we'll talk about it. It's a fascinating book by the way. If you guys want to check it out, go to BenGreenfieldLife.com/C15. That's C15. And I'll put all the show notes over there which promise to be juicy for this one.

Ben Greenfield [00:02:03]: Or should I say fatty? Stephanie, what's a veterinary epidemiologist?

Stephanie Venn-Watson [00:02:08]: It's a nerd who loves animals. As a short answer there. So our job is to basically find patterns related to animal populations, remembering that humans are also animals. So veterinary epidemiologists tend to help not only in large population studies with non human animals, but actually most of us are working for public health and other groups looking at human trends over time.

Ben Greenfield [00:02:42]: You mean you're studying humans or you're studying animals and figuring out if what you find in animals could be translated to humans?

Stephanie Venn-Watson [00:02:50]: Yeah, both. But the latter is obviously is a good reason why we're chatting today because it's like as a veterinarian you really come to understand there are some. So many more similarities between animals than there are differences. So that whole comparative approach has, you know, we're always thinking with regard to, you know, when we go to veterinary school, we learn about 12 species instead of one. So it helps you understand the links between all of us.

Ben Greenfield [00:03:16]: Well, I was walking out to actually record this podcast out of the kitchen. My wife's like, have fun talking to the dolphins. Because I told her last night I was going to be interviewing this dolphin researcher. And she's like, why the heck are you interviewing someone about dolphins on your health podcast? So I should let you answer that question, Stephanie, because you. I mean, this whole story of how this book came to be started with, if I'm not mistaken, dolphins.

Stephanie Venn-Watson [00:03:40]: Yeah. So there I was. I mean, this whole discovery, Ben, was an accident, which is wonderful and gifted to us by dolphins. So, again, veterinary epidemiologist. I was recruited by the Navy about 24 years ago to help better understand health and wellness of aging navy dolphins. The Navy has cared for this sustained population of about 100 bottlenose dolphins for over 60 years. They live in the open ocean here in San Diego Bay, go out into the open ocean every day.

Stephanie Venn-Watson [00:04:15]: Every day they choose to come back. So it's a really amazing population. They get such good care, Ben, that while dolphins in the wild live to about 20 years old, dolphins at the Navy are now living in, routinely living into their 40s, 50s. And I just learned last week when I was stopped by for a visit, two of the dolphins are turning 60 years old this year. So much older dolphins at the Navy.

Ben Greenfield [00:04:41]: I didn't know dolphins could even live that long. That's interesting that they come back. So a dolphin is released into kind of like its native habitat from this Navy base or whatever, and they go out into the ocean, but then eventually just, like, show back up at the front door.

Stephanie Venn-Watson [00:04:57]: They do. And they live, you know, they live in the bay there. So they kind of have a home base in San Diego Bay. And so they'll go out in the bay, do their work, which is easy peasy, and then. Yeah, yeah, come back.

Ben Greenfield [00:05:09]: So you guys count them. Is there ever, like, a rogue dolphin that doesn't come back?

Stephanie Venn-Watson [00:05:13]: It wouldn't work. So the program wouldn't work if dolphins went rogue. Because if you can imagine if you have 100 bottlenose dolphins, each one of those is, you know, a really valuable individual who you spend, you know, decades training and working with and getting to know that if they just kind of went away, the program wouldn't be able to sustain. So it's really good population. Dolphins get really good care. And what we learned is as they were getting older, that about 1 in 3 older Navy dolphins were developing things that are going to sound really familiar like insulin resistance, fatty liver disease, high cholesterol, anemia, chronic inflammation, and as we just published last week, the full suite of changes consistent with Alzheimer's. And so really fascinating parallels between large, large brain, long-lived mammals of humans and dolphins.

Ben Greenfield [00:06:09]: So obviously the diabetic dolphin isn't necessarily like eating, I don't know, seed oil, Doritos or whatever it is people are blaming on diabetes these days or for diabetes. But with these chronic diseases in dolphins, what is it that you were finding that's applicable to humans?

Stephanie Venn-Watson [00:06:29]: Right, and you hit the nail on the head here, Ben, that this was a huge unlock as I was reaching out to experts in the human space on hey, how can we help dolphins? What are you doing in humans and how can we help dolphins? They were flipping the conversation around immediately and saying, wait, wait a second. Dolphins are getting fatty liver disease and Alzheimer's and all the chronic inflammation, metabolic syndrome. Exactly like you're saying without carbs, without trans fatty acids.

Ben Greenfield [00:06:58]: Right. Assuming they're not swinging by like a Navy SEAL tequila bar while they're out there on their journey. When you let them loose, it's a pretty controlled diet and lifestyle, I'm assuming.

Stephanie Venn-Watson [00:07:10]: Exactly. Despite being Navy dolphins, they also are not heavy drinkers. So we were given the good fortune to have office in naval research funding. The Navy archives all of serum that they collect on dolphins as part of their routine care. So we were able to go in and use an advanced technology called metabolomics to study thousands of small molecules that are present in the dolphins archived serum, but also their all fish diet. Right. Because all they eat are fish. And we were then able to look for which small molecules predicted the healthiest aging Dolphins.

Stephanie Venn-Watson [00:07:51]: So those 2 and 3 that aged well, we thought of the Omega-3s because all they eat are fish and. And instead. Right. They completely surprised us by showing that in fact it was C15, this odd chain saturated fat that predicted the healthiest aging dolphins and has emerged today, which we'll talk about, you know, as the first essential fatty acid to be discovered in over 90 years.

Ben Greenfield [00:08:13]: Okay, so C15, you said it's a saturated fat.

Stephanie Venn-Watson [00:08:17]: Right. So that's where we were confused too. We're like, wait a second, a saturated fat? We've all been taught our whole lives all saturated fats are bad. Especially since our primary source of C15 isn't from fish, it's from whole fat, milk and milk, but dairy fat. So C15 is called that because it is a fatty acid that has 15 carbons in it, hence C15. And then you'll see, even though we don't pronounce it, it's a colon zero. And the number after that colon tells you how many double bonds are in it. If a fatty acid has no double bonds, it's a zero.

Stephanie Venn-Watson [00:08:58]: That means it is a saturated fat. So it's particularly resistant to lipid peroxidation. Those double bonds love to get attacked by oxygen. So it just ended up being this Goldilocks fatty acid that is a good saturated fat. We've learned that not all saturated fats are created equal. Those that have an odd number of carbons like C15, C17 and C15 being the Goldilocks fat, have anti inflammatory effects. We'll talk about all the many benefits of C15 and protective. While even chain saturated fats like C16, C18 are pro-inflammatory.

Stephanie Venn-Watson [00:09:37]: Which is why we've for so long we've associated saturated fats with higher risk of Type 2 diabetes, heart disease, fatty liver disease. We weren't wrong, we just are now understanding, we've known that not all fats are equal. We now know that not all saturated fats are created equal.

Ben Greenfield [00:09:54]: Okay, so real quick, not to nerd out on this too much because it's probably not that high up on people's priority list, but thinking back to biochemistry, so when you're saying C15, 15 refers to the number of double bonds.

Stephanie Venn-Watson [00:10:19]: Number of carbons. So it'll tell you.

Ben Greenfield [00:10:19]: Okay, so there's 15 carbons. But because it's a saturated fat, every single bond between each of those 15 carbons is a double bond.

Stephanie Venn-Watson [00:10:19]: So it's not a double bond.

Ben Greenfield [00:10:22]: It's not a double bond.

Stephanie Venn-Watson [00:10:23]: Exactly, exactly.

Ben Greenfield [00:10:24]: And when you say not a double bond, what does that mean?

Stephanie Venn-Watson [00:10:28]: So that's a good point. So it's a single bond. So if you like, we think back to our biochemistry days, right, you'll either see two bars go across, almost like an equal sign versus a single bar. So a single bar means it's super sturdy, it means it can't bend. So if you think about in a fatty acid structure, if it's a double bond, think of it as a hinge. So it allows the bond, allows that fatty acid to bend, which makes it flexible. Which is why unsaturated fats that have double bonds are oils at room temperature. So they're able to be flexible.

Stephanie Venn-Watson [00:11:03]: But those double bonds can also be attacked by oxygen, which then leads to risk of lipid peroxidation and other things. So think about saturated and unsaturated fats as kind of like a yin and yang of the fatty acid world. Saturated fats are sturdy. Unsaturated fats are flexible. And we need both to maintain, you know, a balanced cell membrane. But specifically, we're learning that our cell membranes need C15. This odd chain, saturated fatty acid, plays a very special role with regard to improving the integrity of our cells.

Ben Greenfield [00:11:40]: Yeah, it's a little bit counterintuitive, isn't it? Because you hear double bond, and you think that a double bond would be, like, more rigid, less flexible, twice as strong and unable to bend and more solid at room temp, Right?

Stephanie Venn-Watson [00:11:51]: That's right, Yep. So it goes against, again, where all these things are like, wait, a saturated fat that's good for us, and double bonds are weaker. So we're all learning together.

Ben Greenfield [00:12:02]: Okay, so 15 carbons long, this fatty acid that you find in dolphins, and you're saying that's the first essential, essential fatty acid to be. How many years do you say, 90?

Stephanie Venn-Watson [00:12:14]: 90 years since 1929. 1930.

Ben Greenfield [00:12:18]: Okay, walk me through that. What's that mean that it's essential?

Stephanie Venn-Watson [00:12:21]: Right. So this is a big deal, right? So an essential fatty acid is a nutrient that our bodies must have in order to maintain our baseline physiological health. If we don't have enough of it, we will see a deficiency syndrome. So our health will fall apart. Importantly, our bodies can't make enough of this nutrient, of this fatty acid. Therefore, we have to get certain amounts routinely from our diet. So prior to our discovery with C15, there are two known essential fatty acids. One's an Omega-3, alpha linolenic acid, and one's an Omega-6, linoleic acid, which were discovered way back when by George and Mildred Burr, back in 1929 and 1931.

Ben Greenfield [00:13:08]: Okay, so essential fatty acid doesn't mean you can't make it. It means you can't make enough of it.

Stephanie Venn-Watson [00:13:14]: Exactly.

Ben Greenfield [00:13:15]: Okay. All right. So when it comes to C15, 90 years is a long time. Why is it that you think this hasn't even been discovered before or looked into before? I mean, obviously you'd expect for science to find new things as time progresses, but it just does seem like a long time with what we know about fatty acids, for this not to have been identified as an essential fatty acid before this.

Stephanie Venn-Watson [00:13:43]: Yeah, you're exactly right. And then add on top of that, Ben, that I'm a dolphin veterinarian, right? So it's like we have people who spend their whole lives working on fatty acids. And so how is this not discovered before? When we first, first made the. This link in the dolphins, we went to Dr. Ed Dennis, who is a global leader in fatty acids. He was the editor-in-chief for the Journal of lipid research for 15 years. So we're lucky that Ed was in San Diego close to us. So we went and met with him and we said, hey, this is what we found in the dolphins.

Stephanie Venn-Watson [00:14:19]: Do you think C15 might be beneficial? And he said, probably not, because we all know about C15. We've known about it since the 1950s. It's present at such low levels that we, and it's a biomarker of how much dairy fat we eat. Chances are we didn't miss this stuff. But the dolphin component is interesting. So here are the studies we would need to do to figure out, is it bioactive? At what concentrations, is it bioavailable? What activities does it have? Like a whole slew of core questions that would need to be answered. So we did eight studies over three years. And the culmination of that, of those studies, we published in Scientific Reports with Ed Dennis as the senior author on this paper, in which we showed that C15 is not only a beneficial and active saturated fat, but that it was meeting these rare criteria of being an essential fatty acid.

Stephanie Venn-Watson [00:15:17]: So we published that in 2020. And importantly, this is critical that over the last 24 months, and really 12 months, four independent teams have now looked at the criteria of C15 being an essential fatty acid, including gold standard studies that were used back in 1929 and 1931, where you deprive a pregnant mouse of C15, you let her have the babies. So now the babies are C15 deficient. They demonstrated nutritional deficiency syndrome. So poor growth. And when they gave the babies C15, their growth restored. So another study was done in worms showing that you could remove every nutrient, not just fatty acids, but every nutrient from a baby worm. And if you give it just C15, its normal growth will restore.

Stephanie Venn-Watson [00:16:10]: So really important follow up from independent teams that have nothing to do with us all concluding that, yes, C15 meets the criteria of an essential fatty acid. So lots of exciting work on that frontier.

Ben Greenfield [00:16:24]: Well, I'm sure as a veterinary epidemiologist, you probably get this all the time. You just talked about dolphins earlier and then rodents and then worms. But what about, like, you know, people?

Stephanie Venn-Watson [00:16:35]: Right, there's that. So what's been important with people like. So for example, in this, as far as infant development and growth, there are, there's a whole other team, there are multiple teams working on the early stages of C15 in humans, showing that even from the level of the oocyte, that the more C15 that's present, the better that oocyte multiplies. So it's signs of a healthier embryo for in vitro fertilization. Studies have shown that the more C15 mom has as a human, right, that the more C15 baby gets, and the more C15 baby gets, the better the fetal body growth and head circumference, which is brain development. The better the baby once it's born, its growth and development. And there's a study done called the Eden Cohort study in France that has followed kids all the way up to six years old, showing the more C15 they got from mom during and after pregnancy, the better the cognitive development of these children. So, you know, when all of these add up, these pieces that you know, gets us to an essential fatty acid that you know is meeting the requirements and is relevant to humans importantly.

Ben Greenfield [00:17:49]: A lot of the research I've seen on dairy seems to indicate, and this surprises a lot of people, maybe it's because of our built in bias still about saturated fats being unhealthy, is that full fat dairy seems to be where you get more of the benefits of dairy compared to non fat or fat free dairy. And I've always wondered, is that because something about separating the fats from, from the proteins affects the dairy, something about the extra processing affects the dairy. I don't know if C15 could fit into the picture here, but is there any research that you know of on people eating full fat dairy products being healthier? And maybe some of those health benefits coming from the C15 composition of full fat versus non fat or fat free dairy?

Stephanie Venn-Watson [00:18:40]: Right. So yes, and in part it's because C15 has been used as a biomarker of dairy fat. So it's almost like, you know, like we were saying before, how did people not discover this before? It's been right in front of us. It's just been the interpretation of people with higher C15 have a lower risk of developing Type 2 diabetes, heart disease, fatty liver disease. But the reason why, you know, when you asked earlier, Ben, why hadn't this been discovered before? People were just seeing C15 as a biomarker of dairy fats benefits, not that the fact that C15 itself may be beneficial. So when we isolated C15, right. And we took a look at how does C15 do compared to whole dairy fat? Other folks have shown like Bishop et al did that study in mouse model of Type 2 diabetes and fatty liver disease. And you know, we had shown that C15 improves health, so decreases glucose, insulin, weight, body, you know, body weight on a high fat diet, lower inflammation.

Stephanie Venn-Watson [00:19:47]: When Bishop et al gave the same model whole dairy fat, the mouse got worse. So and it's because. And they attribute it to that whole dairy fat has much higher levels of C16 and C18 of these pro inflammatory saturated fats. So kind of getting to the point where like Thorning et al. Hedge talked about how do we deal with whole dairy fat? It's kind of a mess. You do absolutely have studies saying whole dairy fat can be good for you. There's equal studies saying whole dairy fat or having these high levels of these pro inflammatory fats can be bad for you. It's super confusing.

Stephanie Venn-Watson [00:20:25]: And I think what we're getting to is understanding like you said, different forms of dairy fat have different amounts of beneficial nutrients, which is why the Navy had funded us to say, hey, can we just take C15 and if you're showing that it has these benefits, can we just put that to work absent kind of the confusion and you know, of dairy fat?

Ben Greenfield [00:20:47]: Well, before we close the loop on dairy, because I don't want to just leave people hanging and you know, sitting there in front of their full fat Greek yogurt now asking themselves, do I eat this? Do I not eat this? Like what's your take on the dairy fat thing? Like would you eat or you know, would you drink full fat milk? Would you eat full fat yogurt based on what?

Stephanie Venn-Watson [00:21:03]: You know, I do not shy away from whole dairy fat, but I do think it's in moderation. Like we shouldn't make 90% of our diet dairy fat. You know, if we look at the Sardinian population and the high longevity zone, they have swapped out cheese so we can swap cheese for meat. So eat a lot less meat. They eat a lot of cheese. And their cheese specifically has, has 50% more C15 in it compared to other dairy fats. And so with regard to understanding fats that are good for us, it's dairy fat that comes from animals that are grass-fed have twice as much C15 in it than like cows, for example, that are fed corn. And so when I'm going for my whole dairy fat options, I go for cheeses that are from if hopefully, you know, from grass-fed animals is.

Ben Greenfield [00:21:57]: Okay. That's actually super important to know. So so in Sardinia, the cheese that they eat is special because that cheese is coming from grass-fed animals.

Stephanie Venn-Watson [00:22:06]: Yeah. And even better, there's actually multiple studies showing not only is it about grass-fed animals, and they use sheeps and go sheep and goats. It doesn't really matter if it's a sheep, a goat or cow, but if they are fed not only grass, but grass at high altitude, that has even more C15 in their milk. So the Sardinian high longevity zone is in a mountainous region in Sardinia. So they're really getting, they are hitting that sweet spot of grazing, you know, grass-eating sheep and goats at high altitude, and that's resulting in their cheese. One of which is pecorino, which I love, has, you know, high C15. And it helps except explain why people in this high longevity zone have two to three times higher C15 levels than the rest of us.

Ben Greenfield [00:22:55]: Okay, we are rabbit holing big time. But, but why is it that like a hypoxic Sherpa goat cheese would, you know, would, because of some type of oxygen limitation, produce a cheese that's better than a goat at normal altitude?

Stephanie Venn-Watson [00:23:11]: Yeah, I mean, I think you're heading down the right rabbit hole. I think it's, you know, C15's role is to be a sturdy fatty acid that helps make things, living things, more resilient to stressors. And so hypothesis, Ben, but not yet been tested, is are these high altitude grasses and animals put at, you know, really having to leverage C15 to be able to make them more resilient? And again, in a hypoxic environment.

Ben Greenfield [00:23:39]: Kind of makes me wonder if any type of stress might induce upregulation of C15. Because I have goats, but I don't live at altitude, but I do have cold tubs. So if I like cold thermogenesis my goats, maybe I could induce higher C15.

Stephanie Venn-Watson [00:23:54]: You did not get that from me, but yeah, you're heading in the right direction.

Ben Greenfield [00:23:59]: I don't have mountains, but I have too many cold tubs around here. All right, well, we'll save that for another day. I'll let you guys know if I wind up cold plunging my goats. But back to the longevity piece, because Sardinia is obviously one of these longevity enhanced blue zones. Apparently you talk about longevity a lot in the book. You talk about a lot of these other chronic diseases, but specifically you talk about longevity and you describe these longevity must haves that you've identified in terms of something that a molecule must cause for it to be a longevity must have.

Stephanie Venn-Watson [00:24:34]: Can you get into that a little Bit I can. So as we started learning about C15's role, its activities, how it works and what it's doing, Dr. Nicholas Schork, who's head of NIH's longevity consortium, and he's been playing that role for over 15 years, Nick came in and he's like, I'm reading all these studies are now over 100 peer reviewed studies on C15, available at discoverc15.com for those who want to nerd out. And Nick said, Steph, like C15 is, the evidence I'm seeing is that C15 is emerging as a geroprotector. And I said, great, what's a geroprotector? So that's where Nick described that a geroprotector is the holy grail of a longevity molecule because it slows the rate at which we age to stem the onset of the diseases that kill us. Which means that if it's a true geroprotector, you're going to see clinically relevant benefits within months. Right. In a person who's already going through that process of aging.

Stephanie Venn-Watson [00:25:41]: That's what excited Nick because he's like, we don't have that today. And this has the potential to have a meaningful effect. We worked with Nick and he came up with these five longevity molecule must haves. The molecule needs to show that it targets the human longevity regulating pathway. It needs to show that it targets key hallmarks of aging. There needs to be evidence it slows the rate at which we age, that there are clinically relevant benefits seen within months and that there is strong evidence that the molecule can actually help prevent the onset of diseases. So what we do, we go through the book, is we show that C15 does all of that. It activates AMPK and inhibits mTOR.

Stephanie Venn-Watson [00:26:25]: Right? This is what metformin and rapamycin do, respectively. It targets six hallmarks of aging, including improving mitochondrial function and decreasing senescent cells and decreasing inflammation. It has evidence of slowing the rate at which we age. There's a key biomarker aging rate called Red Blood Cell Distribution Width or RDW. And C15 has been shown to reliably reverse that. So if it goes high, it's a faster aging rate. C15 has repeatedly shown to bring that down. And then we talked about, we'll talk about clinically relevant benefits through clinical studies, in vivo studies within months having to do with liver health, metabolic health, cholesterol.

Stephanie Venn-Watson [00:27:08]: And the last is there are meta analyses. So studies of studies involving tens thousands of people over decades repeatedly showing that people with higher C15 have a lower risk of developing Type 2 diabetes, heart disease, fatty liver disease. Lee et al showed that for every 50% incremental increase in C15, the percentage that we have in our cell membranes and in our blood decreases our risk of Type 2 diabetes by 8% and our risk of getting coronary heart disease by 17%. So when you bring all these pieces together, that's where you get to checking off these must haves of a longevity nutrient.

Ben Greenfield [00:27:52]: Come back to you are what you eat type of idea or you are what you eat, ate. Is it because C15 is comprising our cell membranes with this more stable fatty acid and is it just that or is it doing other things? This is kind of like a mechanism of action question, you know?

Stephanie Venn-Watson [00:28:12]: Absolutely. And this is so important, Right. If you don't understand mechanism of action of something and what concentration. Right. You need to achieve that mechanism of action, it's kind of like game over. Right, Ben? It's like a lot of skepticism around, like how does it really work? So you're spot on. That C15 as a stable fatty acid goes into our cell membrane and it makes it more stable and resistant to lipid peroxidation, which is a major driver of chronic diseases and aging. It is such a simple thing that it does, and we'll talk about it does more.

Stephanie Venn-Watson [00:28:48]: But that is a core mechanism of action. In addition, you know, we and other groups have shown that C15 is a pleiotropic molecule, which means it does a lot of different things. And so I'm just going to name off some acronyms, but we're not going to go into detail. But it, you know, we know that it activates AMPK, Akt, and PPAR alpha/delta. We know that inhibits mTOR, JAK/STAT, HXX, lots of stuff.

Ben Greenfield [00:29:15]: Okay. So by the way, those are all. I mean, interrupt you. You said AMPK, ACT and ppar, those are all the same things that would get triggered via exercise. So it sounds to me like you're saying it might act as a little bit of an exercise memetic agent.

Stephanie Venn-Watson [00:29:29]: That is correct, yes. Especially that PPAR delta. Yeah. AMPK, don't. Not the fact that you're exercising while we're doing this. I'm incredibly impressed.

Ben Greenfield [00:29:38]: Yeah. In my opinion, most. Sorry to interrupt. Most exercise memetics and calorie restriction. Memetics are best combined with respectively, exercise and calorie restriction. If you're looking to maximize the benefits from those. You don't just like pop a pill and watch Netflix.

Stephanie Venn-Watson [00:29:53]: Nope. You don't get any of that you got to do. And in fact, it helps like a lot of people, even for myself, it helps me exercise like I, you know, I'm able to exercise longer, so. And it makes it more enjoyable for me.

Ben Greenfield [00:30:06]: Okay, so I interrupted you as you were going down the Alphabet letters.

Stephanie Venn-Watson [00:30:09]: Yeah, so we've got. Yeah, inhibits, you know, when we talk about activates things, it, it inhibits things like mTOR, HDAC6, JAK/STAT. And so it's like, and the core thing is if you look at all these different mechanisms and we just published last week that it inhibits these two things called FAAH and MAOB. And it does by doing that, this is really critical to cognitive health. So super exciting. To help sustain higher healthier dopamine levels and endocannabinoids, which we'll touch on in a little bit. So the point being, it's an essential fatty acid. Nature takes essential fatty acids and it has them do a lot of things, which is a big reason why we and dolphins and dogs have these receptors.

Stephanie Venn-Watson [00:30:58]: It's because they're waiting for us to eat the right things and trigger these receptors and keep us balanced from a metabolic and immune standpoint. So it all makes sense given the fact again that this is an essential nutrient that every mammal gets from birth.

Ben Greenfield [00:31:13]: You mentioned modulation of mTOR, and then earlier of course, you were talking about diabetes. I think two darlings of the anti aging industry as far as off label drugs are metformin and rapamycin. How do you think about the head to head comparison of something like C15 with something like those?

Stephanie Venn-Watson [00:31:30]: Right, so that's where Nick came in and he had the same question you did, Ben, which is, hey, if we test C15 head to head against rapamycin, metformin and then the third molecule called acarbose, which is also in the kind of anti-diabetic world.

Ben Greenfield [00:31:46]: Isn't that like a negative glycemic index sweetener?

Stephanie Venn-Watson [00:31:49]: Yeah, exactly. We don't use it here as much as in Asian countries is popular. And basically what it does, it prevents absorption of carbs.

Ben Greenfield [00:31:58]: Dr. Sandra Kaufmann, she's big into all these different ways to block glucose absorption. I think acarbose is on her list of supplements. Okay, so you're testing C15 about against or at least comparing it against metformin, rapamycin and acarbose. And what are you guys finding?

Stephanie Venn-Watson [00:32:14]: So what we did is we used this panel that is industry standard for the pharmaceutical world and it's called BioMAP. It's 12 human cell systems mimicking various disease states, heart disease, liver disease, lung disease. And what you do is then you treat these diseases in a dish with 10 concentration. No, let me take that back. Four concentrations of each molecule. It measures 148 different biomarkers and it gives you a profile of how well does this molecule behave across many different human cell systems. So it's a great way to assess safety, but also efficacy. So we did that with C15, pure C15 against these other longevity leaders.

Stephanie Venn-Watson [00:32:58]: And we were able to show that C15 had the most cell longevity enhancing cellular benefits than all of them, most closely mimicking rapamycin. And when you step back and you look at what we know rapamycin and C15 do, it's their anti-inflammatory, antioxidant, anti-fibrotic, so anti scarring, antimicrobial and anti-cancer. So it's this wonky set of tools that if you have these, you're going to live longer. And so the conclusion we came to in the paper that Dr. Schork and I in this paper that we published in 2023 was, hey, maybe we didn't need to go to Easter Island for this molecule, right. That is grown in bacteria that grow in a faraway place. Maybe what we've needed to support our longevity is C15. Again, what all mammals get and we've been taking out of our diets by reducing the amount of dairy fat we eat.

Ben Greenfield [00:34:00]: Yeah, this whole BioMAP measuring thing that you use, I hadn't come across it before, but it's kind of cool because yeah, it's not like a double blinded human clinical trial long-term in living people, but it's almost like kind of a cool algorithmic way of comparing things head to head. I hadn't heard of it before, but I think. Let me find this section of the book. You actually say that you start with a handful of different human cell types like lung cells, white blood cells, vascular cells and skin cells. Then you expose them to a variety of factors that replicate a multitude of diseases. And so you're getting a bunch of diseases in a dish that mimic things like heart disease, cancer, inflammation, arthritis, liver scarring, et cetera. And then it gives you a comparison of what's going on in that dish based on what you test against these diseases. Almost like a bunch of little miniature celebrity death matches in a petri dish.

Stephanie Venn-Watson [00:34:55]: Hey, I love that. Yeah, I think biomath's going to call you up and ask if they could use that as a descriptor.

Ben Greenfield [00:35:01]: It is really cool though, because again, I don't think you would say this either. This is not the same as a human trial, but it certainly gives you some pretty cool data to work with.

Stephanie Venn-Watson [00:35:10]: That's exactly right. And what I tell you, Ben, like as the years have gone on since we first, you know, started using BioMAP, I have become a huge believer in it. And it's because we've been able to see it move forward. Right. So it predicted, for example, that C15 would have anti-cancer benefits in this dish. And then there's a group that then moved C15 forward in cancer studies in vivo and they were able to figure out what was the mechanism of action. So it was a JAK/STAT and HDAC6 inhibitor, which are anti-cancers. It mimicked gemcitabine and paclitaxel, which are two anti-cancer drugs.

Stephanie Venn-Watson [00:35:49]: And most importantly, when they moved in vivo to a mouse model that it decreased the tumor size of mice with breast cancer. So it's remarkably good at being a predictor of what activities it will have. And because these are human cell lines, it's a predictor of what's going to be useful in humans. Again, this is used by the pharmaceutical industry and they are not going to waste. This helps them be much more efficient at honing in on which molecules are most likely to make it across the line.

Ben Greenfield [00:36:21]: Yeah, a few minutes ago you mentioned the endocannabinoid system. Why were you talking about that?

Stephanie Venn-Watson [00:36:26]: Right, so this is a fun component that as people, people started, you know, taking pure C15 and supplementation, we had about half of the people within two weeks reporting deeper sleep, calmer mood and less joint pain.

Ben Greenfield [00:36:44]: Wait, I want to back up, interrupt you real quick. Were they like taking this right before bed or is this just kind of like chronic long-term use effects?

Stephanie Venn-Watson [00:36:50]: Yeah, like it was more like. And it's within two weeks. And so, you know, it takes a few, maybe a few days to. But let's say pretty reliably at two weeks, half of the people, and we're like, you know, hey, we understand C15's mechanism of action. You know, from what we understand today, that doesn't really line up with what we know about C15. But then the science continued and we learned that C15, that our bodies use C15 not only for all the things I just talked about, but Our body uses C15 to make a second molecule, a metabolite called pentadecanoylcarnitine, which we'll just call PDC. And what we found was again, the first step is take the molecule throw it against a bunch of receptors to understand is it active, is it activating relevant receptors? And so that's where we found that PDC fully activated. CB1 and CB2 receptors, where CB stands for cannabinoid.

Stephanie Venn-Watson [00:37:48]: So these are the receptors throughout our brain and body that respond to cannabis. Right. And they're named that because of cannabis. But we don't have those receptors because our bodies were waiting for humans to find cannabis and start using it. Right. Like dogs have it and dolphins have these receptors.

Ben Greenfield [00:38:04]: So you're telling me weed is not an essential plant?

Stephanie Venn-Watson [00:38:07]: We know that was not the big discovery. So. But why are they there? Right. And so what we showed is there's a, previously, there is a one called an endocannabinoid. So it's a cannabinoid that our bodies make that are intended to activate these receptors. Prior to our discovery, there was only one known full acting endocannabinoid. This PDC was the second. So the second ever discovered, which then helped explain.

Stephanie Venn-Watson [00:38:34]: Aha. Deeper sleep, calmer mood, less joint pain, all of which I have experienced myself. And now it's like I get it, like I'm understanding why those benefits.

Ben Greenfield [00:38:45]: So the way that it's working on these receptors, you said it acts on CB1 and CB2 receptors or it upregulates this PDA which acts on those receptors.

Stephanie Venn-Watson [00:38:53]: Yeah, exactly. It's this metabolite that then activates these receptors.

Ben Greenfield [00:38:58]: Okay, so if you're binding to those receptors, would you, and this is just like a total thought experiment and you like smoked weed or had an edible, would you need more of it to actually work with those receptors because the receptor side is already occupied?

Stephanie Venn-Watson [00:39:14]: Yeah, that is an interesting question. If there's what we don't know is competition that if let's say. Yeah, that the, the phytocannabinoids. Right. The non ones that are body non endogenous cannabinoids. Yeah, yeah. If they're stickier right to the receptor, then there may be a competition component. The neat thing about endocannabinoids, which is fascinating, is that our bodies make it on demand.

Stephanie Venn-Watson [00:39:40]: So we store C15 and then when our bodies need less pain, calmer mood, better sleep, our bodies will actually then make the, make the endocannabinoid versus if you take an edible, it just goes up at that time and then goes down based upon how long when you had eaten it. So maybe they'll do a one, two punch that you can store it in your tissues, your tissues will use it when you need it. And then you have your edible, which will have its immediate effect at that time.

Ben Greenfield [00:40:09]: Yeah, interesting. You said you store it in your tissues. What do you mean?

Stephanie Venn-Watson [00:40:13]: So C15. So as we eat C15, it goes into our cell membranes. This includes cells in all of our tissues. So we want to have C15 stored in our tissues because of all the things we talked about. Anti, inflammatory, antioxidant that keeps our liver, our heart, our brains healthy. But it also means we've got a store of C15 waiting, so that when our body needs endocannabinoids, when it needs to deal with pain, when it needs to deal with sleep, it's able to make those endocannabinoids and increase the levels upon demand. Which again, is something I learned while writing the book about endocannabinoids. And just fascinating.

Ben Greenfield [00:40:54]: Kind of makes me wonder too, like if you're kind of a pothead or you're too reliant on CBD or THC, if you could kind of use some form of C15 to wean yourself off that or kind of taper off.

Stephanie Venn-Watson [00:41:06]: Yeah, that's the hypothesis. It helps. Yeah, exactly.

Ben Greenfield [00:41:10]: Interesting. So if it's stored, is there a way to actually get a blood test or some kind of tissue sample or something that the average person could do to see how much C15 they actually have in their bodies?

Stephanie Venn-Watson [00:41:22]: Yes. And so the good news is, because C15 has been used as a biomarker for how much dairy fat we eat, the test has been used for decades reliably. So fatty acid panels, if you, you just, you can ask your doctor to do a fatty acid panel. Just make sure that they check and that C15 is included. Another reason why C15 wasn't discovered until recently is that fatty acid panels before the 1990s for the most part, didn't include C15. So if we had done that dolphin study, Ben, three years earlier, we would have missed the entire discovery because there were. C15 wasn't on the panel. So, you know, a bit of luck came into play here.

Ben Greenfield [00:42:06]: Yeah, but if, if I asked my doctor for a fatty acid panel, I mean, I know doctors are smart, but maybe they're not trained in this specific type of panel. Usually, like even a smart doctor is going to give me like an Omega-3. They'll order like an OmegaQuant or something like that. Like, is there an actual test you could ask for, an at-home panel? Or do you literally just need to go to your doctor and say, hey, C15 is the one I want you to test for?

Stephanie Venn-Watson [00:42:32]: Yeah. So you can do the latter first. And if they don't have it or they're like, what are you. I don't even know what C15 is. And then you're going to give them the book. But what we know is, so what, we worked with Genova Diagnostics to develop an at-home blood spot test. So if people don't have an option, and that's what I used, then you can get this at-home blood spot test and then turn it in, you mail it in and they send you your results.

Ben Greenfield [00:42:58]: Oh, easy. So if I go, if I have like an accountant, direct labs or whatever, would it be on there?

Stephanie Venn-Watson [00:43:03]: Yeah, it should be on there.

Ben Greenfield [00:43:04]: Okay, easy. And it's just at home.

Stephanie Venn-Watson [00:43:06]: Yeah.

Ben Greenfield [00:43:07]: Oh, most people, I mean, most of my listeners are going to do that because they just like to take it into their own hands.

Stephanie Venn-Watson [00:43:13]: I know. It's good.

Ben Greenfield [00:43:15]: That would be that expensive.

Stephanie Venn-Watson [00:43:16]: It's not.

Ben Greenfield [00:43:17]: Yeah.

Stephanie Venn-Watson [00:43:17]: I mean, for people who are used to ordering, you know, tests and to be able to get results, results, you know that it's, it's in the same realm as, as other tests. And so I use that one and that's where I was able to show that my C15 levels in that test. Right. That uses this ref, you know, a different reference range than maybe other tests. But this one showed from the concentration that I have the Sardinian level, so 0.46% and over 5 micrograms per mil.

Ben Greenfield [00:43:46]: So, yeah, you're going to start talking like an Italian biohypoxic goat. Wow.

Stephanie Venn-Watson [00:43:50]: Yes, exactly. See, it's easy.

Ben Greenfield [00:43:53]: So dolphins you mentioned eat fish. They don't eat yogurt, but at least I don't think they do. I don't know what you're doing in the Navy if you guys haven't been at Jerry's there. But the thing about fish oil, because fish oil is often called a source of some of these essential fatty acids that you named earlier, I think. How do you compare C15 to fish oil supplementation? Do you still use fish oil or what's your take on the fish oil piece?

Stephanie Venn-Watson [00:44:21]: I love fish. There's so much, there's so many studies been showing that the more fish we eat, if we eat two to four servings a week, that the better our health. So dolphins are onto something. So we know that fish are good for us. They contain a lot of important nutrients, including the omegas. So with regard to fish oil, you know, fish oil goes back to the 1800s industrial revolution of that was our cod liver oil was our main source of vitamin D and it helped to get rid of, to cure rickets. I mean so fish oils played a really important role in supporting our health. When we talk about, again I think we talked about earlier, the yin and yang, that Omega-3 Omega-3s are important to keep our cell membranes flexible.

Stephanie Venn-Watson [00:45:10]: They have some anti inflammatory benefits. The pure, this EPA, the Omega-3 in that, in that supplement or even better the pharmaceutical, the better the outcomes in the longer term studies because you just have more control over what was in that fish. Every fish has a different life and that dictates the fatty acids that are in that fish's oil. So in comparison C15, again we talked about getting it from dairy fat but that becomes complicated. So again that's why the Navy funded us to isolate C15 and create a pure bioavailable form that you can control. And again this was for the dolphins to control and supplement the dolphins diets so they could get exactly the amount of C15 they needed. So it's a stable powder at room temperature versus an oil. So again, complementing each other.

Stephanie Venn-Watson [00:46:04]: Yeah, I'll leave it at that.

Ben Greenfield [00:46:05]: Okay, so they can complement each other. So, so DHA and EPA. If I look at a fish oil label, what is it? Dose of hexanoic acid and eicosapentaenoic acid. Am I even close?

Stephanie Venn-Watson [00:46:18]: Yeah, that was it.

Ben Greenfield [00:46:20]: So we nerded out before. I want to nerd out again just real quick, just so people kind of understand this. So C15 is 15 carbon atoms with a single bond. And then EPA and DHA, what do those look like? Like if I were to look at like a diagram or a picture of an EPA and DHA next to a circle.

Stephanie Venn-Watson [00:46:38]: Yeah, so they have, they're polyunsaturated fatty acids. So that means they have multiple. So polyunsaturated means double bonds. Polyunsaturated means multiple double bonds. So they're going to have, it's a longer, bigger, kind of more complicated molecule that has lots of hinges and lots of bending points, which is why they're oils at room temperature. It's why you know, Omega-3s are oils and why they're more susceptible to oxygen. So if you're, you know, like leave the oil out of the fish oil supplements, they can get rancid.

Ben Greenfield [00:47:13]: It sits in the Amazon and it sits out in the summer heat for 90 degrees on your doorstep for two days while you're on vacation. And you come back and put that in your fridge, it's still probably pretty damaged.

Stephanie Venn-Watson [00:47:22]: Yeah, exactly. And so that fishy smell you get is the oxidation of those fatty acids. So it's not the manufacturer's fault. Right. It's just. They're just molecules that are naturally more susceptible to attack by oxygen. The nice thing with, you know, with C15 is that whether in the bottle or in our bodies, its job is the opposite. It's meant to protect us against lipid peroxidation and shore up those membranes, but also be incredibly stable in the bottle.

Ben Greenfield [00:47:53]: Yeah. So it sounds to me like your take on fish oil is probably a little bit similar to mine. I love fish. On any day that I eat fish, I don't use fish oil. And so that's on, like, three days of the week. And then on the other days, I take about 1 to 2 grams of a DHA, EPA blend that I keep in the refrigerator. And so I kind of go back and forth. And I recently added C15 into the mix.

Ben Greenfield [00:48:16]: After reading your book, I decided to do, like, a, well, so far, I think I'm two months into kind of trialing using C15 via this supplement called Fatty15. So I've been taking. I think the label says two. I've been taking four of those a day. Is that okay?

Stephanie Venn-Watson [00:48:32]: You know, three? Maybe three.

Ben Greenfield [00:48:35]: Okay. All right. I'm an overachiever.

Stephanie Venn-Watson [00:48:37]: Well, you may be catching up. Maybe you're catching.

Ben Greenfield [00:48:40]: It's like I've been getting bigger. I'm almost 200 pounds now, and I get. I get a little bit of flack for this, but I don't purposefully keep my body fat low, but I'm 4% body fat and 200 pounds, so I have a lot of muscle, and I just feel like I need a little bit more than the average. I don't know if that's true, but.

Stephanie Venn-Watson [00:48:59]: Well, and also, you know, it depends. I think it depends on a person's diet. Like, if you don't eat a lot of dairy, then.

Ben Greenfield [00:49:05]: I'm pretty lactose intolerant. I forgot to mention that.

Stephanie Venn-Watson [00:49:11]: Yeah. So it might be like, again, maybe some ketchup. But we, you know, we have people tell people, start with one, work from there. And you have over 95% monthly retention rate. And it's not because, you know, people are just crossing their fingers and believing. It's that, you know, they're seeing and feeling benefits within months. And so those doses seem to be working for most people.

Ben Greenfield [00:49:34]: How many, like, milligrams is in one capsule?

Stephanie Venn-Watson [00:49:36]: 100 milligrams.

Ben Greenfield [00:49:38]: And in the studies that you've done, you know, because I'm sure you're running this in the supplement industry, people will like make a supplement, but it's nowhere near the dosage that were that was actually used in the study or extrapolated to humans. How does the Fatty15 match up?

Stephanie Venn-Watson [00:49:50]: Yeah, so it matches up. So there have been multiple clinical trials. One of them used 200 milligrams, the other one did use 300 milligrams. But you know what we'll cover is that these clinical trials were done in people who were likely C15 and then we saw C15 deficient. So again, kind of to your point, Ben, that if you're starting from a C15 deficient state, so people are purposely avoiding whole fat dairy then, or have a condition consistent with C15 nutritional deficiency, there's some catch up that's needed. And I think there was a desire by the people who are running the study to say like we really want to kind of push it to a higher amount so that because it's only for 12 weeks, it's not for six months or a year. So they were pushing it higher to say can we see benefits within in 12 weeks?

Ben Greenfield [00:50:42]: Okay, got it. Well, if people want to try the one I'm using, I'll put it in the shownotes at bengreenfieldlife.com/C15 so I want to kind of give you a little chance, maybe slightly lightning roundish here, but you've had some people try and take down your research and I came across it, I do a little bit of stalking, a little bit of my own research in anticipation of these interviews that I do. So there's a really popular podcast called The Proof and more or less like the summary of a YouTube video that they did was they said C15 is non essential for humans and lacks strong evidence for metabolic health benefits and shows inconsistent absorption and effects in studies. What say you?

Stephanie Venn-Watson [00:51:26]: Well, it's easy to say things on YouTube. I'll say that it's a lot harder to get things published in peer reviewed studies. So we'll cover a couple of those things. You know, the. And I will say, Ben, my hope is that the intent of some of these, you know, takedown videos are not. It's because there's earned skepticism in the supplement industry. Right. It's, there's a good reason for this.

Stephanie Venn-Watson [00:51:52]: Right. And it's really hard to keep up with the latest C15 studies. Literally every three to four weeks there's a new paper coming out around the world. So it's real hard unless you're spending all of your life like I do, looking at the latest studies, which is one reason for Writing the book to have one resource for all of these studies, it's hard to keep on top of things. My hope is it's not nefarious, it was just an unintentional misinformation that was provided. When we talk about there's no evidence at all that it's essential. We already talked about not only did we show that it's essential, but now multiple teams have done the gold standard studies to show even beyond what Omega-3 and Omega-6 had to do to get their criteria of essentiality. We have surpassed that thanks to multiple teams coming in and revalidating it.

Stephanie Venn-Watson [00:52:48]: So there is absolutely strong evidence for C15 as an essential fatty acid. So with regard to metabolic health, when we talk about if we walk our way up from mechanism of action, we know C15 activates AMPK and AKT. That was then showed and I should mention activating AMPK is the main mechanism of action of metformin, which is the top leading diabetes drug globally. When moved into cell lines, C15 at those concentrations of activating AMPK and AKT were shown to improve glucose uptake at the cells. Even interestingly, Fu et al showed that C15 actually mimicked insulin. It not only improved insulin sensitivity, then it actually did as well as insulin in these cell based studies. Then we moved to in vivo efficacy studies. So then you treat a mouse that has Type 2 diabetes showing that it decreases insulin, I'm sorry, decreases glucose, the whole suite of components of Type 2 diabetes.

Stephanie Venn-Watson [00:54:01]: Then you move into the human studies with regard to these large scale human epidemiological studies, the higher C15, the lower the risk of developing Type 2 diabetes. So we had a third party come in and actually review our claims for Fatty15 and review the science and to say are these substantiated? It's called KARS process. And they absolutely said with regard to our claim that including metabolic health, that there's clear substantiated evidence that C15 plays a core role in supporting our metabolism.

Ben Greenfield [00:54:36]: Right. And I know that a lot of people will say, well you showed that high levels of C15 in these models, whether animal or human models, is associated with all these benefits. But you haven't shown that taking your pill, your supplement or your Fatty15 causes those same benefits. I've heard that. What do you think about that?

Stephanie Venn-Watson [00:54:59]: Yeah. So when it comes to clinical trials, right, so then you need a clinical trial in which people have the condition and so with supplements. We haven't. That study, absolutely to your point, haven't been done yet. The studies to date on clinical trials have focused on fatty liver disease. And that's because the hypothesis is that fatty liver disease, which didn't non-alcoholic, or it's now called mazzold, it's going through a rebrand, didn't exist before 1980. And so one of the hypotheses is that decreasing C15 levels that happened since the 1970s and especially since the 1990s have gone down population wide, that then these deficiencies may actually be causing fatty liver disease. So the clinical trials are being triaged based upon urgency.

Stephanie Venn-Watson [00:55:49]: One in three people have fatty liver disease today. And so the two clinical trials that have been done with C15 have been on people with fatty liver disease, history of fatty liver disease. The first one, which was 200 milligrams per day, had people go on it. And this clinical trial then was a home run. And the reason for that is two out of three of the people in the study, they were 18 to 24 years old, had what we defined as a nutritional deficiency, right? So they had C15 levels lower than this, 5 micrograms per mil. So first of all, we're saying like, okay, two out of three people with this condition have what's defined by, through cell based studies from the dolphins, from the epidemiological studies, all rally around, we need 5 micrograms per mil, at least to not be deficient. So it showed that two out of three people met this criteria of deficiency. Then among the people who took C15 supplementation and got their levels up and above that, 5 micrograms per mil, they had lower liver enzymes of ALT and AST, which is improved liver function.

Stephanie Venn-Watson [00:57:00]: And again, these people had high liver enzymes at the start of the study. And it also increased their hemoglobin, which again, kind of going back to the whole aging rate and stability of cells, includes red blood cells. This is a marker of improved red blood cell health, which was not the intent of the study, but was really interesting. Which leaves you with why did half of the people who got C15 not have an increase in their C15 levels?

Ben Greenfield [00:57:29]: That's the other question I was going to ask you because Dr. Bill Harris of OmegaQuant, he came out with an article and said, well, half the people who took it didn't even see an increase. So there's questionable aspects of the absorption effectiveness of it.

Stephanie Venn-Watson [00:57:42]: Right. And fair enough. I mean, so what's important is that a couple of things. The first is that extensive clinical trials, pharmacokinetic studies have been done on this pure free fatty acid, C15 ingredient. This was done by Mascarenus et al and Stallings et al. And they did lots of people, they did adults, they did kids, they did people with and without cystic fibrosis. And Ben, what they showed across two papers, an extensive clinical trial trials were that this molecule is 100% bioavailable. So how much you ate reflects exactly how much was in your blood.

Stephanie Venn-Watson [00:58:18]: So that leaves us with the question of what happened in this clinical trial. When you read more into the paper, what they showed was that the people who had the increase had a 95% adherence to the protocol. So they actually took the amount of C15.

Ben Greenfield [00:58:36]: Basically not doing their homework. Yeah, yeah.

Stephanie Venn-Watson [00:58:39]: So if. And it's there and it doesn't explain all of it, but a good portion is that it def. It was significant. Of people who actually took the C15 had higher C15 levels. And importantly among that group that took that adhered to the protocol, they had the increase and they increased their levels by 2 micrograms per milliliter which exactly matches the 200 milligrams, which is what the prior study showed, that for every 100 milligrams you eat, you go up by 1 microgram per milliliter. So when you look at that group, it was spot on. So the big question is, well, if you don't take the supplement, you're not going to increase your C15. And they were 18 to 24 year olds and Jeff is like, it's kind of like the worst group for adherence.

Ben Greenfield [00:59:23]: Okay, so that was a 12-week study. So what I'm getting from what you're saying is that there's probably still a need for longer term human clinical trials of taking C15. But the way I think about this is if somebody's listening in, I'm a total kind of like N equals one guy guinea pig stuff on myself all the time. Somebody could theoretically start taking this. You said 100 to a maximum of 300 milligrams a day and then get pre and post bloods and maybe even this Genova Diagnostic C15 test to see what their absorption or what impact it has on the levels. Lots of people, especially my listeners who are smart cookies, know how to do that. They know how to like get a pre blood test, take a supplement for X amount of time and then do a post test to see what their levels are and see how it changed their biomarkers. But the question I have for you is if somebody was going to do that, how long should they wait between the pre and post test for the C15 to build up or to have its effects based on what you know.

Stephanie Venn-Watson [01:00:28]: Yeah. So we do just like you said, we strongly recommend that every person before they start Fatty15, the supplement to go get your blood work. C15 levels, great to assess, to look at. But what's more important is are we seeing clinically relevant improvements? Right. So start and get your baseline blood work which includes and sometimes you might need to ask for things like ferritin levels and your full red blood cell indices because there are some special things like that RDW measurement that is kind of like bonus measurements of efficacy. But get your standard CBC and chem, go back. We say we recommend between three to six months later. And that's where, if you go to our reviews and that's where Ben, we're seeing again why people stay on Fatty15 and retention is so high.

Stephanie Venn-Watson [01:01:20]: People are doing exactly this and they're seeing the benefits. I mean science works like this is, you know, it's what Nick Schork, Dr. Schork, head of NIH's longevity consortium, it's why he has explained that there is no of all, given the breadth of data across all these different aspects. He said there is no molecule that has more support as its role as supporting its role as a geroprotector, our long-term health and wellness than C15. And this is Nick Schwarzenegger who has seen everything.

Ben Greenfield [01:01:53]: Yeah, well, okay, so three to six months, that's helpful. This whole thing has been helpful, by the way. And we barely even kind of broke the surface of everything that's in this book. I'm holding it up for the video. Longevity, nutrient. If you go to BenGreenfieldLife.com/C15. Yeah, the letter C15. You can check out the show notes, get the book, check out the supplement, et cetera.

Ben Greenfield [01:02:18]: Last question, Stephanie, from my kids and wife. Can you talk to dolphins? Do you speak dolphin?

Stephanie Venn-Watson [01:02:27]: I can speak dolphin by being a nerd that analyzes their data. And I can know, I can tell you how that one's feeling. What they could have. Gosh, I wish they could have told us from the beginning. Hey, Steph, I slept better last night or my arthritis is feeling better. We had to figure that out down the road. But there is new technology coming out that I think we're getting closer to actually being able to interpret dolphin language.

Ben Greenfield [01:02:50]: Which is I do some turkey gobbles and some alcohols and I don't know if they made a dolphin collar. I'd try it out, something like that.

Stephanie Venn-Watson [01:03:01]: Hey, you did that a lot better than me. All right.

Ben Greenfield [01:03:04]: You know, I've got a little dolphin in me, I suppose. I don't know to get a genetic analysis for that. Stephanie this was great. Again, the show notes for everybody listening in our BenGreenfieldLife.com. Dr. Stephanie Venn-Watson, the Dolphin Whisperer. Thank you so much for coming on the show.

Stephanie Venn-Watson [01:03:23]: Ben. It's been an absolute pleasure. Thank you.

Ben Greenfield [01:03:25]: All right, folks, have an incredible week and try Fatty15 if you want to leave the comments, questions, feedback in the show notes at bengreenfieldlife.com/C15 Read the book too. It's great. And until next time, I'm Ben Greenfield along with Dr. Stephanie Venn-Watson signing out. Have an incredible week.

Ben Greenfield [01:03:47]: To discover even more tips, tricks, hacks and content to become the most complete, boundless version of you. Visit BenGreenfieldLife.com. In compliance with the FTC guidelines, please assume the following about links and posts on this site. Most of the links going to products are often affiliate links, of which I receive a small commission from sales of certain items. But the price is the same for you, and sometimes I even get to share a unique and somewhat significant discount with you. In some cases, I might also be an investor in a company I mention. I'm the founder, for example, of Kion LLC, the makers of Kion branded supplements and products, which I talk about quite a bit. Regardless of the relationship, if I post or talk about an affiliate link to a product, it is indeed something I personally use support and with full authenticity and transparency recommend. In good conscience, I personally vet each and every product that I talk about.

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