Nutrition at the Cellular Level: The Dolphin Discovery Behind C15

Welcome, Synergy listeners. Today we are so honored to welcome Dr. Stephanie Van Watson, a veterinarian, epidemiologist, and serial entrepreneur whose work bridges animal and human longevity science, has led research with the CDC, World Health Organization, Department of Defense, and DARPA, authored over 60 peer-reviewed publications, and is the lead inventor on more than 40 patents. She's also the scientist behind the discovery of C15 and the founder of Fatty15, reshaping how we think about nutrition at the cellular level. This conversation was eye-opening. It was inspiring, and it was deeply grounding. And we have no doubt that you're going to feel the same as you listen in. So tune in. We can't wait to get feedback. And at the end, there'll be a special surprise.

Kelly, Lori, wonderful to be here.

We're excited that you took time out of your schedule for us and for our listeners. So thank you. Thank you for your work. And I can't wait for you to be to share that. So listen, your background is so incredible. So let's start there.

What is your story?

Give us a little context behind this discussion today.

Sure. Unexpected discovery, right? Unexpected to be here if I went back 10 years, 10 years ago. So I am a veterinary epidemiologist. I was working for World Health Organization, CDC, helping to set up disease surveillance systems all over the world. And then about '24, just to date myself, right? 24 years ago, was recruited by the Navy to help to come in and help continually improve the health and welfare of the Navy's dolphins. And, you know, which is funny because I, you know, I don't know how to swim, I'm terrified of water. And so the last place I thought I'd be, be working with dolphins. So, but I thought it would be, you know, great to do for a couple of years. And the Navy, you know, has cared for this a wonderful sustained population of about 100 bottlenose dolphins for over 60 years. They live in San Diego Bay, which is incredible, go out in the open ocean every day, and every day they choose to come back, which is, it was important for me, you know, from a, as a veterinarian. And the Navy takes really good care of these dolphins. The, if you look at dolphins in the wild, they typically live to about 20 years, and dolphins at the Navy are routinely living 40 to 50 years, and 2 dolphins this past year turned 60 years old. Wow! Pretty impressive, pretty impressive. And so we did, um, we, uh, the, the team, we, over a period of about 10 years, we were able to really dive into the, um, massive treasure trove of data behind these animals, all because the Navy takes great care of them. So if you could imagine with your patient populations, if you had CBC and chems, you know, 40 different variables measured on them routinely every quarter of their entire lives.

Woo!

What you'd be able to do with that information. This is now what functional wellness clinics are doing increasingly, so we're catching up to the dolphin medicine regimen. And what we found, thanks to those data, was that about 1 in 3 older dolphins were developing a cluster of conditions, aging-associated conditions like high cholesterol, chronic inflammation, fatty liver disease, and even the full suite of changes consistent with Alzheimer's. So that allowed us to go in and say, use advanced metabolomics to look at thousands of small molecules present in their archived serum, but also their all-fish diet to see which small molecules predicted the healthiest aging dolphins. And that's where this wonderful gift discovery, gifted discovery came in which we found that C15, this odd-chain saturated fat, was the top predictor of the healthiest aging dolphins. And off the adventure started. That was 10 years ago.

Well, first of all, I had no idea that dolphins actually had, and correct me if I'm wrong, but they actually have signs of what you just said, metabolic syndrome, that we as humans have. Like, that blew me away. Maybe other people listening to this already knew that, but I was actually— it really took me back.

It didn't. And Lori, when we started seeing this, and it was exactly that— so smart, you know, it's— this is metabolic syndrome. Like, it's how you define— if it's— they had insulin resistance, high glucose, all the pieces and parts. And that allowed us to reach out to experts in the field in human medicine to say like, hey, we're finding this in dolphins. So the first step we did was reach out to the experts on the human side to say, hey, we're seeing this in the dolphins, what are your thoughts on how we can help the dolphins? And that resulted in the experts saying, what are you talking about? Like, the dolphins are not the same— same surprise. And then we were able to work together to help the dolphins and then wonderfully have that turn right back around and help us too.

Incredible. Just incredible. So from you discovering this, and it was probably a conglomerate of, of data that was placed together, like what happened from there? Because it's, it's a very unique situation. It's what we want more of. We want more of organizations and teams of researchers and people seeing things to work together. But that is not common to happen, unfortunately. So how did you get that buy-in? And what, what did you do differently that, that made them want to help?

It's a great question. Um, selfishly, we have the dolphin card. So, so, you know, when you're helping dolphins, uh, and, uh, it's a lot easier to really be able to get experts, um, in the field. And it's experts in nutrition, experts in— you ended up bringing experts in longevity, experts in, um, heart health, metabolic health, and endocrinology, you know, liver disease. And we were, um, and within— we're It's wonderful we're here in San Diego, so we have this hub even locally of experts in biotechnology and medicine where we were able to do exactly that, come together. And we had meetings where it was solely focused on how can we bring our expertise together to help the dolphins, right? And like, how fantastic is that? So then it really enabled us, like you said, when you cross disciplines and you come together, you have a multidisciplinary approach, you suddenly get perspectives and ideas together that you never would have come up with, you know, with, if you had, if we had just stayed like in the dolphin veterinary lane. So it was, it's a perfect example of that.

Yeah. And what advancements in medicine would happen to be if we did more of that. That is right. So I just wanna reiterate that because unfortunately due to, I'm sure a multitude of different reasons, that we could probably spend a whole podcast talking about. That doesn't happen. But this did. And it clearly shows how much benefit there was from those putting pride down, whatever it was, right? Putting pride down, putting priority to this and coming together and being willing to share what they knew. So that's really cool. So what exactly is C15?

Right. So it is an odd chain saturated fatty acid. So a big surprise. That was Another surprise was that we were seeing what was beneficial was a dietary saturated fat that was doing the opposite of everything we've been told about saturated fats, right? So I had never heard of C15 when C15 started popping up in these studies. And then we gave dolphins with a higher amount of C15 in their fish, a higher C15 diet, and they got better. Then we leaned in and said, wait, what is this fatty acid? So it's an odd-chain saturated fat. It has 16 carbons, which is— or sorry, 15 carbons, which is why it's called C15. It's an odd chain because it has an odd number of carbons. So we can get the geeky chemistry part out of the way. And it ends up that when we look at saturated fats, that even today, all dietary saturated fats are still being clumped into one singular category. The new dietary guidelines that came out, very different than they have been in the past, and they're definitely giving some credence to healthy fats. Surprisingly, there's, they still are not separating out these good versus bad despite the fact that it is now unquestionable thanks to, you know, over 100 peer-reviewed studies showing that there was a clear difference between odd and even-chain saturated fats they have completely opposite effects where these odd-chain fats, especially C15, has anti-inflammatory, cell-stabilizing, mitochondrial repairing results in higher levels of C15 in dolphins and in humans now associated with a lower risk of developing type 2 diabetes, cardiovascular disease, and others. Higher levels of even-chain saturated fats like C16 It's the opposite. Higher risk of developing type 2 diabetes, cardiovascular disease, impairs mitochondrial function, is pro-inflammatory. So it is shocking how nature can take one carbon and have completely different effects. But it's, you know, thanks to science that's allowing us to learn and adapt. Yeah.

So how did we bridge the gap from dolphins, those joyous little creatures that everybody wants to help? Over to humans, right? How do we start looking at the, the human effects of lack of C15, and, and how did that evolve, right?

So it ended up— it's a great question, Kelly. So it ended up there was a parallel, uh, accidental experiment happening in both dolphins and humans at the same time. So the dolphins for a long time had been fed, uh, a fish called hulakon fish, and they were really heavy in fats. They had so much fat in them that you could dry a yulekon and put a wick in it and it could be a candle. So they would call them candlefish. That fishery died out, resulting in some of the dolphins getting increasing amounts of fish with no C15 in it. So over— that's why over a decade we started seeing these, um, this cluster metabolic syndrome show up as some dolphins were getting less and less C15. The same experiment has played out in us in which our primary source of C15 is dairy fat. And as we've taken whole dairy fat out of our diets, and then, you know, starting with in adults and children, and then really moving to the pediatric, younger and younger space, especially in the 1990s, we've decreased our intake of C15. Our C15 levels have been declining. And so we're seeing that not just higher levels are associated with a, a lower risk. We're seeing now the question is, as we've been in taking in less C15, have we increased the risk of type 2 diabetes, fatty liver disease, and heart disease, especially among younger and younger people? So we published last year detailed pathophysiology of a nutritional deficiency syndrome called Cellular Fragility Syndrome that was just, for better or worse, it was, has been repeated and re-verified by a second team this last year. So it really seems like we may have induced a new deficiency syndrome through these changes in dairy fat.

Okay, so Lori and I use InBody as a way of measuring body composition in our practices, and one of the measurements on there is a phase angle. Are you familiar with the phase angle? Okay.

Yes, it's a great measurement.

Curious to know if— how you guys measured cellular fragility. And can you— what are the— what would be the symptoms someone would have? How would they show up on their lab testing and maybe their, their phase angle? Like, what would you see?

So C15 does a lot of things. One of its core roles is as a stable anti-inflammatory fatty acid that has no double bonds in it. It is particularly resistant to attack by oxygen. So resistant to lipid peroxidation. This is important because C15 integrates into our cell membranes, right? And our cell membranes are made out of fatty acids. The less, the fewer the double bonds in a fatty acid in the cell membrane, the stronger that cell membrane is resistant against lipid peroxidation. There's a theory called the cell membrane pacemaker theory of aging that was introduced by AJ Holbert in 2005. And what he showed was that the more stable the fatty acids in the cell membrane, the lower the systemic lipid peroxidation, and the longer it dictated how long a species lifespan was. Why a human lives longer than a mouse, right? So, so it's like it's a true evolutionary enabler of longevity. So this all gets back to the phase angle, right? So if the stronger your cell membranes, then that helps feed into these, the measurements if you can use, because you have the fancy schmancy good stuff, right, with you. For dolphins, because we couldn't quite give them that test, for the dolphins, one of the easiest cells to detect it in are red blood cells. So when red blood cells become fragile, um, and for the dolphins it was, you know, C15 levels, dietary levels were going down, they had less in their cell membranes, those cell membranes became more fragile, and the ones we could most readily see were more fragile red blood cells. So what we saw as veterinarians on the blood panel was we saw a decreasing hemoglobin, we saw increasing red blood cell distribution width. So RDW, and right. And so RDW ends up being a really important biomarker that has emerged throughout the literature. It's one of the strongest biomarkers of our biological aging rate. So it feeds into what's called the aging cell phenome. And so now we're understanding that of why that RDW is such an important measurement. It's a measurement of our cellular stability. Not just of red blood cells, but it gets to be a little flag to let us know how the rest of our body is doing with how fragile or strong our cells are.

So for our listeners, you're going to see that show up on your CBC, your complete blood count, that your doctor or healthcare provider may do once a year when you go in for your annual visit. They're measuring that typically. So that's something that you can track and trend for yourself over time to see what way is that going. Right.

But often is one that is just glanced over, much like MCHC or MCV, like, oh, it's okay, right? It's okay. That's not a big deal. Is there a particular reference range and optimal range that you specifically speak to, like, in some of your studies? It's a good—

we're always looking at trends, Lori. So I actually can't give you That's fair. Yeah, embarrassing. I can't, but I can tell you though, as far as you will see that it will pop up as abnormal on the, so just using your typical ranges that you have in the test. So sometimes the first thing you're gonna see even before declining hemoglobin is an increasing red blood cell distribution width. RDW, for the people listening, it's a measurement of how variable the variability in the size of the red blood cells. So they should be stable. They should be a relatively stable size, therefore a low RDW. When our cells start getting fragile and falling apart, then we have to make new ones. So you ended up with a bunch of different sized red blood cells. It means that our cells are not stable and that results in a higher RDW. I was giving a talk just a few months ago and someone in the audience asked, okay, so what would I see if I had cellular fragility syndrome? What would I see if I went on a supplement? What would I expect to see? And I said, well, you would probably see lower RDW, maybe a low hemoglobin. And as you go on it, you would see those come back, or you would see that— sorry, high RDW— you would see your RDW drop and your hemoglobin go up. And then she came up to me after she showed me her blood work. She's like, that's exactly what happened with me. I've been on Fatty 15 for 6 months and that's exactly the right thing. So it's your That is the signal of cellular fragility. But then there's also all the obviously the downstream effects with that we're seeing with low C15 and then really clinically meaningful benefits on the back end from beyond just the cellular fragility component.

So I love that we can see that happen on just a CBC, right? It's not a fancy test. I know in years past I was doing some red blood cell analysis, fatty acid analysis through Kennedy Krueger. And C15 was actually on. I went back to see, well, C15 on there then, and that was probably 4 or 5 years ago. It was, it was one of the biomarkers that they reported out, and they still offer that test. It's a pretty fascinating, fascinating test looking at that whole cell membrane, whether you're looking at odd-chain fatty acids or aberrant fatty acids. It was really cool to see that in our patients that are more complex chronic inflammatory response patients who are really working to repair cell membranes, it was very valuable to have. And I noticed that Genova also has a test now that looks like just C15, right?

Right, right.

So, right.

So that, that others, that others offer the C15 test. Genova Diagnostics has it in their NutrEval panel, but not all of them. Quest doesn't have C15 yet. So you have to look and I know we'll get them. So, but you have to look and make sure that C15 is including included. It's really funny you mentioned Kennedy Krieger. That's who we used for all of the dolphin studies.

Okay.

So we used them to measure the fatty acids in because they were at the time, I don't even, it was just luck that we ended up using them because at the time C15 was not included in a lot of fatty acid panels. And had we not used them or a panel that included C15, this discovery would've never happened.

Right.

So it's— you just sometimes things just turn out and you'll have to forgive my skepticism.

But any time I read the title, you know, the longevity nutrient, right? We're sold so much. That's going to fix one thing. That's going to fix everything. I had to really start digging in and say, okay, is there any validity to this? Like, how can one thing be so powerful? And it goes back to that cell membrane. If we have an unhealthy cell membrane, we can't repair. We simply can't get the nutrients in and can't get the toxins out. And so it is pretty incredible what you guys have done in the way of the research and then bridging it to humans. Right. And then having a product that can go to consumer.

Thanks, Kelly. Yeah, it was really— we brought in, you know, as we were going through this, as more and more discoveries were being made on C15. So yeah, now there's over 100 peer-reviewed papers most of them not by us, right? We, you know, have— we're still doing the science, but certainly not all those papers. And there's an average about 1 paper coming out on C15 per week over the last couple of years, including, you know, today. So as these studies started coming out, we brought in Dr. Nick Schork from the— he's head of the NIH's Longevity Consortium, and he's been in that role for over 20 years. And Nick was really compelled by the dolphin population because of the longitudinal data that we had on them. And he said, "I bet you're gonna be able to show in the dolphins what we've never, what we've assumed in people, what we've never been able to show," which is that people, that individuals within the same population age at different rates. And this sounds really simple, but our lives are so complicated. You know, it's hard to say that, is it because we smoke or drink or eat too much of a bad thing or eat a lot of good things. So the dolphins were this very homogene— relatively homogeneous population where then we were able to go use this, you know, routine blood data, um, for hundreds of dolphins and able to show that, you know, dolphins aged at— indeed had different dolphins age at different rates. These red blood cell indices were some of the key indicators. And So once that started happening, Kelly, then Nick really started leaning in and said, you know, on C15. And now we know that C15 targets key longevity pathways. It activates AMPK and inhibits mTOR. It targets multiple hallmarks of aging. It stabilizes the cell membrane. And then we see the benefits of its role as a geroprotector, right? Which Nick got all excited. He's like, this is going to be a geroprotector. And I'm like, I appreciate your excitement. What's a deroprotectin? I don't know what that is, Nick. So, you know, he said it's a molecule that can effectively slow the rate at which we age to stem the onset of the chronic diseases that kill us. I'm like, well, that sounds pretty important. And he was so excited because there are a lot of molecules out there, Kelly, like you're sharing, that said, you know, this is for longevity and there's a lot of hype around it. But he said, just, you know, just because you tap into a mechanism does not make it a longevity molecule or a nutrient. He said it has to play out and be able to show benefits within certain— meet these criteria of a geroprotector. So Nick spoke among his peers last year in Copenhagen at an anti-aging conference, and he said, um, bar none, that of all the molecules that he has seen, nutrient or drug, he has not seen a single molecule have more supportive data than C15 in playing a core role as a foundation to our longevity. So, to have Nick say that, that helped feed the boldness of the book of saying this isn't getting us to live to 200, this is getting us to maximize our healthspan as long as possible so that as individuals, we can live as long as possible.

So powerful. How does it feel to be a part of that?

Oh my gosh. Every day is a gift, Lori.

I can only imagine. Like, I'm sitting here getting kind of choked up, feeling like it's just, it's amazing. It's amazing to think that. And, you know, before we even, you know, started recording, we were kind of talking about how important it is for both Kelly and I. Integrity is a big deal for us. We know that people listen to us and, you know, there is a lot of hype out there. Around a lot of things, a lot of things. And, you know, we really have to be in it and discerning, and it's certainly not perfect, right?

We—

but, but we have to be insistent on having conversations just like this and scrutinizing the data that's out there. So I love that there's this continuous data, and I love hearing that it is not you guys, it is other people doing it, which is— that's amazing too.

So I want to go back to diet because obviously a dolphin's diet is very different than a human's diet, right? But we landed in the same place, right? We landed with the C15 deficiency or cell membrane fragility that is leading to chronic disease states. And we are finding that dairy is oftentimes very inflammatory for our patients, especially with autoimmune conditions. Like we're testing it out. It's not everyone that's reactive to dairy, but a good bit of people are. And so they pull dairy out of the diet or they're limiting the dairy that they're consuming. And so it can be a challenge to improve cell membrane health is what I'm hearing without this particular molecule. Are there any other ways to get C15 in the diet for humans?

Yeah, it's a great question. So the dolphins taught us that, you know, that fish we did look into the fish to say like, where is the C15? We learned that specific types of fish have— some have C15, others have zero. So it, it depends. So it's not— for them, it's not about just eating fish, it's about eating the right types of fish. And in the fish, it's primarily in the skin and the heads of the fish, which is interesting because in Asian cultures— because the big question is like, well, a lot of Asian cultures don't drink a lot of eat a lot of dairy products, where are they getting their C15 from? And those cultures actually where skin and the heads of the fish traditionally haven't been a routine part of their diet. So there are some without having to eat the skin or the heads of fish. Their fatty fish will have some source of C15. Dairy fat, unfortunately, is such a reliable source for us, for most people, for C15. That for a long time C15 has been used as a biomarker of how much dairy fat one eats. Everyone— no one knew that it was a bioactive beneficial nutrient, but they knew that it was a reliable biomarker of dairy fat. So that means that even though there have been some studies looking at fish, there's a great study that was done looking at how— looking to explain how Fiber helps in mouse models of fatty liver disease. And they did a great series of studies, really fantastic series, where they showed that when a mouse eats the fiber, it uses the inulin in the fiber to feed microbes in the gut to make C15. So there— and then that C15 that's made was what was responsible for the resolved liver condition in the mice. So it means that— and there's nobody who has no C15, right? So it means that we have some level of production, just not enough to get over that threshold of 0.2%. So, but when we say like what recommendations, eating fiber, it doesn't hurt, right? It can help like to help feed those microbes. So that we can have some level of endogenous production. We can, from among dairy fat, if it's coming from animals that were grass-fed, there's higher C15 content in milk, and that comes from grass-fed. The most reliable dairy product with higher C15 that translates to health benefits is from cheese. So there's a study showing that pregnant women who specifically ate cheese had higher C15 in their red blood cells and in their breast milk that then translated to better growth and development in the infant. Association, right? Not causation, but being able to show that the animal studies have shown causation in that. So some types of fish, have some fiber. Those are probably— interestingly, meat, red meat has a sizable amount of C15, but that is not translate— that does not translate to higher C15 in our circulation. And the hypothesis is that there's just too many other fats and it's competing, and C15 doesn't get absorbed, uh, as well as it does from dairy fat.

Interesting. So now we can supplement. With C15. So how do— what is the process to which the C15 goes from animal, right, to capsule, to us? What is that process, right? So, so we understand.

Yeah, so the Navy came in, right, and then— and they had— because they were having a hard time finding enough fish that had C15 in it, they had a different problem than we have, which is like just as you had mentioned, Kelly, with regard to all these pro-inflammatory fats and dairy fat. So we should get milk when we're young. Every mammal does. So we should probably not question that part of evolution. But no other mammal continues to eat dairy when they're older. So I still— I love my cheeses, so I still eat my cheeses. But the question is, how do we solve for getting the good odd-chain foundational C15 nutrient without all of the pro-inflammatory ones. So the Office of Naval Research actually funded us to develop this pure C15 ingredient and supplement for Fatty15 for humans. And the dolphins also get Fatty15 supplementation every day, which is, which is so, so wonderful. So we, because we're able to, you know, have this good funding, we then use a plant-based C14 and we add a carbon onto it. So that way it can be vegan. So we don't need to have it animal sourced and have it be pure. So it's developed in a, in a pharma-grade way that allows it to be pure. And it's the same pure C15 free fatty acid molecule that's readily bioavailable. And importantly, it's the exact same molecule that's used in all of these studies that I've talked about. So, you know, what, what you're getting is exactly what's been used throughout these studies, which is why we're seeing such great response from patients and from customers.

And much of the research that I had originally read was based on, I believe, correct me if I'm wrong, 300 milligrams.

Is that correct? It's a mix. So there's one clinical trial that was with 200 milligrams. Those were in young adults. With obesity and elevated liver enzymes. They were chosen and they were— that population was— they were specifically— they were included if they were purposely avoiding dairy fat. And so 2 out of 3 of those participants had what we defined as low C15 levels, so below this 5 micrograms per mL or 0.2%. For those who took the C15 supplement, 'cause they were 18 to 24-year-olds, those who adhered to the protocol and then got up and over that threshold of 5 micrograms per mL at 200 milligrams per day saw a dramatic decrease in ALT, AST, and then interestingly, an increase in hemoglobin. We weren't expecting that in such a young population, but we even saw that red blood cell improvement even among, young adults. And the study, Lori Esarey MS, that, yeah, you're talking about is a study done in Singapore, women with a history of MASLD, of fatty liver disease, and they give them 300 milligrams per day of C15, and they saw lower LDL cholesterol, increased growth of Bifidobacterium adolescentis. That was above and beyond. It was a, it was a really interesting study, right, because they The groups were the first group, they gave a low-calorie diet, hypocaloric diet. The second, they gave hypocaloric that was Mediterranean-aligned. And the third was hypocaloric Mediterranean-aligned plus C15 supplementation. We're like, well, is C15 actually going to do better than eating a lower, you know, diet and Mediterranean? That's already two huge wins to help with fatty liver disease. And it did. It was able to even you know, get out across all of those wonderful benefits of the first two groups.

So the recommended dosage for the adult population, we'll speak over the age of 18. And I love what you said about the young adults, getting them disciplined and regimented to take something every day. So kudos to you for that. But would be what? Like, what, what would you recommend? What is the science shown for recommended dose for loading? Is a loading necessary? Because that's a question that I have too. And then what is the typical dose and for how long? What's the duration?

Right. So the great thing about— so I'll start with the straightforward answer, which is that we need between 100 to 300 milligrams of C15 per day, of added C15 per day. And that was whether we used to get it from whole fat milk when we used to drink 2 cups of whole fat milk in the 1950s to today when now we're getting it through other means and supplementation. The nice thing about being able to test your C15 levels is it can help guide what it is that you need. So your goals there, we kind of separate the goals of C15 supplementation into two categories. The first is let's not be deficient, right? So let's not have disease because we don't have enough C15 in our cells. So no nutritional deficiency. So to be able to get up and over that is, depends upon, of course, where you start. So we've seen vegans have C15 levels of like 0.04, 0.06. So they are a long ways from that 0.2%. And so Lori, like you're talking about getting a loading dose, and those may be like a 300-milligram dose to get them up and front-loaded. If they're your typical person that's sitting at 0.2%, um, that's the average person, is right on the edge of cellular fragility syndrome reminding people that just because 0.2% is in the middle does not mean that that is healthy as a population. The whole curve has shifted. So you need to get them away, got kind of further off the curve, off the ledge. So 100 to 200 can help to not be deficient. Now if you want to optimize, we can talk about like the Sardinian zone, right? So, and the Sardinians have In the high longevity zone, they have C15 levels that are 2 to 3 times higher than the average population. They're 0.4 to 0.6%. And so they do that because they've got tons of locally— local sheep and goats. They feed on mountainous grass. That combination results. And then they eat it as cheese. Their milk is cheese, as pecorino, as many of us know it, one of the highest C15 levels. And they eat— they've replaced their meat with cheese. And it's this high C15 cheese. So that has allowed them to get these high levels. It's really hard for us to get to those optimal levels. Studies have shown not just the, you know, people living longer in Sardinia, but consistently showing that the higher— for every 0.1% increase in C15, the risk of developing type 2 diabetes is decreased by a whopping 38%. And it's a large prospective dose-dependent meta-analysis that just came out a couple of months ago. When you— the higher you go in C15, the lower the risk of developing type 2 diabetes, as well as a separate paper showing the same thing for cardiovascular disease. So we call that the optimal zone, or long— we call this longevity zone of this 0.4 to 0.6%, uh, based on those studies. So that then is probably going to be more of your 150 to 300, uh, you know, milligram, 200 to 300 milligram, um, dosing.

Is there a reason to consider not using C15?

It's a good question. We haven't found one yet. I, and I think it's because, you know, a couple of things. One is, you know, it's in breast milk, so it really is, it really is a foundational nutrient that we all need. Um, the doses that we're talking about are not, it's not like this is We're offering a supplement that's 100 times more than you could ever possibly get ever that your body was ever meant to see. We're talking about let's like restore and optimize within levels of where we should be. So I think for those reasons, Lori Esarey MS, that's why we haven't seen— it's been extensively tested for safety. That was our number one requirement before we even thought of bringing it to market. And so it's grass and, and now has been, you know, hundreds of thousands of, of customers. And, and once they start on Fatty 15, boy, they stay. So we have a 95% monthly retention rate and people are feeling better.

Yeah, yeah. Um, I— we often talk about, you know, supplements filling in those nutritional gaps, and, you know, a lot of times there are so many gaps in, in one's nutrition that they land with very long list of important things to supplement with. And we're always, you know, asked the question of, is this something that is necessary, foundational? How long will I need to be on it? So there's some critical conversations happening at every visit. And I have recently been talking more about, of course, cell membrane and not just omega-3s, but the use of fatty 15. And so I love what you, you know, I love what you just said. I think that it makes sense to prioritize something that we are not really getting in our diet. And now that we have the ability to test for it—test, don't guess—I think that's going to be very helpful to the conversation, right? So it's not just, I recommend this. No, look, here's where your levels are. Exactly.

Yeah. We should be moving beyond the days of just cross our fingers and hope and pray that it works. That's a big reason why, again, Dr. Shorrock was so excited about C15. He's like, you can measure. It's not just a biomarker. It is the intervention and the effect that it has with regard to red blood cells, with regard to improving glucose control. Of helping with liver conditions, you know, and slowing these measurements of biological aging. These are all tests that are readily available. So it doesn't— it doesn't— it's not hiding behind some fancy mechanism that's like, don't worry, you don't need to understand it, just take it. It's like, no, it really needs to work and it needs to have our healthcare practitioners, you know, use it with confidence, look at it skeptically, Kelly, like you're saying, and then be able to, you know, see the positive impact it has on patients. Yeah.

And so with that being said, is there a particular time of day? Is there a particular combination? Is it better taken with fats? Not? Are there some helpful tips that you can give our listeners on how to take it to get the best outcome?

Right. So most people take, um, take them in the morning, uh, and I'm not sure if that's because it's— if that's better or not, that's just become part of their habit. Uh, impressively, 99% of our customers, a survey of 6,000 customers, 99% said it's part of their daily routine. So it's easy to take 'cause it's a small, teeny tiny small pill, no taste, no smell. And I personally, I take it in the morning because, you know, you were taking C15, VADi15 for the long-term cardiometabolic liver and immune benefits. But it does have an added benefit of it. There is two mechanisms that we found that it inhibits FAAH and inhibits MAO-B. And by doing so, it actually helps boost endocannabinoids and dopamine. And so when I take them earlier in the morning, then I get to enjoy, you know, for the next 4 to 6 hours through the day. It helps me with as far as being calm and having, you know, a good mindset. And it's still— it helps me. I sleep better. I used to roam the halls at 2 in the morning, and so it's been helping me with sleep. That's one of the most common kind of a delight and surprise benefit. Even when I take it in the morning, it's still— I think it's just helping with the circadian rhythm and getting, you know, homeostasis with regard to how our bodies are supposed to be working.

So I want to go back to something you said earlier about the RDA for fatty 15 or C15. And it made me think about vitamin D. You know, we had a standard for rickets, right? And I'm wondering if cellular fragility is going to be part of that same conversation. You know, you may— you need this much to prevent rickets, but you need this much for health optimization. So how far away do you think we are from having conversations like that and for it to be part of the conversation, like not a foreign conversation to be talking about cellular health?

Well, you just made it happen, Kelly. We just did. This is great. You're, I mean, you're spot on. It's exactly that. So it's being able to introduce exactly what you just described, that we really are looking at a deficiency syndrome. You know, we put the paper out there again, a second group reconfirmed that, you know, that it's feeding into these fragile cells. We know that in 2012, Columbia University scientists discovered an entirely new way that our cells were dying. They called it ferroptosis. And the way they describe it is fragile fatty acids in the cell membrane lead to lipid peroxidation and to this new, entirely new form of cell death. So what we learned was that the dolphins actually taught us what was causing ferroptosis. I mean, since that discovery of cell death, 20,000 papers have been written on ferroptosis since 2012. And everyone's like, well, we know it accelerates aging and accelerates the onset of type 2 diabetes and heart disease and cognitive decline, but nobody could explain where it came from. And so now we're understanding exactly, Kelly, that it's increasingly— the studies increasingly supporting that C15 deficiencies are driving this new form of cell death, which then, you know, we are confident will become part of the conversation of, wow, oh, it was a C15 deficiency, just like vitamin D and rickets, vitamin D and scurvy will be, you know, C15 and ferreptosis. So, you know, we'll keep working with the scientific community wonderfully. They're also often running on their own, but it's for folks that are especially working with kids and fatty liver disease and seeing hypertension and seeing aging-related diseases showing up in younger and younger people. They're also the ones on the forefront that are pushing this. Because they say, I'm seeing this be fixable and we have to bring this to the forefront because we can't afford to wait because this is a safe molecule. This is an easy thing that we can test and we should be absolutely be paying more attention to it and do what we've always done, which is follow the data.

So I want to thank you for being here and thank you for your contribution to the world, really. I mean, this is a big deal. And I noticed that you're going to be speaking for A4M in April. Speaking on just the topic you were talking about, which I had not heard until I read it in your book. And so thank you for spreading the word to clinicians like us. Thank you for being here for our listeners today, because this is such an important conversation. And, you know, nutrition is so foundational. But if we can't get the nutrients that we're eating into the cell and have them do their job, then we're not making a lot of progress. You know, we may be keeping them at a certain level and keeping certain things at bay, but we can't really see that health optimization that you've been talking about.

So thank you. Oh, well, thank you both for this opportunity. And well, you've just joined the movement, so welcome aboard. Awesome.

And we're going to have some links in our show notes for, um, a code for Fatty15 for our listeners. So that'll be in the show notes. Is there anything else you want to share that you guys are putting out there, or anything else, um, for our listeners?

Um, I would say, uh, uh, all the peer-reviewed science that's coming out on C15, uh, is available at discoveryc15.com so we can make sure that you can put that in your show notes. And that very soon we will be coming out with Fatty 15 gummies for adults and kids. So stay tuned for those who are gummy folks, just mixing them up throughout the day. But we're excited to be able to get really based upon demand from parents that's saying, I really want my children to be able to get their C15. So we're excited to be able to—

that is exciting. So I think some people have pill fatigue and somehow when it's a food and they can take it as a gummy, it seems more like a food than taking a medicine or a supplement. So I think that'll be a big hit.

And if we can be part of the movement to getting labs, more labs testing for C15, reach out to us. We— I use a ton of Cleveland Heart Lab. Quest and would love for it to be part of their panels. So if there's anything we can do to help with that, we would love to.

Oh, Lori, I'm taking you up on that right now. So yeah, absolutely. I'll follow up. That's wonderful. Okay. Sounds good. Because to me, that means a lot. That's great.

We need it more available because we do— we talk about the data. Data drives decisions. And we're already doing these wonderful wonderful, uh, studies on multiple biomarkers, but that one's not there yet. So next on the docket.

All right, all right. Well, thank you so much. It was such a pleasure talking with both of you.

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