← Biohacking Beauty: The Anti-Aging Skincare Podcast
Biohacking Beauty: The Anti-Aging Skincare Podcast
Dr. Stephanie Venn-Watson: The Essential Fat That Reverses Aging—Why No One’s Talking About It?
01:05:51
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- [00:06]
Amitai
Okay, Stephanie, like we have chatted off air. I am a huge, huge, huge fan, A huge cheerleader. It's not really because it means that you are hearing me, but I am a person that constantly wishes good things for you and what you are doing because I am such an avid user and believer in what you guys are doing. That is why the minute I heard about your new, about new development, I had to have you on again. So welcome back to the Biohacking beauty podcast.
- [00:42]
Stephanie
Oh, Amit, it's always a pleasure, always a pleasure chatting with you.
- [00:47]
Amitai
Yeah. And so I just want to let you know that I think Also thanks to Dr. Mercola, like, our podcast together was one of our most successful podcasts.
- [00:58]
Stephanie
Amazing.
- [00:59]
Amitai
Yeah. So first of all, assuming people did not, I hope listeners listened to the last episode. But maybe we should start just in case. Like, let's go through the quick origin story of, you know, C15. How did you first like identify it as a potential health promoting fatty acid? And let's talk about that aha moment that you had.
- [01:25]
Stephanie
Yeah, absolutely. So, you know, when we talk about longevity molecules, which was not how the, you know, the discovery first happened. Amitabh, when we talk about how our longevity molecules, the molecules that help us stay healthy for as long as possible and stave off chronic diseases, how are they discovered? You know, a lot of most of the research as you know, is done on short lived species. So like mice, worms and flies. And then there'll be a discovery and they'll be like, oh, worm lives two times longer and the head, you know, which means like a week longer, a few days longer. And then the headline on the papers is molecule can double lifespan. Right. And so it's, and that's, and that's an important part of research and the studies that are being done.
- [02:10]
Amitai
But if it's, if it's a molecule, like, no offense, like a molecule that I take, so I can't say too much bad things about it. Like C60, it's like one mouse study and then no one wants to touch that study. Like no one wants to look at it again in case they don't get the same result. They're like, no, no.
- [02:28]
Stephanie
So it's so it's kind of like, you know, it's great to be able. And we will talk about studies with C15 that do have, you know, that do involve, you know, short lived species. But when we talk about longevity, we were given this amazing gift where instead of understanding how, you know, helping short lived species live longer, we were working with, and I Was working with, as a veterinary epidemiologist with an incredible population of long lived large brain mammals. And you know, it kind of now makes sense because it's like, if you think about it, if we talk about how do we meaningfully extend our longevity, nature and evolution has already figured it out. Like how do mammals like humans, dolphins and elephants live 30 times longer than a mouse, right? And which is a mammal. So something is there that is already enabling longevity. Let's use those lessons and then figure that trick out and be able to leverage it from there. So that whole discovery came from you guys working with Navy dolphins with the sole purpose of improving Navy dolphin health. As we had talked about previously, the Navy's cared for, you know, the sustained population of about 100 bottlenose dolphins for over 60 years. So we were. And because they get such great care, Navy dolphins live a lot longer than dolphins in the wild, like two to three times longer. They live in their 50s and 60s versus 20s.
- [03:56]
Amitai
Yeah.
- [03:57]
Stephanie
So because of that, we were seeing, we were able to like watch over a 10 year period, a population of geriatric Navy dolphins and understand that some, but not all were developing chronic aging associated diseases like high cholesterol, chronic inflammation, fatty liver disease, even the full suite of changes consistent with Alzheimer's. And so, long story short, we were able to go into the Navy archives of serum samples.
- [04:27]
Amitai
I just want to ask, it's like did they develop like other things suddenly they preferred like sparkling water to still water.
- [04:35]
Stephanie
See, that's like a really point, right? Because it's like there that was, that left this giant opportunity because unlike us, right, they have a very controlled environment. They live in the ocean, right? So they live in their natural environment. They eat fish. All they eat are fish. But there were five different types of fish which ended up helping us narrow down, right, the secret sauce, right, to longevity. And they all had the same healthcare system, drove the same cars, you know? You know, it's like it was insurance. They don't drink beer, they don't drink alcohol, even though they're Navy dolphins. So it's like we had all these benefits of this very clean population. And the whole question is, why are some aging, well, slower and others are developing these diseases and actually have accelerated aging. So we were then able to go in, use this advanced technology called metabolomics and look at thousands of small molecules, right? That's in these archived serum samples to see which small molecules in their blood and in their all fish diet predicted the healthiest aging dolphins and amitate, to your point, it was such a clean data set that we were able to see right out of the gate that C15 was the top predictor of healthy aging dolphins. And we thought it'd be omega 3s because they eat fish. And it was C15, this molecule that I, you know, fatty acid I had never even heard of. And you know, as an added surprise, right, it's a saturated fat, so that's what started the whole, and this was 10 years ago. Since then there are now over a hundred peer reviewed publications throughout the world demonstrating C15's benefits.
- [06:17]
Amitai
Yeah, that, that. I, I, I, I want to ask you a small question. Is that why I think conventional, I would say, like slow moving dietary recommendation tests don't recommend it yet or don't really isolate it as a molecule, that the needle should be moved there? I mean, I'll give an example. I have a friend who is both an AI researcher, like machine learning researcher, large language model researcher, and someone who is like an avid biohacker. And he plugs everything into different models that he has and he kind of reads the data and he only follows, he's, he's, he's, he's, you know, he's beyond event horizon. All he cares about is what the models are telling him. You could tell him, hey, you know, you, you need to brush your hair, you need to shave. Is like, no, the computer told me not to. So like, and when he plugs in his blood tests, I was telling him about fatty 15 because, because he was interested in skin health. What, what are what, some of the molecules I can take. I told him, hey, blah, blah, you know, spermidine and you know, fatty 15. And he goes, no, no, no, fatty 15. I don't need more because when I plug in my, my blood tests or my metabolomics tests, it doesn't tell me I am deficient. Is that, why is it just that the data is not, is not fed correctly yet?
- [07:46]
Stephanie
Yeah, I mean there's a huge flaw in C15 levels today. Right. And that is, you know, a part of, you know, what you're getting to, which is our, well, the dolphins are getting, we're getting their C15. Some dolphins were getting them from some types of fish that had C15. And there were other types of fish that no C15. So it actually their C15 was driven by which fish they were eating even within the same population. For us, our primary source by far of C15 is dairy fat. And so we've gone through a 50 year experiment of methodically removing and lowering C15 in our diet as we've moved away From it was 1977. If you think about Congress, Congress, it was actually like five senators came out with recommendations for dietary changes for all Americans in 1977. And in that, they said we must decrease our intake of saturated fats. And the best way to do that is to lower our intake of whole fat, milk and butter. So when we did that, our C15 levels have declined population globally. And by doing so, because this is your. Who picked up those recommendations? Like, this is right? So, so what has happened is what's a normal C15 is around 0.2% of total fatty acids in our blood that we have learned and we just published. We published last year, right? The not only is C15 the first essential fatty acid to be discovered in over 90 years, we discovered what you would expect, which is a nutritional deficiency. And if we have low levels of C15, our cell, we'll talk about mechanisms, but our cell membranes become more fragile. It's causing a whole new form of cell death called phoroptosis. And then that accelerates aging and all the downstream diseases. The problem here is that almost everybody is sitting on 0.2% C15. So we're right at the edge of being deficient, and 13 of us are deficient. So when your, your colleague and your friend are looking at the data and saying, hey, I'm right there, I'm at normal levels, I'm not deficient, then normal doesn't mean healthy, because the entire, even a healthy population today has 0.2%. If you go to populations like Sardinia, right, and you look at them and they have a lower. They. The. In the high longevity zone, where they're living longer and they're less likely to die of heart disease, they have C15 levels of 0.6. So they have three times higher levels. So it. There's exactly that. Like, even if you went today to a doctor and you got a test for C15, if you. It would show you, like right in the middle. But what we're trying to help understand and educate is that we actually, we need to be 50 steps from that cliff, not one step.
- [10:45]
Amitai
In other words, I feel like what you are saying as far as, like 50 steps from that cliff is something that I'm trying to explain to people intuitively. I think people look at longevity is what I call the Phoenix model or the car garage model, which is. Which is a model that relies on getting something dysfunctional and nursing it back to health, which we don't. Our body doesn't do Very well. Like, our body is not, we're not built to do that. And the other thing is that even if our body would have done it very well, we actually don't know how to do it yet without insane interventions that currently also cause cancer. Like, I'm obviously referring to the Yamanaka genes and stuff like that. Like, insane things that are very far from being available. Okay. And what you're talking about is a, you know, preventative is a very unsexy word. But what you're talking about is kind of understanding that our body constantly, constantly has disbalances somewhere. These cause accumulated damage. So being anywhere around, like, minimal ranges really means that in some areas you are deficient chronically. Therefore, you are accumulating mistakes and accumulating damage, which our body, again, is not great at. Going back and repair and repair.
- [12:26]
Stephanie
That's right. That's right. And I'll give you an even less sexy word, which is, which is general protector. Right. And so, so, and geroprotectors are like, if you talk to a long, you know, longevity scientist. Oh, it's like, it's a, it's a really important word because it represents a molecule that. Right, exactly what you're speaking to, Amitay. It's like, it protects us against aging. So geroprotectors, so it slows our aging rate and slows the onset of the diseases that eventually kill us. And oh, my gosh, like, from a branding standpoint, it's like the worst word ever, but it makes complete sense. And so C15, that's where Dr. Nicholas Shorick and I, Nick Schor, leads the NIH's longevity consortium. And Nick came in and he saw all the things that C15 was doing. And that's where then he said, gosh, he's like, steph, I bet C15 is going to meet the criteria of a geroprotector. And I said, amazing. What's a general protector? But, you know, we, and then we published that work back in 2023, I believe in, in nutrients of that. It's, you know, a leading. It did had better geriat protective properties than rapamycin, metformin, E. Carbos. So, you know, and that's how, you know, it came to, you know, the name of, of, of the book.
- [13:50]
Amitai
Incredible. I, I, yeah, I think longevity is slightly sexier. So again, I really am excited to nerd out about the molecule in this podcast specifically. And if someone wants a less mechanistic, less deeper of a dive, I refer them to the first podcast with It, But I do, you know, you're baiting me here to ask you questions about mechanisms of action. So you know what, you got it. Let's talk about like cellular physiology a little bit. What do you, what do we know about house? C15, which is, which is trademarked as fatty15. So I'm just going to put it out there that we're going to probably use them interchangeably. So what do we know about C15, about how it interacts at the cellular level, like which pathways or receptors that it does it influence?
- [14:43]
Stephanie
That's right. So C15 is a pleiotropic molecule. And so that means that it does a lot of things, which is what again you would expect of an essential nutrient. Lots of benefits throughout the body. But we're going to talk about the core benefits here. So the first is that C15 is a saturated fat that has no double bonds. We usually think we automatically put saturated fats into the naughty category. We now know that there are odd versus even chain saturated fatty acids. Odd chain are those that have an odd number of carbon, C15, C17. Even chains are C16, C18, and that the odd chain, saturated fatty acids specifically, specifically C15 is the Goldilocks saturated fat that actually has lots of benefits. And because it has no double bonds in it and it's anti inflammatory, unlike the even chain saturated fats, it plays a critical role in strengthening our cell membranes. So it physically goes into our cell membranes which are made of lipids. Right. Of fats. And we've learned that it plays a primary role of strengthening our cells against attack by oxygen. And every time a fatty acid has a double bond in it, which are unsaturated fatty acids by definition. Right. So polyunsaturated fatty acids, multiple double bonds, multiple points of attack, C15 is able to basically fight against oxidation. And that's called lipid peroxidation. Right. So oxidation of fats, lipid peroxidation in turn leads to like a, a whole slew of issues, but it sets up the cell to become more fragile. This sets up inflammation. When we talked about this for optosis, this is an entirely new form of cell death that was discovered in 2012 by scientists at the University of Columbia. And since then there have been over 10,000 papers on fermentosin.
- [16:42]
Amitai
But I think until like 2021, 2022, it was even like disputed as far as like a leading cause of cellular death, like people used to think. I mean, like I remember people pooh, poohing it, saying, no, you would need an unconventional amount of like iron atoms to be excited in order for it to even make a difference. Obviously, since, you know, very early on when ferreptosis kind of came about as a, as a potential disruptor or potential DNA damaging effect, we kind of led the charge as far as like against skin and synthetic vitamin C, which also excites iron atoms. And I remember like, you know, I'm not going to name her by name, but like the leading Harvard dermatologist saying that I'm, that I know what I'm talking about. So like. So yeah, so I think, I think, although you're saying 2012, people need to understand that 2012 is when it was like people started talking about it, you know, as far as like scientific literature, but really we're talking about like three, four years of this being something that people nod when you, when you refer to it, right?
- [17:52]
Stephanie
That, that you're completely right, Amit, and you are right from the get go, like from the beginning. Because we now, you know, we now know that. So this form of optosis, uh, you know, the same year that that was discovered, which you had talked about, you know, it, it, the way the definition of ferroptosis are increased fragility of fats in the cell membrane, increasing lipid peroxidation that then mixes with this free iron, right, that's then available, that's shouldn't be in the cell, but it is that that mixes with the lipid peroxidation results in massive reactive oxygen species and it knocks out the mitochondria. The same year that paper was published, we published the discovery of iron overload in dolphins in the liver.
- [18:38]
Amitai
Wow.
- [18:38]
Stephanie
Yeah. And so we didn't know that it would take, you know, what, 15, 13 years to bring it all together. Where because again, the dolphins were such a clean population, we learn the pathophysiology behind C15 deficiencies or cellular deficiencies or cellular fragility syndrome, showing that when you have, when you don't have enough C15 in your cell membranes, they become weak. They are susceptible to lipid peroxidation. This includes your red blood cells. So when your red blood cells are weak, your liver has cells and it called KUFR cells that are specifically there to take out fragile red blood cells and recycle the iron. So that's great, it's what they do. But when you have a lot of fragile red blood cells, then the Cooper cells engulf those red blood cells. You have so many of them that the corpse is left behind is excessive free iron. So now you have iron in overload in the liver mixed with fragile cells, red blood cells, but also liver cells. Lipid peroxidation, that's then over a period of, you know, years and even decades, spills over into the blood. It then seeds our brain, our hearts, our skin, and all those effects that froptosis has. We have proven that that is what was happening in the dolphins. And there was only one inciting cause, and it was C15 deficiency. We fixed it when we put C15 back. And then there was also a model in which we were able to definitively show that replenishing C15 into the. Into the system fixes the entire, stabilizes the cell membrane, stabilizes red blood cells, fixes anemia, it lowers lipid peroxidation, it stops iron deposition in the liver. So we now understand, you know, a big part of where this all came from. So, Amitay just. That was a long way of saying you were right. Yes.
- [20:40]
Amitai
Anastasia never tells me this ever, so. No kidding. So I do have a question, because you kind of didn't touch on it yet. Is there. Is there evidence that seems C15 exerts epigenetic changes, in other words, like modifying gene expression in a way that promotes either, you know, health at the moment or longevity?
- [21:00]
Stephanie
So there are a couple of new papers that have come out that are supporting. So it's. It's not us, it's other groups that are doing work looking at epigenetic changes and looking at the, you know, epigenetic clock, our biological versus our chronological aging. And. And that was published last year, and it's an ongoing study of looking at biological versus chronological aging in a cohort of people. And one of their first publications out of this study showed that people who had higher levels of C15 in their lipids. So understanding C15 can be a free fatty acid, but when we eat it, it gets incorporated into lots of different complex lipids. So you'll have a 15 carbon chain attached to different lipids throughout your body. And they showed that the more of these lipids that we had that with C15 attached to it, the higher the level, the younger the biological age. And in fact, people with the highest C15 levels had younger biological age than their chronological age, which is what we'd expect. But it's always great to see that, you know, kind of validation for us, you know, one measurement of. Of biological age and epigenetic aging is also a marker called rdw, or red blood cell distribution with that has really come out as a marker. And it's how variable our red blood cell size is, and you want it to be homogenous and the more variable it is, it means that your cells are turning over faster than they should because they're fragile. So the other thing we've been able to show improve is that C15 by stabilizing our cells, including our red blood cells, helps the red blood cell distribution get stable. And so it's actually stabilizing not just the cells, but our aging rate and stabilizing epigenetic aging too. So it's a lot of exciting things coming on that front. But really what's been great over the past year is the work of others. You know, the world working on C15.
- [23:08]
Amitai
Interesting. Well, you did mention cellular turnover. And, and I think anyone who only speaks to their service provider as far as like, you know, I'm going to say something maybe that's not like great, but anyone that, that, that is interested in like skin health or the appearance of youthful skin, and he's only talking to the person that wants to sell them a treatment that is in office. The minute that you say cellular turnover, most people would associate it with a very positive outcome. So maybe first of all, it does lead me to the subject of like, from a dermatological standpoint, how does C15 influence the skin? But we can definitely start with cell turnover because it's not only about the. Obviously when we're older, we turning cell cells over slower normally. But what is the connection here between, you know, C15 and cellular turnover? Especially like skin cellular turnover?
- [24:10]
Stephanie
Yeah, it's a, that's a great question. So when we talk about cellular turnover, like in the red blood cell perspective and others, it's the part of aging where our cells become more fragile and they're. And then what happens a lot of times is they don't. And that's where, you know, a lot of talk around zombie cells and senescent cells where they get weak and they don't work, but they also don't die. So. So right. So then you just get this unhealthy. The whole role of C15 is as an essential fatty acid is to maintain balance. Right. So it's important that it like to your point, that our cells turn over healthily and that when they are, it is time for them to die, that they then know to, you know, get out and move on and let new cells come in. So the senescent cells, which gets to other two other mechanisms as far as just throwing in there with regard to longevity, that C15 also has been shown to activate AMPK and inhibit MTOR. So with regard on the senescent, helping to prevent the senescent cells and the zombie cell situation, with regard to healthy cells, they're specific to skin. There have been some really exciting work done looking at C15's role in cell strengthening from a. From an epithelial barrier hypothesis standpoint. Right. And so we know that whether it's our. Our and our epithelial cells are so critical to protecting our body against the onslaught of everything in the environment. Right. Whether it's what hits our skin or what we eat in our food. So otherwise we would die, like. Yeah, very quickly. And so the epithelial barrier hypothesis is that your ongoing exposure to contaminants, it's a very. It's mainly environmental focused.
- [25:59]
Amitai
Yeah.
- [25:59]
Stephanie
But saying that things to which we are being exposed are making our epithelial barriers so the connection between our epithelial cells weaker. Right. And in our gut, that leads to leaky gut syndrome. In our skin, it leads to like, increased exposure, dryness, inflammation.
- [26:15]
Amitai
I actually called it. I actually called it. Now it's being usurped completely. I'm fine with it, by the way. And people don't use it correctly, but referring to what you have just described, I used to call it leaky skin.
- [26:27]
Stephanie
And I.
- [26:29]
Amitai
And I try to explain. And by the way, Ara, the CEO of. Of seed, told me I'm doing it wrong. So. But what I try to explain is that as opposed to the gut, the leaky skin is leakage of mainly of information that our skin is now being fed information of. Of distress, of stress, of malfunctioning environment, which then leads to increased inflammation, etc. But Ara said that it applies to the gut as well. So I can't just juxtapose it now.
- [26:59]
Stephanie
Okay. All right. Well. And we know, like, exactly both of those are working. So the studies that have been done with C15, there were three that came out just within the last six months have focused on leaky gut syndrome. So they focus on epithelial cells within the gut. And what they all three showed in multiple mouse models of colitis and IBD and others is that C15 supplementation successfully shores up that the gut lining stops. Leaky gut syndrome decreases, actively decreases inflammation. So that's a key thing we need to talk about with the skin and helps basically calm everything down. So that's great from a gut perspective, from our skin, you know, when we talk about nutritional deficiencies, especially fatty acids like linoleic acid and alpha linolenic acid, a deficiency in that is in the models, in the mouse models are, is dry skin, right. And poor hair. And so it's standard understood that a fatty acid deficiency or having low amounts of fatty acid is going to have one of its direct effects on your skin. And so it goes in, it plays a role as a lipid. It helps. The main thing is also being able to maintain water right within our cells and not becoming dehydrated. And so the lipids help do that. And then in addition, C15 has been shown to decrease 18 different Pro inflammatory cytokines directly, not just through decreasing lipid peroxidation. And it does that in part as a JAK STAT inhibitor, which is one of my favorite mechanisms personally for me from a skin point, because I, my whole life have had atopic dermatitis and eczema that resulted in my hair falling out. And it just got worse with age. And when I hit like menopause, just forget it. And C15 helped fix that. It helped calm things down. I got moisture back in my skin, the redness went away. And so it, it helps. I know personally that it helped with my skin health. Is it one, you know, the one stop shop to fix everything? No, but I think it's a critical part of just maintaining our cellular health, including and for me, especially for the skin.
- [29:17]
Amitai
I'm sure you know how correct you are, but I don't think it came through the level of correctness because I, we don't talk about this often, but I do mention it sometimes. And you, and you've, you, you've introduced two key, key, key terms as far as skin health. One is obviously barrier function and the other is what we call transepidermal water loss. Okay, so the way I normally explain transepidermal water loss is if you live in Florida like ourselves, you go to Vegas immediately or your lips are, you know, they are zombies themselves. They are. You are lipless for the next couple of days. So. And the reason is, is because there is a, there is a. You are losing more water to the environment. Your skin is not prepared to deal with it. And you're basically, there is a, there is more loss of water to the environment and that is what, what your lips are experiencing. And that happens to your skin all the time. And one of the things that we're trying to do is maintain that so lipid. So skin barrier as a whole is, is important for that and especially the makeup of lipids there. And why am I saying that you're touching on something very important is because a lot of People, especially in the kind of clean skin care world, which obviously I give them respect for their efforts, but they are using oils as moisturizers and it's very in most plant oils arrive to the client in a subpar state, but 99.9% of the time in a not in the state that they got into the bottle to begin with. And what happens is, is that you are now diluting your skin barriers ability to, to protect from environmental stressors and prevent that moisture loss. Oils don't actually provide moisture to the skin directly. They don't go to the skin and tell it hey, here is more moisture. Actually our skin, because it's designed to deal with, you know, water, etc. Consistently is not designed any way to receive moisture from the environment. Whether you're putting hyaluronic acid or jet fuel, I don't know what. But don't do that. But don't do that.
- [31:27]
Stephanie
No, it's not a recommendation for this podcast.
- [31:29]
Amitai
No, absolutely not. But the sure fire way to, and we know like, people know that like stuff like castor oil or things like that will actually dry your skin. There is a reason so you're providing oils that are more permeable. And the reason we, you know, myself I have been extremely interested in trying to get, you know, fatty 15 into skincare. You know, is because our journey constantly is a journey of how do we improve the lipid makeup of the skin barrier because it improves everything else. Everything else. By the way, the one study we published around, around, around lipids and dry skin is attaching the lipids that you've just described in a very pristine state to retinol and showing that it prevents the dehydration of the skin that is, that is associated with retinol or retinoids, vitamin A's. So there is a lot of like. So you could even push the skin further. You know, if you're interested in all of those ideas of like hey, let me go to my specialist and stimulate, you know, renewal and turnover cells, et cetera, that even as a modality on its own will benefit from, from something like fatty 15 like this pristine, resilient fatty acid added to the skin barrier.
- [32:53]
Stephanie
Well, that was fun.
- [32:55]
Amitai
Yeah, that's me rambling on. So, you know, maybe we'll talk about, you know, specific skin things a bit later. But I do want to ask something about, you know, giving the, given the, I think the main, the main excitement I've heard about fatty 15 from users is neurobiological effects. So, and you've alluded to that as well. What are the known effects as far as like cognitive function? Neuroprotection.
- [33:32]
Stephanie
Yeah, yeah. So the initial work, so if you look at the body of work, it's really been focused around metabolism, like, so metabolic health, liver health, you know, and heart health, like lots and lots, I'm a tea on that. And increasingly now about things like pregnancy and infants and the essentiality of C15 at that stage. The new frontier for C15 is understanding what is its role in cognitive health. And so it's the area that has the least information, but obviously the most, for a lot of us, the most exciting potential. And you know, our brain is made of lipids and our brain requires oxygen. So those are two knowns. When you mix oxygen with, you know, lipids, as we talked about that, especially the ones with the double bonds, it's kind of like a. Our brain then becomes particularly susceptible to the effects, the aging associated effects of lipid peroxidation. Right. And because we can't have the recommendation of don't send oxygen to your brain. Right. So we don't have that option. And so. But we do have the ability to influence the lipid makeup of our, of the lipids in our brains. So that's where, you know, studies with C15 are coming into play.
- [34:53]
Amitai
Yeah.
- [34:53]
Stephanie
So that's early work. Meanwhile, you know, we had launched fatty 15 and we, the research continued and we have a chapter in the book, you know, and, and I haven't, I don't think I had said actually the name, but it's the longevity nutrient there. And it where the folks at the Navy said stuff. Hey, it's great that you discovered, you know, C15 from this work. This is awesome. But like you discovered like a hundred molecules that predicted healthier aging dolphins. So let's get going on what else you got. And so we're like, okay, okay. So we went back to the data and we found a handful. So we kind of went to the next five in line and one of those really stood out as remarkably promising specific to cognitive health. And it ends up that this molecule is called pentadecanoyl carnitine, which is a metabolite of C15. So our bodies take. And we're talking about. We're looking at thousands of molecules.
- [36:01]
Amitai
Yeah.
- [36:01]
Stephanie
And like, no. And we did not pick this one because it had anything to do with C15. So here we go. Number two. Candidate number two from the dolphin work was this gray molecule which behaves completely differently than C15. And so it's its own. I call it like the baby sister of like the star, like C15 is the super was the rock star. And this is like the baby sister of the rock star. And so it, this molecule PDC is basically our bodies take C15 and attach a carnitine to it and that's all it is. So it's an acyl carnitine. When we ran that against a bunch of receptors, we found that it fully activated both CB1 and CB2. So cannabinoid receptor 1 and cannabinoid receptor 2. So it's the second ever discovered full acting endocannabinoid like ever. So we published that back in 2022 and you know, we know what cannabis is and we know what it does. But. And that's why the receptors were named that. But we don't have those receptors for cannabis. Right. We have those receptors throughout our brain and body to help us sleep better, to help us have, you know, better cognitive health, to be able to decrease inflammation in our brain and in our body. So why do we have them? We know that we use arachidonic acid, which is an Omega 6 to make the first discovered full acting endo, like our endocanna, our body makes it and PDC is the second. So we were meant to get C15 not only to strengthen ourselves and to help support longevity, all the things we've talked about, but also to make this metabolite which helps our mental decreases anxiety, helps us sleep better, you know, helps with joint pain and you know, it just feeds into this bigger picture of the what if. Right. I'm gonna tell you what, that if we've been given a scenario where the world has decreased its intake of C15 and we're all sitting on base or at C15 deficiency, how much has that not only impacted our aging rates and sped up, but how has it also impacted our mental health?
- [38:15]
Amitai
Yeah, yeah.
- [38:16]
Stephanie
So that's a really. I'm super excited about where that's heading. C15 deficiencies really kicked in at the baby level in the 1990s. So we're really looking at the generation of that were that are now in their 30s and younger. And this is the same population of people that are undergoing, you know, just really alarming increases in mental health issues, in increases in type 2 diabetes, coronary heart disease, even certain types of cancer. So it's, you know, you can, there's urgency to be able to say, let's have these types of conversations. And you know, you just can't explain C15 away.
- [38:55]
Amitai
Yeah.
- [38:55]
Stephanie
You know, anymore.
- [38:57]
Amitai
100%. Hey, there.
- [39:04]
C
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- [41:08]
Amitai
I want to go over some clinical preclinical evidence. I do have a question. We're talking so much, you know, we're talking about different impacts on the body, you know, different approaches. And it seems to me, I wonder why write a book now when there is so much that has been studied 100% but so much that is happening currently. And a book is something so obviously it's not finite. There are iterations, stuff like that, but it's. So we're in the midst of this storm. So I wonder how is the book play a part in all of this?
- [41:53]
Stephanie
So the book is to help get the conversation going because we are at the point now, Amitay, where you're absolutely correct. Like the, it continues like literally as I was writing the book and turning in the last, like the last last. I'm like ah, there was like, I like since the book, you know, the final draft was submitted or the Final version was submitted, three papers came out revalidating C15 as an meeting the criteria of an essential fatty acid from independent teams, you know, in, in three different countries and like oh man, if I could always. So yes, you're right. We are in the middle of a very exciting time.
- [42:32]
Amitai
You're adding like a note to the end of every book like oh, and this happened.
- [42:37]
Stephanie
I just having some incidents right at the, at the meetings. So yes, and I'd say Probably once every two weeks there's a new paper coming out on season 15. However, because of the urgency of what you know, we're talking about that if you look at the USDA duck guidelines, dietary guidelines today, the ones that are active today, not 1977, they mention avoiding all saturated fats 161 times and a 164 page document. So there's too much information. And again those, even chain saturated fats that are present at much higher levels in dairy fats, like 40% of dairy fat have pro inflammatory saturated fats. It's not that they were all wrong, only 1% of it has C15. But for our kids and infants, they probably do need that milk fat, whether it's for mom. But mom can't be C15 deficient, right? And to be able to. We know now studies showing that babies that get more C15 from mom are more likely to have healthier growth, healthier brain development and healthier cognitive skills all the way up to six years old. So we're at a point where there's so much, there's a hundred papers here that we cover in the book and we walk through, you know, obviously the, the adventure of the discovery story, which you know, it took place over a 20 year period. But it's also really telling the story about all the research teams throughout the world who we now have enough that this is a movement, Amanda. I mean you've been part of it since the beginning, so you can't. It breaks my heart when you know, you could still probably talk. Well, not you because not your community. But most people could ask 9 out of 10 people or 10 out of 10 people, have you heard of C15? And they'll say no. And so we can't be at that state anymore. So the purpose of the book is to say, you know, we've had our blinders up on saturated fats. We understand the need for the science world to have to prove out what we, the stake we put in the sand in 2015 or in the ground. But now it's proving out so it's just, it's, that's why now it's like, let's get this going because we can't afford to wait. If fatty liver disease in fact is the reason why we went from the first cases of fatty liver disease diagnosed in 1980 by Mayo Clinic to 38% of people today. And if what the data are supporting are that C15 deficiencies are a major driver of a phenotype of this syndrome and our kids are aging faster than they should, we just, it's, it's time movement is on.
- [45:26]
Amitai
I agree and I think there is something about, even if you are someone who is very, who's drinking the kool aid, the C15 enriched chol aid, I think there is a reason, like placebo is 30% of the positive results. I think even for myself I would want to read the book because I believe that there is a psychosomatic effect to loving what you're doing, having a positive connotation to what you're doing. Even the most cerebral, intelligent, whatever person in the world should, should, you know, should encourage the psychosomatic effect to work as well. So I'm selfishly interested in reading the book. Obviously we don't have like a lot of time and I want to go to practical applications. So maybe you can run me quick, run quickly through human trials, animal studies, where they're at and if there are any skin related studies.
- [46:32]
Stephanie
Yeah, so animal studies, in vivo studies, there have been a lot. Now most of them have focused on mouse models of fatty liver disease, of type 2 diabetes, obesity. And those have repeatedly shown that C15 supplementation within 12 weeks successfully decreases insulin, glucose inflammation, IL6 and MCP1 and TNF Alpha, as well as lowering the amount of fat in the liver and lipid peroxidation. We talked about the studies in the gut of mouse models with inflammatory bowel disease, multiple models showing that it helps heal the gut and help decrease inflammation in models of colitis. Then there's this model of rodent model of ferroptosis in which it's the whole suite that we talked about earlier of this pathophysiology and showing that C15 supplementation helps fix the entire suite of ferroptosis and cellular fragility syndrome, including treating anemia, stopping iron deposition in the liver, lowering inflammation, lowering cholesterol is another consistent outcome that we've seen and others have seen across various models. So, so then when we moved to people, There have been two randomized control clinical trials with C15 supplementation. Both were published last year or the beginning of this year. And one was both of them focused on fatty liver disease for the reasons we mentioned. One was a young population, so they're young adults, 18 to 24 years old, had a history of fatty liver disease. They took C15 supplementation for 12 weeks. And it showed a couple of a key, a few key important things. One is two. Two out of three of the people in the study had our definition of C15 deficiency. So less than 0.2% that 2 out of 3. So that was meaningful for those who took the supplementation fatty 15 and got their levels up and above that definition of deficiency. They had significantly lowered ALT and AST liver enzymes, which is the primary issue they had at the beginning of the study. And we also saw an improvement in hemoglobin. They not we an improvement in hemoglobin which was indicative of these, you know, improved red blood cell health. And again, this is just within 12 weeks. The second study was done in Singapore with women average aged in their 30s with fatty liver disease. And they showed that C15 supplementation in 12 weeks lowered LDL cholesterol and also increased the growth of Bifidobacterium adolescentis in the gut. So it helped to improve, which is like a mama microbe that does a lot of things, right. And it has even been shown to extend longevity and worms. And yeah, I could tell it's a microbe you like. So in addition to helping to lower enzymes and fat in the liver, so there's, you know, again, two of these clinical trials focusing on the most urgent needs right now for C15 to help fix this crisis. And that's kind of where the world is at. And then we have these large scale epidemiological studies, prospective cohort studies, which all which are there now, meta analyses. So studies of studies tracking thousands of people over tens of thousands of people over decades, repeatedly showing that the higher the level of C15 people have, the lower the risk of type 2 diabetes, heart disease, fatty liver disease and certain types of cancers. So you bring that all together mechanism, in vivo activity, cell based dose response activities and you know, and now these clinical trials and prospective cohort studies. And it gets to what Nick Schork says, right? And he says there's no molecule that has more evidence of supporting our health and longevity than C15. Amazing that he has seen.
- [50:39]
Amitai
Let me ask you, so what about do we have anything even in animal models showing, you know, specific improvement in skin health? You know, whether it is hydration, whether it is again like obviously like skin quality, skin aging markers of skin aging, anything like that.
- [50:59]
Stephanie
They haven't, so they haven't done studies on, on with, with regard to dietary C15 and skin health. So Amitay, we're, we're ready, we're ready for those studies. There was a study done a while ago in a mouse where they would, they would look at its effect on inflammation and they would like create a little cut in the mouse's ear and it would swell and they would apply C15 topically and they saw that the inflammation went down. So there was a top. There's an example of a topical application.
- [51:31]
Amitai
I'll take it. But this is a good start. I mean most, most like I would say like rejuvenation supporting molecules. That's how they start, right, like with some kind of wound healing application. And we obviously can extrapolate that to longevity. I think that would be, it's an entire podcast. But I mean this is promising. So I'll just refer to a couple that we now know started that way and are now know ubiquitous with skin health. One is obviously red light therapy and the other one is GHC or copper peptide, but really I could name like a million. So let's talk about practical application and usage. We talked about supplement form. Why offer Fatty 15 as a supplement instead of, of dietary sources? You kind of did touch on it, but you know, we talked about foods rich in C15. Why is it difficult to incorporate it naturally at the adequate levels?
- [52:30]
Stephanie
Right. And you know, because if, if we could have fixed this just by changing dietary recommendations, you know, we would, that's what we wouldn't have done. And the Navy really invested 10 years of funding. All the studies I've talked about on were were funded by the US Navy. So you know, which required submitting a grant proposal defining your objectives, helping to understand. So the Navy understood from the beginning that there are limitations in the food supply with regard to, and especially changes in food. Like with the dolphins, it's getting harder and harder to find fish that have adequate C15 levels in them. Sadly because of overfishing and warmer waters are resulting in fish with less fat. So Navy dolphins are actually getting supplemented with fatty 15 now. So they really did have a need. And so at the military it's what we do. We find a need, invest. The Navy invests the money to fix it and then you fix it. So the Navy funded even the development of this supplement for this purpose. So that is important.
- [53:32]
Amitai
So it's a military grade supplement.
- [53:35]
Stephanie
Military grade supplement. It is, it really is. I love it. That'll be the next, the next label. So, so when we look at foods, you know, like I mentioned, our primary source is dairy fat. And they're, you know, when you look at dairy, there have been thousands of clinical trials with dairy fat and they are crazy inconsistent, right? You can find just as many saying that they're good for you as they're bad for you as they're null. If I had to lean toward anything, it's saying, at least in general for most people, dairy fat is probably not bad for you. So we can start there, right? But you don't see the benefits that we were seeing, that we're seeing with these clinical trials. And in fact, you know, an example of a mouse study where if Bishop et al, where they had a mouse got C15 and it had lower glucose, better lower liver fat, you know, improvements across the board, they gave it C17 just to test and see a different odd chain and it was kind of meh, it had some anti inflammatory effects, but not nearly as well as C15. Then they gave it just straight up milk fat and it got worse. So it had increased inflammation, increased fat deposition and they attributed it to the extraordinarily higher levels of C16, which is again this even chain pro inflammatory saturated fat. Again 40% of milk fat are these pro inflammatory saturated fats. So there is a study, a series of studies that they showed a surprising finding in which when you gave a rodents high fat diets, which is how you, by the way, you induce diabetes and obesity, their C15 levels actually went down despite the fact there was C15 in their diet. And so what that showed was that the Hypothesis is that C15 is competing with these other high fats in the food. And it, it just, it's like a little kid in a subway station trying to make it on the subway when it's busy and it's just not going to make it on the subway. So yeah, I'm, hence the theory.
- [55:36]
Amitai
I'm tempted to, I, I can't stop myself. I'm gonna say something has nothing to do with our discussion. I would say that in game theory, odd number columns or odd number games that rely on odd number of of turns are more easily resolved. So maybe we have something there like as far as, like the ability of the body to, you know, to process. Yeah, odd chain fatty acids. I love it. Anyway, so recommended intake for adults. You know what dosage seem beneficial? We talk about why you decided on 100 milligrams, which is the dose right now in fatty 15. And for idiots like myself, you know, if one is good, you know, 10 might be. Must be significantly better. So a few questions. So I have, that I have, like why. Why the dosage that you've chosen? Does timing matter for absorption? And then what if. What if I'm an idiot?
- [56:34]
Stephanie
Okay, so what? You're never gonna be an idiot.
- [56:37]
Amitai
But I am gonna again ask. You should refer to.
- [56:40]
Stephanie
I'm gonna tell you not to take 10. So. So the first is the dose. Again, this is a free fatty acid, pure C15 molecule, right in C. In fatty 15. And so it's readily absorbed. It's 100% absorbed. And that's been shown in extensive human clinical trials. It's 100% absorbed. So we know. And there are not genetic drivers for C15 levels, which is extraordinary. Like you very rarely not see a genetic influence. A big study was done on that. So we know that for every 100 milligrams of C15 of the free fatty acid C15 that we take and then we absorb that, we. Our levels go up by about 10 micromolars. So I'm going to use this or 1 microgram per mil. This is equal to around the 0.2, 0.3%. And so we know we need to get 1 to 200 milligrams added C15 in our diet per day to get above and beyond, you know, get further from that threshold. So on one point, what you're saying, you're correct that the more you take, the further you are from that threshold. I myself have a 0.46% C15. And that gives me lots of leeway from being on the edge of that cliff. And I take two capsules per day sometimes. And other times I just kind of let my body kind of feel where it's at. And other times I'll take just one capsule. So one to two capsules a day is the recommendation. And those were chosen because the reason why I said the micromolar level is that studies consistently have shown of all those mechanisms we talked about, of, you know, inhibiting jak, stat of activating AMPK and inhibiting these pro inflammatory cytokines. The, the optimal concentration is almost always around this 20 micromolar level. So we, everybody is sitting on around a 10 micromolar level because our gut microbes can make some C15, but not enough to get up and over. So if we're all sitting on around 10, we need to add another a hundred micromolars or sorry, a hundred milligrams to get to that 20 micromolar level.
- [58:50]
Amitai
Did they See any point of diminishing returns?
- [58:53]
Stephanie
So that's a great question with regard to set. In some cases, the higher the better. So that's with heart health. And then the population in Sardinia, right, where they're at 0.6, the higher you get, the lower the risk of developing heart disease, which is association, as well as in Sardinia, which is association. So there's promise there. There is evidence in like mitochondrial health that there's diminishing returns. So when you get between 20 and 50 micromolars or should be equal to 200 to 500 milligrams per day, it's the height is that it's like 20. Then you know, if you have 20, then 40 and 50 and then you just kind of get back to baseline. So. So I will tell you that we really do mean, like holding to that, like two, one to two capsules per day and then just seeing how your body responds. And, you know, physicians are watching. If they're more like looking at a person who is dealing with ongoing nutritional deficiency syndrome, there may. There's a need for catch up.
- [59:56]
Amitai
Got it.
- [59:56]
Stephanie
Right. Um, so it's really being able to tailor it because there are C15 tests. We can now tailor our dosing to, to our level.
- [60:05]
Amitai
Got it. And, and speaking about tailoring and customization, are there any known adverse effects or drug interactions, um, like who, if anyone, should be cautious about taking C50?
- [60:19]
Stephanie
Well, we haven't seen any signs of negative effects. I think it's more of amitay, the diminishing returns. So. And this is based upon extensive clinical, extensive safety studies. It was included in NIH's Tox 21 program in which they ran it through 450 safety tests and it passed all of them. We did our own safety. It is generally recognized as safe. We went through that, you know, FDA process us to ensure that it's a safe molecule. And the two clinical trials showed there were reports of side effects that were equal in both the placebo and the C15 side. So safe to take. We haven't seen. Everybody is different. We always include that as a caveat. And so just making sure that, you know, as you take it, you're in ongoing communication with your healthcare team and just being able to mostly for the most part, pick up the benefits that are coming.
- [61:25]
Amitai
This is awesome. I love this conversation and this ingredient. I have another, like, one more question, which is more, I would say, application wise, you spoke about bioavailability. Is there anything that we can do to ensure the active ingredient, the C15, is absorbed optimally or like other co factors like other fats or fat soluble vitamins that improve its uptake or. No.
- [61:58]
Stephanie
Yeah, it's, it's a great question. At first we were saying no, but as we're starting to learn more, especially with. Okay, so if you, if, if you eat C15 at the same time you eat a hamburger, you know, if you take your C15 supplement at the same time you eat a hamburger, that actually might work against you. Right? Because again, because, and then again these are rodent studies. But if I were to hedge, what I do in the morning is I have my supplement, I take fatty 15 with my coffee in the morning and get to enjoy its benefits throughout the day. But obviously it's long term benefits. So we may be, we really need to do the studies to say if, is that the same in people? But if you eat a high fat diet, it's not that you can't, you won't benefit from the supplement, it's just maybe not taking it when you eat that high fat meal.
- [62:47]
Amitai
Last is skin health and interaction with other ingredients should people want to improve people who want to improve their, their skin combine fatty 15. Are there evidence to any combination with other supplements like certain vitamins or collagen or topical regimen that have synergistic effects?
- [63:08]
Stephanie
That work is currently underway.
- [63:12]
Amitai
So we'll.
- [63:13]
Stephanie
Just need to have another, another chat I guess.
- [63:17]
Amitai
Done. Okay, fantastic. Steph, continue doing what you're doing and we will make sure that we support in any way we can. We love what you're doing and we don't kind of play the game a little bit of like hey, here's our coupon code and do that. But if someone wants to get a product, is there a kind of an offer that is available for like maybe first time users or something like that? I know I get the refills which is pretty cool. But is there an offer, something that people can do?
- [63:52]
Stephanie
There is, there's that if you go on to fatty15.com and you sign on for the 90 day starter kit with subscription, it's an extra 20% off. It is super easy to cancel. So if you don't, it's not one of those like oh man, I got it and now I can't get out. Like we actually have a very high retention rate and it's not because it's, it's difficult to cancel because people are feeling better. And then I do have to plug that for the buzz. Like if you want to read it like it's, it was, it's really been an amazing adventure on the day. You know, 20 years in the making of the Longevity nutrient and that is by Simon and Schuster and available wherever books are sold.
- [64:32]
Amitai
Amazing. So also like Amazon and online.
- [64:35]
Stephanie
Yeah, it's everywhere. So we're real excited. Just finished recording the audiobook.
- [64:41]
Amitai
Who is narrating the audiobook? Oh my God. So if you love the voice of.
- [64:47]
Stephanie
This sounding so great. It's so great today but you know I'm sure they are able to bring it down. Nice. And Roman sex.
- [64:58]
Amitai
Amazing again Steph, thank you so much. We will make sure that we have the links in the description. Stay tuned for the newsletter associated. We're going to talk more about the book and where people can get it which is everywhere. And yeah, you are awesome. Thank you so much Steph.
- [65:21]
Stephanie
Great. Thanks Amitay. Always a pleasure.
- [65:23]
Amitai
Thank you everyone. Bye.