Increase C15: SHOCKING New Cause Of Insulin Resistance (Not Carbs)

People with higher C-15 levels have lower risk of developing type 2 diabetes, heart disease, fatty liver disease, and not just in single studies but meta-analyses. There's no other molecule that has stronger support as being a longevity-enhancing molecule than C-15, even above rapamycin. Dr. Stephanie Ven Watson is a leading expert in C-15, a saturated fatty acid that is vital for health. She has found the link between C15 deficiency and insulin resistance, and there's an easy fix.

What can people feel in the body that might indicate C-15 deficiency? Understand that it's accelerated aging. Think about fatigue, joint pain, poor sleep. That's what a C-15 deficiency is doing. It's really going to get picked up when you go to your doctors and you get a test; your hemoglobin may be declining, your ferritin may be increased. You then may see the downstream effects then of type 2 diabetes, heart disease; signs of insulin resistance.

Can you get enough C15 from the diet? You cannot be deficient. The average is 0.2%, and just because that is the normal, that's not healthy. Dairy fat is such a reliable source of our C-15. Reena, that how much C-15 we have tells you how much dairy fat you ate. Cows that are fed grass have twice as much C15 than cows that are fed corn, and just 1 to 2 tablespoons of butter can get you that 100 to 200 mg of C15 per day.

This episode features Dr. Stephanie Ven Watson, and we're talking about the new cause of insulin resistance, and it's got nothing to do with sugar or carbohydrates. Now, if you're learning from enjoying these free episodes, please hit the subscribe button, because we know that real food is medicine, and by the simple act of subscribing you can help share the message to millions more people that need to hear the truth. And now for the episode with Dr. Stephanie Van Watson.

Dr. Van Watson, welcome.

That was wonderful to be here, Reena. If someone is just watching this, most likely they have insulin resistance and at least one chronic disease, and we're told that just comes from sugar, but that is not entirely the case. You see, there is one newly discovered cause of insulin resistance that doesn't come from sugar. So today, Dr. Ven Watson is going to share this new research and the one deficiency that is causing insulin resistance and chronic disease. We're going to talk about how to naturally fix it and why you need to eat more butter and pecorino. So Dr. Ben Watson, my first question: what is this newly discovered cause of insulin resistance?

Right, so it's uh, C-15, or what we're going to talk about, lack of C15, uh, nutritional deficiency—the first nutritional deficiency, Reena, discovered in over 75 years. So we'll talk about how that's happened, and um, you know, also be able to talk about how dolphins helped, you know, get us there and a shared evolutionary driver for insulin resistance between both dolphins and humans.

Absolutely. I think people will be thinking, "What is C-15? What is C15 deficiency?" Um, firstly, it doesn't just affect or cause insulin resistance; this deficiency also causes every other chronic disease that people are facing. Can you explain those and what is that connection?

Yeah, absolutely. So C15 is an odd-chain saturated fatty acid—yes, saturated fat—uh, that's present in butter. Uh, our primary source of C15 is from whole dairy fat, and uh, we—it has uh, now recognized as the first essential fatty acid to be discovered in over 90 years, and so we put that stake in the ground uh, back in 2020 uh, in Nature Scientific Reports. And since then, Reena, there have been four independent studies that have been done by other three other teams, and they have come up with the same conclusion, even using gold-standard studies of that originally um, defined the first two essential fatty acids, one which was an omega-3 and omega-6. So wonderful to get that validation. So C15's primary role is—it does a lot of things which we'll cover—but one of its primary roles is it's a stable fatty acid that has no double bonds, so it is not susceptible to attack by oxygen and lipid peroxidation. So it's stable; it goes into our cell membranes; it stabilizes our cells against aging, age-driving lipid peroxidation. So it's a really simple mechanism, and what we've learned and we published in Metabolites last year is if we don't have enough C-15 in our cell membranes, they become fragile, and that's where uh, it's tied into an entirely new form of cell death called ferroptosis, which was discovered by Columbia University uh, scientists back in 2012, where they published this paper, Reena, of an entirely new way that our cells were dying, which is a really big deal because like in cell biology class, right, we learned there's apoptosis, necrosis, and autophagy, and those are the three ways that our cells die. So they discovered a fourth, and it was very specific; it's where cell membranes, the fatty acids in them become fragile; it increases lipid peroxidation; that lipid peroxidation combines with iron that is in the cell that shouldn't be there, and when you combine lipid peroxidation with iron, you get massive reactive um, oxygen species; takes out the mitochondria; kills the cell. So since that paper was published, 10,000 papers have been published on ferroptosis showing that it accelerates aging, accelerates the onset of type two diabetes, heart disease, fatty liver disease—all these, a lot of these conditions, you know, that we're talking about, cognitive health, all of these things—and but nobody understood why ferroptosis showed up in the first place, and that's where we learned that and have shown that deficiencies in C-15 in our diet are now causing the cellular fragility syndrome, causing ferroptosis and all the downstream complications.

The good news is with nutritional deficiencies is—right, they're fixable.

Absolutely. I want to talk more about this process in detail, because even when I was researching it, you know, I really understand the sugar and carbohydrates hypothesis regarding insulin resistance, and I feel that my audience really understands that, and that still stands true. So with regards to sugars and carbs, yes, a lot of carbohydrates, processed foods, and sugars does still lead to insulin resistance. What we're saying here is this is another possible mechanism towards insulin resistance and disease. Would you concur with that?

Yeah, I concur with that, and what's um, what has been helpful with regard to providing insight into insulin resistance not driven by carbs—again restating what you just said, Reena, which is yes, carbs can cause insulin resistance; there's another way—and the way that we know this is because it came from dolphins, right? That we understand that in while studying and uh, continually improving the health of dolphins who have no carbs in in their diets, we were seeing about one in three older dolphins developing insulin resistance, fatty liver disease, iron overload, and this, you know, syndrome with ferroptosis, and obviously it didn't have to do in this case with this phenotype with uh, sugar; it had to do with C-15 deficiencies.

Absolutely. And that's how you—well, not you, but this whole discovery of C-15 and the deficiency in C-15 actually occurred. Let's dive into that story. So you are—your background is a veterinarian epidemiologist. What does that mean exactly?

So I'm a veterinarian, uh, so got check that box, and then but I went—I became a veterinarian, Reena, in or to be a veterinary epidemiologist, which is uh, you know, a veterinarian who tracks diseases and looks for patterns of diseases in populations to understand risk factors and most importantly protective factors against diseases. So um, I was originally, you know, working with a CDC and World Health Organization—like 20 years ago—was recruited by the Navy um, and good on them for looking for veterinary epidemiologists to continually improve the health and welfare of a growing population that they had of aging Navy dolphins. Um, the if you look at dolphins in the wild, they have um, they live to about 20; the Navy has cared for this population of about a hundred bottlenose dolphins for over 60 years; they're now living into their 40s, 50s, and even to 60 years old. So they had this growing population of older, geriatric dolphins. Over a period of 10 years, we published a series of papers showing that about one in three of these dolphins were developing insulin resistance, fatty liver disease, um, iron overload, ferroptosis. So that really gave us this unique opportunity um, with, you know, the pure intent to help the dolphins understand, you know, healthy aging in dolphins, but then it had a spin-out benefit to humans too. So we use this advanced form um, advanced technology called metabolomics, and we were able to very easily, because this is such a clean population, right, from a compared to humans um, because all they eat are fish and they have the same environment, same health care; they don't drink, they don't smoke—you know, a very stable population—we were able to use metabolomics to study thousands of small molecules present in their archived serum, but as well as their all-fish diet to see which small molecules predicted the healthy aging dolphins. We thought it'd be omega-3s 'cause all they eat are fish, but instead we were completely surprised uh, by the fact that it was C15 was the top predictor of healthy aging dolphins who did not have insulin resistance. And then, you know, add on top of that, like we shared, this was a saturated fatty acid.

So what you're saying is that um, in studying these dolphins, looking at the levels of C-15, when they were not elevated but in normal ranges—and we'll talk about the ranges that are normal and good ranges—when they were high um, in the presence of everything else controlled—a good diet, obviously they eat fatty fish, don't drink alcohol, etc., etc.—they lived the longest, to age 40s or 50s, which for dolphins is quite long—equivalent to a human living for 90 to 100.

Yeah, that's a great—that's a great equivalent. Okay, and I just want to make this connection between dolphins, 'cause people might be thinking, "Well, who cares about dolphins? How does that relate to humans?" They are mammalian species, warm-blooded species. How is that connected or relevant to humans, and how can we make that connection of C-15 in dolphins to, oh, C15 and humans?

Right. So there's—it ends up there's a lot of uh, common ground between dolphins and humans. We are not just mammals, which is a really important as you pointed out, but we're also long-lived, large-brain mammals, right? And so we have co-evolved to develop the same mechanisms to ensure a long lifespan um, and so but what's come with that is the burden of—as you're allowed to get older beyond the—the opening—to be able to develop these chronic aging-associated conditions. So that's where we started seeing—when we started seeing one in three older dolphins getting things like chronic inflammation, high cholesterol, insulin resistance, fatty liver disease, even changes in the brain consistent with Alzheimer's disease, Reena; this was mind-blowing to human health experts who are like, "What do you mean dolphins are getting fatty liver disease? This is a—this is a disease that's purely from from sugar, right?" And and they're like, "How is this happening?" So it's really that started opening up the parallels. We know like if you look at things like human chromosome 1 uh, that is uh, you know, an important chromosome that has a lot of genes related to chronic diseases, or we—or we can flip it and to say health over time. Very few species have the exact same—what's called synteny—the exact same type of order of genes as human chromosome 1. It's humans, bottlenose dolphins, the two-toed sloth, and gorillas—so of all species. So it's this conservation of genetics of long-lived um, of certain long-lived, slowly evolving species that explain things. We also have shared glucose-carrying mechanisms. So all other mammals aside from cetaceans and primates are able to rapidly um, move glucose using red blood cells as infants, but they lose it as adults. Only cetaceans, which include dolphins, and primates, including humans, continue to have that capability as we get older, and that's because we have big brains that require glucose demand. So all—when you start kind of put looking at these pieces and parts, it starts explaining why it's really actually a very special connection between dolphins and humans. The last is uh, under the carnivore hypothesis, where we showed—were able to demonstrate that dolphins um, appear to have developed insulin resistance in part as a way to uh, evolve that when they were—they were land mammals that ate carbs; they moved back into the ocean about 30 million years ago and then moved to an all uh, you know, into a carnivore diet, and when they did that and now they had these big brains that needed glucose, so when they did that they actually developed insulin resistance as a means to have their liver generate more glucose to support that glucose demand. So it was a healthy evolution. The carnivore hypothesis is that the same thing happened in humans when we moved from—during the ice ages—when everything with carbs froze, right? And we moved to an all-meat diet, and in that point we developed insulin resistance again for a way to be able to provide glucose to our brain. The problem is when um, you know, the plants grew back, the ice melted, the plants grew back, and then we went to all kind of crazy town on the carbs, and it really fed into insulin resistance to then becoming a disease state. So a lot of these really special connections between the two.

I think it's good to understand the um, epidemiology of, I guess, species, because there's so much controversy around what is the right diet, but it appears to be that a meat-heavy diet with a good saturated fats seems to be very, very important, and how this deficiency in C15 in humans has occurred is the changes in the dietary guidelines, which is less whole dairy fat, less saturated fat. Can you speak more about that?

Yeah, absolutely. So um, at the same time um, that we started seeing this deficiency show up in dolphins—and this happened because uh, the dolphins for a long time had been eating eulachon, which were really fatty fish; they're so fatty that if you dry the eulachon uh, and stick a wick in it, you can—it's a candle; they were called candlefish; they had so much fat in the marina—the eulachon died out. So around the 1990s, that's when the Navy dolphins moved to lower-fat fish um, and as a result—by accident, right—moved to a lower C-15 diet, where we started then seeing the syndrome kick in. With regard to some dolphins who were eating much lower C-15 fish compared to others, at the same time as you had shared, we started taking whole-fat milk out of our diet, and not only as adults, but then in the 1990s, because that was in the like 1977—Congress, Congress, right?—released recommendations saying all Americans—not just men who are at risk of heart disease, but all Americans—shall decrease their intake of butter and whole-fat milk with the intent of lowering the risk of type two diabetes and heart disease. Um, then in the 1990s, it was double down, right? So you had uh, pediatric groups saying, "Hey, as soon as a child turns 2 years old, they need to come off whole-fat milk and move to low-fat milk, regardless of the health status of that child." And then they double down again to say if a child was at risk—in a family way—of obesity or type two diabetes, then they should never have exposure to whole-fat milk um, even as a 1-to-2-year-old. So that we had these kind of co-occurring—dolphins and humans getting C15-deficient diets—and then we watch over the decades things like fatty liver disease show up, you know, non-alcoholic fatty liver disease or NASH—that is now called—didn't—you know, the first 30 cases were reported in uh, humans by Mayo Clinic in 1980; today one in three people have this condition. We were seeing the same thing happening in the dolphins, and we now know that for the dolphins and now um, in humans, stronger and stronger evidence showing that C-15 deficiencies are at least a driver of at least a specific phenotype of fatty liver disease in humans.

It's incredible; when you lower what is actually needed in a human body, you can develop so many different diseases, whilst increasing ultra-processed food. So obviously we're going to have a population of sick and obese people, which is what we have today.

I want to talk about the cells and the cell membrane, so people can understand where C15, a saturated fatty acid, fits in the cell membrane and why that's important for body function, hormones, and health. So my question for you: let's explain cell membranes and the phospholipids and where C15 fits in.

Absolutely. So uh, our cell membrane—our cells are protected by an armor, which is the cell membrane. The cell membrane is made up of what's called a bilayer—so two layers of fats and fatty acids—probably a lot of us from thinking back to our cell biology class and the drawings. And so what's really important about the cell membrane is based upon the fatty acids that are present in the cell membrane helps to dictate not only how well does it protect the cell, but it also plays a role in cellular signaling; it also and how it communicates with our body and keeps it balanced; it also helps with what comes into the cell and what makes it out of the cell. So the cell membrane is really important, and what's um, you know, we've learned a lot about in the last 10, 20 years is that we literally are what we eat uh, as far as when our cell—when it comes to our cell membranes; the fats that we eat in our diet make it directly uh, are directly translated into the fatty composition that we have in our cell membranes. So if you eat a lot of stable fatty acids like saturated fats, your cell membrane is going to be more stable; if you eat more polyunsaturated fatty acids, which have double bonds and uh, which is why they're oils at room temperature and susceptible to attack by oxygen, you're going to have more fragile cell membranes. So and this is fixable—that you know, within 3 to 6 months based upon your diet, you can completely change the structure of your cell membranes and then how whether or not they're going to be good or bad for you. So conversely, if someone does um, a normal fat diet to a low-fat diet, how quickly do their cell membranes change?

Yeah, so probably—I mean, to be fair, like different cells have turnovers at different times, but on average within 3 to 6 months, Reena, you'll have most bodies, most cells throughout your body will have undergone that change. So when it comes to the C-15, it's a saturated fatty acid, so as you mentioned, in the cell membrane that is important for structure and integrity, so it's very stable as opposed to polyunsaturated fats, which includes omega-3s and omega-6s. Because people hear about omega-3s, they're like, "Well, I take a fish oil; that's probably good enough." Do you think that's a good enough?

Well, no, I think, you know, so I know—surprise, surprise—so I think we're—you know, we're continuing to learn; we're—we're getting so much smarter about fats, right? So we thought all fats were bad. Well, back in the 1920s, it wasn't believed that fats actually did anything but add calories, right? And then they realize, oh, there are—they're active, but there are good ones and bad ones, and the good ones are the unsaturated fats, and the bad ones are the saturated fats. And then we get to the omega-3s versus omega-6s, and the 3s are good and the 6s are bad, right? Again, kind of over-categorizing. And then with saturated fats, we were saying that they're all bad. We now know that some um, that not all saturated fats are created equal—that these odd-chain ones, the ones with an odd number of carbons—C15, C17, and really C-15 as Goldilocks odd-chain saturated fatty acid is the one that meets the criteria of essentiality, right? This first essential fatty acid to be discovered in over 90 years. So it—it plays this role, but it's almost like saying we—we discovered vitamin E, but we wouldn't say don't take vitamin A, right? So so it's about that we need the—all of these different fatty acids, but it needs to be in the right balance so that our cells can still be flexible, thanks to the—the unsaturated fatty acids and polys like omega-3, but it can also have resilience and stability by having that C-15.

As Dr. Watson mentions, all the fatty acids, including saturated fat, is so important for our health, and later in the episode we'll talk about how to naturally increase your C-15 levels from whole food fats. But as you can imagine, the way that our food is produced with chemicals and pesticides, this can really limit the absorption of nutrients into our cells. So to support my health, I have been using a whole-food supplement called Armor Colostrum, and this only has one ingredient. Since using Armor Colostrum, I've noticed so many benefits, especially with my skin, as colostrum has growth factors that stimulate collagen production and skin elasticity. And with all the clearer skin I'm seeing, it really makes sense because colostrum is the first milk that mammals produce after giving birth that has all the vital nutrients that we need to thrive. And Armor Colostrum is a nutrient powerhouse with over 400 bioactive nutrients in every serving, and most importantly, Armor Colostrum only uses grass-fed colostrum in its most bioavailable form, and it's 100% carnivore. And I use four full scoops of the unflavored Armor Colostrum per day in chilled water. So if you'd like to try Armor Colostrum, just head to tryarmorra.com/theprimalpodcast or just use code theprimalpodcast to get 15% off your first order. I've also linked them in the description down below. And thank you to Armor Colostrum for sponsoring this episode.

So now we understand the importance of C15 in the cell membranes in terms of structure and stability; let's move on to ferrapto—ferroptosis—so cell death and then disease. So how is that connected to a C15 deficiency?

So what we now know is that we need a certain amount of—specific amount of—C15 in our cell membranes in order to avoid ferroptosis, and um, in general, that's greater than 0.2% of fatty acids in that cell membrane needs to be C15. So it's not like 20% of the cell membrane; it's like they're these little bricks in the cell, you know, in—in our cell membrane, and we need just enough of them in there to avoid deficiency and falling apart. There is evidence that if we can double or even triple that amount—to to point 4 or 6—that it can further support heart health. And like, for example, the Sardinians in the high-longevity zone, they have levels that are 0.4-0.6% um, because of their diet; they also have a lower risk of dying from heart disease. A separate study showed that these higher levels of C-15 are protective against uh, development of of heart disease. So we're seeing that there are these optimal levels, and but we also want—we just want to start with like, let's not be deficient. So when we talk about ferroptosis, what happens is we have low C-15 levels, and our cells become more fragile; this includes our red blood cells, so our red blood cells become more fragile, and we have cells inside of our liver called Kupffer cells, and the job of the Kupffer cells is to basically take out any weak red blood cells that are in our system and they recycle the iron, and that's great. The problem is when we have lots of fragile red blood cells, the Kupffer cells then work overtime, and they're engulfing all of these red blood cells; what's left behind is of the corpses of these red blood cells is iron. So now we have iron overload in the liver that again is accumulating over time—like we're talking about over a decade—what patients will see or what doctors will see in patients is called hyperferritinemia—so high levels of ferritin in the blood; often gets interpreted as inflammation, which it is—that it's that too—but it's also a key measurement of too much iron in the tissues. So you have iron overload now in the liver, paired with lipid peroxidation—rate of weak red—weak cells, including the liver cells. So you have that lipid peroxidation paired with the iron, and then that then kicks off—kicks off ferroptosis in the liver. And so this is—this phenotype is a liver-centric, really red blood cell first, liver-centric disease that then progresses to the iron um, and reactive oxygen species and lipid peroxidation spill over systemically, and it seeds our brain, our pancreas, our heart, and you know, our different organs. And if you go and you do a Google search for iron overload, um, this is where you understand that just in last year alone was the highest number of papers ever published on iron overload um, because it's really come to be understood as a problem—all getting back to this core uh, base issue—and that's where the insulin resistance comes in is really it's a later-stage component of impacting the liver but also the pancreas um, with regard to impairing glucose metabolism.

I think it sounds complicated, but I think it just highlights that there's multiple ways that we can get diseased when we overeat poor nutrients or if we have a deficiency in something. So, just to summarize, we have cell membranes, and in that you have C-15. If they become fragile, meaning that you don't have enough C-15, that leads to more heme iron because I think it's the heme iron. So you have hem in your hemoglobin red blood cells. Um, the first site is the liver, uh, because that's where things get recycled, and then you just have more heme iron left over building up that becomes toxic, that becomes problematic, and then that feeds into your pancreas potentially, and that can elevate hormones like insulin, causing insulin resistance. It to feed to your eyes, your heart, your legs, everywhere, causing disease. Is that the correct pathway? Am I getting that right, man?

Rita, put that in a can, and you're done. Yeah, well, because if you say ferroptosis, it sounds so complicated, and when I was researching this, I think people just want to understand plain and simple what does this mean? Like, okay, I understand the sugars and the carbs, but if I have a C15 deficiency, how is that leading to a problem that I'm feeling, which is called insulin resistance? How then does that lead to fatty liver disease as well? Yeah, so, so that's exactly the same problem, right? So that we're basically wreaking havoc in the liver, um, and so you know, there are studies that have shown, for example, Dr. Jeff Schwimmer, when he first read our paper, um, in 2012, coincidentally the same year, right, that the ferroptosis paper was published, and we just didn't know that there was a name for it when we published, um, fatty liver disease and iron overload in the liver in dolphins. Jeff Schwimmer, who is a leader in pediatric fatty liver disease, he opened the first fatty liver disease clinic for kids in the world, and so Jeff reached out and he's like, "I don't think you're calling it fatty liver disease, but I don't think it's what we're seeing in humans. Send me some slides." So we sent him a bunch of liver slides from dolphins, and I'll never forget he sent an email and he said, "We are a go." He's like, "This is the exact same disease under the microscope that we're seeing in humans. What the heck is going on?" Because they don't eat carbs. So Jeff then did a follow-on study in which he looked at over, he included over 300 kids with fatty liver or 300 kids and measured the amount of fat in their liver, and he showed that the higher their C-15 levels, the lower their uh liver fat. So he's like, okay, which we're seeing that same association you saw in dolphins, and then he followed up with a clinical trial using C-15 supplementation in young adults with a history of fatty liver disease and elevated liver enzymes, and he showed that the participants that reliably took uh C-15, because they're 18 to 24 year olds, uh, that reliably took the C-15 supplement, uh, had raised C-15 levels, and if they got above that threshold, right, for deficiency, they had lower liver enzymes. So all, you know, these components that we keep pointing to, and we've it's been, you know, already demonstrated directly in in um in animal models of fatty liver disease and in masold that restoring C or getting C-15 back into the system reverses, stops iron, it stabilizes the red blood cells, it stops iron deposition in the liver, it decreases fibrosis, all in models of fatty liver disease. So a key component, I'm left a little bit with the question of how does it cause, how does C15 deficiency cause excessive fat in the liver, which is what Jeff showed. I think it's, it plays a role, but I think more so it's if there's fat in the liver, and then you have a deficiency in C-15, it's just like throwing like a flame of a match onto, you know, dry kindle, and as you have all these lipids in the liver just waiting, and then you add the iron onto it, and you add lipid peroxidation, and it's just these livers are just prime for, you know, rapid damage.

I would say it's very similar to what you said with the dolphin studies that, you know, they are very a well-controlled species that they're not having other like tobacco, alcohol, ultra-processed foods, but when you introduce humans, and that's why you can't really do a dietary experiment because they're probably having carbohydrates or other sugars on top of that C15 deficiency, and perhaps that's why it shows um fat in the liver not coming from saturated fat, the fat in the liver, but sugar and carbohydrates. Because people might be thinking, well, fat in the liver, that's coming from fat, shouldn't need butter. No, no, no. Okay, let's talk about some signs and symptoms of C15 deficiency. First of all, what can people feel and see in the body that might indicate C-15 deficiency?

Yeah, so it's these are broad effects, so it's there's no single thing where it's like, oh, you feel this, you're C-15 deficient. The good thing is C-15 has been measured, um, has been routinely measured in humans and animals for decades. So C15 actually has been traditionally used as a biomarker of how much dairy fat people ate. So they didn't know that it was an active fatty acid, but it's such dairy fat is such a reliable source of our C-15, Reena, that how much C-15 we have absent of supplementation tells you how much dairy fat you ate. So the good thing is that there is a reliable test for C-15. So that would be as far as understanding what your C-15 levels are, that's accessible. What do you feel? So if you think about when we talked about ferroptosis, right, it's really accelerated aging of ourselves. So, um, what, you know, Jeff is showing, um, is that kids are aging faster, right, or that people with C-15 deficiencies are aging faster, which means like, so what he's seeing is that the kids are developing diseases of their grandparents before their parents. So, so when we understand that it's accelerated aging, so you think about fatigue and joint pain and poor sleep, and it's like imagine like you're fast-forwarding where your body is going to be 30 or 40 years from now, and that's what a C15 deficiency is doing. In most cases, it may be poor sleep, it may be, um, you know, fatigue, things like that, but it's really going to get picked up when you go to your doctors and you get a test. Your hemoglobin may be declining over time, your ferritin, like I said, may be increased because it's showing the increased deposition of iron in your tissues, um, you then may see the downstream effects, right, then of type 2 diabetes, heart disease, fatty liver disease, so elevated liver enzymes, signs of, um, insulin resistance, um, and then, you know, kind of again all these other key components that are more of secondary to the primary problem.

Interesting, because I was thinking about the symptoms and looking at it, and it's very much like any other chronic disease, so you wouldn't actually know by just relevant symptoms, but you did say in terms of the signs. So, so if you look at your blood work and your red blood cells, you mentioned the width of the red blood cells varies, is that correct?

Yeah, this is so this is this uh measurement that's called red blood cell distribution width or RDW, and it doesn't sound like a very sexy uh like exciting test, but it has truly emerged as a very relevant measurement of our biological aging, um, so lots of papers not having anything to do with us have shown that the higher the red blood cell distribution width, which what that means is it's really a measurement of the variability in size of red blood cells, and what that's telling you in the case of C-15 deficiency and ferroptosis is that our red blood cells are dying too early, which means that we have to keep producing new red blood cells to make up for those that have. So then you've got new red blood cells, older red blood cells, and so you have a lot of variation in red blood cell size. So that RDW measurement, the higher it is, is a measurement of a faster biological aging rate, and so what's fascinating is with C-15, right, it it stabilizes, it decreases red blood cell distribution width because it's stabilizing the red blood cells. So, and then extrapolating that, right, then that would be a measurement of slower biological aging. There was a in an independent study looking at epigenetic aging showing that the more C-15 people had on their lipids, C-15 tails, the those people were the higher they had of that the um younger their, sorry, let me re-restate that, that among people who had higher C-15 in their lipids had a younger biological age than their chronological age. So we're seeing kind of again looking at things from multiple angles supporting that C-15 really is meant to be there, um, to help support longer, you know, to help our health to stay healthy for as long as possible.

I'm so curious what is my C-15 levels. So you mentioned there's a test now. Can you just go get your blood work done and just ask for C-15? I'm sure that they're going to say, "What is that?" No, how can you get a test done?

So most physicians can get a fatty acid panel. So when you ask for a fatty acid panel, they'll say, "Yes, I have that." Then you have a second question for them is, "Does that fatty acid panel include C-15?" And chances are, Reena, exactly to your point, they're going to be like, "I have no idea." And so they'll go back and check, and if it includes C-15, that's uh the way you can do it. We did partner with Gova Diagnostics to develop an at-home blood spot test, um, that is their test, uh, I I used it, um, and was able to show I have C-15 levels of 46, which is all right, Sardinia, the longevity zone, which is great, um, and that provides that test provides both, um, percent as well as concentration, the total amount, which is which is really nice.

Okay, I need to get that test done. Is that is that only in the US because I'm in Australia right now?

You know, I think if you have GOVA in Australia, because I know they have multiple countries, then they would probably be able to get you that blood spot test, but you can also again go to your, you know, vet doctors. Most doctors now have access to a fatty acid panel. It was interesting, we were talking with, you know, Dr. Mark Hyman, um, and he's been following our story for a while, and and he's like, "Oh my gosh, I I actually think I've been measuring C-15 in my patients this whole like for like a decade." And so he went back and he's like, "Oh my gosh." He was he was shocked at how many people of his patients are low in C-15. So and that's even based upon a test where the average is 0.2%, and just because people that is the normal, right, today we're that's not healthy, like that you're right at that edge of fragility syndrome because as a whole population, right, we've decreased our intake of all saturated fats, and so now this lower level of 0.2 versus wanting to get point four to point six, this lower level is actually normal, it makes sense. So, so 2% is, so that's what you might see on the test, 2 or 0.4, 0.6. So 2 is the minimum you want, 4 to point or 6 is there a higher level or too much C-15 that is too toxic?

We haven't seen any toxicity. I think it's just, I think it might be diminishing returns over time. So we always encourage people with regard to the supplement of just take one capsule a day, which is 100 milligrams, and see what it does for you, and in most cases, you know, our customers that we have, 50% of our customers report feeling benefits within two weeks, 72% within 16 weeks, and then but if you aren't feeling benefits, then they might take two capsules, but we're we're big fans of just take the minimum amount that you need to be able to achieve your personal goals, um, and and and then we're just going to continue to learn more about, um, you know, about what may be, let's not be deficient, and then the gains from optimal levels, which again seem to be more of a Sardinian level of that at least is is circling around improved heart health. Okay, so two things there, we're not trying to sell a supplement, but you do have Fatty15, which is incredible. We're going to talk about some whole food sources of C15, but some people might be thinking, oh, you know, we're just trying to sell a supplement or mentioning that no, this is very, very important as an essential saturated fatty acid that if you cannot get it from whole food forms, potentially a supplement might be beneficial, and you've seen incredible results, which we can talk about. Fatty15. Let's talk about sources of C15 that people can actually just do it. Can you get enough C-15 from the diet first of all?

You cannot be deficient uh with dietary sources. So, so no, no, but that's good, Reena, this is really, really, really because like this is a really, really important point, right? Because what we're seeing is increased chronic diseases, especially among people born since the 1990s, right, and that we, you know, the hypothesis is that C-15 deficiencies are what's, you know, a component of what's driving that. So that's terrible, like, so let's fix that. So we need to get, and that happened because we took we're taking these whole-fat dairy products out of our lives. So there's a reason, there's a fix for that, which is putting them back into our lives, right? And so yeah, and especially for kids, especially for kids. And the other part is that as Sardinians, they're not supplementing, right? So the big thing is what are they doing? So let's talk about whole uh full-fat dairy. Um, this is not the dairy that you just go to your local supermarket and get because let's say, for example, milk, whole-fat dairy is that good to increase your C-15? Um, it so we're learning it depends on what the cow ate. So, so chances are, no matter what type it is, if it's whole-fat milk, the there will be C15 in it. So it's not that it won't have C15, will it have what it used to have, you know, back in the day? Um, to your point, Reena, it's we now know that cows that are fed grass have twice as much C-15 in their milk fat than cows that are fed corn. So grass-fed, if you know that it's a grass-fed, um, product, um, butter is a great source of grass butter from grass-fed animals is a really good source of C-15, um, and just one to two tablespoons of uh or two tablespoons of butter can get you that 100 to 200 milligrams of C-15 per day. So it's not a lot, we don't need a lot, um, and as long as we know and what we're trying to push for for the industry is to report how much C-15 is in your product because I'm going to go buy the product that has the highest C-15 in it, and I think what we'll probably be working on or what where the world will evolve is kind of like the omega-3 to omega-6 ratio that there may be like a C15 to C16 ratio and really finding kind of optimal ratios, um, based upon different foods. What's C16? Is that like the antagonist or the complimentary part of C-15?

It's so C16 is it's a saturated fat, but it's an even-chain saturated fat, and so when you look at different cell-based studies or animal studies that pure C16 can actually induce disease states. So it can be pro-inflammatory, it can induce insulin um resistance. C15 does the opposite. I mean, it's just amazing, um, what nature, how specific nature gets with fats that C-15 is anti-inflammatory and C15 activates AMPK and AKT, which help improve insulin sensitivity and glucose handling. So I think it may be we're going to kind of see that parallel, um, that we're seeing in the omega world with the saturated fat world.

Interesting. Okay, so getting back to the sources, one to, so two tablespoons of butter can actually increase your C15 so that you're not C15 deficient. Grass-fed butter, grass-fed butter, uh, and then in Sardinia, a really good lesson is that uh they um have so they are heavy cheese eaters, um, and their cheese comes from local goats and sheep that feed on grasses, and in this high longevity zone in Sardinia, it's high altitude. So there have even been studies, repeated studies showing that sheep and goat and cows, goats and cows that eat high-altitude grass have even more C-15 in it. So the Sardinians in this high longevity zone are kind of in this sweet spot where it's high-altitude grass, it's local uh ca cows and sheep that are feeding off of that grass, and then they create the they make their cheeses. One of them is called Pecorino, and so Pecorino has um some of the highest C-15 levels among dairy products. So they just had the right conditions to be able to get their C-15 levels uh, you know, at this really great point 4 to point 6 level. So cheeses is another good thing, and then another component, um, is fiber. So it's interesting that fiber, um, has been shown to feed microbes within our gut, and our microbes use inulin within that fiber to actually make C-15. So microbes in our gut, it's not enough alone to get us up and over from being deficient, but we'll take everything we can get, right? So that's another source, and then there's another study showing that exercising increases our C-15 levels, and the understanding from that is it's helping to release C-15 that might be stored uh in our tissues and in our fat. When we exercise, we release C-15 to be able to put it into circulation and work. So those are multiple ways that we can increase our C15.

I'm so glad that you said the Pecorino. I love Pecorino, it's delicious. I follow a high-fat ketogenic carnivore diet. So, so it's so interesting everything that you're saying is so aligned. So all the foods that we're going to go through is so aligned with that lifestyle, maybe not so much the strict carnivore, but definitely a ketogenic higher-fat approach. Just to mention about the fiber because some people are pro-fiber, uh, some people are against fiber. You're talking about, um, a prebiotic fiber, which is inulin, is that correct?

Yeah, it would be the the studies that were done, um, were with mice. I believe they were mice, and they showed that when they gave mice fiber, and I can't remember, Reena, the source of the fiber, that their fatty liver disease got better, um, so then they kept, they did a reductionist approach. So they said, "Okay, what within fiber was actually attributing the benefit?" And it was inulin, not insulin, but inulin. So they're like, "Okay, inulin." So then how is inulin helping? And then they found out, oh, inulin feeds specific types of bacteria in the gut, okay, and then those bacteria produce C-15, and then in the end, it was C-15 that then led to the benefit. So hopefully that helps with some understanding of that of fiber's role. It makes sense. It's just some people are like yes to fiber, some people are no to fiber, but it's just that inul, the inulin piece, which promotes some sort of C-15 production, and that's where that one is. So getting back to the sources, so whole milk is fantastic, but it has small amounts of C-15, and you have to balance that with the negative, not negative, but I guess the sugars and all the other things in milk, is that correct?

That's correct. Yeah, I mean, it's when you look at milk fat, whether it's whole-fat milk or butter, only 1% of the fats in milk fat are C-15. So you got a lot of other stuff going on, you know, um, that and and so again it's it's, and that was a that was a reason for the Navy funded us to develop the supplement was kind of like, can we get better control over over this? But this is the supplement is really intended, Rea, to a point that you're always really good at getting to, it's meant to be part of a solution to a global problem, right? It is not the solution. It's saying, how do we look at industry practices? How do we push for, you know, more grass-fed, um, you know, dairy products, whole dairy products? How do we get dairy products to report how much C-15 they have in them? So it's like it's it's meant to be part of a of a larger ecosystem where we can support healthy C-15 levels.

Okay, so milk has a bit of it. If you can get good quality milk, butter, two tablespoons of butter will give you enough C-15 to not have a deficiency. Pecorino, how much each day or every? I love Pecorino. I know 3,000 ounces. How's that? No, I'm just kidding. No, I'm kidding, justified. Uh, Pecorino, it probably be about two to three servings, so two to three ounces. Happy, happy with that. Okay, what about things like yogurt? Is that a good source of whole-fat dairy for C-15?

Yeah, yogurt, yogurt can be a good source. Really, anything that is whole-fat, you know, and again, the more concentrated the fat is, and again, like you said, yogurt, yogurt can have the added benefit of fermented, uh, you know, being fermented, which can help create more free fatty acid forms of saturated fats, including C-15, which makes them even more bioavailable, uh, so a lot of times fermented products can be a good source, just like you're saying, of C-15. Sour cream, I mean, pretty much anything that you think about, and then again, the more we can understand is, you know, if it's coming from grass-fed versus, um, you know, other just basically under if there's a grass-fed version, which I just found a really nice grass-fed whole-fat yogurt, and I'm like, we're getting there. Like the fact that that was a marketing call-out was great to see. Does it have to be grass-fed and grass-finished for dairy? I don't know, because that's the thing that the the next one, well, okay, before red meat would be fatty fish and salmon as a key uh drive for C-15. Why is that important?

Um, so dolphins don't eat cheese, so or so, right? We get back to like, okay, wait, this whole thing came from dolphin stuff. So it's not a dairy issue with with dolphins. So we talked about it, certain types of fish have C-15, while others have none, um, so when we look at, so it's worth looking, and and when you look at human populations, you have entire Asian populations that, you know, are many are lactose and or many just populations that are lactose intolerant, right, and/or dairy is not a rout has not been a routine part of their traditional diets. Those tend to be cultures that have a lot of fish, um, so chances are that's where those cultures have gotten their C-15. We've learned, learned that it's primarily in the skin and the heads of fatty fish, so which is what most people don't eat. So C-15 hasn't been a reliable marker of how much fish we eat, but my bet is is that if you ate whole fish, but you know, like anchovies or like where you were eating the whole fish, it would actually be a reliable C-15 would actually be a reliable biomarker of eating whole fish. It's like when when I went to Italy, they just have all the fish, they like they love fish and seafood, and you just eat the whole fish, whereas when you're in kind of maybe the US, Canada, Australia, they have all these fish fillets, the skin is not there, the head is not there, everything. I mean, in Italy and in Europe, everything is not like clean, and I mean, sorry, it's clean, but it's not, you know, it's a whole food. I'm just trying to say, yeah, whole food.

Yeah, that's exactly it. It's like I'm I'm half Chinese, and you know, on my my Chinese side of the family, the, you know, you'd have the whole fish on the table, and the head went to the person of honor, right, and it's usually the elder, and it's like, ah, they didn't know it, but what they were doing was they were giving the oldest person the biggest dose of C15.

Are you really half Chinese? Amazing. I would never have seen that from your beautiful face.

Oh, well, thank you, thank you, thank you. I know nobody would. Nobody ever guesses. Well, I'm full Indian, and nobody ever guesses that I'm Indian. So really interesting. Yeah, they they think I'm like South American, or I don't know, but like quite interesting. Anyways, moving on to C-15 foods, um, so this is interesting, grass-fed red meat, yes, so especially from Australia, um, so I was like, so you we want to look into what grasses are, you know, cattle eating in Australia. So we saw both a um grass-fed, um, beef and lamb from Australia were some of the highest C15-containing meats. So there's something there, and then when

There's another study that looked at pregnant women and looked at their breast milk. Australians had the highest levels of C-15, uh, in their breast milk, which is really important because studies showing the more C-15 mom eats and that she has, she then passes on to her infant, and the better the body growth and the better the cognitive development of children with the more C15 they get from mom. So, um, yeah, Australians have a have a a head start. Absolutely. As a fellow Australian, I was just like, yeah, that's why like our lamb and beef are fantastic, as well as other parts of the world, but I mean, you know, the lamb and the beef here is quite incredible. Uh, but then it would be important to get grass-fed, grass-finished.

Okay, let's move on to um supplementation. So you said that if we eat all of this whole fat dairy, fish, butter, grass-fed red meat, that we can just not have a C15 deficiency, but if you really want to up it, do you recommend a supplement of fatty 15? Um, I I do, and I'm gonna sound biased though, right, Reena? So, but I I will say that um, you know, this work was funded by the Navy um because of the understanding of limitations of how far we can get with food um and so, but understanding again the Sardinians are doing it with no supplementation, so it is absolutely possible. They also walk, they're herders, so they walk three to five miles a day, they keep their calories under 2,000. You know, there there's it's there multiple components that lead to that healthy lifestyle. Um, so with regard to being able to reliably get these higher, you know, optimal levels of C-15, I think that in most people um case that the supplementation truly serves as supplementation. So, you know, at the military arena, you know, like, you know, our job has been, you know, to find the problem, and the problem was one in three older dolphins were developing insulin resistance, fatty liver disease, and these other aging-associated conditions, then to figure out how to fix the problem. So we figured out, okay, with C15 deficiency, and then you go and fix it. So that's the military; it's not keep doing research to do for research sake, it's to fix it, and the Navy funded us all the way through, including developing the supplement. So again, to be part of the solution, I love my cheeses for sure; I don't shy away from dairy fat, and I think it's because I'm eating, you know, the cheeses and um and whole dairy fat from grass-fed animals, plus supplementing, which is the point of supplementation, that I'm able to achieve, you know, these higher optimal levels.

Yeah, I just wanted to make that point because you do have to get things tested to know if you have a deficiency before just adding in any supplement because I mean, I think a lot of the times in the health space there is a push towards, take this and take that and do this, but usually you can just get everything you need from the diet. I think people appreciate that as far as your perspective when you say, okay, hey, do this and eat whole fat dairy, red meat, and everything, exercise, live a healthy life, check your C15, if you need it, take fatty 15. Do you have any success stories or before and afters of people just feeling great or any transformations by increasing C-15?

Yeah, so that was the delight and surprise, uh, because it's what the dolphins uh couldn't tell us uh or maybe they were trying to tell us, but we weren't smart enough to understand their language. Um, but when once we started putting Fatty 15 out to the world, and this includes, you know, me again, how said I don't avoid um, you know, whole fat dairy products, I embrace them um and reliably um so we launched it in 2020, we have almost 100,000 um active subscribers, and reliably half of our customers report feeling better within 2 weeks and 72% within 16 weeks. And at the two-week mark, the most common feedback we get is, "I'm I'm sleeping deeper, I have less joint pain, I have a calmer mood." And we're like, "Well, that's a placebo." We're like, "That's great that you're feeling it, but that's a because that's not what C-15 does from what we understood." And then I experienced those benefits and I'm like, I know like I've had pain in my, you know, in my elbow for years, and it went away like, you know, like it went away. So I'm like, okay, this is not placebo. So, but what we've come to understand since then is because the research has continued, not just from us but from over 100 peer-reviewed papers on C-15 throughout the world, that's at discoverc15.com, but one thing we um learned is that our bodies use C-15 to make a second molecule called pentadonoyl carnitine or PDC, and this is the second ever discovered full-acting endocanabonoid, so it fully activates CB-1 and CB2 receptors, which they're called canabonoid receptors because it's what cannabis activates, but we didn't evolve to have cannabis, right? Because like dogs have these receptors and dolphins have these receptors, they're there for us to have molecules in our body that then naturally activate them that helps support homeostasis, especially with regard to inflammation, sleep, and mood. Um, so then all of a sudden, Reena, that all then came together where it's like, oh, this is why we have a really good explanation of the repeatability of these benefits reported in reported in people. So there may be differences in how well people convert C-15 into PDC, and that might uh influence who gets feels those near-term benefits um and not to undermine them because sleep is critical um to our long-term health and control of pain and and calmer mood. Um, but we continue to really lean in on these long-term metabolic, heart, liver um and and healthy insulin um responses.

Oh, it's so so interesting. Even my husband was saying that he goes down the stairs and has some like clicking in his knees. I'm like, you just need more fat, and then maybe he just needs more, for example, C15, because as we're not even old, I mean, we're in our 40s, but as we age, we have all these little wears and tears, and especially as we get older, things just start happening, but it's the what's important is that these nutrients get abs that you first intake these nutrients, and our food is so deplete in nutrients, secondly, is that we can absorb it. So you mentioned that, and this is pure C15, not trying to push it, but I just think that fatty 15 is just a great solution for people that if they're feeling like crap because they can't get it from the diet, some people can't get really good whole fat dairy, C15 can be an option. I just want to switch gears as a last thing just to talk about longevity. We spoke about how to prevent disease because people have disease, but C-15 is also a very important nutrient for longevity, hence why you wrote your book, The Longevity Nutrient. Wasn't that a good segue? I know. Oh, I got it already right there. Goodness, it's already back there. All right. Yeah, yeah. So that it came out um March 25th, so two weeks ago, uh, made the USA Today bestseller list uh its first week out, which is which is awesome. Yeah, so right, so the longevity nutrient um so then as we were understanding, so the benefits that C-15 strengthens cells um we also and the world has learned that C15 does a lot of things uh that supports our health, which is what nature does with essential nutrients, but uh and so we now know that that C15 activates AKT and PARS, it inhibits mTor uh uh jackat 6 and or sorry, DA Jackat and HDAC 6. So it has these mechanisms that are understood to help lower inflammation, to help uh target the longevity-enabling pathway. There's actually a a human longevity-regulating pathway, you can look it up, and you put keg ke GG and it'll show you the map to longevity, and um and in the heart of it is that then goes to inhibiting mTor. So these are two key mechanisms: the first one is how metformin works, the second is how rapamycin works. So C15 has the two mechanisms of the top two two of the two of the top longevity-enhancing compounds out there. So once we really came to understand all these benefits of C-15, Nick Shorr, who's the head of NIH's longevity consortium, and he's been in that role for over 15 years, Nick came in and he's like that I bet C-15 is a geroprotector, and I was like, awesome, what's a geroprotector, what is it? And so he shared a geroprotector is a molecule that can slow our aging rate and slow and therefore slow the onset of the chronic diseases that kill us. So um we've done a series of studies with Nick, and one of them was we went head-to-head against um rapamycin and metformin using this assay called BioMAP, which is an extensive um human cell-based uh assays, there are 12 of them that mimic different disease states, and what you do is you treat these diseases in a dish with four different concentrations of C-15, rapamycin, metformin, and it measures 148 different biomarkers. So it's typ it's used a lot in the pharma industry to try to to look for compounds that are going to tell you, we predict it's going to be good for X, Y, and Z. So we used that assay, and we showed, we published back in 2023, that um C-15 had the most uh longevity-enhancing cellular benefits, even above rapamycin. But when you look at them head-to-head, both rapamycin and C-15 are anti-inflammatory, anti-cancer, antioxidant, um antimicrobial, um and anti-apoptotic, which is kind of a wonky list of benefits, but if you have that toolbox, you're going to live longer, um and you know the whole kind of conclusion of that paper was that maybe we didn't have to go to Easter Island to find this uh, you know, this um rapamycin that is made by bacteria that grow on Easter Island, maybe it's been in front of us all along, which is a molecule that every mammal gets from birth. So we the book goes through these seven must-haves of a geroprotector and shows how kind of checks off the boxes of how C-15 meets all these criteria to the point where Nick went to ARDD, which is one of the world's largest anti-aging therapeutics conferences, he presented in Copenhagen, and Nick shared with his community, right, that there is no other molecule that he has seen, and he's seen them all, and in Nick's opinion, there's no other molecule that has stronger support as being a longevity-enhancing molecule than C-15. So that means a lot to us, and we're just excited for the research to continue, and in the meantime, you know, it's it's moved from this surprising discovery in dolphins to a global movement to, you know, get our health back on track and hopefully even be able to optimize them.

Absolutely. I'm going to leave the link for The Longevity Nutrient in the description of this episode as long um as well as Fatty 15. Um, how come this is not in the mainstream, C15? Is it because it's a saturated fatty acid and saturated fat? How did you know that? Because I mean, the whole my whole channel honestly is about satur meat, saturated fat, dietary interventions to treat chronic disease; that is what I interview people about, and that's what the message is about, and more people are talking, and any it's so interesting, anything that lowers that anything that contradicts that message around saturated fat is just lowered in the mainstream; they want to push some other agenda. It's very frustrating, but um, yeah, so is it that it is, and and what was, you know, kind of most telling, Reena, was, you know, when we found this association between higher C15 and healthier aging dolphins, we then turned to the human literature, and when you go digging, it was this was starting to emerge in on the human side too, that people with higher C-15 levels had lower risk of developing type 2 diabetes, heart disease, fatty liver disease, and not just in single studies but meta-analyses of large prospective co like 18 prospective cohort studies all combined into one meta-analysis, and they made these conclusions, and like I'm scratching ing my head thinking, wait, this has actually already been seen in humans, but you look at the paper, and the paper will say saturated fats are bad for you, and what they focused on were the outcomes of C16, right, which showed that higher levels of C C16 was, you know, this was a higher risk of type two diabetes, heart disease, fatty liver disease, and then the fact that these odd-chain fats, C-15 and C-17, had the opposite effect, we're kind of like, eh, and by the way, we also kind of found this thing, but it's probably not important. So even though peer-reviewed literature, you know, in prestigious journals had actually been showing it, like you said, we kind of were just it just didn't fit the pattern, and so even though it was found over and over and over and over again, it just society wasn't ready to be able to hear it. So your channel is doing tremendous work in being able to you just have to keep, you know, and again, we're kind of to the point where it's like you can't you so the way it's frustrating for Nick and for Jeff Schwemer is just like you can't explain C-15 away anymore; like there's so much science there; like we have to force the conversation, which is why we call their supplement Fatty 15 because we're like, we're going to own the word and force the conversation to say this isn't a bad word.

Yeah, it's an awesome word; I love I mean, anytime I can wave but the butter flag and the well now it's the whole fat dairy flag, it's good because it's just so um, you know, demonized, and people are like, oh my god, um, cuz I actually slice butter and eat it as like, not big slices, but salted butter, grass-fed is delicious; it's good, and if you put that on some smoked salmon or if you put that on some any meat, it's just delicious. Again, because I follow a high-fat ketogenic approach, so if somebody does two tablespoons of butter, uh, some whole fat dairy, some red meat, and they take maybe fatty 15, is that good to increase your 15 levels? That is going to increase your C-15 levels. Yeah, easy. I'm like, I like this lady cuz I like butter and I like dairy, and I just need to get my fatty 15 and maybe The Longevity Nutrient book. Again, I love absorbing myself with all this information cuz just fun, it's a bit nerdy, but you know, at the end of the day, we feel better, you feel better, the world feels better, so why not? And embrace butter and embrace whole fat dairy.

Steph, if people want to find you more, where can they find you? So uh, going to fatty15.com uh is is you know, we keep keep uh all the information as far as with regard to um what's the latest happening in the news and media and stories like that. Um, the longevitynutrient.com is where uh the book, but it basically links to wherever books are sold. Um, and then I'm on LinkedIn; I'm I'm old school, Reena, and so with I I love the conversations and engaging with folks on LinkedIn, and we're having some some wonderful wonderful conversations. Awesome. Well, thank you so much for your time, Steph, and I'm sure we're going to see you very soon. Absolutely, Reena. It's a pleasure. Thank you for joining me today on this episode with Dr. Stephanie Ven Watson. If you'd like to know more information about how to naturally increase your C-15 levels, just go to the description of this episode, click on naturally increase C-15, open that up, and you'll see all the information there and how to fix insulin resistance. If you're learning from and enjoying these free episodes, please hit the subscribe button, and you can also find me on other social media accounts; I'm on Instagram and I'm on Twitter under the name of The Primal Podcast. Now, if you love this episode, you'll enjoy another episode I did with Dr. Robert Lustig; we spoke about insulin resistance and the easy way to fix it and the seven types of fats that you need to eat. Finally, thank you for your interest in root cause healing, and I'll see you next.