The Fatty Acid We May Be Missing: From Navy Dolphins To Human Health

Leigh Ann Lindsey (00:00.92)
Well, Sharlyne, welcome to The Accrescent Podcast.

Sharlyne Poggio, MS (00:04.792)
Thank you so much, Leigh Ann. I’m so happy to be here.

Leigh Ann Lindsey (00:08.112)
We were getting ahead of ourselves a little bit off air, diving into introductions and some of our past stories. So I am excited though to get a little bit of the deeper story just so the audience can get to know you personally, because we’re gonna be talking a lot about C15, fatty acids, Fatty15. But let’s just start with an introduction to you and maybe a little bit of your personal journey and what ultimately led you to be working with Fatty15.

Sharlyne Poggio, MS (00:34.582)
Absolutely. Okay. So well first of all, my full name is Sharlyne Poggio. And so I started off with military service, coincidentally. And so as you might know, some of their co-founders actually started off in the military too. So I was an Army medic and that looks like practicing medicine either in the field, in a combat field environment, or force health protection. So things like preventative health, right? How can we keep troops healthy?

At a larger scale, right? Whether that’s a small squad of five soldiers or whether that’s a whole battalion of hundreds. Started off there, and that really made me feel passionate about just medicine in general. But you can really fall down the rabbit hole. Like there could be so many avenues to take when it comes to medicine. And so I really wasn’t aware of where I wanted to go, right? Like you’re a 19-year-old soldier and then fast forward 10 years, you’re like, okay, where do I want to go now that I know all of these things? And so I went back to school and I got my bachelor’s in biology and then I went on and got my master’s in biology with an emphasis in molecular biology.

So it’s really figuring out root-cause mechanistic, molecular reasons for why we experience certain conditions, right? And so coincidentally, I came across Fatty15 by literally just seeing Dr. Stephanie Venn-Watson’s TED Talk and it blew my mind.

Because I understand all there is to know with legitimacy and credibility when it comes to science, literally, Leigh Ann, down to where I’m gonna put my hummingbird feeder, like the first thing I do is look at all the peer-reviewed studies. Like, where’s the best place to put your hummingbird feeder? When’s the best time to neuter my dog? All of these different things. It’s like the first thing I wanna look at is how credible is the science behind anything, any decision that I make. And so in looking at Fatty15, I understood the science.

Leigh Ann Lindsey (02:32.256)
And I realized, I was like, gosh, I need to be a part of this. And so I reached out and I was like, surely you need somebody to help educate your community on all the deep science and all the complex pathways that are going on here. And I want to be that person for you. And so here I am. And it’s been an absolute joy. It’s exactly what I thought it was gonna be and more. And we continue to learn more every week. There’s a new paper on C15. And so the science is just exploding on this as it should be, right? Because there is still so much to know.

Leigh Ann Lindsey (03:36.155)
Mm-hmm, exactly. And that’s exactly why you’re here to walk us through this in a really digestible way. And I’m gonna do my best to guide us in kind of a linear way as best we can. So why don’t we start though at the beginning with Dr. Stephanie Venn-Watson? She’s one of the founders of Fatty15 and her work with Navy dolphins. I think already, I mean, even just hearing like, wait a second, what do dolphins have to do with this, gets people really intrigued. So walk us through the origin story of Fatty15 a little bit.

Sharlyne Poggio, MS (04:10.966)
Absolutely. So first and foremost, I think I should tell you who Dr. Stephanie Venn-Watson is and what she is by trade, right? Before Fatty15, right? So she has many, many accolades. She’s worked with the World Health Organization, with the CDC. And then finally, she was recruited by the Navy to care for their aging dolphin populations. So by trade, Dr. Stephanie Venn-Watson is a veterinary epidemiologist. And that’s actually a big deal, right? Because when we think about epidemiologists, what do they do? They study large sets of data, they identify patterns, and then they figure out how to fix a problem.

She was recruited by the Navy to care for their Navy dolphin population. So many people don’t actually know that the Navy even has dolphins, right? We’ve had them for decades and for several different missions. In the Navy, they actually already live longer than they do in the wild because they’re so well cared for. They have the best diet, the best exercise, the best veterinary care. So they age. But what they were starting to learn is that these dolphins are living longer, but what is their actual health span starting to look like? Well, one in three of them were starting to develop age-related diseases that we typically see in humans, things like insulin resistance, dyslipidemia, anemia, even the full suite of changes consistent with Alzheimer’s disease.

And so the big question is why? Why is this happening? This is a clean population, and by clean I mean they are not all smoking cigarettes and eating junk food and sitting on the couch all day the way humans do, right? They get a lot of exercise, they get a great diet, and they get great veterinary care. So that’s kind of where the detective work started.

Across several different studies, they started to identify that it had something to do with their diet. And then even further than that, they did what they call metabolomics, which is just measuring all the different types of metabolites that are in the dolphin’s blood system. And so what they started to learn is that one in three dolphins are presenting with these age-related diseases and that one in three dolphins also have low levels of C15.

They thought maybe it was gonna be omegas, but it wasn’t. It was C15. And so actually, Leigh Ann, what it is is that prior to the 2000s, the Navy dolphins were being fed eulachon fish, which are really high in C15, but there was a shortage of that fish. And so they replaced the diet. They didn’t think anything of it, like, well, we’ll just give them this other fish. And unknowingly, what they did is that led to a nutritional deficiency.

Throughout doing these modified fish diet studies, what they found is that upon incorporating fish that were rich in C15 back into the Navy dolphin diet, they actually saw a lot of those biomarkers resolve. So the anemia was resolved. RDW was lowered. There was also the insulin resistance was improved, so their glucose was improved. So all of these biomarkers essentially resolved three months into this modified diet.

Leigh Ann Lindsey (08:33.214)
Well, I think where I’ll take us before we dive even more specifically into it is so they started observing this in dolphins and going, okay, whoa, C15 seems to be a factor here. When it’s taken out, all of these biomarkers start declining. When it’s put back in, they start rebalancing themselves. So what I’m very curious though is there had to be a jump from somewhere from like we’re talking about dolphins to, hang on, how does this connect to humans?

Sharlyne Poggio, MS (09:03.791)
Absolutely. So that’s where we go, right? We do these modified fish diet studies and they find the first hint of a threshold. We need to have in our red blood cells a threshold of 0.2% total fatty acids. That’s what we see in the dolphins, that when they cross that threshold of 0.2% in the red blood cell membrane, that’s actually when these biomarkers resolved, and that’s actually three months in.

Our red blood cells have a life cycle of about 120 days. And more specifically, what we know about red blood cells too is that they actually don’t have the mechanisms to repair themselves. So really, whatever cell membrane structure you start out with in the red blood cell, that’s what you have throughout your whole life cycle for that specific cell. And so that was the first hint that there’s something here related to red blood cell health and C15 levels and these age-related diseases.

What she found five years after that, and she published this landmark study in 2020, is cellular fragility syndrome. It’s this pathophysiology that basically starts with low C15 levels, which leads to fragile red blood cells. And that actually drives something called ferroptosis, which is a new form of cell death, which drives inflammation, lipid peroxidation, and then eventually iron deposition in the liver cells. And then that has spillover effects that present as dyslipidemia, insulin resistance, and all of these symptoms and biomarkers that we started to see in the dolphins.

This isn’t just across the dolphin population. These studies have been repeated not just by Dr. Stephanie Venn-Watson, but by scientists throughout the world. We’ve seen it in several models: dolphins, rabbits, rats, in vivo studies, and epidemiological studies across human populations. So we’re sitting at over 150-plus papers on C15.

Leigh Ann Lindsey (11:22.852)
Yes. Okay, so for the audience, Sharlyne just hit us with basically the whole premise of all of this, but I’m gonna break it down. We’re gonna break it down because everything in there are all the points that I really want to talk about. Cellular fragility, the ferroptosis, but I want to make sure they each get the time that warrants so that we can really understand it. So even though we’ve already said it, I do want to come back to, so it’s really, really clear for the audience, what is C15?

Sharlyne Poggio, MS (11:50.105)
C15 is an odd-chain saturated fat that is typically found in whole-fat grass-fed dairy for the Western population. So for most of our lives as a society, humans have been getting it from whole-fat grass-fed dairy. Now in the dolphins, they’re getting it from fish, but they’re eating the whole fish. So they’re eating the skin, heads, eyes of the fish. They’re not filleting it.

We know that cells need both unsaturated fats and saturated fats. Think of oil versus butter. Butter is solid at room temperature because it’s got a lot of saturated fats which pack really nicely. When you think of something like an oil, whether it’s olive oil or any kind of seed oil, that’s really high in polyunsaturated fats, which does not allow them to pack nicely. So what that looks like is a liquid at room temperature.

C15 is a saturated fat, so that means it has no double bonds and can pack really nicely. But taking it even further, it’s odd. So that means it has an odd number of carbons, which is why it’s C15 and not C16. That’s actually a really important distinction because dairy is a mixed bag of saturated fats. So it only has trace amounts of odd-chain saturated fats like C15 and much higher amounts of C16.

C15 is also what we call an active fatty acid, which means that it activates many key pathways in our body. There are certain microbes that can make C15, so if you’re eating a lot of fermented foods, or again, the whole fish, you’re probably getting C15 that way. There are also certain types of seaweed that have high levels of C15, like brown algae.

The human body and actually the mammalian body can’t make enough C15 on its own. And so that’s why we’re starting to learn that it’s actually an essential nutrient. I don’t just mean essential as in it’s important, but in the biological sense, that it’s important for basic physiological function and we need to get it from our diet or supplementation.

Leigh Ann Lindsey (15:51.631)
I do want to get into that rabbit hole a little bit of what are some of the compelling findings around what C15 is doing in the body on that cellular level. You know, it’s affecting things like metabolism, liver, heart, red blood cells. I know we might not be able to get into the weeds of all of that, but just a general idea so that people understand, ooh, here’s what this saturated fatty acid is doing in my body and why it’s so important.

Sharlyne Poggio, MS (16:20.625)
Whenever you have an essential nutrient, whether it’s vitamin C or whether it’s your essential amino acids or whether it’s an omega, if you pull it out of the diet for long enough, it’s gonna have a negative effect. But when you put it back in, it should hit several different body systems. It should be what we call pleiotropic.

So a pleiotropic nutrient is a nutrient that hits several different body systems. And that’s exactly what we’re seeing with C15. We’re seeing that it’s important for liver health. We’re seeing that it’s important for metabolic, cardiovascular, gut health, brain health, and cognition. It activates 36-plus cellular pathways and benefits us in many different ways. A huge part of that is its ability to lower pro-inflammatory cytokines.

It strengthens cell membranes to protect against ferroptosis. Strengthening your cell membrane is really important for communication because nothing is static even at the cell membrane level. Everything has to move and communicate.

Beyond that, it activates AMPK, a key metabolic regulator. Metformin activates AMPK. Statins activate AMPK. Exercise activates it, fasting activates it, and C15 activates it. Following that pathway, AMPK is involved in inhibition of mTOR complex 1. Rapamycin is an mTOR inhibitor, and C15 can affect that pathway through activating AMPK.

There are also papers showing that C15 improves mitochondrial function. It strengthens biological membranes because all of them are made up of phospholipids, which have a fatty acid in there. By strengthening the mitochondrial membrane, we’re making it more resilient to lipid peroxidation. When we’ve got a lot of reactive oxygen species in the body, they can attack polyunsaturated fatty acids within the cell membrane and eventually degrade the membrane.

When C15 is metabolized and broken down, it feeds into the citric acid cycle in the mitochondria, making more energy.

Leigh Ann Lindsey (22:16.41)
One of the things we do, the InBody 970 here for all of our patients. And one of the things that looks at is phase angle, which is what is your cellular permeability? Are your cells able to excrete things from them, take nutrients into them? And when that cellular permeability gets hardened, things can’t get in well, things can’t get out well. We’re gonna start seeing issues downstream. So that’s actually something we measure and it makes me really curious to wanna do an experiment with Fatty15 of like, huh, I wonder if phase angle goes up with Fatty15.

Sharlyne Poggio, MS (22:56.678)
That would be really interesting, like if you get somebody’s C15 levels, because there are a few labs that test for C15. That would be really interesting to get maybe somebody’s red blood cell C15 level and then couple that with exactly what you just said, phase angle.

Even just from a structural standpoint in that cell membrane, because C16 is even, it stacks too neatly. If you’ve got a ratio of high C16, not too much C15, and a little bit of polyunsaturated fats, those places where the C16 may pack and stack too neatly, now you kind of have a little bit too much rigidity in that cell membrane.

Whereas because C15 is odd, it doesn’t pack as neatly. It still packs quite nicely because it’s a saturated fat, but it doesn’t pack as neatly and so it’s not as rigid. It’s almost like I picture C15 in the cell membrane as a flexible anchor. It’s still an anchor and still very sturdy, but it’s not gonna create as much rigidity.

Leigh Ann Lindsey (24:16.476)
Yeah. So that mitochondrial support, supporting the cellular function. And when we support the mitochondria, everything our cells do, they can do better.

Sharlyne Poggio, MS (24:28.334)
Absolutely. Mitochondria really are essential to life.

Leigh Ann Lindsey (24:53.22)
I remember you guys were kind enough to send me some to test. But in the handout, it also was talking about blood sugar. And I would love to hear a little bit more about this specifically because it’s really fascinating in our complex chronic illness and cancer patients. Blood sugar is so important. It’s something we’re working to balance for almost everyone. And almost every patient who comes in, their blood sugar is all over the place.

Sharlyne Poggio, MS (25:24.368)
To date, there haven’t been any randomized controlled clinical trials related to measuring those glucose levels, but there’s a lot of compelling science at the cell level. There are studies showing that C15 can mimic insulin in relevant cell models. They looked at muscle cells in mice, and a lot of the genes for mice, specifically for muscle cells, are conserved and very similar to human muscle cells, so it is a good starting point.

They compared giving these cells insulin with different doses of C15. Even at the lower dose, C15 mimicked insulin in the amount of glucose it was able to bring into the cell and in the expression of GLUT4, which is responsible for signaling glucose uptake into the cell. There have also been in vivo studies with A1C, but nobody’s done the randomized human clinical trial on glucose yet.

Leigh Ann Lindsey (27:29.766)
We’ve talked a little bit about some of the ways it affects our physiology beneficially. What I wanna ask now is when C15 isn’t present in high enough levels, what starts to deteriorate?

Sharlyne Poggio, MS (27:57.02)
That takes us full circle back to cellular fragility syndrome. When we see the starting point of low C15 levels, we follow that pathophysiology down where it’s like, okay, we get ferroptosis, which is a new form of cell death, driving inflammation and reactive oxygen species that spill out into different tissues and organs. That can present alongside many of the age-related diseases we’re familiar with, such as type 2 diabetes and heart disease. Cognitive health is affected too. We’re also looking at MASLD.

There was a consensus statement put out by a consortium of scientists and doctors that describes metabolic hyperferritinemia, a liver-centric condition involving iron dysregulation. What’s interesting is the overlap with the fragile red blood cells and iron deposition seen in the dolphin work.

We also have large observational studies and meta-analyses across human populations that have associated higher C15 levels with lower risk of conditions such as type 2 diabetes, heart disease, and stroke.

People in Sardinia, Italy who live to be very old have high levels of C15 and they’re not supplementing with Fatty15, right? But they do get good-quality dairy. They eat a balanced diet and exercise is built into many facets of their day.

Leigh Ann Lindsey (31:02.786)
I thought it was interesting that at the beginning you said whole-fat grass-fed dairy, which is a specification that maybe levels are also declining because dairy has changed and the dairy we’re consuming in masses is not the same and is not as nutrient-dense as dairy maybe should be.

Sharlyne Poggio, MS (31:29.403)
There have been studies that show that grass-fed cows compared to those fed corn have higher levels of C15. Going back to Sardinia, Italy, the dairy there is from grass-fed sheep and goats. There’s even a geography aspect. Hard cheeses and aged cheeses can also have higher levels of C15.

Not everyone can have dairy, and not everyone has access to good-quality dairy. So this is why we’re seeing a steady decline in dairy consumption mirrored with a steady decline in C15 levels. And on the flip side, we’re seeing age-related diseases in younger populations. It goes beyond Fatty15. It raises broader questions about diet and food quality.

Leigh Ann Lindsey (33:59.271)
The marker there that really catches our attention is that quote-unquote age-related diseases are showing up in people who aren’t at that age where that disease is expected. It just shows us that we’re getting to that depleted state so much earlier.

Sharlyne Poggio, MS (34:35.86)
Absolutely. And what Dr. Stephanie Venn-Watson laid the groundwork for is that it could potentially be ferroptosis-driven. If you have fragile red blood cells, who’s responsible for cleaning fragile red blood cells up in the body? In the liver, there’s something called a Kupffer cell that engulfs the red blood cell. If they get overwhelmed, you start to get iron deposition in those Kupffer cells. That spills over to other cells. It’s a cascade.

Ferroptosis is literally an iron-dependent form of cell death. So it’s the spillover effect of that iron coupled with reactive oxygen species, coupled with too many polyunsaturated fats in the cell membrane.

Leigh Ann Lindsey (35:35.967)
Can you say more? I’m really interested. I’ve never heard of ferroptosis before. What I’m thinking of is apoptosis, which is cellular death, which we actually need. But it sounds like this ferroptosis is not good. It’s not the kind of cellular death we’re wanting.

Sharlyne Poggio, MS (36:05.001)
That’s exactly right. There are a few types of cell death we’re familiar with. There’s apoptosis, which is programmed cell death. Then you have autophagy, which is cellular recycling. And then there’s necrosis, which is not as orderly and can leave behind inflammatory debris. In 2012, scientists at Columbia University identified ferroptosis, which is an iron-driven, iron-dependent form of cell death that can also generate inflammation.

The science on ferroptosis is expanding rapidly and it’s being studied in relation to brain, liver, gut, and other diseases.

Leigh Ann Lindsey (37:28.754)
How is that ferroptosis affecting some of these diseases? If it’s iron-dependent, does that mean it’s causing excessive iron depletion because it’s requiring so much iron? And then you talk about the mess it’s leaving. What is the mess it’s leaving behind? That inflammation.

Sharlyne Poggio, MS (37:53.064)
The mess it’s leaving behind is driving up inflammation, cytokines and reactive oxygen species. That contributes to lipid peroxidation in the cell and eventually in the tissues. In metabolic hyperferritinemia, there’s concern around iron deposition and dysregulated iron handling.

Each red blood cell carries a lot of iron. If fragile red blood cells are being cleared and that iron isn’t recycled properly, iron can accumulate in Kupffer cells and spill over to other tissues and cells. That’s where you can get ferroptosis happening across other cell systems.

Leigh Ann Lindsey (39:31.266)
Is there something about C15 that allows correct apoptosis and autophagy to happen?

Sharlyne Poggio, MS (40:01.949)
We didn’t even talk about C15 as a geroprotector, which means supporting longer health span. We did mention AMPK. By AMPK being activated, that drives autophagy, supports apoptosis pathways, and is involved in clearing senescent cells. AMPK also supports mitochondrial biogenesis, so we’re clearing away old cellular components and supporting the creation of new mitochondria.

Leigh Ann Lindsey (41:12.348)
I’m gonna take us a leap further, which I know you guys can’t make claims like these, but I’ll bring in this big-picture view. Healthy apoptosis and healthy autophagy are important parts of cellular regulation, and in integrative oncology we’re interested in why the body may no longer be able to perform those functions appropriately.

Sharlyne Poggio, MS (41:55.703)
Absolutely. And again, you’re right, we’re not allowed to make claims. What I will say is there are very early studies related to cancer and C15, and I’d be more than happy to send those over to you. There are early studies looking at breast carcinoma, and then HDAC6. C15 is actually an HDAC6 inhibitor, which is being studied in certain types of cancer.

Leigh Ann Lindsey (42:26.15)
It’s fascinating. What I love about it is, especially in integrative medicine, we’re always trying to then look higher upstream. And what is most upstream is the cell. So what can we do to figure out what is causing your cells harm? What do we need to get out that’s causing harm? What do we need to get in that’s gonna support repair and higher function?

Sharlyne Poggio, MS (43:22.324)
A lot of times people are like, well, what am I gonna feel? But sometimes you don’t feel it right away because it’s happening at the cellular level. That’s why we have our 90-day starter kit, because it does take 90 days to really feel outward benefits sometimes. If somebody’s very deficient, like some of my colleagues who haven’t eaten dairy for decades or vegans that have been vegan for decades, when they take it, they may notice it sooner.

For me, when I first started taking it, the first thing I noticed was deeper sleep. We don’t have sleep studies, but C15 affects endocannabinoid pathways that are relevant to mood and sleep. We also didn’t talk about how C15 inhibits JAK-STAT and activates PPAR-alpha and PPAR-delta. Those are pathways that are being studied in cancer and inflammation too, so it’ll be very interesting to see where the science takes us.

Leigh Ann Lindsey (45:14.332)
Okay, I know we’re close to the end here, but let me bring it back to what is Fatty15. We’ve talked about C15, this saturated fatty acid. Who and what is Fatty15 as a brand, as a supplement?

Sharlyne Poggio, MS (45:48.118)
Fatty15 was brought into the world by our co-founders, Dr. Stephanie Venn-Watson and Eric Venn-Watson. She didn’t set out to go discover a new supplement when she started her work with the Navy dolphins, but they realized the potential importance of C15 and brought Fatty15 into the world.

Fatty15 is a C15 supplement. It’s 100 milligrams of C15 per capsule. Its outer capsule is vegetable cellulose, and inside is a pure synthetic C15, which is important because we do have people with certain allergies, people trying to stay away from dairy, or people who are vegan. So it’s vegan-friendly.

We’re oversimplifying this, but a C14 is sourced from something like nutmeg or coconut and then the final carbon is added to make C15. Then of course it’s tested for purity and contaminants. So that’s Fatty15. It’s a C15 supplement.

Leigh Ann Lindsey (47:05.51)
If someone’s looking to take this, are there any contraindications? Is there anyone this might not be for? Or in general, is it pretty safe for everyone?

Sharlyne Poggio, MS (47:17.555)
In general, it’s pretty safe for everyone. We recommend that somebody with sickle cell anemia check with their doctor because of that red blood cell membrane component. As far as medication interactions, people who take psyllium husk may already be aware of this, but if you take psyllium husk, you want to space that out from supplements to support absorption.

Fatty15 is easy to take. You don’t have to take it with a meal. We recommend starting it in the morning because some customers report more energy throughout the day, but we also get people who report taking it at night because it helps them sleep. So you can take it at the time that works best for you.

Leigh Ann Lindsey (48:56.966)
So is it a 100-milligram capsule a day?

Sharlyne Poggio, MS (49:06.431)
One 100-milligram capsule a day would be the maintenance dose. With some practitioners, we do get into what we call a therapeutic dose, which is 200 to 300 milligrams a day. There are randomized controlled trials evaluating 300 milligrams a day in specific populations, including outcomes such as liver enzymes and cholesterol. We also launched a practitioner version, the advanced formula, which is 150 milligrams per capsule.

If somebody can test their C15 levels before starting, that can be useful. If they’re very deficient, a practitioner may decide on a higher starting dose and then drop down to a maintenance dose. If they don’t have access to testing, then reflecting on diet is another piece.

There’s a threshold framework. Roughly 0.2% to 0.4% of red blood cell total fatty acids is described as a healthy range in this body of research, while levels above 0.4% have been discussed in relation to Sardinian populations and longevity.

Leigh Ann Lindsey (51:23.674)
If you do blood work for C15, first of all, is it a blood test?

Sharlyne Poggio, MS (51:31.618)
There is a blood test. Genova Diagnostics does it, and other fatty acid panels may include C15. TruDiagnostic has also looked at C15-related measures through epigenetic testing, although that’s different from reporting red blood cell concentration.

If you’re testing C15, the red blood cell percentage is the key number we were talking about. A result around 0.2% to 0.4% is the range being discussed here. Anything below 0.2% would be considered low in this framework. Small changes can be meaningful because these are small percentages at the cellular level.

Leigh Ann Lindsey (54:32.178)
This also opens up a whole future dialogue around, even if we are getting it, what’s happening in our system that might cause C15 depletion much quicker? What if we’re not able to absorb and utilize the C15 appropriately? So consumption isn’t the only factor we’re looking at here of why C15 levels might be low.

Sharlyne Poggio, MS (55:08.61)
Absolutely. It goes back to not just the consumption piece, but also eating a balanced diet, because we do have microbes in our gut that can make C15 at trace levels. Think about Sardinia again. They get good fiber and they exercise. There have been studies in pregnant women showing associations between exercise and circulating C15 levels. So I think it’s those components together. Here in the Western world the primary dietary way is through whole-fat, grass-fed dairy or whole fish.

Leigh Ann Lindsey (55:52.026)
I love it. I know we could go down so many more rabbit holes, but we’ll land this plane. So just for the audience, anything really important that we didn’t touch on otherwise, where can they learn more? Where can they get Fatty15?

Sharlyne Poggio, MS (56:06.996)
They can learn more at DiscoverC15.com. We have something called the Nerdy Do-Gooder Connect program. This is something we offer to customers and practitioners, where you can book a time with somebody from our team to learn more and ask questions. Discover C15 has the studies and Fatty15.com is where you can purchase Fatty15.

Leigh Ann Lindsey (56:45.446)
Sharlyne, thank you so much for coming on and walking us through all that science in a really comprehensive way.

Sharlyne Poggio, MS (56:54.402)
I’m so happy to be here and I know it’s a lot. It can be overwhelming, but I hope it was fun for you. I hope it was as fun for you as it was for me.

Leigh Ann Lindsey (57:03.763)
A hundred percent. It’s the best whenever we get to nerd out over here.

Sharlyne Poggio, MS (57:08.384)
Absolutely. And please feel free to reach out, Leigh Ann, if you yourself have questions. I’m happy to send over any resources that you might need and to your community as well.

Leigh Ann Lindsey (57:19.419)
Yeah, I will absolutely.