← The mindbodygreen Podcast
The mindbodygreen Podcast
632: The science of skin aging & how to slow it down | Saranya Wyles, M.D., Ph.D.
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Saranya Wyles, M.D., Ph.D., a dermatologist, regenerative medicine scientist, and the director of the Regenerative Dermatology & Skin Longevity Lab at the Mayo Clinic, joins us today to unpack how the skin reflects systemic aging and the emerging therapies shaping the future of regenerative dermatology.
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Welcome to the MyBodyGreen podcast.
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I'm Jason Wakab, founder and co CEO.
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Of MyBodyGreen and your host.
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Your skin is one of the most powerful windows into how well you're aging. Those freckles, fine lines and sudden overnight changes we all notice were actually reflecting deep cellular shifts happening throughout the body. And today's guest is here to change the way you think about skin altogether. Dr. Sranya Wiles is a dermatologist, regenerative medicine scientist and the Director of Regenerative Dermatology Longevity Lab at the Mayo Clinic. Her research sits at the cutting edge of aging biology, looking at how cellular senescence, wound healing, inflammation and regenerative therapy shape not only how our skin looks, but how it functions as a true longevity organ. In today's show, we'll dive into some fascinating topics, including how your skin reflects systemic aging and why it may be your most visible biomarker of long term health. We also cover what zombie cells actually are and how they accelerate both skin aging and whole body ag aging as well. Plus, you learn about the five pillars of skin longevity and the future of regenerative dermatology. This episode is packed with actionable insights.
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A
Let's dive in. So you started in dermatology and regenerative medicine. What shifted your focus from aesthetics toward the deeper biology of aging?
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D
Skin Skin health is an incredible part of how we age systemically. Skin is our largest organ. Think about it as our longest relationship, and it's our most visible biomarker of how we're aging on the inside. So looking at skin was a natural way to see how cues of systemic aging and systemic health could just present on your skin. So at Mayo Clinic, I lead a research lab called the Regenerative Dermatology and Skin Longevity Lab and we started exploring these different biomarkers starting from how the skin ages naturally with age and how inflammatory skin diseases like atopic dermatitis psoriasis, and even aspects of wound healing can be disrupted with age.
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A
And so how do. How does one get a sense of how their skin is aging?
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D
Yeah, so the skin is the naturally largest regenerative organ. So our skin turns over every 30 days. So every 30 days, the skin rebuilds, and the rest becomes, I call it, dust on the floor. Right. So it basically sheds over. And this process is how we can kind of time the different ways that the skin is showing healthy barrier and healthy barrier repair. So when the skin starts to age, there are two aspects of change that we can look at. There is structural change, and there is functional change. So structural change, this is what we're seeing physically. Some things, like how our melanocytes are aging. You know, we lose melanocytes over time, and about 10% or 20% with each decade, you lose melanocytes. And this is your active melanin production, this is your active pigment production. When you lose that ability, it actually contributes to dullness, to dispigmentation, to ineffective ways of combating UV protection. So when this happens, you're losing both functional ability for skin protection against UV damage, and you lose structural change. So you start to see dispigation. And a lot of my patients come in and say, all of a sudden, I notice this brown spot on my skin. It's happened overnight. All of a sudden, I'm seeing this change. So skin aging can feel like it happens overnight, but really it's years of molecular underlying biological damage that accumulates, and it manifests as structural and functional change.
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A
And so with melanocytes specifically, is there anything we can proactively do to stop this from happening or potentially reverse the damage?
- [04:30]
D
We look about. Look at the skin as a collective unit. So think about it as epidermal aging, epidermal regeneration and dermal aging. And dermal regeneration. So melanocytes live in the epidermis. They're part of that milieu or microenvironment. They interact with keratinocytes. And then in the dermal aging, this is fibroblasts, macrophages, immune cells are also there. Really, it's this collective home of epidermal and dermal aging that interface together, and that influences how each player is activated. So if you look at senescence, for example, senescence is this state that can happen with aging. These are zombie cells or cell cycle arrest that happens over time. So when a fibroblast or melanocytes undergoes senescence cell cycle arrest, it influences that entire skin homeostasis. So you really want to be Thinking about the skin as a unit and how each cell contributes and influences its neighbors, and what are the influences that can then shift or disrupt this natural homeostasis?
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A
So zombie cells, how do they accumulate? Why do they matter? I think this larger idea of it's not just about your skin health, it's not just for aesthetics, like the wrinkles, but can you talk about zombie cells and what this looks like in terms of overall skin health and systemic aging more generally? Because I think it's just this idea that it's not just your aging esthetically, because no one likes that. It's you're actually aging systemically. And no one wants that either.
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D
Exactly. And the idea is that the skin is your reflection, right? It's your mirror for systemic age. But the skin also has this incredible dynamic function. So the skin is your thermoregulator. It keeps our ability to heat the body. The skin is a sensation organ, so we can sense and feel the outside environment. The skin is your barrier protection. So everything that you're getting exposed to, whether it's smoke, pollution, UV damage, it's your active barrier from the outside world, your largest extrinsic organ. So it plays a lot of these dynamic roles. I should also say it also is an organ that actively secretes and excretes. So it's secreting sweat. And we kind of detoxify the body's waste through that portal. And we also absorb different topicals and moisturizers within that skin layer. So it's a very dynamic, hyper functional organ. And when you talk about senescence, when senescence accumulates or these zombie cells accumulate, they actively disrupt this functionality of the skin. So it's not this esthetic change, but actually this underlying functional change of how you're playing a role that keeps the whole skin functioning as a unit. Right. And let's talk a minute about senescent cells. So you asked about the zombie cells and why this happens. So senescent cells are. It's. It's a. It's an evolutionarily conserved process. This is a good thing. We actually want senescence because it's our cancer evading mechanism. So even in skin being predisposed to skin cancers, melanoma, et cetera, when a cell gets these DNA damage from UV light, from other exposures, there's a DNA damage that occurs and this cell is mutated. Now a cell becomes senescent because it kind of undergoes a growth arrest. So it says, I see that the cell has a mutation. It's going to take a lot of energy for me to put this cell under apoptosis. So I don't have that energy to spare right now. So instead I'm going to put it under this cell cycle arrest or house arrest, if you will. And that's how these senescent cells accumulate. So it's a good thing. Most cells that become senescent are bad players or bad apples. But the immune system comes and clears out these senescent cells. So it's it. It kind of gets arrested. And then your active immune system comes and says, these are bad apples, we're going to clear them out. What happens with age is your immune clearance slows down and you start accumulating senescent cells haphazardly, or senescent programs turn on even without a DNA damage mutation. And that's where chaos and havoc create trouble because basically these cells start accumulating and you don't have an efficient way of clearing them and they start to release factors. They're called senescence associated secretory phenotype that kind of affect their neighborhoods.
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A
So if we don't want that to happen, what should we do? Are there therapies available to us? Does it go? Is there anything beyond the common sense of, you know, don't smoke, don't expose yourself to high UV during peak UV times during the day. Like, how do you think about that?
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D
Yeah, so we've thought a lot about skin health and skin longevity. And we've created five pillars of skin span, which is this idea that we have. Our health span, lifespan and your skin span is how well our skin is functioning over time. And these five pillars, we kind of think about them as fundamentals. A lot of it is actually comes down to consistency. But the five pillars encompass sleep, diet, exercise or movement under one, and stress management, Then finally topicals recovery, what you can be doing topically to kind of help promote and retain a healthier barrier. So I'll start with sleep. There's a lot of evidence around sleep. Of all the factors, sleep is the number one factor that we can influence to have healthy skin over time. In fact, there was a study that was done looking at women who are good sleepers, so getting about seven to nine hours of sleep a night. And they'd found in these patients with something called tape stripping, where they look at the top layer of their skin or the stratum corneum, that These patients had 30% better barrier recovery than patients who did not get seven to nine hours of sleep. So that sleep is a really key aspect in better recovery. Better recovery from UV Induced redness. And they actually found that there's fewer signs of intrinsic skin aging compared with poor sleepers. So it really affects not just external skin aging, but internal skin aging too.
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A
Makes sense. And what about diet and exercise?
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D
Yeah, so diet, think about this as your edible spf. Right. So this is how we can manage to eat in ways that we can kind of create a healthier skin barrier and a healthier skin protection against UV damage. So keeping those melanocytes active and healthy is very important. They we looked at a study in older adults, a pattern with high vegetables, legumes, olive oils, and we found that about 20% of the variation in sun related skin damage actually patterned with eating eating healthier. So patients that had more meat or butter heavy patterns, there was actually a higher correlation with certain types of skin damage and wrinkling compared to a more vegetarian and Mediterranean rich diet. A lot of this is based on studies of skin disease. So a lot of times we look at psoriasis as an example. So psoriasis is a condition where patients have haphazard turnover of keratinocytes, which is that top layer of skin and the epidermis, these cells kind of regulate how psoriasis plays a role on skin. And it's an immune mediated disease. So what we found is there was a study that looked at a 16 week Mediterranean diet intervention. So by optimizing diet to have more Mediterranean rich foods, these 40, 47% of these patients actually had a better PASSI score. So Pasci score correlates with 75% improvement in psoriasis severity. So about nearly 50% improved by being on just a Mediterranean diet. And this goes on and on. We can. We've also seen similar studies related to acne risk and looking at patients glycemic load and glucose intake and how that correlates with patients that have different episodes of acne and acne flares. So really eating, you know, when it comes down to it, I think we're still learning about what are the gut rich microbiomes that will translate to the skin microbiome and how that connectivity and which, which foods are the key players. But right now we're kind of just highlighting, you know, eating colorful plants, Mediterranean olive oil, nut seeds, fatty fish, those types of simple prescriptive habits.
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A
Makes sense. And how do you think about exercise? Movement?
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D
Absolutely. So movement is so key and movement is so important in looking at aerobic exercise resistant training. It really allows the skin to perspire and that's a really important ability for the skin to get rid of toxins. So you want to sweat, you want to be able to actively create an environment so that the body and the skin is excreting toxins. So there has been studies that small trials, they've looked at elite athletes and looking at their cardiorespiratory fitness and looking at it with how it correlates to improvement in skin elasticity and resistance training. I think we need more evidence on how exercise contributes to skin turnover. We don't have good data on that yet, but what we can say is that exercise and movement contributes to the ability of the skin to perspire and kind of excrete toxins in that way. So I think that that plays a very important role. We always tell our patients to do two, two or three times a week strength training. And I know you've recently had Peter T. On your podcast and thinking about zone two training. Those are also important in connecting it back and sprinkling, those short, high intensity efforts. I think all of that collectively plays a role in keeping your skin barrier stable and strong.
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A
Makes a lot of sense. And in terms of topicals, the fun stuff, what can we. What can we do topically?
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D
Yeah. So topically, the number one product that I talk about for skin longevity is sunscreen. And there's a lot of things that we don't understand about sunscreen that we can demystify. So first, not all sunscreens will cover both UVA and uvb. So really, you want to look for the label that says broad spectrum, because that's the one that's going to be comprehensive of UVA and uvb and reapplication of sunscreen. This is so important. Important. People think, oh, I've put on sunscreen in the morning, I'm good for the day. But really, your sunscreen has an expiration date of our time of two hours. And this is regardless of whether it's a cloudy day, a sunny day, you really want to make sure you're reapplying that sunscreen every two hours. There's a lot of different ways that you can do that. I know a lot of my male patients don't prefer to feel like they have something thick or heavy on. You know, they're. They usually equate having sunscreen as well. If I'm golfing or if I'm out at the beach or if I'm doing an outdoor activity or hiking, I sunscreen on. But not as a daily habit of. I'm doing this on my way to work because most of us get a lot of sun Exposure actually just in the car ride to and back from work. So I'd put sunscreen right at the very top as the number one thing you could be doing. And then I really wanted to highlight how the skin works. So to understand what to apply for the skin, we have to understand that the skin has its own circadian rhythm. So the skin functions differently during the daytime than it does at nighttime. So the skin during the daytime, it's a barrier, it's a, a defense system. This is why your AM routine should really include products like sunscreens and antioxidants. So you really want to include vitamin C and other antioxidants that are really rich in being able to prevent oxidative stress or free radical damage from getting UV exposure, pollution exposure, et cetera. So I would highlight the importance of vitamin C and antioxidants in the morning and then at nighttime your skin circadian rhythm switches so it goes into a more repair. So it's just endured all the stress during the day and now it flips into repair mode where it gets rid of toxins and it starts to rebuild and repair. So at nighttimes there's a lot of more moisturization ceramides that you want to be including in your regimen. You want to be including peptides. Exosomes are talked about a lot these days and you really need to filter through which is the right one. But there are certain exosomes like platelet derived exosomes that I include in my skincare regimen. So those types of rebuilding ingredients are key to use at nighttime. So daytime routine as more defenses and then nighttime routine as more regenerative repair.
- [17:15]
A
So a couple, couple of follow up questions, one on sunscreen and so my view here, I'm curious what your take is. Sun is good, you need, you need your morning sunlight, you want sun in the, in the late afternoon. Sun exposure is good with the exception of you don't want to be when UV index is very high. You don't necessarily want to be out in that bright sun when the UV index is, you know, north of 8 or 10. I'm curious what number you think it is like and like you want to limit sun exposure, high UV index and Absolutely. Where sunscreen when you are out in the middle of the day and the UV index is very high, but you're probably okay if it's the morning or evening and the UV index is low with not applying sunscreen. Is that a fair take?
- [18:08]
D
Yeah, absolutely. I think sun avoidance, especially those high UV indexes, I actually say it's greater than three. So it's.
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A
Wow. Greater than three?
- [18:17]
D
Yeah, greater than three. So three to five is actually a caution zone. So you should be wearing sunscreen, seeking shade. This is like early morning, late afternoon. But people underestimate those low level exposures of UV. So 0 to 2 is your safe window. Very low exposure, minimal time to be outside. And then certainly where it's limited, unprotected sun time is a UV of 6 or higher. That's really your super cautious time. But I would, I would include three to five as a caution zone.
- [18:47]
A
And do you think so? I live in Miami now. I've been here for three and a half years. And I've noticed and I noticed with my kids, I'm relatively fair skinned. And our kids are fair skinned. My kids especially, they don't really burn a lot and they're fair skin. It's like their, their body is almost adjusted to living in South Florida. And if they're out and it's super high UV index and they're playing soccer or something, we always apply sunscreen. But like it just doesn't happen. Sometimes in the morning or even like we just. There's just a lot going on. It doesn't happen, but they don't really burn. It's interesting because they are bare skin, but I'm not seeing the burning. Are we like adjusting, Are our bodies adjusting to the climate we live in?
- [19:28]
D
Yeah. So kids actually have a lot of melanocyte resistance. And you can start to think like in areas like Miami, it's sunny throughout the year. But typically we start to see in other areas like springtime, so usually in March, April, kids get outside, they start playing baseball or you're just going outside. And we start to see these populations that do come into dermatology clinic where they're having what we call juvenile spring eruption, where they do get a little early burn. And this goes away entirely after maybe six or seven weeks of exposure to that early spring sun. And we do see this. The skin has this ability to gain resistance over time. And usually in climates that are in the, in the south or just more sun exposure throughout the year, you're going to see a lot more resistance with these kids because they're continuously getting sun exposure throughout the year. In contrast to kids that are kind of seeing more seasonal changes with the environment, they do have that early spring change where they're kind of needing to build up that resistance again before the summer. So the skin's very dynamic and it does adapt to different climates in different Ways.
- [20:43]
A
And so you mentioned peptides for the evening routine. Peptides, very hot topic. I feel like peptides are everywhere. And peptides are powerful, but they're everywhere. And I think we're just starting to learn about them. What's your view on peptide? Like, what specific peptides are helpful as we think about our evening routine?
- [21:02]
D
Yeah, that's a great, great point about peptides because it can be really confusing. It seems to be one of the most promising categories. But there's a lot of brands that I think overhype them. And this is, you know, we need to filter through and see when peptides are correct, are they stable, are they bioactive? So just defining peptides, they're just short amino acid sequences, 2 to 50. Think about them as like a biological text message. And when you have peptides for the skin, you want to think about which receptors are they going to be talking to, those signals and text messages. So in the skin, we, we look at receptors like retinoids. So, you know, topical retinoids and retin A and tretinoin. These are nuclear recept. So they are really important for skin turnover and maintaining collagen, elastin. So which peptides are currently modulating that versus aha bha. So these are alpha hydroxy acid. So these are more exfoliating categories. So looking at signaling from peptides, you really want to understand where are these signals going to and who are they talking to. So let's talk about an example of a peptide that has entered and has been in the skin space for a long time. Copper tripeptide. So copper tripeptide is GHK copper. And this can support collagen formulation or collagen formation by talking to the fibroblast receptors. It has antioxidant ability, it has wound healing support. And so think these are, these are really key in kind of supporting the skin barrier. But it really comes down to how these carrier peptides are manufactured and how stable are they and how well are they penetrating the skin barrier. So we know a lot about key ingredients that could be helpful. But where we are still exploring the science is how well they penetrate the skin barrier. And there's a lot of different types of peptides too. So there's carrier peptides, there's signal peptides, enzyme inhibitor peptides. So you're gonna see a lot of different words and ingredients and know that each one contributes to, like talking to different cell types and kind of creating what we call the extracellular matrix. At the end of the day, your skin scaffold really matters. And that dermal layer where you're having collagen, elastin, hyaluronic acid, that scaffold is what kind of keeps your skin taut and well balanced. If you get a wound, if you get an injury, that scaffold is what brings everything back together. So certain signaling peptides that can promote pro collagen and pro elastin. So those are the ones that we could be looking for like Palmitoyl Pentapeptide 4. That one was recently described to have good penetration into the skin barrier. So. So yeah, so I think, I think overall there's a lot of excitement within the peptide space and even a lot of companies talking about combination of peptides and I think that's where we're headed. So we really need to be looking at. There's not one peptide that's gonna sing the song of victory. Like you need to have a combination.
- [24:08]
E
Rei Co Op knows when you're up at 4.30am on a Saturday for a long run and you're actually excited. Not everyone gets it, but we do at rei. We're here for people who get outside gear up for your next run in store or@rei.com so, so what are your.
- [24:36]
A
Top three for someone who's listening and is about to go shopping for peptides?
- [24:40]
D
Yeah, so I think my top three would be the Palmitel Pentapeptide 4. So this was just described and trademarked as Matrixyl. So this can increase collagen 1, which we really want. And they, they'd shown up to 200% increase in collagen 1 in in vitro studies. So when it comes down to in vivo and topical application, it's going to be a lot less than that. But that's a really encouraging number for translating in vitro to human skin. So I would put that in the top. Copper peptide is, is great. It's kind of helped and shown support for collagen, elastin, glycosamino, glycans. We've been talking about copper tripeptide for a long time. So it also has a lot of antioxidant activity and some of that activity is comparable to vitamin C. So I'd put that up there as well. I'm also a big fan of hexapeptide 12. So there products that are out there that have hexapeptide and these really go into dermal collagen and dermal density. So there was a study that did a split phase study. So half the face had hexapeptide 12 and tripeptide 12 other half didn't. I always think if they're gonna then do a crossover later on to this poor person. Exactly. Split phase studies are interesting. So but that showed, that showed a lot of improvement in collagen benefits these patients. I should add that in a lot of these studies you have to have a vehicle control or a proper placebo because you can't emphasize enough the fact that moisturization or just hydration of the skin is going to have considerable benefits. So you really want to make sure that all of these studies that are looking at actives also have a vehicle control or placebo control in their arm.
- [26:24]
A
So cosmetic dermatology has exploded. Med spas are popping up everywhere and there are a lot of new treatments. So like lasers, specifically lasers. And there are certain types of lasers from my understanding, not only have, you know, aesthetic benefits, but they're also longevity benefits. In your view, like what are some of the treatments that are out there that do have aesthetic benefits? Because I think that's probably the number one reason why people walk into a cosmetic derm or a med spa. But also there are actually like, like longevity benefits. So like the butt lift probably not going to have a longevity benefit. It's like a very dangerous. But like what's a treatment that's going to, you know, give me the aesthetic outcome I'm looking for. And I'm also going to have some longevity benefits.
- [27:11]
D
Absolutely. Oh, I love talking about lasers. I'm so glad you brought this up because lasers I think are key of how you can interface with your dermatologist twice a year at least to have, have a non ablative laser. And let's talk about lasers and like why the science behind lasers is so strong. So what do lasers do? Lasers induce a controlled thermal injury. So they're like little micro columns of thermal heat injury that can then activate fibroblasts. They can then produce collagen and elastin and healthy blood vessel formulation called angiogenesis. So lasers are a dose controlled way to stimulate these exact pathways that decline with age. And we recently did a study looking at patients before and after an ablative laser and looking to see how they influence the senescent cells pathways. And what we show is that when you have a fractional CO2 or erbium laser, this can actually reduce your P16 senescent cells and restore a healthier fibroblast function. So they're actually helping to reset the skin function and kind of clear out the weeds of the senescent cells, if you will. Um, so Really, I think lasers are underestimated in this way to reset the skin and kind of create like healthier skin turnover. So there's a lot of different types of lasers. You could do a laser that has low downtime. So for some patients, downtime's really important to consider. They're not able to afford a week or two of taking time off and having a long recovery period. So if, if patients just have the shorter recovery period time, you can have them come in for a monthly laser, kind of a low energy type of laser that you could be doing once, three months or once a month, where picogenesis is a laser that I commonly use in my practice and we call it the lunchtime laser because it's super low downtime and people can come in and kind of get a, get a quick re energy or reset of their skin and then kind of follow up over time. Or you can do more non ablative lasers twice a year. They do have about a three to five day downtime, depending on the laser type. Or you could do a more ablative laser which depending on the depth of ablation could be done once every three years and you'd be good. So a lot of potential.
- [29:24]
A
And what do you mean by downtime? Does that mean. So I like not doing anything sitting down or avoiding the sun. Like, how do you define downtime?
- [29:33]
D
Yeah. So some lasers you're going to have, it's essentially creating a wound on your skin that is a very raw wound, especially with these ablative lasers. So you could have swelling, redness that can last up to two to three days. Some patients where it's an active wound, you can have oozing and a lot of debridement that you need to be actively doing. So you can get crust formation on the skin. A lot of times we, we talk about vinegar soaks that we're doing. So patients are actively doing something on their skin multiple times a day to kind of taking care of an open wound, if you will. So it takes about five to seven days with these truly ablative lasers. But you can also have much lower downtime where maybe you're experiencing a little bit of light redness, which results in improvement by the end of the day.
- [30:20]
A
And that's like non ablative. If I'm understanding correct correctly, it's non ablative.
- [30:25]
D
You can also do low procedures like microneedling. There's also micro focused ultrasound. So different lasers or different ways to kind of stimulate or activate the fibroblasts. Think about it like you, you just need to, it's almost like an injury mediated collagen stimulation. You need to create some sort of a trigger for these cell wake up, clear their senescent cells and start to rebuild and rejuvenate. You're sort of rebooting that space. So whether you're doing that by microneedling and waking them up, or whether you're doing it by micro focused ultrasound or a low level laser, a non ablative laser or a very aggressive ablative laser, it's all about kind of rebooting that system.
- [31:05]
A
I'm guessing. I'm trying to recall which I did a laser. I went in to the derm and the use case was I had some, I started to have a little bit more broken blood vessels when I moved to Miami and so I went in for that. And the derm's amazing. Michael Abruch and he was like, I'm going to give you a special laser. And this is actually his longevity benefits. I was like, oh really? And you put on the little glasses because it's super bright and it's like a little painful. I was just like puffy for like maybe a day or two and it went away and I did them. So like, I think it's, it's so interesting in that there are aesthetic benefits, but the more I learn about lasers, like there are real benefits as relates to your overall skin health and longevity goals. And they're easy. There's all different. Like there's a whole Chinese menu, if you will. It's like, do you want, how much downtime do you want, do you want a day? How frequently do you want to do this? Do you want to do it once a year? Do you want to do it once a month? Lots of options to choose from.
- [32:01]
D
Exactly. And to that point about longevity benefits, it's, you know, the laser that you probably had was a vascular laser. It's 595 nanometer wavelength, which is great.
- [32:11]
A
Because, because I love that you know that.
- [32:12]
D
Yeah, I mean it's, it's, it's. What did you see? Benefit, by the way. Did it help your redness?
- [32:17]
A
Yeah. And I'll probably go back that now. I went like four times the first year and now I'm like, like once a year, twice a year. Ish. But yes, I did.
- [32:26]
D
Yeah. And that's probably targeting. So it's, it's chronic low level inflammaging. So inflammaging can present on your skin in a lot of different ways and it's usually with redness. That's how we can, we can Target now.
- [32:37]
A
Yeah, Sun. I'm like, for sure I have sun damage. I'm 51. I have so much I did not take care of in my youth, and I'm paying for that now. What else do you think? Just staying on med spas and cosmetic derms. What do you think is completely overrated?
- [32:53]
D
Completely overrated? I think oral supplementation of collagen is completely overrated.
- [32:58]
A
Really?
- [32:59]
D
Yeah. So a lot of people think that collagen supplementation translocates to the skin directly, but it actually. It does not assist. Probably a good source of protein, but oral collagen is often marketed as a great supporter for skin, hair, and nails. But it's. You know, we really need to. We don't have a good way to promote rejuvenation of the skin collagen from oral supplementation. We could do it through all the ways we talked about with lasers and topical barrier protection and other biostimulators for the skin, but not from oral collagen supplementation.
- [33:36]
A
What about in terms of procedures?
- [33:38]
D
In terms of procedures, I think we have to be really cautious in the regenerative medicine space right now. I'm a big fan of platelet exosomes. We've actually done a lot of clinical studies in evaluating the efficacy of topical platelet exosomes, which has been great. But there's a lot of places that are utilizing these regenerative injectables, which is an area of where we need to pause and be cautious. You know, I think Kim Cardiff Kardashian talked about the salmon sperm facials, and everybody started to talk about, like, getting these injections from. They're called pdrn. They're basically just nucleotides, atcg, that you can inject, but they're sourced from salmon sperm. And it became. It is a big thing in Korea, and people were starting to utilize them here in the US but it's not FDA approved for injection. So you have to be really cautious of what med spas are marketing because most of them are not FDA approved.
- [34:31]
A
Right. That just sounds gross to me. But so what? On the flip side, what. What do you think is underrated where there is science and maybe not getting all the attention that it deserves?
- [34:42]
D
Yeah, I mean, I. I think the power of consistency. I can't emphasize enough what the research around skin span that we've done and the power of consistency with simple habit, whether it's, you know, know, diet, movement, sleep, stress management, and then combining with doing simple habits of skin skin barrier repair. Right. I should also mention colloidal oatmeal, which is in a lot of products like Aveeno, which is something really simple. But We've have over 50 years of research on it as a topical way to strengthen your skin barrier. So I think what's underemphasized is really the power of consistency. And then from a, from a more interventional approach, I would talk about biostimulators. I'm a big fan of injectable biostimulators which have been around for decades now. And they are, they, the protocol has been optimized over time and it's really creating very nice changes in the skin for collagen, elastin. So these are polylactic acid or Sculptra and calcium hydroxylapatite like radiesse. So these are injected, you have to go to a well trained injector because they, all of these procedures do carry risk of complications depending on the injector and how they're procuring their practices. But the products itself, they have really good science behind, behind them of retaining skin structure over time.
- [36:02]
A
So where do you think we're going here? You know, I talked to Teo Solemn Soleimani, who's a really respected derm on the podcast and his view was I've got young kids, I got two girls, 6 and 8. He was like, when they're in their 30s, they might actually be able to experience eternal youth. Youth, given how fast things are moving. When I think about when he was like non invasive procedures, whether it be lasers or I want to Talk about by 3D bio printed skin, like where is like are there going to be some treatments that just like completely disappear? Like does Botox just completely go away? Are we entering a world of lasers and bioprinted skin? Like how, how fast? And my. I just remember in the 80s and 90s, like if you were getting any quote unquote work done like it was you, you'd read it in Us Weekly or People magazine. Back in the day, like it was a full on like facelift. People disappear for months now. Like that still happens, but there are more non invasive treatments that are just incredible. How do you think about that?
- [37:13]
D
I think we have entered a very exciting time in science and medicine where we're meeting artificial intelligence and advancements in innovation that's really opening doors in a big way. At Mayo Clinic, we've launched a registry called Salud S A L U D. It stands for Skin Aging and Longevity Understanding Database. We are looking to profile 500 patients across three to five years. The same patient over time through a lot of different biomarkers. So looking at systemic health, your, your heart ecg, your heart function and cognitive function, and looking at specific biomarkers like your buccal swabs. We take your skin tape stripping your microbiome. We're looking at skin biopsies, blood, urine samples, peripheral vascular imaging, all this really rich data set over time, over five years. This is the first time we're going to be able to understand how one person ages over time and then look at it across different populations and couple that with our ability to automate this data and utilize artificial intelligence to understand and make these different connections. I think this is really going to change the level of what we know for what is aging at the level of the skin. We're doing some very advanced spatial sequencing. It's called spatial transcriptomics, spatial proteomics. And these sound really fancy, but what it actually is is mapping out tens and thousands of cells at the same time and how they correlate and what signals are coming at, coming from them. So think about it as before we used to know. I'm in Minnesota, so I'm going to talk about Rochester, Minnesota. Before we used to know just what's happening in Rochester, Minnesota. And now with these spatial omics data, we can look at what's happening in the entire world and to look at it and map at all these different pathways. So I think we're just entering this really data rich era right now and we can couple that to technologies like 3D bioprinting. So one of the things that we're doing in our lab is bioprinting to your skin blueprint. So we could actually take Jason, your skin cells and do an omics profile and create like an architectural blueprint of where your skin is, where are your senescent cells, where are your melanocytes, your fibroblasts, and then superimpose that into a CAD drawing. So this is basically how you can then, you know, build the blueprint of the, of the skin and then have our 3D printers with melanocytes, fibroblast, keratinocytes, all specific bioinks and print these skin layers to match your specific skin profile.
- [39:54]
A
Wow. So do you think we're getting to a place where aesthetically some, someone might be able to stop how they're aging as relates to their skin health, but at the same time, how have. It's not just the aesthetic benefit, actually have the benefit of slowing down aging internally, essentially like treating metabolic issues through the skin and also looking good.
- [40:17]
D
Exactly, exactly. That's that's our ultimate goal is to see how we can biohack from the level of the skin. Right. In a very tangible, scientifically validated way. By having all this data. This is gonna inform the science of how skin and systemic aging are connected. We're actually working closely with the NIH National Institute on Aging on a project on the largest study on aging called the Baltimore Longitudinal Study on Aging. It was started in the 1950s and they've collected skin samples. So we've partnered with them to look at these skin samples and then profile it with their systemic factors like their neurocognitive aging and their heart health. And then see how the skin and systemic health are interconnected and see how we can, what we can learn from that. So, so we're at the tip of the iceberg. It's really, really exciting.
- [41:05]
A
Any early findings from that?
- [41:07]
D
What we're finding is that there is a correlation with senescence in the skin and senescence burden in the skin affects neurocognitive function. And we actually published this work in a mice model in aging cell last year. And what we found was when we artificially introduced senescent cells in these young mice at the level of their skin, and then we looked at different cognitive function, they started to decline in their cognitive function and they also had increases in senescence associated markers in their hippocampus. So just by localizing senescence in the skin, you're actually creating end organ damage at the level of the brain.
- [41:49]
A
So zombie cells in the skin are impacting your cognitive health?
- [41:53]
D
Yes.
- [41:54]
A
And so do you think we're getting to a place where we can stop the zeta. Like well, we can't stop zombie cells. But what's like. That's fascinating.
- [42:02]
D
Yeah. We can, we can turn down the noise from zombie cells, right? So we can, we can clear zombie cells. And that is an, that is through products like senolytics and we can turn down the noise from zombie cell and that is through products called xenomorphics. So there are actives that we are exploring through clinical trials right now. There are over 50 clinical trials in the United States that are looking at senolytics and looking at the benefit of senolytics for different chronic diseases. So there's a lot of research.
- [42:31]
A
Is that over the counter? I'm not familiar with senolytics, so c.
- [42:35]
D
There are some that are over the counter. Like fisetin is over the counter. You have to be careful with how you're taking it, cuz it's, it's pulse dosing. It's not meant to be taken daily. So there are some over the counter flavonoids, they're called like supplements. And then there are more medical grade versions, D and Q. Dasatinib and quercetin are the ones that are often in clinical trials.
- [42:55]
A
Got it. But are they. So is it in, in an ingestible form or is it topical for these like quercetin for example?
- [43:02]
D
Yeah. So the quercetin. We have a study going on. We actually partnered with University of Colorado and we're doing a study on sheep and looking at sheep wool. And we've applied topical dasatinib and quercetin and seeing how the wool production is changing. We don't have the results from the study yet, we're just analyzing the wool. But there's a lot of benefits in looking at, at animal models from a topical perspective and looking at topical senolytics as an avenue.
- [43:30]
A
It's just unbelievable. It's so exciting. Do you think hair loss will eventually go away?
- [43:34]
D
Hair loss is another big area that I think is understudied and there's a lot of potential by understanding pathways in senescence and how senescence pathways we actually call them, you know, senescence induced alopecia in, in a lot of our studies because there is a, a high concentration of senescent cells that accumulate with hair follicles on age related hair, hair loss. So I think by targeting these pathways and starting early and this is where you know that prejuvenation, the idea of starting early, Even in your 20s, when you have family history of certain conditions and what can you be doing that's consistent and low level intervention that can be sustained? I think we're just learning about this.
- [44:17]
A
Those to me, is it fair to summarize that so much of what we've talked about today comes back to zombie cells and if we can really figure out what's happening with zombie cells, we're not only going to be able to potentially improve our aesthetics and skin health, but we may improve our overall health, including our metabolic health, cognitive health. Like this is really interesting and key.
- [44:42]
D
Absolutely. We've Talked about the 12 now 14 Hallmarks of Aging which include cellular senescence. And we look at cellular senescence as the linchpin within these different hallmarks. Like it really influences how the other biological factors are playing a role in overall health.
- [45:04]
A
It's incredible. We covered so much today. Is there anything we didn't touch on as relates to all the work and studies you, you've, you've got. I know, there was just a recent one. What. What else would you like to touch on before we wrap?
- [45:15]
D
I think this is awesome. I wanted to talk about. Yeah. The senescence work that we're doing. We talked about Solude, which I'm very excited about, the skin Aging Registry. It'll be about five years before it amounts to something, but eventually we'll get there.
- [45:29]
A
Are you still looking for participants? Because we could.
- [45:32]
D
We are.
- [45:33]
A
Well, we'll have to get a link from you. We'll put that in the show notes because I think a lot of people are going to raise their hand. Hand.
- [45:37]
D
That would be. Yes. Let's do it. Yeah.
- [45:39]
A
Amazing. Well, thank you so much for coming on. Fascinating work and please keep us posted.
- [45:43]
D
Thanks Jason. Good to talk to you today.
- [45:48]
F
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