Latest / The Science of Skin / Can Skincare Reverse Aging? Inside Epigenetics with Dr. Elke Grönniger

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Can Skincare Reverse Aging? Inside Epigenetics with Dr. Elke Grönniger · The Science of Skin

• 0:05
  SPEAKER_01: Hello and welcome to the Science of Skin Podcast.
• 0:08
  SPEAKER_01: My name is Dr.
• 0:09
  SPEAKER_01: Ted Lane.
• 0:10
  SPEAKER_01: I am a board-certified dermatologist and your host for today.
• 0:13
  SPEAKER_01: And I have got a very special guest.
• 0:16
  SPEAKER_01: I am in Humburg, Germany, and have the ability to interview Dr.
• 0:20
  SPEAKER_01: Elka Groniger.
• 0:22
  SPEAKER_01: Now, Dr.
• 0:22
  SPEAKER_01: Groniger is the lab manager at ByerSdoor for skin rejuvenation and longevity, which really doesn't sound as impressive as what she developed, which is a new product that really focuses on the epigenome.
• 0:37
  SPEAKER_01: And the epigenome, if you don't know, is what turns on and off genes in our cells.
• 0:43
  SPEAKER_01: So, for example, why does one cell in your body become a skin cell and another become a brain cell when they all have the exact same DNA?
• 0:52
  SPEAKER_01: Well, it's because certain genes are turned on and off.
• 0:55
  SPEAKER_01: And that's due to the epigenome.
• 0:57
  SPEAKER_01: So it's an incredibly important part of our cell, of our biology.
• 1:03
  SPEAKER_01: But unfortunately, as we age and due to other factors, the epigenome can be altered.
• 1:09
  SPEAKER_01: And this new product by Beiersdorf really focuses on trying to revert the alterations in the epigenome so our skin cells can act younger and we look younger as well and function at a younger level, which is what we're all trying to do with longevity.
• 1:29
  SPEAKER_01: So, Dr.
• 1:30
  SPEAKER_01: Groniger, thank you so much for being with us.
• 1:32
  SPEAKER_00: Thank you for the very nice introduction.
• 1:35
  SPEAKER_00: It was already explained very, very perfectly.
• 1:38
  SPEAKER_01: Thank you.
• 1:39
  SPEAKER_01: Well, can you please tell us, first of all, I always like to get the background of our guests.
• 1:43
  SPEAKER_01: And you are a PhD, a biochemist by training.
• 1:48
  SPEAKER_01: How did you get to start working on the epigenome?
• 1:52
  SPEAKER_00: Yeah.
• 1:53
  SPEAKER_00: Yeah, exactly.
• 1:54
  SPEAKER_00: My background is in biochemistry.
• 1:57
  SPEAKER_00: Um, this uh was a field uh yeah, which which uh already early on uh interests me very much because it links the molecular processes uh to a biological reaction or biological effects.
• 2:12
  SPEAKER_00: And um after finishing my PhD, or honestly, no, after finishing my studies, I joined Biersdorf as a PhD student, and it was already in cooperation with the University of Heidelberg.
• 2:27
  SPEAKER_00: So there it was really the first step um into epigenetic research.
• 2:33
  SPEAKER_00: And yeah, the collaboration uh was for me really very, very interesting because it gave me the chance to do cutting-edge research on epigenetics while also already seeing how how the fundamental research we are doing can be translated into um into meaningful applications for the skin.
• 2:55
  SPEAKER_01: Yeah.
• 2:56
  SPEAKER_01: So when we talk about the epigenome, I mean I've defined it at a very broad level, and and I appreciate the fact that you that you said it was good because you're the expert.
• 3:05
  SPEAKER_01: Uh, but when we, you know, in in our space, we hear a lot about cellular reprogramming and using Yamanaka factors to cause a mature keratinocyte or skin cell to revert to a stem cell, for example.
• 3:20
  SPEAKER_01: Is does that have anything to do with the epigenome?
• 3:24
  SPEAKER_00: Yeah, I mean, this is really fascinating, this uh cellular reprogramming process.
• 3:29
  SPEAKER_00: And yes, absolutely, the epigenome, I would say, is is the heart of the cellular reprogramming.
• 3:36
  SPEAKER_00: Um when when when people talk about uh these reprogramming or also the German ACA factors, they are referring to these uh four transcriptional factors that can take a mature or specialized skin already as you described it, and reset it back to a more youthful or stem cell-like state.
• 3:58
  SPEAKER_00: And um yeah, asking to what actually is really to be reprogrammed or reset, this is uh exactly it's not the DNA sequence itself, but the epigenome.
• 4:11
  SPEAKER_00: So as uh as we age uh or or also as uh as cells specialize, these epigenetic marks, uh in this case also DNA methylation, accumulates and uh and locks certain genes to to an on or an off position.
• 4:27
  SPEAKER_00: And the Geminica factors work by by um wiping those marks away by reopening the chromatin and re-establish uh re-establishing then a pattern that is uh typical more for the young-like and the flexible cells.
• 4:46
  SPEAKER_00: So um, in short, I would say the cellular reprogramming is kind of an epigenetic reset, and the Jamaneco factors are the tool to rewrite the epigenetic instructions.
• 5:00
  SPEAKER_01: Okay.
• 5:01
  SPEAKER_01: So for everyone listening, when you hear cellular reprogramming, maybe the Yamanaka factors, we're talking about that today.
• 5:07
  SPEAKER_01: We are in that theme today.
• 5:09
  SPEAKER_01: And just like we try and keep our bodies young and flexible, we want to keep our cells young and flexible as well.
• 5:16
  SPEAKER_01: And that's what we are discussing with reversing DNA methylation of the epigenome.
• 5:24
  SPEAKER_01: Because as you as you mentioned, Elka just wants to highlight this as we age, and because of intrinsic aging or because well, and or because of extrinsic aging, like your exposure to UV radiation or smoke or other pollutants, stress or sleep or diet, you get these little marks on your epigenome that turn on and off genes.
• 5:48
  SPEAKER_01: And those marks are called methylation.
• 5:50
  SPEAKER_01: And so if we're able to reduce or remove some of these methyl groups, demethylate, then we can have our cells act younger, which is the whole purpose for both regenerative medicine in terms of acting younger, but then in terms of longevity, we want our cells to be in that young state for as long as possible to extend and prolong our skin span, just like we are with our health span.
• 6:13
  SPEAKER_01: So uh just I know that's at a very basic level, Dr.
• 6:16
  SPEAKER_01: Groniger.
• 6:17
  SPEAKER_01: I know that that I'm, you know, you can go into much more molecular detail than I am, but I think that just to give our audience some idea of what we're talking about now, um, I wanted to lay that foundation.
• 6:29
  SPEAKER_01: And and now that we have that foundation, let's talk about this compound that you discovered.
• 6:35
  SPEAKER_01: I mean, it was well known in medicine, right?
• 6:37
  SPEAKER_01: But you realized it had great potential for demethylating the epigenome.
• 6:43
  SPEAKER_01: How did you do that?
• 6:45
  SPEAKER_00: That's uh exactly uh how you described it.
• 6:49
  SPEAKER_00: Uh, we are talking about dehydromercetin or DHM.
• 6:52
  SPEAKER_00: Uh, this is actually uh a compound which has been already, yeah, or has already a long history in the traditional Chinese medicine.
• 7:02
  SPEAKER_00: It's it's known for its uh its uh beneficial uh uh um effects on uh the overall health, like it's an oxidative uh compound, it's also inflammatory.
• 7:14
  SPEAKER_00: Um and um it's it's uh really a very uh very good compound, but nobody yet thought about epic um uh thought about DHM really being a rejuvenating uh active ingredient.
• 7:28
  SPEAKER_00: And well, we also didn't do.
• 7:30
  SPEAKER_00: I mean, um when we started to look for interventions or to look for cosmetic compounds, um we are first, yeah, we we we first needed to set uh the status uh actually.
• 7:47
  SPEAKER_00: So before we really start a screening for active ingredients, we need to build a kind of a solid uh scientific foundation so that we need to understand what is really happening to characterize the specific epigenetic changes that are occurring up on age.
• 8:05
  SPEAKER_00: I mean, you you described it uh quite nicely that we accumulate some uh DNA hypermethylation, but uh how this is really um yeah, how the dynamics are up on age.
• 8:18
  SPEAKER_00: This is really needs to be understand quite well before you really can look for um for approaches or intervention strategies there.
• 8:27
  SPEAKER_00: So this was the first thing we did, understanding what is changing and why it is maybe changing, uh, and then looking for a specific target, because this is another one which you really need before you screen for compounds.
• 8:42
  SPEAKER_00: You need to define a specific um target, an enzyme or a protein that you can tackle with active ingredients.
• 8:52
  SPEAKER_00: And once you validate it that you really have the relevant target to introduce the um uh DNA methylation changes you want to see in the end, then you can start to set up a drug discovery phase with a compound screening.
• 9:10
  SPEAKER_00: And therefore, you systematically test large libraries with compounds and molecules, which in the best case really are a kind of a range about uh the whole chemical space you have.
• 9:24
  SPEAKER_00: Uh and in this uh in this uh kind of uh epigenetic screening we did, we looked into uh more than 50,000 compounds uh in the end.
• 9:33
  SPEAKER_00: And yeah, our outcome was definitely that still until now we really haven't found a single molecule which is really outperforming dehydromersage.
• 9:43
  SPEAKER_00: So so it's really a unique uh and a powerful active ingredient we found in the sense.
• 9:49
  SPEAKER_01: So you mentioned a target, right?
• 9:51
  SPEAKER_01: You identify the target first, and then you find something that can affect that target.
• 9:56
  SPEAKER_01: What is the target for DHM?
• 9:59
  SPEAKER_00: So the target is uh an enzyme which is uh responsible for setting DNA methylation.
• 10:05
  SPEAKER_00: Um so it is uh maintaining the epigenetic pattern uh in the um or cell cycle, so to say.
• 10:14
  SPEAKER_00: And this target is so interesting because this uh enzyme um it sets the epigenetic pattern and it maintains the epigenetic uh pattern also um um uh during several um cell proliferation phases, but it gets a little bit less precise upon age.
• 10:34
  SPEAKER_00: And this is why we accumulate DNA methylation, which is not uh supposed to be there.
• 10:41
  SPEAKER_00: So we accumulate faulty DNA methylation.
• 10:45
  SPEAKER_00: Uh and what we are doing now with epicilline, uh what we are doing now with uh DHM is we we partially inhibit this enzyme.
• 10:56
  SPEAKER_00: So this enzyme has just a reduced activity.
• 11:00
  SPEAKER_00: Um and this reduced activity is now used uh really concentrated or focused.
• 11:06
  SPEAKER_00: So the enzyme is now really concentrating uh on the the most relevant, on the on the right uh epigenetic pattern, which is simuli, like in uh in the younger ages.
• 11:18
  SPEAKER_00: And this is how it it definitely uh or how how uh DHM is working.
• 11:24
  SPEAKER_00: So we need to be sure, of course, that it's an effective target, but also a safe one to address.
• 11:31
  SPEAKER_01: Yeah, and I'll get to safety in a second, but you mentioned that DHM has is well known in in Eastern medicine and traditional Chinese medicine.
• 11:40
  SPEAKER_01: I did a little bit of research and it's been shown to help with the hangover.
• 11:44
  SPEAKER_01: For example, if you drink too much alcohol, I I guess it it reduces the uh the hangover symptoms.
• 11:51
  SPEAKER_01: And then for liver toxicity as well, I've seen it's used in traditional Chinese medicine.
• 11:56
  SPEAKER_01: Um, does it have any effects on the cell that are worrisome at all besides its effect on this enzyme?
• 12:04
  SPEAKER_01: Are there any other off-target effects that we should know about?
• 12:08
  SPEAKER_00: I would say uh DHM is the flavonoid, and uh flavonoid uh has uh is is or flavonoids in general are known to have uh not really single effects, so it's not really um uh like um um specifically, it's not specifically targeting uh just uh the the one enzyme, but it's um really working uh on on several mechanisms here.
• 12:36
  SPEAKER_00: So I would say definitely there is still uh some things that we haven't looked into.
• 12:44
  SPEAKER_00: Um, but also as it has already such a long history, I would also say um that there is already also a lot of uh things uh um um uh studied uh in the context of DHM.
• 12:58
  SPEAKER_01: Yeah, so so that benefits us, right?
• 13:00
  SPEAKER_01: Because we know that it's been used in the human for for decades, if not centuries.
• 13:04
  SPEAKER_01: Exactly.
• 13:04
  SPEAKER_01: A flavonoid is an antioxidant as well.
• 13:07
  SPEAKER_01: So we know it has beneficial aspects just be by being an antioxidant and quenching free radicals, and then it has this other effect of it's a flavonoid plus, because it helps to uh reduce the activity of the the uh the DNA methyl transferase enzyme that uh is so important as you mentioned.
• 13:26
  SPEAKER_01: So that's really interesting.
• 13:29
  SPEAKER_01: And this reminds me, Elke, it reminds me of the process used for thiamidol in terms of screening so many compounds with, you know, again, a novel um tarosinase model.
• 13:40
  SPEAKER_01: Uh just that just rang a a bell in my mind for that.
• 13:44
  SPEAKER_01: But but coming back to DHM, you mentioned, you know, we talked about off-target effects.
• 13:51
  SPEAKER_01: We think it's okay, so it's it's we understand it's a flavonoid, probably extremely safe.
• 13:55
  SPEAKER_01: But you know, if you are reducing the methylation, right, some methylation is good.
• 14:01
  SPEAKER_01: You you you know, you don't want to turn on oncogenes, for example.
• 14:04
  SPEAKER_01: Um, and so how did you assess what genes were being affected by the reduced activity of the enzyme through DHM uh use?
• 14:17
  SPEAKER_00: Yeah, I mean, this is really a good point.
• 14:20
  SPEAKER_00: We have, of course, also methylation that needs to stay, uh, that we need to keep uh because we do not want to uh activate oncogenes.
• 14:29
  SPEAKER_00: And uh when we did our studies um for DHM, um of course we did a lot of in retro studies where where we also looked into several uh safety readouts um and and endpoints.
• 14:44
  SPEAKER_00: Um this is something we make always sure because the safety of our active ingredients is is really one of our utmost importance.
• 14:52
  SPEAKER_00: So there is a comprehensive uh safety uh um and toxicity assessment before we go into any kind of products and before we are going really into uh into the real situation, into the real uh clinical studies.
• 15:10
  SPEAKER_00: But once we are there, of course, specifically uh for this um for this active ingredient, we also looked into the gene uh activation.
• 15:20
  SPEAKER_00: Um so we conducted uh a clinical study where we asked our volunteers to use either a vehicle cream on their skin or a virum containing DHM.
• 15:32
  SPEAKER_00: And they used uh this or both uh creams for eight weeks, and afterwards we took or we obtained skin samples, we uh analyzed the gene expression, and on the one hand side, we looked really for the age-related silence genes that we wanted to reactivate with this active ingredient and which we indeed could see.
• 15:56
  SPEAKER_00: And on the other side, we used the same sample set and uh also analyzed oncogenes, which are already um described to be very relevant in the context of skin.
• 16:07
  SPEAKER_00: And here we couldn't see any effect at all.
• 16:10
  SPEAKER_00: So these were, I would say, um the the studies uh I would highlight in this context.
• 16:18
  SPEAKER_01: Thank you.
• 16:18
  SPEAKER_01: And and Dr.
• 16:19
  SPEAKER_01: Grandjugar, we there's a concept called pre-aging, right?
• 16:23
  SPEAKER_01: Where we are starting to use uh dermocosmetics or cosmosceutical products earlier and earlier in life in order to extend longevity, but also to stop the uh the symptoms of aging, right?
• 16:40
  SPEAKER_01: If we think of aging as a disease, then we we are trying to stop or delay them as much as possible.
• 16:46
  SPEAKER_01: Would you recommend that DHM be used in both the population that already has methylation on their DNA?
• 16:54
  SPEAKER_01: So in other words, those those who either through intrinsic and or extrinsic aging need the demethylation?
• 17:01
  SPEAKER_01: Or do you think maybe it's both, do you think that this product should be used for those who are young in order to prevent that bad methylation?
• 17:11
  SPEAKER_00: This is a very good question, I would say.
• 17:13
  SPEAKER_00: And uh it would be really, really nice to have uh even more studies uh on long-lasting effects.
• 17:21
  SPEAKER_00: Right.
• 17:21
  SPEAKER_00: So far we looked um at time points um which are uh four weeks or eight weeks after starting our treatment with uh DHM, but we do not have really long-term studies.
• 17:36
  SPEAKER_00: This is something I would definitely go into also in the future to see how far we really come and um also looking at the consumer range.
• 17:48
  SPEAKER_00: I mean, so far, of course, we we when we um started to set the fundament of uh and the basis of the epigenetic um research, we looked into age-dependent changes, which means, of course, we looked at younger people and also uh to mature skin and tried to divide those uh also in into groups.
• 18:11
  SPEAKER_00: But the question is when uh is mature skin really starting to be mature skin?
• 18:17
  SPEAKER_00: Uh this is a question we haven't answered yet, honestly spoken.
• 18:21
  SPEAKER_00: But what we can see in our clinical study is that uh starting uh, I think with a um with a consumer age from 40 years on, that we do not see any age dependency uh in the response to uh DHM.
• 18:39
  SPEAKER_00: So it's it makes no difference if you start uh with uh in within your 60s or your 40s, you would um always come to a reduction of the biological age.
• 18:51
  SPEAKER_00: So from my perspective, I would say it makes definitely sense to start early on.
• 18:56
  SPEAKER_00: Um, but it's also never too late, I would say.
• 19:00
  SPEAKER_01: Yeah, it sounds like you have data to support those statements.
• 19:03
  SPEAKER_01: Um and so that's that's great.
• 19:05
  SPEAKER_01: And it like I said, there's a theme right now in skincare, and I think in dermatology overall, to start preventative care as early as possible, whether that's a broad spectrum sunscreen and these different products that are now affecting the UV pollution intrinsic and intrinsic uh aspects of aging that can affect the DNA.
• 19:29
  SPEAKER_01: And I I think we wanted to highlight this on the podcast because this is really the first product to hit the mass consumer market that targets one of the hallmarks of aging in such a precise manner.
• 19:41
  SPEAKER_01: Um, and it was really developed in a bespoke manner to do that.
• 19:46
  SPEAKER_01: Uh, so it's not like we're looking at a niacinamide that has been on the market forever and understanding how it affects the hallmarks of aging.
• 19:55
  SPEAKER_01: This is this is purposefully built for a hallmark of aging, which make it unique.
• 20:00
  SPEAKER_01: And I think um we believe that the future of skincare is going to be squarely within the realm of longevity.
• 20:08
  SPEAKER_01: We believe that skincare needs to target the hallmarks of aging, 13 now.
• 20:14
  SPEAKER_01: I understand there's going to be more in the future with the new publication.
• 20:17
  SPEAKER_01: So uh this is you know, the future is happening now, actually, with skincare with this product.
• 20:24
  SPEAKER_01: Um, not available yet in the United States, but uh it certainly is important for us to keep an eye out.
• 20:30
  SPEAKER_01: But Dr.
• 20:31
  SPEAKER_01: Groniger, because you know, you develop this product, you're at the very cutting edge uh of skin skincare science.
• 20:38
  SPEAKER_01: What do you think is next?
• 20:40
  SPEAKER_01: You know, I as I mentioned, I believe we're we're targeting the hallmarks of aging, but what do you think is next?
• 20:46
  SPEAKER_00: Yeah, maybe I can uh also uh comment uh also a little bit on uh on the skin longevity and uh also how we see skin longevity because I think this is really uh changing at the moment.
• 21:02
  SPEAKER_00: There are a lot of uh products and companies who are really talking about skin longevity, but just using uh old uh or the the former anti-aging solutions uh and just referring now to skin longevity.
• 21:20
  SPEAKER_00: And I think there's really a difference between those angles.
• 21:23
  SPEAKER_00: Um for for us at Biostoff, skin longevity means really, as you mentioned, to uh to target the hallmarks of aging.
• 21:32
  SPEAKER_00: Why?
• 21:33
  SPEAKER_00: Because the hallmarks of aging are the root cause of aging.
• 21:36
  SPEAKER_00: So our understanding is that it uh does not really um make sense if you want to have a long term um maintenance of skin functionality just to correct superficial uh um um um deficits.
• 21:54
  SPEAKER_00: But you really need to tackle the problem at its root, and this is what we are trying to do.
• 22:00
  SPEAKER_00: That we are really targeting the root cause of skin aging and referring to these hallmarks of aging you mentioned, there are, of course, they are all relevant when it comes to aging.
• 22:15
  SPEAKER_00: But also there are some which are called primary hormones.
• 22:21
  SPEAKER_00: And these primary hallmarks I would say are really defined as causal for aging, while the others are more the response of the cells or the consequence of the damage.
• 22:34
  SPEAKER_00: So when it comes really to tackle the root cause of aging, from my perspective, it makes really a lot of sense to tackle one of the primary hallmarks.
• 22:44
  SPEAKER_00: And there we are with epigenetics, we are really on the page.
• 22:50
  SPEAKER_00: This is why I really believe that we are tackling a very relevant main driver for aging and why we also contribute to the skin longevity topic at the moment.
• 23:03
  SPEAKER_00: But your question was a different one.
• 23:05
  SPEAKER_00: You asked what the next hot topic could be in skincare.
• 23:12
  SPEAKER_00: And here I would say a lot of groups are really looking into understanding the complexity of skin aging and skin health.
• 23:24
  SPEAKER_00: It's not only superficial, it's not only one cell type, it's not only the skin, but also the whole body.
• 23:32
  SPEAKER_00: And the system itself is feeding into how the skin structure is developing.
• 23:41
  SPEAKER_00: And I think today, with all the technological possibilities we have, and also with all these advanced AI tools we have, I think there is really the future that we really understand even better the complex biological processes to then in the end uh define also new breaking through interventions in skin science.
• 24:14
  SPEAKER_00: I think this is really the way to go, to have a broader, holistic look uh at the skin and not only uh looking at uh at the tissue itself.
• 24:26
  SPEAKER_01: I just want to remind everyone listening that the hallmarks of aging are considered hallmarks because, first of all, they're related to the aging process.
• 24:34
  SPEAKER_01: And second of all, when they are targeted by therapeutics, they they reverse or delay the aging process.
• 24:40
  SPEAKER_01: So every one of those hallmarks is a therapeutic target.
• 24:43
  SPEAKER_01: Uh and so just by its very nature.
• 24:46
  SPEAKER_01: And that's what companies are doing now is they're able to, through all of the techniques that Dr.
• 24:51
  SPEAKER_01: Guniger just mentioned, develop molecules to target the hallmarks of aging.
• 24:57
  SPEAKER_01: And so we'll see more and more of that.
• 24:59
  SPEAKER_01: And it's not just going to happen in in dermocosmetics.
• 25:03
  SPEAKER_01: As I've said before, what happens in dermocosmetics usually precedes what's happening in medical therapeutics, just because it's it's just a faster development process.
• 25:14
  SPEAKER_01: And so we are now starting to see early companies, young companies, come up with products that are going through the FDA process to target precancerous lesions, for example, uh, on the skin, internal cancers, but also inflammatory disease.
• 25:31
  SPEAKER_01: So it's important for everyone to be fully aware of the hallmarks of aging because they are going to be targets for both therapeutic uh diseases, that they're going to be targets therapeutically for both inflammatory diseases, malignancy internally and on the skin.
• 25:48
  SPEAKER_01: Uh, so so that's why it's a call to action for everyone to be intimately familiar to with the hallmarks of aging, which are constantly evolving.
• 25:56
  SPEAKER_01: Um, Dr.
• 25:56
  SPEAKER_01: Groniger, we we could go through so much more.
• 25:59
  SPEAKER_01: And I thank you so much for your time.
• 26:01
  SPEAKER_01: Uh, we've we personally had a long day today reviewing a lot of data, and I uh really appreciate you doing this for us.
• 26:10
  SPEAKER_01: Um, we learned a lot.
• 26:12
  SPEAKER_01: I think we will uh I think everyone will probably need to listen to this a couple of times to really understand and absorb all the information that you gave us.
• 26:20
  SPEAKER_01: But I think we need to do a follow-up uh podcast episode again where we can talk more, even about epigenetic clocks, because I know you were developed a very unique epigenetic clock, which stay tuned.
• 26:32
  SPEAKER_01: That'll be another episode.
• 26:33
  SPEAKER_01: But thank you so much.
• 26:35
  SPEAKER_00: Thank you for your interest and also for the nice questions.
• 26:38
  SPEAKER_00: And I would be happy to have a uh part two uh on epigenetic clocks.
• 26:43
  SPEAKER_01: Okay, let's do it.
• 26:44
  SPEAKER_01: I'm Dr.
• 26:45
  SPEAKER_01: Ted Lane.
• 26:45
  SPEAKER_01: Thank you so much for listening to the Science of Skin podcast.
• 26:48
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• 26:52
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• 27:02
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• 27:08
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• 27:10
  SPEAKER_01: Thank you again.