Understanding Barrier Repair with Dr. Carl Thornfeldt of Epionce

Skin Anarchy

Dermatologist Dr. Carl Thornfeldt, founder of Epionce and holder of 22 patents, shares the scientific origins of barrier repair skincare dur

Key takeaways

The stratum corneum functions as a regulatory tissue that actively repairs itself when damaged.
Barrier repair involves rapid synthesis of cholesterol, ceramides, and free fatty acids within minutes of injury.

Main topics

Skin barrier biology
Epidermal self-repair mechanisms

Notable quotes

The stratum corneum is a regulatory tissue—not just a passive barrier.

Conclusion

Dr. Thornfeldt's journey from personal struggle to scientific breakthrough

Transcript preview

Speaker 1 (0:00) Hey guys, welcome back to Skin Anarchy. It's a very, very special episode today because we're going to be interviewing a true pioneer in the skin health space. He has brought a brand to us that has been paving the way for so long. Epionce has been around, I think, long before any of the skincare brands that we see right now that are now focusing on barrier health. They were doing this way before. And, you know, it's just one of those trailblazing brands that has really paved the way for so many. So without further ado, please welcome Dr. Carl Thornfeld. Welcome, Dr. Thornfeld. I'm so honored to host you. Speaker 2 (0:28) Thank you very much. And it's a pleasure to be here. And thank you for inviting me. Speaker 1 (0:32) Yeah, I know. It's a pleasure to host you and to learn from you today. I can't wait to dive in. You know, I know that your journey has been, you know, long before the brand even started. You know, it was really rooted in innovation, rooted in trying to understand the science of the skin. And I'd love for you to walk us down memory lane and tell us, where did the science really begin? And how did that evolve into the brand? Speaker 2 (0:53) I was afflicted, unfortunately, with significant atopic dermatitis when I was a child. And even though my dad was chief of pediatrics at Oregon Health Sciences Center and the second board-certified allergist in the state of Oregon, I was still... in and out of treatments and really suffered significantly from this time. So I always had this interest of being able to understand what actually happened to me and why was that occurring. So I was called to rural America. And after I did my training at my undergraduate at Oregon State and then my medical school in Oregon Health Sciences Center, I should say I trained in family practice because I felt I could be a better specialist if I truly understood the whole human body. But when I got out into practice in the high desert area of Eastern Oregon, where I was the only dermatologist, full-time dermatologist for 30,000 square miles, 140,000 people scattered over 10 counties, what was interesting about that is I really... got to see the extremes of skin insults. It's an agribusiness type area. So there was ranching, farming, as well as lumber and mining and so on. With big variations in temperature from 20 below in the wintertime to 115 in the summer, you'd really get to see how many of the skin reactions would occur. And by that, what I meant was that when I went into training, I thought, you know, if I trained at the top, programs, I'm going to really know how to fix people. And when I got out into practice, I thought the reason people didn't get well, the doctor wasn't quite smart enough. Well, when I was in San Diego, UC San Diego, I'd see patients like 15 times for a disease. Now, I didn't see them anymore. I thought I cured them. Well, I came out to this rural area and realized after I'd see a patient 15 times and I didn't see them, I'd see their families at the one hospital or at one of the high school football games. We had one mall serving all that area. And all the major roads to go to Boise all went through. And so I'd see the family members and I would ask, oh, how's such and such doing now that he's cured? Well, you know, doctor, he isn't really cured. He's really not doing very well. And I'll tell you, after 18 months, I was just like, how come people aren't responding? Now, you have to go back to what it was like in those days in the early 80s. Most effective agent for inflammatory skin diseases had a 56 percent cure rate. OK, or clearance rate, I should say. But I never had a patient come in and say, hey, can I get 56 % better? And I never wanted that. I wanted to completely get clear and stay clear and not have recurrence. I was actually on top of a mountain. I relaxed by punishing my body with physical things, climbing mountains, open water swimming, things like that. And it really struck me going up over 9,000 feet how the sun felt stronger, the wind was stronger and so on. And it struck me that, you know, what the major purpose of skin is. protection. Everything we were doing, all the research we were doing in the retinoids and the work I was seeing done on others with hydroxy acids and all the pioneering work we were doing with steroids and other topicals that resulted in some of my 22 US patents. Anyway, I really realized that all of those were really destroying the barrier more. And could that be the real issue? And there were particularly two diseases that I thought were important. So I'll let you hang on that for a minute. Speaker 1 (4:11) Yeah, no, I'm very curious because, you know, it's interesting what you're saying, because we don't talk about extreme environments to study anything. We have to understand the extreme. So it's very, very interesting what you're explaining here, because the skin is usually discussed in a way of like, okay, you know, we're all living in the same place, but we're not, you know, and we don't have the same conditions. We don't have the same exposures, environmental, whatever that might be. So that's very fascinating. But what were those two conditions? I'm very curious. Speaker 2 (4:38) Okay, so the first one was winter itch. And what we would see then, that's also known as eczema estivale. And about right after Thanksgiving, when we get our first really hard freezes, usually early November, about a month later, people would start getting itching, particularly starting on their lower legs, hands, and feet, and could become quite widespread. What was interesting about that condition, it really didn't matter what we did for treatment. It always burned out about spring vacation time, about mid-March, it would go away. Speaker 1 (5:08) The Speaker 2 (5:08) other condition was another disease that also afflicted me, which is called polymorphous light eruption. And that's that true sun allergy that people talk about. It's triggered by ultraviolet A. And that would start about mid-March and would burn out about the 4th of July. And I often wondered, how does that do it? How is the skin regulating itself? And what's actually going on there? Well, at this time, no research had really been done on the epidermis itself. And so I started looking at that and biopsying and found that, in fact, there was, they moved into. winter itch, the skin barrier, the epidermis and the stratum corneum where the barrier resides became thinner and more disrupted. And the amount of sebum being produced, which provides key barrier oils, was also diminished. And then in the spring, under the auspices with the UV light particularly and more activity, you would see the epidermis thicken, the stratum corneum thicken and repair, the sebum production increased. And that accounted for the spontaneous resolution. So then the question, because I had the mind of an investigator, how does that happen? What are the regulatory pathways that actually regulate the epidermis and the sebum production? And so that's... started a nine-year odyssey for me in understanding the molecular and cellular biology of how the epidermis really regulated itself. And so, as you know, the vast majority of inventions are not done by just a single person. It's usually a team. And there was one other individual, true renaissance man, Dr. Peter Elias, who was working in skin lipids as well. I went to him and said, you know, let's go ahead and form a research organization focused right on the epidermis. And we were the first ones that did that. So we found this group. We put together a whole team, including Dr. Man Mao Guing, who I worked with very much, and then Ken Feingold and a whole really great group there at UC San Francisco. And so working together, we made significant discoveries. And I think one of the major points was that we then learned how the skin regulated itself and realized the stratum corneum was a regulatory tissue. Profound concept. So what we found that when the skin was injured for any cause and the stratum corneum was disrupted, That would trigger not just a mild erythema and acute inflammation to increase blood flow to the skin, but it also, within 10 minutes or so, would trigger synthesis of cholesterol, a number of the ceramides, there's 11 ceramides, and certain free fatty acids, especially linoleic acid. And within 45 minutes, these were being synthesized by the epidermal cells. And then that was also being deposited out in the stratum corneum barrier. So that provided the mortar. for the stratum corneum. And then what we also found is that would increase basal cell proliferation and would also trigger an acceleration, a significant acceleration of the cellular differentiation to form the bricks in the outer layer. Now, Peter Elias is the one who came up with the phrase bricks and mortar, and that's really exactly what it is. So you have the key protective barriers, the stratum corneum, and it has these protein bricks that are a-nucleot cells, but all also hold water packets as well as 97 % of it being protein. And then you had it embedded in these layers of these key lipids. And it turned out it was those three key lipids were critical. And so we did more research into that as well. Speaker 1 (8:37) Yeah, that's, you know, what's fascinating, what you're saying is I had this argument with somebody like, I mean, you discovered this, but we're, you know, the students that have learned from this. I mean, I was arguing with somebody, I'm like, you need those three lipids, you know, you need them to be able to actually create the lipid architecture, you know, the actual three to one to one ratio, as many call it, you know, and people don't believe when you say that they don't believe that. And I want you to go into that, like, if you don't mind, like explaining the importance of this, because most of the time, the stratum corneum is looked at as it's just the dead layers. You know, it's just the dead layers of the skin. No one discusses exactly what you're talking about, which is that downstream signaling that happens and why the integrity matters so much. Because can you dive a little bit more into those pathways? Sure. Yeah, Speaker 2 (9:20) I'll gladly do that. Thank you for that comment. And also it's... Great to hear that you have that interest as well. And of course, with your background in medicine, I know that's very interesting for you as well. So what we found is that normal baby skin has a one-to-one-to-one ratio of cholesterol, ceramide, and free fatty acid. The question then was, what triggers the repair process? And so what we found was that when we looked at various ratios of the components, so the cholesterol, the ceramide, number of ceramides, and the free fatty acids, which we found that for optimum activity of barrier repair, 50 % of those free fatty acids needed to be linoleic acid. We found that there were two concentrations or two ratios, I should say, that actually triggered a barrier repair. And this was work that Dr. Manmau-Ging and I did. We did... many, many experiments looking at all the different ratios because the cardiologist several months previously had published about the ratio of the omega-3, omega-6 for cardiac function. And I thought, okay, could that be actually the signal that was going on in the skin? Because there's variations as people mature and get exposed to all these environmental insults, there's got to be a protective mechanism. And sure enough, we found that the three to one to one ratio triggered a dramatic. epidermal proliferation and differentiation. And then it dramatically increased the production of the stratum corneum. Instead of taking normally 28 days, we could get it produced in about three days. And we also found that a two-to-one-to-one ratio also had some function. And there's a company now that sells a product, a 242, which is similar to that. But that was 40 % less effective than the three-to-one-to-one. And the 3-to-1-to-1 is still considered the gold standard. I mean, we did a literature search just a month ago or so, and it's still considered the gold standard for barrier repair as far as the amount of data proving its functionality and clinical studies and so on documenting that. So that was really critical. But the fact that the problem then was, all right, now that we have this ratio, how do we apply it to the skin? to keep it going, not just put it on for temporary later, but we needed to upregulate the regulatory aspects of that. So the regulatory lipids of various protein signals, various elements that were important. And so the formulas that we made really had not just the three to one to one. but also triggered all the metabolic pathways to make more. So you continue to have benefit throughout the day when you're getting all these exposures to the expososomes, which is all the environmental insults. And so that was also one of the big aspects. At the time, keep in mind, this was in the 80s, there was really no... synthetics that we could formulate together that would actually trigger any of those aspects. I mean, it's really complex. I mean, there's eight inflammatory pathways of the chronic inflammation going on. There's five barrier pair pathways. So you have to activate those four, suppress those eight. And so having had experience with herbs and primarily growing up with my dad on a sheep farm, I said, well, let's go to the herbal arena and see what we could find. So we screened a number over a hundred. different herbs that have been reported to have any benefit in skin diseases. And we wanted to see, do they actually work? How do they work? Is it berry repair? Do they work on the inflammation and what concentration is required to produce the effect? Because as you know, as a physician, really anything you put on, there is a peak. It's a bell-shaped curve and you want to be in that therapeutic concentration. And the fallacy, one of the fallacies in America is that more is better. Well, it Speaker 1 (13:07) doesn't happen that way in the human bodies, you will know. Speaker 2 (13:10) So we really wanted to find out what those therapeutic concentrations are, and we were able to discover all of that and figure out the interaction of how barrier disruption played a role in triggering the chronic inflammation. As a matter of fact, I first published that in 2005 in Cosmetic Dermatology, that the chronic inflammation was actually, as a result of the barrier damage, was actually the trigger for most of the damage that we see. in photoaging. Since that time, other people have now labeled it as inflammation, but that was subject to one of my patents many years ago. Does that answer your question pretty well? Speaker 1 (13:48) Yeah, no, it does. And it leads me to so many other questions because, you know, you brought up, for example, linoleic acid, and I really would love to learn more about linoleic acid because I know it's behind creating one of the ceramides that's an anchor for that orthorhombic formation of lipids. And so can you talk to us a little bit more about linoleic maybe, because we don't really see this a lot in the ingredient list. It doesn't come up anymore for some reason, but it's so essential. Speaker 2 (14:11) It is essential, and you're exactly right. With the 11 ceramides and... That also includes phytosphignosine, which we used a lot of because that's the master one. All the others come from phytosphignosine. So that was our major ceramide that we used. But back in the 80s, there weren't any really good sources of ceramides. And the phyto ones had not really been well characterized. There was an animal one that we had a lot of interest in. But being a physician, I wondered, well, what about the safety of that particular organ extract? And what do you know? It had prions in it. So we completely decided not to use that.