In this episode of Derms on Drugs, the hosts discuss atopic dermatitis (AD) as a multi-organ disease through the SING (skin, immune, neuro, gastroendocrine) framework. Dr. Peter Leo explains that AD involves skin barrier defects, immune dysregulation (TH2 cytokines), neurogenic itch (substance P), gut-skin axis (microbiome and short-chain fatty acids), and stress-related endocrine effects. He advises clinicians to validate patient concerns about diet without promoting elimination diets, which lack evidence and may worsen outcomes. Instead, he recommends a healthy diet and probiotics to support gut health, while emphasizing that topical treatments and biologics (e.g., dupilumab) are primary therapies. Dr. Tim Patton presents a study on diet and AD severity in children, which found no correlation between food choices (including ultra-processed foods) and disease severity. Despite 30% of patients using elimination diets, often based on perceived triggers, the study and guidelines from major dermatology and allergy organizations conclude that elimination diets provide little to no benefit and may be harmful. The hosts agree that while diet influences AD through the microbiome, effective management relies on standard medical treatments, and clinicians should steer patients away from restrictive diets that may lead to non-adherence to proven therapies.
Welcome to season two of Derms on Drugs and Video Podcast brought to you by Scholars and Medicine, the best educational platform at dermatology and provided no cost to medical providers. Derms on Drugs is we're cutting it's term meets, yeah, it's a miscommunity. A Matt Zyrish from Dr. Dermotology in each week, I'm joined by my residency, buddy, Dr. Laura Ferris from the University of North Carolina, Dr. Tim Patton from the University of Pittsburgh. And we use our 60 years of combined degree experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be on the cutting edge of GERM and you actually have some fun listening. New episodes drop every Friday on Scholars and Medicine, Apple Podcasts, Spotify and other major podcast platforms. And a reminder that the video, the podcast is of a video component that has the key figures and tables from the articles we talk about. And today's episode is supported by Lilly, a medicine company. This week we have a guest that we are so excited about. We've got Dr. Peter Leo from Medical Dermotology Associates of Chicago joining us this week. Dr. Leo, how you doing? I'm doing great. Thank you so much for having me. I am a longtime listener and first time caller and it is really a thrill to be here. You know what that phrase I bet two thirds of our listeners, they probably never listen to A.M. talk radio, right? It's true. Lock that listener first that color. We'll in their 50s love us. That's why I get the references. Exactly. Well, let's go ahead and get started. So let's see, here, why don't we start with Dr. Ferris? Dr. Ferris, what do you got? All right. So I have a paper that is the skin immune neuro gastroendocrine or syng system lighting the fire on a topic dermatitis research. This is by Paz and Dr. Leo and this was published in dermatology, practical and conceptual. I think it's the name of the journal. And so I thought this would be great to be able, I love having a paper and then being able to talk about it with the author. So this is really thinking about a topic dermatitis, you know, not just as a skin disease, but as sort of a multi organ system disease. So syng, skin, immune, neuro gastroendocrine. And so, you know, I think we've thought about a topic dermatitis as being skin and immune system, but this really brings in sort of the neuro gastroendocrine aspect of it. So I thought it was an interesting paper. So let's start with, we'll go through it alphabetically, S skin. So we know, we've all learned the phlegm mutation is important in atopic derm, tight junctions are important. So what they really emphasize is yes, the epithelial barrier matters, but they also talk about like the role of impaired care tenacytes. So the care tenacytes being important in sort of being cells that are involved in the pathogenesis of AD and the itch scratch and barrier dysfunction and sort of how that interacts with the rest of the immune system. So emphasizing yes, amolians, barrier protection, all of that is like is really, you should think of it as upstream disease modification. That's police. So it's, we're talking about it more. I'll let you get in. We'll talk about it more. I, immune, Axa, Axis. So we know that there's, you know, TH2 cytokines, IL-451331, we know we've got biologics that target those, but that in chronic disease, you also get TH1 and TH2 responses and that there's a skin associated lymphoid tissue that is sort of driving the whole process and that that involves also the care tenacytes and longer on cells sort of beyond, mass cells, eosinophils beyond just the T cells. So you know, that's why we know that, you know, we know the immune systems involved, we know that this is why most of the drugs that we have that work for this actually target different arms of the immune system. And you know, they also point out that, you know, not every drug works well for every patient or equally well for every patient. So we ought to think about more precision, precision medicine, like, you know, there's probably different endotypes within AD and, you know, we can maybe try to find biomarkers of response to particular drug types. We can talk a little bit about what's maybe out there coming and is neuro. So, you know, the itch is what drives the disease. It's an important concept, but then they also mention that, you know, we need to think about neuropeptize substance P, CGRP. So mentioning that, you know, these are involved in driving the immune response, but they're also potential future targets. So pointing out things like substance P is overexpressed in AD, drives things like mass cell, digger, annihilation, fuels the itch. So you know, we could think about, you know, novel sort of novel therapies that might be based on this G. So this is gastro or gut. So this is, I think, the thing that is really different. So I think, you know, I used to kind of think, oh, patients, always are like, is this related to my leaky gut? And I kind of thought that was a bunch of BS. But the point here is that, you know, there is actually a connection to the gut and the skin. And I like one of my favorite papers. The last year was a story that showed a paper that showed in mice. If you have cutaneous damage and then you get sensitized to it, or you get exposed to an antigen through the gut, you actually will be more likely to make an alert to develop an allergy to that. So there really is this like skin gut access. So you know, there's the microbiome and they talk about, you know, specifically bifidobacterium and lactobacillus are sort of good and protective for the skin versus C diff and E. coli are worse and can make disease worse. So probably related to short-chain fatty acids like butyrate acetate and propryonate that modulate T cell functions. So, you know, what does that mean? You know, focusing on things like, you know, asking about GI symptoms or thinking about diet diets that maybe we can talk with Dr. Leo about what are the diets that you would recommend. But things that sort of promote a healthy microbiome. We've also in the podcast talked about free about what's that? Whatever you want. Whatever you want that you actually presented a paper on using one of the what the probiotics that's as close to with improved disease. So that's right to eat whatever you want. All the junk food, processed foods, all of it. Just take a probiotic and you'll be fine. Okay. We'll see. We'll see. And then E is endocrine. So stress activates the central HPA axis. So C-R-A-C-T-H cortisol. The skin actually has its own local HPA-like system. And that cortisol signaling, which you would think, right, steroids make atopic dermatitis better. It should be protective, but that it's actually those are that topical steroids and probably even like endogenous steroids are contributing to barrier dysfunction. So we ought to a rethink the topical steroid model, but be also think about how endogenous steroid production through stress might be making this worse. So where does it leave us? That kind of gives us a more integrative approach to think about the skin barrier, the immune system, the neuro axis, the gut skin axis, and then stress. So I thought it was a nice summary. I would encourage people we can put this there, the link that there's, you know, a couple nice figures that sort of show how these all interact with each other. So Ferris, all right, that the Leo guy, he likes to publish all this weird, I know clinical relevance at all. So Ferris, was there any, was, was there any clinical takeaway from this of like, oh, so we should do this, right? Is. Yeah. I mean, and that's what I want to ask. And maybe since he's on, we'll just ask him. Like for Dr. Leo, I thought this was really, you know, I thought it was an interesting way to put it all into a framework. So I guess to Matt's point, I think what, what do you practically tell people to do? So do you give people, so think it's starting with like the gut. Do you recommend a certain diet and do you recommend certain probiotics? No, thank you. And that was beautifully, beautifully presented. I think on one hand, if you step back, you could look at this and be like, well, duh, this is just saying that like, eczema is not just skin deep. Like yes, it affects every organ. The body is connected. Like it sort of seems ridiculous and maybe overly reductive. But on the other hand, I think it is kind of magical to start, you know, with the deep dive on the skin and really look at that separately, but then say, wait a minute, you're right. This is very much connected. I always show my patients. I'm like, when you think about it, it's skin, skin, skin, skin, skin. And as you round the corner of your lips, it's gut. You go to your own gut epithelium, right? That's your gut. They're part of the same tube inside and outside. And we think about how deeply connected they are. And I love that you alluded to that leaky gut thing because I started in the same place. I thought it was sort of a metaphor or some way of thinking about it, but it turns out there like legitimately is a way to measure gut leakiness. Like it's a thing and it correlates with AD severity. So I love just looking at all these different connections. Now, the heart part is what does it mean for us as clinicians? Can we act on this? and the truth is, I don't think we can act.
easily on all of these factors, at least equilaterally, right? And that's why I say also to my patients, I say, yes, your gut is part of the story, but I can't reach your gut. Like what I can reach is your antacubital fossa where you're scratching right now. I can put something there. We can change that environment. We can fix behavioral pieces too. We can use things like everything from habit reversal therapy, this kind of quirky thing where you give a replacement behavior to stop that sort of itch scratch cycle to acupuncture to help with some of the nerve aspects. So we have these little pieces of the puzzle we can do. And I think when you explain it this way, it's sort of, I think it puts the patients at rest. It's like, okay, this clinician is really thinking about me broadly. They're not just talking about the skin, but they're also being practical in that you can't necessarily do much with the endocrine part of this at this point in time. And that's maybe going to be something that's downstream. So patents habit reversal therapy is drinking beer. So that's the every time he wants to scratch, he just drinks. But the thing that I think is like the liver is starting to fail and I'm much more itchy. So this is really not working as I plan. So the one other thing that I find super clinically relevant here is the idea that the gut is playing a major role in the disease. And where that changes it is, right? What's one of the questions that y'all we all hate, right? So what food should I avoid last three months ago? I ate tomato and I flared. So I've been avoiding red and I was good, but then I ate a banana and I was okay. But then when I ate a tomato or a banana together, I didn't flare. So I think maybe orange foods are the prop. And you're just like, shut up. Go see an allergist, right? But right, historically what we told people is you're not allergic to any foods. Food allergy is not driving your AD. And I think that if that's where we stop, the patient then leaves our office, cause their mom says mom, that dermatologist doctors never listened to you. They didn't think that tomatoes were playing a role. They don't know what they're talking about. Remember whenever I ate that tomato, I'm going to go see a naturopath and they're not going to use that medication they told me. I want to, but now we can really say, you know what? Absolutely. Your gut is playing a huge role in this and the things that you eat absolutely are playing a big role in your exema. But we don't know. It's not an allergy. It's more the overall, you know, what are all those healthy bacteria in your intestines doing? Some foods are going to, you know, make them better. Some foods are going to make it worse. It's going to, they're always changing. So it might be a tomato is a problem this week and two months from now, it might not be a problem. So you can't really, you know, there's not going to be a magic bullet stop eating this. If you to healthier diet and if you take a probiotic, that might help over time. And then that person feels listened to. Right. They feel like you really, you didn't say no, it's not food. Like you gave them a food is playing a role. Right? That's the, you know, Peter, what's your spiel whenever a patient says, what food should I avoid? You're having no exactly as in so many things. You and I converge almost in exactly the same place. Me. Yeah, that's exactly how I say it. I wish it were one food. I'm like, it would be so much easier. You and I wouldn't even have to be it or we could be out golfing or something like it would be simple. But it's not. You've already tried it. You told me you went gluten-free and you cut dairy and you cut tomatoes and nightshades and all that stuff. It's like, so we know it's not that. Like that can't be the root cause. So what is the root cause? I'm like, well, I don't know, but it's probably not just food. And we understand that food is playing a number of different roles. You're glycemic index and just pro inflammatory foods. And there's a contact dermatitis from food's little babies. They're eating stuff and their skin gets all irritated on their face. And the mom's like, maybe he's allergic. It's like, well, or maybe eating citrus is really irritating. Like, I don't think that's an allergy, but it's just irritation. So we can put a barrier to help with that. So we have all these pieces. And I said, part of the problem is there's a threshold effect when your skin is a mess. And the system is in a bad spiral. It is really tough to know anything because there's so much variability. Let's get you better first. And then we're going to have a much better insight into that baseline and what could be making things worse in most of the time. And I'm very honest. Most of the time, you know what my family say to me, I guess it wasn't food after all because now we're kind of eating everything. And I really like that. That let them come to that conclusion because I'm not trying to tell them what to do, but I want them to feel heard. And I really want them to know that we're not just saying it because it's a shortcut. We're saying it because it really doesn't seem to give results. It's right on. So let's let's in this vein. Let's go on to Dr. Patins article. And for anybody who's watching the video component, Dr. Patins middle name is literally Luddite. So he I think is using a Commodore 64 and it broke down. It's a Texas. It's a Texas instrument. Texas instrument. So he's like, he's on his phone. Yeah, it's pronounced Luddite. It's a time. All right. So yeah, along that vein, November, deep dive, November 2025 edition of nutrition and is titled Can Food Choices Be Associated With Nutritional Status in Atopic Thermatitis Severity and Children in Adolescence. It's by Bikeli et al. So right, AAD published guidelines in 2014, pretty unenthusiastic about the idea that Diet FX AD in 2023, both the American Academy and the College of Allergy, Asma in Eonology. Like if you like, is it harder to get into the college or the Academy? Or is it, are you in either? I don't know. I mean, they just like they can't be in the AAD. We, but they, so yeah, they've got like the, the Quad AI. And I think the Quad AI is bigger than the college. Right? There's the American Academy of Blubblubblubblubblubblubblubblubblubblubblubblubblubblubblubblubblubblub. I think the Academy is bigger than the college. It sounds like it's fancier, yeah. Yeah. Alright, anyways, they published an atopic dermatitis guideline, and regarding elimination diets, they determine that, quote, most individuals pursuing a diet elimination strategy would most likely experience little to no benefit. And that it actually may be harmful, leaky gut, making like potential food allergies worse by leaving it out and not exposing your gut to those allergens earlier. So not a ringing endorsement for the idea that diet and atopic dermatitis severity are related at all. E and miles, we had him earlier on, he published this in the chat as Matt likes to say in tenacity and I'll which listed and I kid you not 42 different environmental and behavioral strategies to mitigate 80 symptoms and includes the line. Well, no specific dietary plan or avoidance is recommended. So it seems to me patients ask their ex most role to diet. I'm not on the same page with you guys. I am like, no, experts have determined conclusively, like get out of my office. If you keep bringing that up, like I people get better on Dupy and they don't change their diet at all. Like I'm not engaging you on this at all. Maybe that's why I press gaining. You're making our point for us. The point is you tell them yes, diet is involved, but changing your diet is not going to help is if you say your diet is not involved, they're not going to take the dupexant. So, so diet and elimination diet are two different things though. So, right. So, healthy diet that encourages a healthier microbiome and more short-chain fatty acids is not an elimination. I mean, it's like an elimination of twinkies. Okay. But other than that, like it's not like, I don't eat night shades. No, I get that. But you put somebody on Dupyxant, you put somebody on Dupyxant and they get better and you didn't counsel them at all about diet. Like it's not the diet, but I digress. Let's move along. So, so this study even need to be done. It was done by nutritionists, so a different perspective maybe. And the authors actually they hypothes, they went against the grain. They hypothesize food choices can be associated with AD severity. That was their hypothesis going in. So, 104 patients between one and 18 years of age recruited from few dermatology offices in Brazil. They underwent nutritional and AD assessments and completed questionnaires related to diet medication supplements, blah, blah, blah. Basic takeaway. There was not an association between diet and AD severity. It's kind of a weird study. It was like a one-time thing. So, like, I don't know how you say, oh, diet's not helping this person. Like, you don't know what they were previously. It was like, it's like a one-time visit. And they're like, what do you eat? How bad is your eczema? Okay, your eczema is really not that bad and you eat terribly. So, therefore, there's no association. There wasn't really a table or figure that presented the data was more narrative. And the results section author state quote foods classified as ultra processed by the Nova classification were grouped and submitted to correlation analysis regarding AD severity. There was no correlation between the food consumption of the ultra processed food group and participants score at. At the end of the same paragraph, they state that none of the other foods in the questionnaire were associated with disease severity. So, you know, what were the patients doing about 30% patients were on an elimination diet. A table four list of foods that were restricted topping the list lactose eggs, dyes, cow's milk. A table four also lists the reasons for following it. 75% said. That eliminated food that seemed to worsen the dermatitis so that's why I eliminated it. 30% of patients said they adopted the diet on their own. The rest of the patients said that the diet was adopted following a device from a healthcare provider. Most often a pediatrician but 17% of patients said it was a dermatologist that were recommended that that dietary change. So that's a. That's a Brazilian dermatologist not. I married. Yes, I thought it. Stop it Brazilian dermatologist. You know, I had a Brazilian resident who told me how to say stop it. And I didn't write it down so I don't know how to do that. But Brazilian dermatologist stop doing that because.
because this is not like 70% had that conversation about, well, I don't know, they were like, hey, you should cut out eggs, right? I mean, that seems too high to me. 70% of, no, 77.4% of patients confirmed that there was a decrease in symptoms by following the diet. So it didn't help with patient perception at all. So we're fighting an uphill battle. That's almost 80% of patients that were like, you know what, I did cut out oatmeal, and my skin is way better. So that's all. It didn't really add a whole lot. It was a weird way to do that sort of study, but I think when their hypothesis was, we're gonna find junk food diets and that's gonna be with the worse eczema and healthy, healthy diets is gonna be with the mildest eczema and that was not the case. So just adds more fuel to the fire of, diet doesn't make a difference. - Yeah. So two quick thoughts, number one, I think it's useful in the sense that it gives us, yeah, there were this group of nutritionists who really thought that eczema was driven by diet, and they did this big study. It asked people about all about their diet and the takeaway was that it often seems like your diet is playing a big role or eliminating something helps. Blah, blah, blah. The other point though that is super useful. So Eric Simpson published a great article, maybe two years ago now, where they looked at like 70 some patients, old people who had examinist drug eruptions and they looked at drug discontinuation trials and I think 70% of them initially got better, right? So we meaning the normal waxing and waning, but not a single person had a long-term improvement. Like it got a little better and then it came back despite still being off the drug. I think that's what we're fighting against is the natural waxing and waning of the disease. You're like, oh, two weeks ago I started avoiding tomatoes and now I'm getting better. Must you take it that long to work a way out of my system? No, it's just, you know, yeah. But so that's what I thought this was reassuring, gave us more ammunition. I don't know. - I was gonna just add, there's a great quote from Ruchi Gupta. She's a pediatrician in Chicago and she's focused on food allergy and it's really kind of summarizes what we've brought up a little bit too about the dangers of avoiding foods, right? We know that of course part of the reason we think people get sensitized to foods is through their skin, broken skin. So we want to heal the barrier. And the other piece is that if they're not eating those foods as we learned with the leap study from Gideon Lack and his group that if you don't expose it then you don't become tolerant. So her little mnemonic, the little poem and I say this to patients all the time is through the skin, allergies begin, through the diet, they stay quiet. Ooh, I love that. So that tells them, you know, we don't want to just start cutting stuff out because we know an anemory saying is a great allergy stuff in Wisconsin. She did this beautiful study showing that a proportion, I think it was almost 20% of patients who cut a food because they thought the food was driving their eczema. When they cut the food they, they agreed that, okay, it wasn't this food, this wasn't the cause of it. When they added it back, one out of five, then actually became allergic to it. They actually got either hives or angiodema or even anaphylaxis for some of these patients. So that's a real risk. The only other thing I'll say just disclaimer because I just want to be careful because when we, and I'm with you guys, 100% that I agree that for the vast majority of patients, this is not the right path for most people. But I agree, haters are going to hate people are going to bring it up. Are there people for whom a food or foods is really a major driver of disease? Yes, it's true. I think there are a few patients. The problem is those patients become kind of evangelist for this idea and sort of poison everybody and say, well, I found it for me. So it must be the case for everybody. And I think our pushback is just that in general for the vast majority of patients for at least 95%. It seems like it's not going to be the major piece. That doesn't preclude the fact that there are some people out there and many blessings to them. They're so lucky they don't need to see us anymore, right? I would even argue that if your exoma was solely driven by a food, you didn't have exoma. You did not have a topic dermatitis. You had a food driven examinist eruption. That's something different, but good for you. Now please go do other things and quit torturing our patients about this, right? That is exact. So Susan Netterost, who is the case question for a long time, is that one of my partners, she and I have this conversation a lot of like systemic contact germ and particularly nickel and balsamaparu. But potentially lots of other things as well can drive something that's essentially indistinguishable from a topic germ. Other than you avoid it and you get better. And I was making it so what her and I's argument is like, look, if I was the patient, I would rather just give me a shot and do picks it once every two weeks. And I'll eat whatever the hell I want. And she's like, oh, we need to avoid these, you know, drugs can have side effects that we don't know. And I'm like, yeah, I know they can. I know they can. But I, you know, I'm more of a if food, if dietary changes were an effective way to manage disease, we wouldn't need statins or blood pressure meds or diabetes meds, right? Everybody, because those are diseases and works out 100%. Your diet is completely causing your disease. No, they can't get better without the meds, right? It's an interesting thing. - But it's not an all or nothing, Matt. So you could say obesity is not at all related to diet because if I put you on high enough dose of teazepotide, you will not be obese. Therefore, it's not related to diet, but it is. You're just overcoming something that is dietary related. - Yes, I do. - My point is more that even if it is diet related, telling people to change their diet rarely works, right? Because if people get it's hard, it's really hard. Like the time that it takes to make the healthy foods and you know, you do this and the that and the other, like it's hard, even if it takes a lot of effort for dietary changes to do anything. - Yes, I actually think we should teach people how to cook. I think that is like probably one of the most important things we can do is to teach people how to actually cook real food. I think that's probably one of the biggest drivers of poor health in our country, but that's it. - I agree. I agree. Pat, would you have something you want to say? - No, I do want to say, I don't, I'm not harsh with patients like that. I do kind of go along and be like, yeah, well, maybe it could be, but you know what, it's probably a different food for every different patient. And so that's just impossible to counsel against. And hey, if if if deal, if deal flavor potato chips flare your ex-mom, but the old bay ones don't, then yes, makes sense to avoid deal. That's been reported. I mean, I'm making that up. I don't know if that's true, but whatever. So I do do that. I'm not as harsh as I say, but man, I really want to be like, no, no, we're going to be wasting time. Not only could it be harmful, that's totally stressful. Like, you know what, yes, here's this diet and avoid it. And then they're like, okay, well, I'm going to read this package. And oh my gosh, I think this had this in it. And like, who, why live your life that way? Like you were going to be a freer, happier person because you're not going to be stressing about every little thing that goes into your mouth. So I had a patient who like, I can't remember what it was that they got allergy tested and they came back positive to something. And then it was like, well, okay, this particular ingredient can be derived from like corn or from some other vegetable. And if it's right from corn, then it can have this in it. So they were contacting companies to be like, where do you get your, what do you make your something from? And it's like the, yeah. - So can I ask though, so probiotics, right? We've read some papers on probiotics. So we're not going to make everyone change their diet. That's fine. But Peter, do you recommend a probiotic? And what do you tell patients about them? So I'm sure they ask you about them. - I do. And I'm a big fan of them. I think that, you know, I kind of tell the story. I say there's pretty good evidence that if you give expectant moms and then newborn babies, lactobacillus raminosis GG, that actually seems to prevent some atopic dermal at least delay the onset. But by the time they're seeing me, they already have it. And there's pretty convincing data that the lactobacillus raminosis GG doesn't do much at all for existing eczema. They've looked at that over and over. But I think the most compelling data are for some of the mixed strains in particular, like there's lactobacillus paracaceae, salivarius, there are a few like that. So there are a number of different companies that make them. Now, there's a general caveat. And this is one of the hardest things about any kind of supplement. It's like, first of all, does the actual ingredient do what we think? And here, it's not even proven. It's like, it seems like maybe these strains are more helpful. We hope we think, OK, then does the actual supplement contain what they say it contains? You hope? Does it have it in the level they're saying it is? And is it consistent? And is it safe? You know, it was the background, you know, going to be something like heavy metals or some other bad stuff. But I do think there are some relatively affordable, probiotic combinations. The one I've switched over the years to different ones. There's one now on Amazon that comes as a powder, which is really nice. It seems like it's pretty good company. They have independent verification by batch. And I like it because it's really cheap. It's like $17 for a one month supply for an adult. But for kids, for like, adolescents, I'll have them do half a sachet. And then for the babies, they'll have them do a quarter sachet. And it's really great. What's your call? What's the brand? What's the-- Let me pull it. Have it in my-- I keep it actually-- If I print out at work, but the next.
keep it in my Amazon cart for when I'm doing telemedicine. - 'Cause I have one that is, it might be the same one. The one that I recommend is from a company called Now, probiotic 10, it's got 10 strains, but four of them are the mix that is known to be good. - Basically, yeah, so this one, the one I've picked, it's called, though the company's Zabora, Z-E-B-O-R-A, I have no conflict of interest, probiotics, super nutritional powder, 50 billion organisms, 13 probiotic strains, really inexpensive, $16.99 for a one-month supply for adults, but that would be multiple months for kids and really long, like, four months for babies. - Spell it again, Z. - Z is in zebra, E-B-O-R-A, so it looks like almost like zebra, Zabora, probiotic, super nutritional powder. - And as a, this was in a relatively obscure journal, you probably have heard of it, there was a study recently out of Italy, this probiotic called Visbio, that had this unbelievable, but it's like $120 a month, it's very expensive, and so it's even though the results were phenomenal, I'm still like, oh, that's a pretty darn pricey probiotic, but it just confirmed for me again that there are probiotics that work, the other thing that is an interesting thing about talking to patients about probiotics, is the idea that the probiotics, I mean, there's pretty good evidence for this now that it's not that toxins are leaking out of your gut into your circulation, it's that the healthy bacteria are making good stuff, right? They're making the short-chain fatty acids that are anti-inflammatory, they're making these indomitabolites that activate their hydrocarbon receptor pathways, so the same thing that Vitamid does, just systemically, it's really cool, like it's really cool, and it fits well into the idea that there's gotta be a reason that Xima, dermatitis in general has gotten so much more common than it was 50 years ago, and food is one of the easy things that's kind of a low-hanging fruit. All right, now for our last deep-dive paper, I wanna jump over to one that I picked, and this was a out of Denmark, and so it's not terribly relevant because it, anything that is socioeconomic that comes out of Denmark, you can't really like listen to because it, their socioeconomic situation is so different than ours, but the title of this was "New Insights Into the Bird" in the beta-bigurmatitis, "How holistic care" and also consider socioeconomics. Main takeaway of this one was in Denmark, even if you were born with Xima, your life outcomes were basically the same as everybody else. They did a pretty good sibling study where they were like, okay, if you come out of the same family, so presumably similar parents and upbringing and everything else, your outcomes were pretty much identical long-term, okay, great. What I find much more interesting about this is, when I hear people talk about the expense of the drugs that we now have for AD, whether we're talking topical or systemic, all I'm thinking, when we talk about that, we're talking about society, and I'm always thinking about the patient in front of me and the truth is, if I can give somebody one of these expensive drugs, whether it's a topical or systemic, and it really works, not just the better sleep and you're not itchy, you're more productive of work and you do better at school, but also you're gonna spend less time and money on moisturizers and on doing things, like you becoming normal person. And it's one of the reasons I kind of went over with the beginning when Laura was talking about, the cutaneous and the barrier in the moisturizers. Like one of my goals whenever I put somebody on Dupy or Observer or Vertama or Zaree or Rindvo or whatever, is so that they don't have to put moisturizer on anymore, because it's, if they want too great, I'm not like don't, but I'm like my goal is that it becomes something that you can do, not something that you have to do, right? Is it, so that's, so should be a mefactor. - Maybe the world from moisturizer. That's what you're doing. You're saving the world from moisturizers. - That's exactly right. These people could spend hundreds of dollars a year on Zaree, and Avino, and all of that stuff, some saving society money with the $60,000 baby books. - All right, I'm not buying this. This is a load of BS. - No, okay. So I think one of the analogies I had was, it's like if you had a lion locked in your basement. Like you could say, there's a lion locked in my basement, but he's locked in the basement. But you would think about that constantly. You'd be like, oh my gosh, is the lock locked? Did we update it? Is it rusting through? Going to bed at night, like is the lion gonna stay locked? As opposed to getting rid of the lion. And then it's not a constant part of your life. And Eczema is the lion in the basement. I'm coining that. Take it to the back. - That's what that pretty, patent, that's good stuff. Usually I'm like, when we talk about like what you say to patients, I'm usually like, my god, like they're really desperate for germs and Pittsburgh. That one's really good. - Yeah, yeah. That one's really, really good. All right, so be, - Me? - Never meet up with an alligator. - We don't have basements, so we don't worry about this. We still have to moisturize. - In your attic, but our whole space, we're gonna have a lion there. So be, all right, so we covered our article just, peer before we sign off, what do you think is gonna be, so the last few years in A-topic Durham have been unbelievable, right? The last 10 years, the new drugs, the new understanding of kind of some of this dietary stuff, some of the air pollution and environmental stuff, this is the O'Bareira hypothesis, the best, what do you think is, 'cause you publish a lot, and you publish a lot on stuff that most people have never heard of, right? 'Cause whenever I look up, when I look up Peter Leo, what's you publishing the last six months, I'm like, "Shit, I've never heard." Like, what do you think is gonna be the big A-topic dermatitis stories in 2026? The reason you haven't heard of it is because it's obscure crazy stuff, that's the only reason it's not anything useful or mainstream, of course. But no, I think a couple of things, I love the fact that we are finally distilling it down, we actually can say something relatively intelligent about why, the environmental story, and I give so much credit to Ian Miles for that, he really pushed that forward. The staff, the serious story, I mean, that really Heidi Kong, a national in suits of health, she turned that completely around. I mean, that to me was a revelation. When I first read that paper in 2012, where staff was a driver of disease, I was like, "Oh my goodness, this changes everything." So now we're finally seeing the ramifications of that. Now I always call it the virtuous cycle of drug development that we get some new treatments that help, but then more importantly than they being just helpful, they teach us more about the disease, and we build on them and build on that. So we're finally in that cycle, which I think Saraias has got about a 10-year head start over A-topic derm. I also think the microbiome, both, we talked about oral probiotics, but also on the skin, we have some amazing stuff in the pipeline, looking at topical probiotics and other ways to manipulate that microbiome. We finally have opened the door to really interacting with itch and the nerves themselves. I think the IL-31 is the beginning of a new, a whole new frontier. So I think we're gonna get to the point where I love the way you put it, like this idea of freedom from eczema, but keeping, getting rid of the line instead of just worrying about it being locked up, but that freedom from disease, it's a big deal. And I know, I guess if you're really, if you're pessimistic, you'd say, well, you guys are just trying to spend the health care dollars, you can do fine with a moisturizer. And we're not arguing that for sure, if you can, by all means, but for these patients who are really struggling and we see the impact to be able to take that equation and change it fundamentally, I think it's unbelievable, it's a miracle. - Can I ask a couple questions? One, I wanna, do you tell patients to moisturize their skin? Or do you say, okay? - I do, yes. I'm a moisturizer fanatic. In fact, my little signature move is, I get a lot of patients with sensory issues, they hate all moisturizers or super sensitive skin, and I'll come in with a palette of different moisturizers, and I'll be like, try this one, try this one, and we do it together. I'm like, I take 10 minutes, I'm like, I want you to show me, and the best is usually, it's little kids, but they'll put one on and be like, oh, I like this one. I'm like, all right, that's your moisturizer. Here's a whole bunch more. Here's where you can get it. This is the one you're gonna use. I love that moment, 'cause I feel like there's, it's also here, right? It's very psychological. They like the feel, I want that enthusiasm about it, because then we know it's gonna work. - Okay, that's cool. That's super helpful. That's so helpful that I forgot with my second question one. Is it like a painter's palette, like you come in with a palette, and there's little smudges of moisturizer? - Or you've got a four-thousand beauty. - Is that awesome? - And do you have a beret now? - I like both of those. I both know that you've been kind of with the big handful. I was gonna say that you wear a little beret at a jaunty angle. - Jauntia, I like that. So, Lauren, did you have something else you wanted to ask before I, I want to talk a little bit more about staff, but was there something else you wanted to ask before you were-- - No, no, that's good. That's good. Go on. Talk about staff. - So, Peter, I may, and I'm, I'm actually not familiar with the name of the woman who you mentioned from the NIH from 2012. I think of staff as driving AD by producing superantigens that can penetrate through the impaired barrier, right? Normal people don't have an impaired barrier so the superantigants can't penetrate. Is that kind of what, is she the person who sort of figured that out? - She's done so much work, but I think her major paper. or in 2012, the one that I always cite was the one that has that cool graph where she was able to show that you see staff or is become dominant and then you see diversity of the microbiome drop and then you see a flare up. So that the temporal, you know, because I think we were all trained. It's like, yeah, you have a broken skin barrier. People are scratching. They have grubby hands. Their staff all over the place and staff is an opportunity. It sees an opportunity. It goes in and makes a mess and they can get infected. But Heidi made the point where no, actually the staff was there first and it's driving this change. Presumably, it's in its favor, right? All these, these different factors like alpha toxin and delta toxin and the V8 protease, like they're driving this whole process to make it perfect so that it can essentially improve its colonization and drive the disease. And of course, it's not for everybody. We know the majority of patients have this, not all. And we know that just killing the staff isn't enough either. Like this is a more complex system. And that's why it's so exciting to me to think about how else can we manipulate the microbiome? Can we change the environment? Can we change the pH? Can we add probiotics to help put the good guys there? Can we do things to stop this? You know, they have these, these quorum sensing genes. Can we turn them off? And like in the pipeline, we have all of these things. It's like holy guacamole. So right now, do you do anything? So rarely I, well, there are some moisturizers out there that actually hand sanitizers that are lotions that have benzoconium chloride in them. Rarely I will recommend those. There's a hands-handed tizer code, Zuno, that is this weird stuff that it has 24 hour efficacy, but you really can only use it on your hands because you can't get enough of it. But is there any, I rarely do either of those. Is there anything that you do, say, if you're looking at somebody, think, and I think staff is playing a big role in this person? Or is there anything you do in particular in general or for people that you think staff is more likely to be playing a role? I think a couple big things for me. One of them is the hypocloris acid sprays. And I think they are fundamentally different than a dilute bleach bath because as Dr. Gallo pointed out, that's probably not the same level of strength, but the stabilized gels, I think are more bacteriocidal. So they're important. I really, I'm a huge fan. I know it's controversial, but of the Dr. Aaron compound. And that is purely that you're telling people to put it on eight times a day. If I can get people to put anything on eight times a day, they will get better. I cannot rule out that possibility. I promise, but it does seem to help in those patients, particularly well. And then I really do think that coconut oil, there was a couple of great studies where they showed that you were able to decrease colonization by using virgin coconut oil. So I have patients do that, not to replace anything. It's just part of the regimen. So I'll say, you take your shower at night, you put your coconut oil on, then your medicine, then your moisturizer because it's not sufficient by itself. But wow, does that make a big difference? And again, it may be multifactorial though, the adding an extra layer of oil is great. It enhances everything, maybe by telling them to stay on it, they're much more likely to be adherent, etc. But I love that and I feel like that can make a big difference. What's your favorite hypocorus accent? What's your favorite one? Is it that CLN or what do you recommend? The one I recommend the most and again, I have no conflict, but it's actually the cheapest one on Amazon. It's called Skin Smart. It comes in a big sprayer. It's great. It's really economical. And I love that one. I know Tower 28 makes one. And the founder of that is a, she's a board member for National Examus Association. And then she's a big advocate for Examus. So I respect that too. It's just a bit more pricey, but I love the Skin Smart from Amazon. I do the Skin Smart as well. Two quick thoughts away. So the Aaron Regimen for anybody doesn't know. It's basically, if you look it up, you'll be able to find it, but it's basically mixing together moisturizer, beta methazone and some mupericin in a particular ratio. Both Dr. Leo and Lisa Swanson. So the two best pediatric dermatologists in the world as far as I'm concerned believe that this stuff is amazing. I say it's below me. So you should believe me, not the pediatric dermatologist who actually know what they're talking about. So obviously that's tongue in cheek and it tells me that this stuff does actually work. And then one other thing, but now I've totally forgotten about what the coconut oil. Here's my favorite thing with the coconut oil. Whenever they say, oh, I've already tried coconut oil. Well, it has to be virgin cold pressed unrefined coconut oil. Is that what you tried? Oh, no, yeah, that's and it's true. It does have to be that because it's the medium chain triglycerides, which get lip out of it as soon as you do anything to it. Yeah, I love it. I love it. This is great. We've got like totally practical stuff here of a spray. You can get on Amazon, a probiotic. You can get on Amazon probably coconut oil. You can get on Amazon and patients. This is like gold for patients, right? They love this kind of stuff. We should, if we are allowed, we'll post the links to all these so people can have an easy thing to recommend. Sounds good. All right. Thank you. Got some trivia for us. Let's go patent. Let's go to trivia. All right. It's it's root causes. That's the category. So you know, you know, you know the rules. You got to wait till patent finishes reading the question and then shout it out whatever you think it is. All right. So the word root is going to be in the question or the answer. All right. Number one, the Bible verse, one Timothy, six, ten states that what is the root of many evils? Money. No, it's the love of money. Dr. Zairus is right. A lot of people, the quote is often misquoted. It's not money. It is the love of money. So yeah, I don't love money. I just like it a whole lot. All right. Number two, what American rock band saw their 1994 song, Send Me On My Way, Gain Renewed Popularity, or about a decade later when it was featured in the animated movie, I say rusted root. It is rusted root. That's a Pittsburgh band. Yeah, that's a Pittsburgh band. So definite advantage for the podcast team on that one. All right. Number three, original recipes for root beer used primarily the root from which trees? Will. Sassafrasse. Or Sassafrasse was like the main one. Sassarilla was used a lot, but it was Sassafrasse bark root. That was one of the main things. Apparently, in 1960, the FDA banned the use of saffron, and that's the compound that's in Sassafrasse. So it was felt to be carcinogenic showing once again how the government ruins everything. So now it's all artificial labor Sassafrasse. Pat, this is something you might know that I wonder all the time. What is the definition of beer and ale? Because like why is root beer a beer and why is ginger ale and ale whenever they either let them has any alcohol in them? Do you know? I have no idea. The original root beer actually did. It was made from molasses and then it was flavored with these things. And it was fermented to give it a little bubbles, but it was really low. It was like 2% alcohol. Okay. So it's a little like the original. When they originally made it, they did market it as a beer because technically speaking, it was a little bit alcohol. And I have no idea why ginger ale is an ale and root beer is a beer. Okay. Good question. Maybe something for the next episode. All right. Well, Peter, I want to thank you for coming on. This has been such a fun, fun, fun episode. I want to thank all of our listeners for joining us this week. We hope you learned a few things. We hope you laughed once or twice. Mostly we're hoping you're planning to join us next week. And until then, I'm Matt Zyrus. I'm Tim Patton. I'm Laura Ferris and we are Germs on Drugs.
Podcast Summary
Key Points:
The podcast episode features Dr. Peter Leo discussing a paper on the skin-immune-neuro-gastroendocrine (SING) system in atopic dermatitis (AD), emphasizing AD as a multi-organ disease beyond the skin.
Key components include
Clinical implications
Dr. Tim Patton presents a study on diet and AD severity in children/adolescents, finding no association between food choices (including ultra-processed foods) and AD severity; 30% of patients were on elimination diets, often self-initiated or advised by pediatricians/dermatologists.
The hosts agree that while diet plays a role in AD via microbiome and inflammation, specific elimination diets are ineffective, and biologics like dupilumab effectively treat AD regardless of diet changes.
Summary:
In this episode of Derms on Drugs, the hosts discuss atopic dermatitis (AD) as a multi-organ disease through the SING (skin, immune, neuro, gastroendocrine) framework. Dr. Peter Leo explains that AD involves skin barrier defects, immune dysregulation (TH2 cytokines), neurogenic itch (substance P), gut-skin axis (microbiome and short-chain fatty acids), and stress-related endocrine effects.
He advises clinicians to validate patient concerns about diet without promoting elimination diets, which lack evidence and may worsen outcomes. , dupilumab) are primary therapies. Dr.
Tim Patton presents a study on diet and AD severity in children, which found no correlation between food choices (including ultra-processed foods) and disease severity. Despite 30% of patients using elimination diets, often based on perceived triggers, the study and guidelines from major dermatology and allergy organizations conclude that elimination diets provide little to no benefit and may be harmful. The hosts agree that while diet influences AD through the microbiome, effective management relies on standard medical treatments, and clinicians should steer patients away from restrictive diets that may lead to non-adherence to proven therapies.
FAQs
It's a podcast where dermatology experts discuss and debate hot topics in dermatology, drawing on 60 years of combined clinical experience.
The hosts are Dr. Matt Zyrish, Dr. Laura Ferris from UNC, and Dr. Tim Patton from the University of Pittsburgh.
SYNG stands for Skin, immune, Neuro, Gastroendocrine, representing the multi-organ system view of atopic dermatitis.
The gut-skin axis involves the microbiome; beneficial bacteria like Bifidobacterium and Lactobacillus produce short-chain fatty acids that modulate T cell function, while harmful bacteria can worsen disease.
They recommend a healthy diet and probiotics to support the gut microbiome, but avoid specific food elimination diets as they rarely provide consistent benefits and may cause harm.
Stress activates the HPA axis, increasing cortisol, which can contribute to skin barrier dysfunction and worsen the condition.
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