279: Chemical That Triggers Eczema (Oh My!) w/ Dr. Ian Myles

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You could be doing all the right things- eating clean, whole foods, tossing out all itchy clothing, and making sure you drink plenty of water. But you're still flaring. Today's guest speaks on possible external triggers that he's been researching that may be causing flares, and it can be everything from where you live to what specific chemicals are in your environment.

My guest today is Dr. Ian Myles. He did his undergrad at Colorado State University, received his M.D. from the University of Colorado, then trained in internal medicine at The Ohio State University prior to beginning fellowship training in allergy and clinical immunology at NIH. He became a commissioned officer in the United States Public Health Service Commissioned Corps and has supported several US and international missions. Dr. Myles received his MPH from George Washington University before becoming the head of the Epithelial Therapeutics Unit to evaluate the efficacy and safety of a topical, live bacterial treatment for eczema.

Have you changed anything in your environment or home and saw improvements in your rashes? Share with me in the comments below!

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In this episode:

  • How the gut microbes prime the immune system to function properly and can affect cellular response in the skin
  • FYI – Staph on your skin isn't the only thing to worry about
  • Stats on how allergic diseases have increased since the 1970s
  • Possible external triggers for eczema (Hello clothing, sheets, and air quality!)
  • Which chemicals show up in the zip codes with more eczema?
  • How these chemicals trigger signals in your body to cause or flare rashes (WOW!)
  • Thoughts on why eczema is not a drug deficiency according to a doctor at the NIH


“There's only seven chemicals you can use to give a mouse eczema so that you can then treat it, two of them are diisocyanates.” [18:25]

“In terms of the fabrics, I think laying that chemical up against your skin, or particularly polyester bedsheets I would worry about for children, if they're laying on that, that chemical is touching the skin, it's going to disrupt the bacteria's ability to do its job and it's going to directly activate the defects in the skin, or the receptors in the skin.” [23:54]


Find Dr. Ian Myles online here and on Twitter

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Healthy Skin Show ep. 253: Eczema Expo 2022 Recap

Healthy Skin Show ep. 266: Eczema-Gut Connection (PART 1)

RESEARCH: Exposure to isocyanates predicts atopic dermatitis prevalence and disrupts therapeutic pathways in commensal bacteria – Science Advances 6 Jan 2023; Vol 9, Issue 1


279: Chemical That Triggers Eczema (Oh My!) w/ Dr. Ian Myles FULL TRANSCRIPT

Jennifer Fugo: Dr. Myles, thank you so much for being here on the show. I really appreciate it.

Dr. Ian Myles: Thank you for that invite.

Jennifer: So do you want to share with listeners what your background is? I know many of them heard me speak about you when I went to the Eczema Expo and many people wanted to know more about your presentation. But could you share a little bit about your background, because you're not the standard dermatologist that I've had on as a guest in the past.

Dr. Myles: Well, yeah, I'm not a dermatologist at all. I'm an allergy immunology researcher, so I grew up in Colorado, went to school, med school there. Did internal medicine training at the Ohio State Medical Center and then came to NIH to be a allergy immunology fellow and have stuck around ever since.

Jennifer: And what do you think in terms of a lot of these different diseases of the skin, just from your perspective, do you think that at this point in time, do you feel like there's a lot more to what's driving these issues than perhaps, you go to the doctor and they might tell you, “Oh, you have an allergy to laundry detergent and here's a steroid cream and here's this medication.” Do you feel like there's a lot to this that we're still researching and figuring out?

Dr. Myles: Yeah, I think a lot of the questions… So as an immunology specialist, so we're talking about the immune system in the entire body, you start to ask the question, is this a systemic disorder of the entire body that primarily manifest in the skin or is this a skin disorder? And there are examples of both, but the more you think, “Okay, this is a full body, the whole system's involved, everything is going wrong,” then that is going to take a different approach in a different solution, than, “Okay, well just deactivate the immune system in your skin using this steroid or simply avoid X and then you'll be fine.” So I think, yes, I definitely think that we're learning that these diseases involve other parts of the body, particularly the gut, for example, and that therefore they're going to require a little bit more sophisticated response than just topical or just even drugs that only target one particular receptor, that kind of thing.

Jennifer: Well it's funny that you mentioned the gut, and that was something in your presentation that I appreciated because you were really jumping around and connecting a lot of different dots that sometimes can be difficult to ascertain just from reading articles. So in terms of, let's just say, eczema, for example, and obviously there's cytokines associated with psoriasis as well, do you think in your experience as an immunologist it's possible that those cytokines that these various drugs target could actually be generated from something possibly happening in the GI tract?

Dr. Myles: I mean it depends on how you want to define that. But if you're saying the first domino that falls falls in the GI tract and then that leads to too much particular cytokines somewhere else in the body, absolutely. I think at this point it'd be hard to even argue against that. The types of bacteria that live in your gut, you have to have them to train the immune system to function properly. The immune system has… Basic tenets are you find something that doesn't belong here, let's destroy it, and then let's all quiet down and get everything back in order and then let's put everything back the way it was. Those are the stages of this inducive inflammation, kill the thing off, and then put everything back the way it was so that we don't leave damage behind.

Every cell that does that. You have to have an organism in your gut to prime the immune system to figure out how that works. So if you can grow a mouse in a lab with no gut bacteria, every aspect of its immune system does not function properly. So I think that it's really unquestionable that you need the gut microbiome to prime the immune system in a lot of ways. And if that gets thrown off, which is a lot easier to do, diet and antibiotics and other things you might consume, then yes, I do think that the subsequent downstream effect could be disrupting a cytokine on the skin far away from the gut.

Jennifer: Do you think that… And this is just my curiosity, do you think that if there are alterations within the gut microbiome, could there be possibly a connection with dysbiosis of the skin's microbiome?

Dr. Myles: Yes, that too. That can be shown pretty straightforward in more extreme examples. So people who have genetic mutations that just preclude… Just completely ruin some part of their immune system. That's obviously a little bit subtly different than what we're talking about. But yeah, the bacteria in the gut, those cells that get trained by the bacteria in the gut pack up and then go to live in the skin, and that's their job. They go live in the skin and then they go protect the skin. And if they're trained improperly in the gut, then when they go to the skin they don't function properly. So that's pretty clear. Something called Omenn syndrome, O-M-E-N-N if people want to look it up. But again, that's a different universe than what you're talking about. So the short answer is just absolutely that those things that disturb the gut will alter the cellular response of the skin.

Jennifer: And one thing that you shared that was really eyeopening to me was this connection between I guess an eczema flare versus the amount of staph aureus on the skin. Do you think that maybe… Because here's the challenge is that… I have a lot of listeners and whatnot who will go to their doctor, they're in this horrific flare, they have the symptoms of an infection and they're doctor will literally tell them that everybody has staph and just blow them off and send them home with more steroids, unfortunately. This isn't an uncommon experience for many of my listeners. Do you think that we need to rethink that maybe in considering the whole role of staph aureus and how it can impact eczema and its severity?

Dr. Myles: Yes and no. So I think the standard academic answer, there's a field, a subset of a field that really thinks staph aureus is the cause. Just everything, you get staph aureus, and then that generates a flare. The problem with that, as we discussed at the meeting, was eczema is unquestionably not contagious. There's mountains of epidemiologic data, it is not a contagious entity. So because of that, that tells you that staph could certainly make things worse, but it can't be the primary cause. In terms of, “Okay, well what do I do then to treat it?” If somebody comes in with overt infection, so cellulitis and things that really scream this is infected tissue, then definitely antibiotics would be appropriate at that point. But all of the studies have really been fairly clear that if all you do is kill off the staph aureus, that's not going to help in the long run.

So just taking topical antibiotics or oral antibiotics flat out doesn't work. So if you have a treatment where the only thing you think it's doing is killing staph aureus, in the long run just it's just not going to be beneficial. I mean it's hard without seeing the actual patient to say should they have gotten it because it was a real infection or not. But I would just say short of overt infection, then you shouldn't treat. And I think the rethinking is staph aureus, what it's really good at is jumping into inflamed tissue and taking hold and then making things worse.

It's an invasive species that it requires you to till the soil for it to give it a disrupted environment to thrive, and then if you can fix that environment, staph aureus doesn't really survive very well, which is why injectable drugs that have nothing to do with staph can actually get the staph aureus to go away, because you're curing the skin and now the staph has nowhere to live. So now the question really should be not we get why the staph showed up and created a problem. Why did the staph have an opportunity? What really threw off the skin that then allowed the staph to step in there and make everything worse and the deeper questions.

Jennifer: And that's where your talk, which was wildly popular… I was in there first session and all the seats were filled, and then people were coming in for the next session and I just remember everyone just kept having more and more questions, and I think that this underscores the point of what you were talking about, is that there may be environmental factors that we're not really considering at this current moment. So for example, you had mentioned something about fabrics and fabrics can impact your skin. Can you talk a little bit about that?

Dr. Myles: Yeah, so the fabrics are one aspect… So specifically to answer that one, patients, it has been published that it's pretty clear, do not respond well… Atopic derm patients do not respond well to spandex, nylon, and polyester. They will just… And then super itchy wool sweaters, but who's wearing that in this day and age? They'll avoid those. And the original thought was, “Well spandex and nylon tend to be tight, so maybe it's just too restrictive and it is too occluding,” which is a little odd because the whole point of slathering yourself with ointments and the lotions is supposed to help you to make it more occlusive. But of course that wouldn't really explain polyester. Like a polyester shirt that isn't tight or is loose fitting, why do patients tend to tell the interviewers or doctors whatever, “I can't tolerate this, I need the cotton and I'm fine with cotton.”

So that's part of it, this kind of like, “Well what is going on here?” And then our work really started with the observation that atopic derm has… And all allergic diseases have really exploded in their prevalence since about 1970 or so. And it's not because suddenly we got better at diagnosing atopic derm. When you see a big explosion of disease, it either means it's real or that a new detection tool was invented or something like that, or that we were missing it before. But it's pretty clear that it's real. There's a large increase… I think everybody, most of your listeners would probably appreciate food allergies as one. None of your grandparents went to a peanut free school, but anybody who's listening probably sends her kid to at least a minimum a peanut aware school. So we know that these things are increasing. So that was part of our question is well why all of a sudden now is so many more kids developing eczema?

And then I think tied to that, whether we appreciated it at the time or not is that the parents and the patients are saying what's driving them crazy, one of their biggest questions is, “Why am I having a flare today? I'm doing everything else the same, I'm eating the same, I'm taking my meds, I'm doing what I'm supposed to be doing. I didn't do anything different and today I decided to flare.” And that's the part that can be very frustrating is to try to nail down what these real triggers are. So those two questions I think led us down the environmental path and the fabrics became part of that. And we started to examine what other things have patients said are inducing a flare or epidemiology has said.

And you see unhealthy diet practices. So processed foods are associated with an increased risk, early life antibiotics increase risk. Again, those speak to that gut microbiome aspect. But living near a highway was a strong increased risk for eczema, atopic derm. Wildfires is probably the more recently appreciated one, particularly Australia and California, those wildfires kick off and you start to actually watch flares radiate out from those sources. So nylon, spandex, and polyester as the fabrics. In-home products that are associated with increased risk are… Anything that you'd basically think of renovating a nursery before the age of two. So paint, polyurethanes, stains, wood sealant, wallpaper, wallpaper glue, particularly, new carpeting. These are things that are all associated with increased risk.

So at on face it's hard to explain that, because you'd say maybe that's just a marker of being rich, that you're wealthy enough to renovate your whole home for the new baby versus not. But even controlling for income that still ended up being case. So that's where we were when we started our environmental survey to just say, “Okay, there's a lot of things that none of them feel connected. Why would carpeting and polyester shirts both have a problem and wildfires?” But we felt like our investigation led us to particular chemicals that are shared in all of those exposures.

Jennifer: And I wanted to ask you specifically, let's hope I don't butcher this. Diisocyanate. I think I got it. It's a bit of a mouthful and I'm sure listeners are like, “I have never heard of that before.” So what is that?

Dr. Myles: So the first time I had ever heard of it is after we took… We had two different databases. So one is clinic visits for eczema or atopic term. So we ask basically per capita… So obviously there's more eczema visits in Manhattan than there is in the middle of a rural town. But per person, which areas, which zip codes are seeing more eczema than you would anticipate or less? And then the second database comes from the EPA, and they're two different sets of databases that basically say if you burn a big ton of whatever out front, you have to tell the EPA, “Hey, by the way, I released this much this year.” Or if you dump stuff into the river, you have to tell them.” And there's 500 chemicals on that list. So what we're basically asking is which chemicals seem to show up in the zip codes that have more eczema than you would anticipate?

So the med student in the lab, Jordan Zeldin, he put together these mathematical models and diisocyanates was basically the top. So it was the only thing more predictive of whether or not you would have a clinic visit for atopic derm was how many pediatricians, allergists, and dermatologists basically live in your town, which makes sense. You're not going to see the doctor if there's no doctors living in your zip code. So diisocyanate was far and away the number one chemical and I had never heard of that in my life. So I start researching it. And diisocyanate is a chemical that came on the market, became manufactured in the United States starting in 1970 and has basically slowly increased ever. What it's normally manufactured for are wallpaper glue, polyester, polyurethane, spandex, nylon. All of these different chemical exposures and these environmental exposures require diisocyanates for their construction.

Not to get too heavy into the chemistry, but iso diisocyanates a side group called isocyanates. So diisocyanate means the molecule has two of them, so isocyanate is just one. If you want to say, “Well, where would you come across isocyanate?” Isocyanate come out of car exhaust. So living next to a highway would increase your exposure to but only if you burn it through a catalytic converter. So normal gasoline does not cause increase in isocyanate. It causes an increase of a lot of other horrible things that'll kill us in other ways, but having a catalytic converter, suddenly now you get an increase in isocyanates. And that became mandatory in the United States in 1975. The other sources of isocyanates would be cigarette smoke, which is strongly associated with increased risk of eczema, and the only natural source of isocyanates that exists that is known are wildfires.

So it just seemed like every box started to be ticked, if you're like, “Why would wallpaper…” Well it turns out wallpaper glues made out of diisocyanates. Well what about spandex, nylon, polyester, all created, made out of diisocyanates. I told you things really start kicking off in the '70s, which screams out that something entered the market in the '70s to drive some of this. Well suddenly it starts to become manufactured in the '70s, it starts getting into people's homes in the '70s. Foam mattresses. I left that one off the list. Those are made out of isocyanate. And then it started to become part of car exhaust in 1975. So you start putting these things all together and it really screamed out, “Oh man, this seems concerning,” that when we just were randomly looking, “Hey, are there any chemicals associated with atopic derm?” The one that comes back is in every one of these products.

And then that really made it concerning was that when you want to… Any drug, it doesn't matter what pharmaceutical you can name, at some point in its development gave a mouse eczema using a chemical and then used their drug to take the eczema away. And then they went to the FDA to say, “Hey look, it works. Maybe we should try it in people.” Sometimes it works, sometimes it doesn't. But every successful drug did that at some point. There's only seven chemicals you can use to give a mouse eczema so that you can then treat it, two of them are diisocyanates. So it's just became overwhelmingly concerning that you say, if I wanted to give a mouse eczema, I would use the one chemical that I happened to find most associated with human eczema, and that is across all the epidemiologic risk factors and correlates in time and space and risk factors. So that's really made us start thinking, “All right, this could be a problem.” And then from there we try to figure out why it's creating the problem, what is it doing that's then creating these problems?

Jennifer: Yeah, because I was wondering, I'm thinking to myself as you're going through this list, obviously with wildfires and exhaust, it's in the air and obviously could be coming in contact with the skin physically, but you're also inhaling that. So would, for example, you mentioned wallpaper glue, is it that it off gases, the chemical?

Dr. Myles: Yes, it off gases. So what we did is I literally just went to a hardware store and started buying all this stuff and then would put it in the lab and put it next to one of these monitors to measure… This is a monitor that measures diisocyanates, and would pick up these diisocyanates coming off of drying wallpaper glue or drying polyurethane glues, anything like that. So yeah, I think there's off gassing. Diisocyanate are pretty well known in terms of occupational asthma. So that would be inhaling it generating a response, and then every time you inhale it after that you get asthma. That has been really well researched, and the exposure level you need to induce pulmonary response is pretty high. And I mean high in terms of… I wouldn't think wallpapering your house would be enough to do it. It's more the guys in the factories who are manufacturing this and… When you manufacture, it's head to toe covers, it's the big gas masks, those kinds of things. So I think the lungs damage needs higher doses, but yes, I do think in the air is where the problem is. Other than [inaudible 00:20:36]-

Jennifer: And when you talk about the fabric, how… And you may not know the answer to this, but any thoughts on how nylon or spandex or polyester, it's part of that it's on your skin. Is it that it's like an irritant? Does it get absorbed into the skin?

Dr. Myles: When we were looking at what we think is going on, it's basically two tracks. So the first one goes to the microbiome that lives on the skin. So all the microbiome… I'm sure it's more complicated in terms of what you need the skin microbiome to do. There's lots of things, but one of the big ones is it makes oils, I'll use the word lipids, but that's the kind of… They make these lipids that your skin needs in order to be healthy, that without them you're not going to have good barrier function and immune system's not going to work right. So these bacteria help make some of that for you. And isocyanate in short prevent that bacteria from being able to do that. We work on a bacteria called roseomonas mucosa. We also tested staph epidermidis and staph cohnii, which are coag negative staphs.

And what's interesting is staph aureus isn't affected at all. So when you expose staph aureus to diisocyanates, it has learned tricks to protect itself from that. Not because of that, I think, but learned tricks for other reasons that it now uses to protect itself against diisocyanates. And in our bacteria, when we expose them, the bacteria that survive develop those tricks and they start to use that. So basically your good bacteria on your skin either die or change their physiology in such a way that they're no longer functioning in a beneficial way anymore. In order for that bacteria to survive it, it has to change so it's no longer helping you do the things that you needed. So that was one major pathway in terms of it's poisoning your bacteria, preventing it from making the lipids that you need in a beneficial way.

The second one is that there are receptors on your skin that are… They pick up hot and cold. Now everybody knows the one… It's called TRPV1, whether you know it or not. It's the reason why chilies taste hot. So there's a receptor that's supposed to be hot, and then the chilies hijack and make you think that it's hot. Well there's one called TRPA1, and that's supposed to be for cold, and diisocyanates, a particular one called toluene diisocyanate, or TDI, the most common one in products, that is directly activated by this chemical. And when you activate TRPA1 there's a signal that goes to the brain that says, “We need to scratch this off of me.” There's a signal for itch and then the signal that comes back is pain and rash. And while it's in the brain, it actually processes through the anxiety and depression centers, at least in mice.

So what you've got is you got a chemical that will poison your skin bacteria and to keep them from doing what they're supposed to do and then activate a receptor in your skin that will immediately induce itch, rash, and psychological stress at least. So that's what I think, those are the two things going on. So in terms of the fabrics, I think laying that chemical up against your skin, or particularly polyester bedsheets I would worry about for children, if they're laying on that, that chemical is touching the skin, it's going to disrupt the bacteria's ability to do its job and it's going to directly activate the defects in the skin, or the receptors in the skin. So what we need to do now is really start connecting how much can you expect in house? What's the normal day to day fluctuation of this stuff? How much is too much for the skin? Those kinds of questions or what's outstanding.

Jennifer: Yeah, because I'm thinking for someone who's a mom dealing with a child with eczema and listening to this going, “Oh my gosh, what do I do?” Obviously you've stated you've got to make some choices in fabrics and different household things. I mean obviously you can't get a device that's just going to suck up this chemical from the air. Is there any potential remedy or actions that someone could take to possibly reduce their exposure?

Dr. Myles: Yes, definitely, spandex, nylon, and polyester I would stay away from. I would not get a foam, those memory foam mattresses. Get a more traditional cotton type thing. I wouldn't paint polyurethane, wallpaper… If you're listening to this and you had plans to remodel your baby's nursery, don't. The baby's not going to notice. I would stay away from those. But one of the worries is that the exposures that matter for eczema happen before you're two, maybe before you're four is more of a gray zone. So if you're the parent whose kids already six or seven has been dealing with this, I don't know that avoidance at that point's going to be the cure all, but it's worth a shot. I would say we did test the ability of just your routine air filter to pull this out is. I shouldn't call it routine, but it's like the carbon… They all sell something, but the label for VOCs. That'll be the volatile organic compounds. So we were able to pull a pretty good amount out of a control room.

We put a room and filled it with this stuff and we could pull it down to zero on the monitor, but it's not low enough for the bacteria to be okay. So my take home on that is if you can get an air filter, I think it would… There are studies, actually only two, but somebody did use air filters for eczema and could see an improvement. It's just hard because there's no placebo control? How would you fake an air filter? But there's some evidence that at least… And I can't imagine it's going to hurt, other than the financial bite it might take. But if you try that, what we're trying to do next is validate a air filter that really can suck this all out. Because there may be one. There may be some particular filter that really could completely eliminate this from the air, at least in your home. You're not going to be able to do much probably when you're out and about. But if we can validate our detection system now we can tell you these filters will actually get things down to zero and these ones won't

Jennifer: So I just want to ask one quick question, so the VOCs that you mentioned, the diisocyanate, is that a VOC?

Dr. Myles: Technically, but if you see something that says… You can go on Amazon… I shouldn't name any brands, but you can go on the internet and get a VOC monitor. It will not detect this. So chemical class, it's a VOC, but not in what you would think of in terms of like, “Oh, I'll get a VOC monitor for my room.” It will not pick these particular chemicals up. There's only one detection system and it's really built to go in a factory. It's like thousands of dollars and the size of a suitcase and needs this cartridge that you have to replace every month. So it's not really a viable thing for consumers right now.

Jennifer: Well I think that what you're offering is a different side of the conversation that doesn't often get heard. Because like I said, a lot of the environmental factors that are considered are allergies to pets, so dander, pollen, allergies, allergic to different chemicals in your detergents and cleaning supplies and things and food allergies. But what you're talking about is something that I think some people do have sincere concern about, but they don't have any real proof, and I know you're working on this, which is really exciting because I think it will help people, like you said, not just now but in the future make better choices and hopefully it will guide some of the decisions at a higher level than the normal citizen of like, “Should we even be using this? Should we do we have to do something to potentially control for this particular chemical in our environment?”

Dr. Myles: And don't know anybody who works in that field in terms of the chemical companies, but I will give them partial credit for this there we didn't see a lot of denialism when you look through the literature on, “Hey look, this can cause problems in the lungs.” It wasn't like cigarette companies where they started lying and hiding things. So now that's very clear. If you want to use this, you're supposed to use a mask and head to toe. Now does every worker actually do that? No, but you can't… If you're using it appropriately, I don't know how much more you can ask of the companies, but I hope that these chemical companies would engage with this because in our data it showed that… There's two different things that show up in the EPA database. It's whether these are just released out in the wild, on the first… This is called fugitive. So it's like if you burned it in your garage or your driveway, versus something called stack, which is a chimney, which if you think of a cartoon picture of a factory in your head, you probably envision the chimney that comes up.

The stacks weren't associated. So it might be that what we really need is to just make sure anybody who's using this pumps it out of a stack, which dissipates it in a different way, or that maybe they need a particular filter to help deactivate it before it comes out. I think there's probably a way in which we can mitigate this at the source that won't necessarily require across the board bans or anything like that. We'll see. I guess to your larger point of getting at this a different way, I agree. I was struck and it was very nice to see that people at the expo, which was overwhelmingly patients or caregivers, seem to respond very favorably to this conversation. Because again, I think deep down, I think maybe patients intrinsically know that they don't have a drug deficiency. They or their kid do not have a steroid deficiency that can be treated. There is such a thing as steroid deficiencies, it's called Addison's disease, but it doesn't manifest as eczema at all.

So you're saying, “I don't have this problem because I lack this drug. Something else is going wrong.” And I think early in eczema research, the thought was, “Oh, it's all going to be genetic, so it's just you're genetically broken or something like that, and that just has not panned out at all in any way. So there are a few monogenic versions, but those are super rare. So the really issue is something is out there driving this, something is causing this in my community, something is causing this to be a flare, and whatever it is, it feels like people aren't really looking for it. So yeah, I do think that that's what people appreciated, that it does feel like there's got to be something… Because all the other stuff, dander and… We actually did a project where we looked at lotions under the thought that maybe all of a sudden we started using soaps that cause a problem, and we can find soaps that are bad in terms of…

You see the soaps that love to brag, “Oh, we kill 99% of organisms.” And you're like, “Well, okay, is the bad guy the part of the 1% that survives, because that's a really big difference. If staph Aureus is the 1% that survives or is part of the 99% that gets killed.” And we can find soaps that represent both of those versions. But then you step back and you're like, “Okay, it's not a soap.” If it was one soap or one ingredient of a soap, I feel like this community would've pieced together by now, “Let's just avoid these things. This is obviously a problem.” Soaps didn't get invented in 1970 and dogs and cats didn't suddenly come into the home in 1970. So all of these exposures that typically get blamed for skin reactions, you're like, “I need you to…” Putting it into the larger picture. Would that help you explain why this has suddenly become such a more modern phenomenon or is an industrial only society problem, basically?

Jennifer: Wow. Well, thank you so much for sharing all of this and I'm excited to continue following your work and your research. I honestly was so grateful to have… I didn't know who you were before I saw your name and you got up on stage and started speaking and I was like, “I have a feeling I am going to deeply appreciate what this man is about to share. And it was one of the best talks and discussions of the entire conference, and I'm so grateful for you making the time to be here. So hopefully we can have you back some time and dive into other topics because I always love different perspectives on things, and I think you're right, people have that inkling that there's more to this than just a drug deficiency of some sort. And I think we need to give voices to those different perspectives, because there is something else more to this than just your genes or your laundry detergent.

Dr. Myles: In the talk I'd mentioned, I didn't want to leave it out, the groundwater hypothesis or the groundwater approach, which actually comes from social justice conversations, but the crux of it is if you came across a lake and there was one fish floating dead in the lake or two fish floating dead in the lake, you would say, “What's wrong with those guys?” But if you come up to a lake and 30% of the fish are floating dead, you're saying, “There's something wrong with the lake and I'm not getting in.” And I think when we look around and we see this much burden of eczema and skin disease and immune disease, it's becoming obvious there's something wrong with the lake, and we haven't spent a lot of time looking at that.

Jennifer: Well thank you so much for being here. I'll make sure that we'll include your email address, since you did say you work at the NIH, so you have a public email address that people can contact you at. And I know we have doctors and other practitioners that listen who may also be equally interested in your research as well. So I'm just so appreciative for you to be here, and I hope that I'll be able to get you to come back sometime.

Dr. Myles: Sure, yep, sounds good.

“There's only seven chemicals you can use to give a mouse eczema so that you can then treat it, two of them are diisocyanates.”

Jennifer Fugo, MS, CNS

Jennifer Fugo, MS, CNS is an integrative Clinical Nutritionist and the founder of Skinterrupt. She works with women who are fed up with chronic gut and skin rash issues discover the root causes and create a plan to get them back to a fuller, richer life.

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