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What are the causes of eczema? Can you get eczema genes? Is psoriasis genetic? These are common questions especially since many doctors still blame skin conditions like eczema and psoriasis on genetics.
Many people have been told “Oh, you just got bad genes!”
So is it true that the genes are the reason explaining WHY you got the skin condition that you have? Or does this attitude overlook and ignore other possible triggers.
With the ability to sequence the genetic code (and even get your own DNA report), genes have essentially become the convenient excuse according to my guest today. And that leaning on them as THE reason you have skin problems (and other health concerns) is something of a flawed approach.
In reality, there are a multitude of reasons or triggers that can cause skin problems that include the environment, your microbiome, chemical exposures, nutrient deficiencies, hormonal imbalances, and even what fabrics you wear. But if we ONLY point to genes, it becomes really easy to see how these important factors are overlooked.
So if you’ve been told that eczema is genetic or what causes psoriasis on the skin is because of your genes, this conversation will blow your mind. My returning guest Dr. Ian Myles is head of the Epithelial Therapeutics Unit at the National Institute of Health tasked with evaluating the efficacy and safety of a topical, live bacterial treatment for eczema.
He did his undergrad at Colorado State University, received his medical degree 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. Also, Dr. Myles received his master’s in public health from George Washington University.
And he’s the author of a fantastic book called Gattaca Has Fallen: How Population Genetics Failed the Populace now available that seeks to answer the question about how genetics research has led care for chronic health conditions (like skin problems) very astray.
Or, listen on your favorite app: iTunes (Apple Podcasts) | Spotify | Stitcher | TuneIn | Subscribe on Android
In This Episode:
- True or false: Is eczema is genetic?
- How genetic research has changed the way medicine views chronic health conditions
- The dark history behind using genes to guide treatment
- Is there an eczema gene (or even a dyshidrotic eczema gene) or is psoriasis genetic?
- How does your environment (and chemical exposures) influence your genetic code?
- Can different fabrics INCREASE Staph aureus on the skin?
- New research on topical eczema treatments using the skin microbiome
Quotes
“It is an easy excuse and it comes from a dark history, but comes from a long time ago where it was just an assumption as to, why would one person get a disease and one person not? And particularly within siblings, right, why would one of your children have eczema and the other one never suffer a second of the disease? And it was just this assumption that there's got to be something innately wrong with the individual.”
“…With the advent of the microbiome and a new appreciation of that, now it's finally expanding out to skin organisms, gut organisms, all these other things, which, it's become very clear, there is no you without those organisms. So a mouse that is raised without any microbiome, there is not one single organ system that functions correctly…Not an immune system, the brain, the gut, the heart, the liver. Not one single immune system functions properly in a germ-free, what the term would be, germ-free mouse, so no microbiome.”
Links
Find Dr. Ian Myles online here and on Twitter
GET THE BOOK → Gattaca Has Fallen (book)
Healthy Skin Show ep. 279: Chemical That Triggers Eczema (Oh My!) w/ Dr. Ian Myles
357: Is It Just Bad Genes? (What Are The Causes Of Eczema + Psoriasis On Skin) w/ Dr. Ian Myles {FULL TRANSCRIPT}
Jennifer Fugo (00:09.67)
Dr. Myles, it is so great to have you back on the show. Thank you for being here to talk about what are the causes of eczema and to answer questions about whether eczema is genetic or psoriasis genetic.
Ian Myles (00:14.734)
Thank you for inviting me back.
Jennifer Fugo (00:16.878)
So I wanted to have this conversation because, like other eczema patients, I had previously been told when I developed dyshidrotic eczema that I just got bad genes and that eczema is genetic. Basically, I feel like to some degree, eczema has just been blamed on genetics. And it's maybe led to a lack of curiosity about other potential triggers. What's your take on whether eczema is genetic?
Ian Myles (00:49.534)
Yeah, without a doubt, it's a lazy out, so to speak. Saying that eczema is genetic is an easy excuse and it comes from a dark history, but comes from a long time ago where it was just an assumption as to, why would one person get a disease and one person not? And particularly within siblings, right, why would one of your children have eczema and the other one never suffer a second of the disease? And it was just this assumption that there's got to be something innately wrong with the individual. There's something broken in you and even if you need the environment to bring it out out or whatever, it is still your intrinsic failure to protect your body from eczema for whatever reason, and the genes were the easiest way to blame it on that. And it does lend itself to kind of giving up and saying oh well, this must just be a genetic trait and we don't have to do anything more about it. So I definitely empathize with the idea of just blaming an innate defect.
Jennifer Fugo (01:47.762)
Do you think that it also allowed for, say, the medication option, like we just have to manage this? Like this is just a management thing, because it's the genes and you can't change your genes. Maybe in my head that's what I'm saying, but is there some truth to that kind of thinking or logic?
Ian Myles (02:11.754)
In my opinion, absolutely. I think that, if there is something innately wrong with your biology, the only solution is a pharmacologic fix. So if I give you a drug that corrects your physiology, then that's good, right? And that works fine when it genuinely is an innate defect. Let's take something like cystic fibrosis. No one's going to disagree that that's a single gene mutation, just as one example, that mutation prevents their pancreas from putting out enough pancreatic enzymes for digestion. So what do we do? We give them a pill filled with pancreatic enzymes, we've corrected their physiology. Ideally, you do gene therapy one day, we'll get there, I don't know.
But the idea is like, well I need this medicine to fix you because you're broken, versus if it's an environmental factor, well I could protect you from that. And so you don't have to worry about ever getting the disease in the first place. And that tends to be a lot harder, or at least has not had anywhere close to the same amount of attention. So I absolutely believe that it leads one to a mindset that even if you are not in the pocket of big pharma or any type of accusation like that, if you only can envision the cure for these disorders is fixing a person's physiology, your imagination will be limited to pharmacology. And then you'll just kind of be in service of that whether you want to or not.
Jennifer Fugo (03:37.658)
So I feel like there is so much in the universe, and I'm going to say the universe, that we do not know. And we're included in that. My dad, who was a medical doctor, an ophthalmic surgeon, and a researcher, he developed a lot of technologies and such specifically for eye surgery. The one thing that I learned from him, because he always had his nose in a book, he was always researching things, he said what we currently know is a mere fraction of what's actually going on. And maybe the research into just genetics in general was this intentional leap forward? Like maybe we thought that it was gonna give us answers to everything, including answering question about if eczema is genetic or is psoriasis genetic. Can you talk a little bit about what the idea was behind looking at genetics and really understanding them, and using them as a basis for how we looked at our bodies, physiology, disease, et cetera?
Ian Myles (04:41.034)
Yeah, so it really goes all the way back to when the word gene just meant packet of heritability, before even the concept of DNA, it was a hundred years away when they started talking about this. So it begins with twin studies, which, I won't belabor their methods, but it's just how similar are identical twins from fraternal twins. And they would do these calculations and come away with statements like the love of sailing is 80% genetic, because there's a difference between whether your fraternal twins both want to go sailing versus identical twins. It didn't take very long for people to piece together that, well, identical twins are treated the same, they're confused for one another, they share the same identity, so of course, they're going to be more similar. That's ridiculous. But that set the number of expectation. So when somebody does, it's easy to laugh at love of sailing, but eczema is 85% by that exact same calculation. So 80% love of sailing, eczema 85%. And so now you have to ask yourself, okay, well, that's the expectation. We expect 85% of the disease is going to be somewhere in the genome. It makes sense to throw an enormous amount of effort and energy to go find what exactly, what gene is it? And then if we can figure that out, just like with cystic fibrosis, which was successful, can you then start to design therapies around that, or start to tease out why that genetic mutation really matters?
And so there was never a reset, or has not yet to be a reset to say, why did we ever think it was gonna be 85% genetic in the first place? And as I said, this gets much darker and much more abusive when it starts to become education, whether somebody goes to college, how much of that do we think is encoded into the genome, how much income, criminal behavior. These are the basis for eugenics policies and race science. In the book, I'm trying to argue that even the researchers who do not have any racist intent or might be of any background, they will still contribute to this with the constant insinuation that all of these modern phenomenon, which eczema is, are somehow encoded into our genomes. And when you hear somebody say, you have bad genes, of course, when your first questions were, well, either my mom or my dad must've had those same bad genes and my grandfather and great grandfather. So why wasn't it a problem for them?
Jennifer Fugo (07:05.179)
Right.
Ian Myles (07:10.838)
And I use allergy as the example because I think most people understand, at least at minimum, food allergy. Where, if you are over 40, you did not go to a peanut-free elementary school. And if you are over 40, you absolutely had to fill out a form if you sent your kids or grandkids to elementary school attesting to whether or not they have allergies. And I guarantee you your school nurse has access to epinephrine, when that wasn't a thing in your grandfather's era. So it's just something has clearly changed in the environment, and the assumption that it was all pre-programmed has kind of fallen apart. And I don't think we've yet had that reset to say this is not a genetic trait.
Jennifer Fugo (07:51.41)
Do you think that overall, getting access to all this genetic information, and I assume when you talk about genetics, is it just the human genome, or does it also include the genome of all of the organisms that live on us?
Ian Myles (08:10.03)
So the ones that people have spent all their effort and energy throwing in have all been human.
But now with the advent of the microbiome and a new appreciation of that, now it's finally expanding out to skin organisms, gut organisms, all these other things, which, it's become very clear, there is no you without those organisms. So a mouse that is raised without any microbiome, there is not one single organ system that functions correctly.
Jennifer Fugo (08:37.958)
Really?
Ian Myles (08:46.196)
Not an immune system, the brain, the gut, the heart, the liver. Not one single immune system functions properly in a germ-free, what the term would be, germ-free mouse, so no microbiome.
Jennifer Fugo (08:49.935)
Wow.
Ian Myles (09:15.856)
It'll still develop, it looks like a mouse, but the bones are brittle, all of it is a problem. And we know maybe, you talk about the universe, I mean we maybe know half a percent as to how to explain each of those individual shortfalls. But yes, when I talk about genetics in a negative term and kind of saying this has been overblown, it's been human. The assumption that a gene difference between you and me will explain our different paths in life. And that's where this stuff started. And I think it's been, unfortunately, it's corrupted the well-meaning research as to why one person would have skin disease or lung disease or so forth.
Jennifer Fugo (09:32.474)
You mentioned some interesting concepts in your book called Gattaca Has Fallen, which I have a lovely copy of. I bought it myself. I love getting books that really make me look at things from different perspectives. I love that. You mentioned something called the selfish gene idea. Can you talk about that?
Ian Myles (09:53.294)
I mean, that is the founding, the springboard for the good old Richard Dawkins, who is not a geneticist, but who came up with this kind of anthropomorphized idea that genes don't, he didn't insinuate genes had sentience or they’re like making decisions or whatever, but he's implying that they act as if they do. And so, like, your gene for oxygen consumption wants to predominate. Or he takes it for genes and memes, so like the meme for certain behaviors wants to spread. And he makes it seem like it's a zero-sum game, that one gene has to out-compete another gene for it to proliferate and survive. And a lot of the geneticists that I've talked to, they mentioned, hey, I read that book in high school or college or whatever. And they were like, oh, this is great, they liked it, they thought it was very insightful. For most of the people, especially now, it has not held up well in terms of this argument.
And again, he wrote it in an era before the Human Genome Project was announced. And before that, there was an assumption that the human genome might have trillions of genes. And so there would be a gene for being a basketball player, a different gene for being a cello player, a different gene for being, you know, there's going to be a gene for liking cheddar and a different one for liking Swiss. And if that were true, then it would kind of make sense, how it was spread out and might dictate your personality. But not only is there not three trillion genes, there's 30,000, and so it's not even anywhere close to being able to explain that. And the difference between one person and another is infinitesimally small.
Again, it can matter if that if a part of that difference is a mutation in the cystic fibrosis receptor, or in hemoglobin for sickle cell. So it can matter, but it has not been able to explain these personality differences and outcomes the way that the selfish gene implied.
Jennifer Fugo (11:54.918)
And so if we take that maybe a step further to what are the causes of eczema, for example, there's different forms of eczema. If you look at psoriasis and what causes psoriasis on skin, there's different forms of psoriasis. Was the assumption that there were just different, you have some like unique version of an eczema gene or something, or a psoriasis genetic component that causes you to have scalp psoriasis versus plaque psoriasis? I have no idea. Was that sort of the thinking?
Ian Myles (12:21.27)
The idea was going to be, yeah, you'd have a dyshidrotic eczema gene and an atopic dermatitis gene. And I don't know how much that penetrated the people who were actually doing that kind of research. But once the Human Genome Project came back and said, we're not even going to be in shouting distance of anything like that, let alone a cello-playing gene. As I talk about in the book, I remember distinctly when it came out, I really wish I had saved it, but there was like an ESPN The Magazine article, to date myself. And it was like, what are sports gonna do now? Everybody's just gonna be able to custom-print their child to be the next Michael Jordan, and so it won't be fun to watch because everyone will be of equal great talent. And that has not come about because, again, they thought, we're going to have one gene for Michael Jordan's skill set, he just happens to have it. Or, say, 20 genes that add up to skill sets, and every kid will just, we'll be able to put it in there. And so, yeah, they really did think it was going to be individual genes. And that has shifted towards, okay, well, there'll be like predisposition genes.
But then, then it starts to break down automatically, as you can already guess, right? If you say, well, there's an eczema predisposition gene, what would, even if that were true, what would determine who got what kind of eczema, and how severe it would be, and why does some psoriasis stay on the skin, and for some people it becomes psoriatic arthritis and starts to destroy the joints? And if you continue, I think the idea was, well, let's just keep sequencing more people, getting stronger computers and we'll figure this out. Like somehow, some way, we'll figure out that there’s a psoriasis genetic trigger in the genome because again, they still believe the twin studies that told them it was gonna be 80, 90%. And I do think at some point, there's a mounting breaking point coming and people will say, okay, even if there was a predisposition, some other environmental factor must be what's dictating who gets what kind of eczema and where. And now we can start to look for those.
Jennifer Fugo (14:28.99)
I have talked with other doctors about, like, methylation, right? There's gene SNPs and your environment can, I've even heard the phrase, what is it? You have your genes, but then the environment loads the gun or something or other. Some phrase, most people who listen to this probably have heard it, some on functional medicine podcasts and whatnot. So they're familiar with it. But is it possible, then, that this has prevented us from really caring about the environment that we live in? You and I have talked about some environmental factors in the past. So is it possible that the environment, you could have a gene, right? You could have theoretically a gene that maybe, I don't know, 70% more people tend to have this gene if they have a particular diagnosis. But is it possible, then, that the environment plays, perhaps, an equally important role in how that gene maybe expresses itself?
Ian Myles (15:34.794)
Yeah, I’d go further than say equally important, and say just overwhelmingly dominant important. And I tell this story that a guest lecturer came, and he was talking about sodium lauryl sulfate, which I'm sure has come up on your podcast as being just something that is gut rot, is the short way of saying it. It will destroy the barrier function of the gut. And it's in a lot of toothpaste, even ones that market themselves as green and have like big pictures of leaves on the front or whatever. And he goes through intimate detail of how this is ruining cell cultures, harming mice, is almost certainly toxic. And one of the people in the room who's in charge of the purse strings for grants, his first question was like, oh, what are the genetic predispositions? And my question was, who cares? If my kid has a genetic predisposition to toxic toothpaste, or he doesn't have a genetic predisposition to toxic toothpaste, I'm not buying that toothpaste. I don't understand why I would even care.
And so even if there were a gene, like for example, if you and I both had a gene that said, if we got Ebola, we would spontaneously combust, I don't worry about that. Like it's not something, our environment in the United States has rendered that irrelevant. There may very well be a gene that makes it more likely that you or I get scurvy, not gonna happen in modern American times, right? And certainly not with the knowledge that we now have about how easy that disease would be to prevent.
So this idea of, it came up a lot, it came through eugenics, that even if you have a gene that required the environment to make relevant, let's say, their argument was it's still a genetic problem because without that gene, the environment would no longer hurt you. And they used that as an argument to say, well, if you have a kid, a child of somebody with schizophrenia who does not have any symptoms themselves, we should still sterilize them, is their argument because if we don't, we risk whatever gene they have percolating in the population, and then who knows when the environment will bring it out. So we'll sterilize all people with schizophrenia and all of their children because that will prevent schizophrenia from happening anymore. And there were, it is not like, only Nazis who thought this. It is not only people on the political right at the time who thought this. There were plenty of liberal individuals and, you know, people who believed themselves to be doing right by saying, wouldn't it be better to cure all future generations of schizophrenia if we could just do this one time? And understanding they may not like it, but everyone's cured.
And like, I guess on paper, I'm sure the ethicists would disagree, and certainly the patients would disagree, but that was their argument. And obviously, newsflash, schizophrenia has not been cured, nor has any other disease by systematically killing or sterilizing people. And I think that's where, whether we want to or not, we still live with that kind of ingrained dogma to say that, okay, it's still your problem, right? Because that's the argument. Two kids in the same home, and one has atopic derm and one doesn't. And in the book, I'm quite harsh on the genetic lottery, because you know, the author of that book would presume that, well, one of your kids lost the genetic lottery.
Ian Myles (19:11.478)
And the problem is, there could be, just because we haven't put any effort into it, there could be immense differences in the environment that we just haven't picked up. And when I was on your show last time, we talked about isocyanates and these different pollutants that are out there. And to bring it home, the worst polluter that we saw in our database was one factory in Southern Florida. And it went online in 2019. So that would mean that if you had a child in Southern Florida in say, 2014, and had another one in 2019, your first child was not exposed to any of this during the early part of their life, at least not from that factory. But your second child would be. And so the assumption like, well, I have two kids, they're both in my home, they were both born to you and your spouse, so shouldn't they be the same? I guess one just lost the genetic lottery.
You have to start to think like, hey, you know what? Even if you tried your best, you can't control every environmental exposure. Some of them may have been harmful, and disproportionately hit you when you were pregnant with one child and not the other. And I think it's a laziness, and I think it is a complacency now, of saying like, oh, I don't have to worry about the environment, or that's just a modifier. Because if I work hard enough, I'll find the gene, I'll find the cytokine that's the problem, and if I just block the right cytokine, all of this is gonna go away. And I'm not buying it.
Jennifer Fugo (20:36.614)
Yeah, I'm reminded as you were talking about sort of where these ideas have come from, that phrase the road…
Ian Myles (20:44.33)
Yeah, the road to hell is paved with good intentions.
Jennifer Fugo (21:04.015)
Exactly, the road to hell is paved with good intentions. It is horrifying.
Ian Myles (21:13.598)
Yeah, the problem is, with genetics, I would say the bike trail next to the road was paved with good intentions. The road was paved by Nazis and eugenicists and murderers whose stated intent was mathematically calculating why Jewish people were inferior. And that equation is with us today. Whether you want, obviously I do not believe the overwhelming majority of researchers today, even if any, want to use that equation to come up with those same kind of purposes. But it's like, you're using an equation from somebody who wanted to calculate inferiority of non-white people to tell me that 85% of eczema is genetic, that feels weird. And it feels like there's some things that might have been missed.
Jennifer Fugo (21:41.895)
Yeah. Interestingly, in your book Gatteca Has Fallen, you talked about, and I do try to explain to people about studies, right? How we do research and how you can't take, like, there's all these little studies. 14 people took X, you know, a probiotic of one billion CFUs of X and we saw this. And I'm like, well, that's not a lot of people. You talk about this concept of having negative controls in a study, and that they're often missing. So in layman's terms, what should listeners understand, just generally speaking, about research, and why would this concept of negative controls be so important?
Ian Myles (22:22.922)
Yeah, negative control is any time that you're going to run your test and you expect it to be negative. You might get some static, would be probably the best word, but you know that that's irrelevant. In the book I use the analogy of, if you listen to a car accelerating, and I joke now that everyone's going to electric vehicles it doesn't sound quite as cool, but you have that revving sound. In your brain, you can guess how fast that car is going, right? How accurate you are at guessing it, I don't know, but you can hear when the car is accelerating or not, or when it's shifting gears, versus when you sit next to a car and it's idling. An idling car makes noise. But if I asked you, listening to the sound of an idling car, how fast is that car going, you will know it's going zero, because it's like, hey, this is background noise. I need to subtract that, and everything above it is what I need to start to care about.
And so as it would relate to genetics, you would want a situation where you know, whatever it was you're measuring, is not genetically encoded, or at least not meaningfully enough that you even need to worry about, because you want to know, hey, what's the background noise? And so I joke in there about using, like, I want to know French-speaking Canadians versus English-speaking Canadians. Only a lunatic would think speaking French is encoded into the genome, like there's a gene for speaking French. Or, I shouldn't say lunatic, somebody from like 200 years ago would have thought that. So if you have a gene, you know there are gonna be genetic differences, because French people are gonna be more likely to mate with other French people and English Canadians with English Canadians.
So just run that. And that will tell you, what is my background noise? How different can human beings separate their gene pool? Because any two people are 99.9% genetically identical. So how much can a population shift themselves apart? And now I can use that. So I can do French versus English speakers. And now when I go to do eczema versus healthy controls, it'll give me a better sense of how much noise is in my system so that I can dismiss low-level things. So for the twin studies, loving sailing should have been a negative control. So that tells you that 80% is background noise. And now you can only really go up above that. So that's what's important.
Jennifer Fugo (24:36.542)
You talked about how, for example, if you use a virus to maybe insert a gene or do something, that, what happens if the vehicle, to affect a change, actually in and of itself affects a change? Is that another example?
Ian Myles (24:59.178)
Yeah, those are, I guess the best one is always the placebo. So you take a drug that for all the world you think is real, you believe it's a real drug. And so now just taking a drug, and believing the drug is real will give you a certain amount of improvement, the placebo effect. And so, open label studies, early on, when you're talking about these early studies, right? I do 14 people just with a probiotic, let's see what happens. You can compare to what would happen if I did nothing, but that's always considered kind of the first stage, right? You're like, hey, look, they got better, they didn't get better, compared to nothing alone, but you say, all right, and now I need to go compare it to placebo. And that would be a kind of a good negative control. And the geneticists have never, ever run what would be considered a placebo.
And every time they run anything, I talk about very heinous ones in there, about this insinuation that being molested as a child is a genetic trait. Which, again, you would think like, just from an evolutionary standpoint, you're like, what was the selfish gene that was trying to get this kid abused, right? Insane.
Jennifer Fugo (26:03.622)
They thought that was a gene?
Ian Myles (26:16.342)
Yeah, The Lancet Psychiatry paper claimed that it was a gene, and their justification for it was the genes associated with being abused were also associated with depression, but not with heart disease. And there was no insight whatsoever to say, I can think of multiple reasons being abused would be linked with depression and not heart disease that don't involve genetics. At no point do they even mention that or bring it up. And so, yeah, that concept of just saying, oh, everything we find, we will assume to be real, because they haven't run a negative control to say, what is my background noise?
Jennifer Fugo (26:47.994)
I did want to go back to your point, how we talked about your research on the diisocyanates. In your book, you actually mentioned how one of your research assistants had this idea about, “why don't we look at fabrics and how they interact, for example, with Staph aureus,” which I feel like a lot of people in the eczema community can appreciate because there's so much information about Staph. Can you talk about that? Because obviously, there's not a genetic piece to this in this regard. This kind of shows that the genetics argument is extremely limited and short-sighted. What did you guys find in terms of how fabrics could interact with this organism living on the skin?
Ian Myles (27:34.782)
Yeah, so we did the isocyanates through, the technical term would be a non-spatial. And so then we added one that's just trying to, a slightly better model, that's the best way to say it. And then added another group of molecules called xylene and benzene, benzene might have been something you hear about. But they are all automobile exhaust, wildfires, and cigarette smoke, and a lot of things that are associated with atopic derm risk, and eczema risk, and started to rise right about 1970 when we start to see this explosion in the rates of atopic derm. And so we thought, all right, let's test them in your house. And so it would be spandex, nylon, and polyester. So nylon is made from benzene, spandex made from isocyanate, and polyester is made from xylene. And you can't make them without it, so there's no xylene-free polyester that exists.
And so what she did, Grace, in the lab, she sprayed the exact same amount of good bacteria and bad bacteria, so Staph aureus, Roseomonas mucosa, which is what we use for our treatment trials, and Staph epidermidis, so good Staph, you've probably heard of. And then just look, and just let them sit on the bedsheet with nothing else, and then come back and see how well they survived. And Staph aureus does not survive for more than three days on natural fibers. So cotton and bamboo, Staph aureus is all dead. Nylon, a nylon spandex blend, it proliferates like crazy. Polyester, it proliferates. Silk was hard because silk doesn't have the same regulation, but there was some there.
And so you compare it to the commensals, the good guys, right? And all of the commensals will also grow on every fabric. So it'll grow on cotton and all the synthetics. But in order to grow on synthetic fabric, the good bacteria have to change the way they behave. So the way I've described it is, the good bacteria are being choked by the synthetic chemicals, and the only way for them to survive is to alter their physiology, right, adapt. Just like if you made a blanket out of penicillin, what do you think would happen to the bacteria on your skin? And so they have to adapt, and the way they adapt is they shut off production of those lipids that we know are beneficial. So ceramides, sphingolipids, phospholipids. Ceramides had a big year this year because of the Super Bowl ad, and I don't endorse any particular product, I don't know.
Jennifer Fugo (29:53.126)
Wow. Yeah.
Ian Myles (30:00.726)
But the bacteria on your skin, you have to have them. And one of the reasons is they make these ceramides for you, or help your body make more of them. In the presence of these fabrics, or in the presence of these chemicals, that shuts off. So it is a survival mechanism for the bacteria on the skin at your expense. And we really think that there's some critical developmental window, because these environmental exposures tend to occur before you're four. Because you don't really hear somebody, sometimes.
For genuine atopic derm, it would be rare to have like a 50-year-old suddenly develop it out of nowhere. You'd start to think like, oh, I don't know, we should look at other things, right? Not impossible. But we think that something happens in childhood early on, and so we think that these exposures are poisoning the microbiome, so to speak, and that the child gets stuck with that, and that lasts for the rest of their life, and turns into the atopic march and everything else.
Jennifer Fugo (30:57.362)
So what you're saying, I'm just trying to imagine this, is that a child is born into a home with fabrics. I mean, obviously fabrics are a part of our life. We wear clothes, we sleep in beds with fabrics. They're all around us, plus paints, like, we got to get the room ready for the baby, right? So you buy all these new furniture a lot of times, you'll get the floors redone, new carpeting, whatever. So you have a child, this wonderful little child, that you're saying that the there is a really good possibility that all of the chemicals involved in their environment. And again, it's not to blame anyone, right, because we're understanding this better now. But that those chemicals could influence how, your skin microbiome thinks it's essentially under, it is, it's under some sort of pressure, and it shifts in a way that is potentially not to our benefit, or to that child's benefit. Is that what you're essentially saying?
Ian Myles (32:02.698)
Yeah. In my book Gattaca Has Fallen, I have a whole part where I go through to say, within just twins. So I say, let's take two twins home from the hospital, and let me walk you through all the different ways that I can expose one to more isocyanate or xylene than the other. Now, identical twins would be less likely, because you're going to dress them in identical clothing at the same time, more likely. And then I go through siblings. And there is a part in the book where I do say that it can sometimes be comforting to believe that your kid lost the genetic lottery and there was nothing you could have done. Because you do have to be careful that it's not implying guilt. Like, oh, well, if the parents had only not remodeled, their kid wouldn't have got eczema. And it's not their failing, it's the failure of the biomedical research community to not inform them, to not first off look to see what might've been the way to protect their kids from eczema, and then not to inform them about the things that we already know. Because we knew remodeling behaviors were problematic and would increase your risk. Most of that research, by the way, is done out of South Korea more than the United States for various reasons. But the reality is, I walk through and say, the mattress that you may have picked, and particularly eczema tends to afflict the first born more than subsequent kids.
Jennifer Fugo (33:20.602)
Interesting.
Ian Myles (33:21.05)
I mean, at this point it's pure conjecture, but my hypothesis is that if you are going to remodel your nursery, and buy the brand new mattress and the brand new crib that's freshly lacquered, it's more likely gonna be on your first child, and then the fourth kid just gets whatever the first three didn't destroy. But I have to be cautious,it's not just gonna be things in your house, right? It's not just the fabrics, like, I wouldn't wrap a baby in a blanket that has chemicals that came out of a car exhaust, but the air in these factories and how close you are to automobiles are also a problem. And what we don't have the data for at all is, let's say we have two different factories and they both put out the exact same amount of isocyanates per year, we'll say 365 pounds. If one factory puts out one pound a day all year round, and another factory, just because of it's manufacturing procedures, just puts out 365 pounds one day out of the year. I have no idea, we don't have that data, it's only aggregated by the year, so I have no idea which one of those is better, but there's no way they're the same, right? There's gonna be differences.
And so it could be that you did everything right. You had the most organic, you know, your crib is made out of unicorns. And yet that day or that week that you brought your kid home, a factory 25 miles away put out a massive ton of a particular chemical that is not traced by the EPA in the air, will not show up on your air quality index. They put out a massive amount of it and it wafted into your house. There's nothing, short of better detection systems and better filtration systems that don't yet exist, there's nothing you could have done. And so I don't know that, like we don't want to get into the blame game, but like absolutely I think that you bring a kid into a certain environment, expose them to all of these different chemicals, you should anticipate something bad is going to happen.
And that's what I think is happening, and not just for eczema. I'm sure it's true for all kinds of things. I bring up constantly in the book the example of lead toxicity. When we used to have leaded gasoline, lead would be in the air, it would get in, it's neurotoxic. It could drive up violent behavior, it would drive down cognitive performance. And so whether you did anything right, two college professors, they're doing everything they're supposed to do, they think their kid is going to be blessed with some brilliance because they both got good genes. Hey, guess what? If they take their kid somewhere and he gets a big huff of lead and gets neurotoxicity from it, that's gonna cause harm. And there's just nothing that you can do about it. And we need to be much more cognizant about how much these modern exposures are driving various diseases.
Jennifer Fugo (36:02.67)
Yeah, I think the underscoring thing as a layman I'm concerned with is, that we really can't go by “it's just a gene problem” anymore when talking about topics like what are the causes of eczema or is psoriasis genetic. And I love that we were able to kind of bring this conversation full circle back to the conversation we had, which I'll definitely link up for anybody who missed that conversation on the diisocyanates. Oh my gosh, it's been like a year and I'm close to saying it correctly.
Ian Myles (36:27.114)
You got it. That's pretty good.
Jennifer Fugo (36:32.93)
That research was really shocking. And I know too, when you presented it, you were like, we were surprised. We were like, what's going on here? Wildfires are a producer of this chemical, and all of these different things. And no one ever bothered to look. And you can't blame that on a gene problem. That's an environmental problem. And by just focusing on genes, we ignore everything else, it gives us tunnel vision, almost. So with that being said, I want to try and leave this on a positive note. So you're in the research world. Is there anything that right now you feel is hopeful or fascinating on the horizon for eczema treatment, eczema research, or what are he causes of eczema?
Ian Myles (37:23.59)
Yeah, I think the hope is that it is an impossibility for any of the next generation of researchers to make it through, at this point, high school even, but college, med school, RD training, whatever it is, it is impossible for you to go forward to become an eczema researcher and not have heard about the microbiome. And then at that point, because the microbiome is so important, it's impossible to not think about the exposures that drive it. The most obvious one is always the gut, because of the diet and how overwhelmingly controlled the gut microbiome is by what you eat. And that'll just change the calculation, right? Because now if somebody comes to you and says, eczema is 85% genetic, you'll know that that's ridiculous, because you'll know, well, wait a minute. How are you explaining, how does the microbiome play a role or what, why would the diet matter? It's gonna help.
And I think that as future generations come along, I just think that they're gonna start to move slowly away from the idea, not even just genetics, but just the idea that a lot of who you are going to become is somehow encoded into your genome. That if you are born today, and we just teleported you at birth to some other family halfway across the world, you'd be a completely different person. And I think people are better appreciative of that now, and I think they'll start to build their research programs with that in mind.
Jennifer Fugo (38:55.378)
Yeah, my hope is that we start asking “what if?” more often. I always like that question. It allows me the room to be creative. And some of the things that you've shared with me, that I can't wait, that we'll talk about in a future episode, is like, well, if we don't change things, if we don't start to really look at and question what we're seeing, we're not going to look for the right things. We're not going to pay attention to the maybe subtle things that are happening under the surface that are really, really important. So I think it's a really important question to ask, what if. I don't think we should have unbridled creativity, because that can take us in some very dark places, but it is warranted in this.
And that's one beautiful thing that I love about researching, and seeing how things play out in real life in the individual, is what if, in this particular person this is actually a problem, and it's not just because they got bad genes. The genes are what they are, fine, cool, let's look at everything else and let's see what we can do about it. I think that is most fascinating. It’s why I love having you on this show, I'm excited to see you again in person this year. So thank you so much for being here, and I am very excited to have you back for another episode.
Ian Myles (40:23.273)
Thank you.
Jennifer Fugo (01:46.255)
And as we mentioned earlier, Dr. Myles has a brand new book out called Gattaca Has Fallen. It's a pretty big book, but it isn't necessarily written at a level that would make it challenging for you to understand the concepts. That's something that I really appreciated about the book. It's very poignant. Dr. Myles shares some really sad and shocking historical context that helps to explain how we got here and, of course, what we touched on in this interview. And I do think that if you have been told that the reason that you have your particular condition is solely because it's, you got bad genes, right? I got told that I got bad genes when I had eczema. That is not entirely true for many of these conditions that we're seeing, especially that we talk about here on the Healthy Skin Show. So I highly recommend the book, and we'll put all of the links so that you can grab a copy of Gatteca Has Fallen into the show notes.
