NurseCE4Less Podcast
The NurseCE4Less Podcast delivers concise, engaging audio summaries of continuing education courses designed for busy healthcare professionals.
Each episode highlights key insights from accredited CE courses available on NurseCE4Less.com, covering essential clinical updates, emerging healthcare topics, and practical knowledge professionals can apply in their daily practice, using NotebookLM's AI podcast hosts.
Whether you're staying current with licensure requirements or expanding your professional expertise, the NurseCE4Less Podcast makes it easy to learn on the go.
NurseCE4Less has helped over one million healthcare professionals meet their continuing education needs with affordable, accredited courses for more than 20 years.
NurseCE4Less Podcast
Atopic Dermatitis: Contemporary Strategies for Durable Control - N593
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This CE podcast summary provides a comprehensive examination of atopic dermatitis, outlining its biological origins and the heavy socioeconomic burden it places on patients.
The authors emphasize that effective management relies on a layered treatment approach, starting with consistent moisturization and the identification of environmental triggers. This course details various pharmacological interventions, comparing traditional topical corticosteroids with modern biologic therapies and JAK inhibitors for more severe cases. Beyond standard treatments, the sources evaluate adjunctive options such as phototherapy, wet-wrap therapy, and the specific role of allergen immunotherapy. Clinical guidance is further supported by a pediatric case series demonstrating the successful use of targeted biologics in complex genetic syndromes. Ultimately, this resource serves as a guide for healthcare professionals to provide individualized care and achieve long-term disease control.
The NurseCE4Less Podcast delivers concise, engaging audio summaries of continuing education topics designed for busy Nurse professionals.
Each episode highlights key insights from accredited CE courses available on NurseCE4Less, covering essential clinical updates, emerging healthcare topics, and practical knowledge professionals can apply in their daily practice.
Whether you're staying current with licensure requirements or expanding your professional expertise, the NurseCE4Less Podcast makes it easy to learn on the go.
NurseCE4Less has helped over one million healthcare professionals meet their continuing education needs with affordable, accredited courses for over 20 years. To receive CE credit for this course, visit www.NurseCE4Less.com.
Welcome to the Nurse CE for Less Continuing Education Podcast. Each episode provides an engaging podcast style overview of individual continuing education courses to enhance your learning experience. These episodes utilize Notebook LM's Deep Dive AI audio to provide a podcast style conversation. To receive CE credit for this course, please visit NurseCE4Less.com. Use promo code podcast15 to receive 15% off an unlimited CE plan.
SPEAKER_03Imagine treating a skin rash like a part-time job. I mean, literally clocking in 20 hours every single week.
SPEAKER_00Yeah, it's exhausting just thinking about it.
SPEAKER_03Right. You are applying these heavy ointments, you're wrapping limbs in wet bandages, uh washing specialized linens, and literally staying awake through the night just to physically stop a child from tearing their own skin open.
SPEAKER_00Aaron Powell Exactly. And if you're listening to this right now, uh you or someone you love might be dealing with these exact, really frustrating realities.
SPEAKER_03Aaron Powell You know better than anyone that atopic dermatitis is just not a scratch on the surface. So welcome to today's deep dive. We are taking a massive stack of clinical guidelines, contemporary research, and dermatological reviews to sort of uncover the hidden mechanics of this disease.
SPEAKER_00Aaron Powell Because culturally we tend to view the skin as I don't know, merely a wrapper for the body. Like if the wrapper is dry, you just wet it.
SPEAKER_03Right. Just put some lotion on it.
SPEAKER_00Aaron Powell Yeah, a comforting, simplistic view. But stepping into the clinical reality of atopic dermatitis or AD, it forces a complete paradigm shift. I mean, we're looking at a systemic internal meltdown that just happens to manifest on the surface.
SPEAKER_03Aaron Powell Which is exactly what we're going to show you today, why your skin interacts with your environment the way it does, and why medicine is moving totally away from that old dry skin narrative. But uh let's start with this bizarre global trend from the research.
SPEAKER_00Oh, the prevalence rates.
SPEAKER_03Yeah. Cases of AD are rising rapidly worldwide, but specifically in industrialized urban areas. Like, why is a skin condition tied to living in a modern city?
SPEAKER_00Well, it points to this framework researchers call the hygiene hypothesis. In industrialized regions, you know, we spend the vast majority of our time indoors. We're breathing air-conditioned, filtered air. We are constantly sanitizing our hands, wiping down surfaces.
SPEAKER_03And sanitizer everywhere.
SPEAKER_00Exactly. But our immune systems are actually designed to be trained in infancy. They need to encounter soil, diverse environmental bacteria, a huge variety of natural microbes.
SPEAKER_03Like you would get on a farm or something.
SPEAKER_00Aaron Powell Right, in a rural environment. So without that early, messy training, the immune system essentially grows up bored and hyper-vigilant. It starts looking for threats that aren't actually there, which heavily skews the body toward allergic inflammatory responses.
SPEAKER_03Aaron Powell Okay, let's unpack this. Because if the immune system is hypervigilant, what does that actually look like at the physical surface?
SPEAKER_00Aaron Powell Well, down at the microscopic level, AD is driven by what we call a perfect storm. It's three interconnected failures.
SPEAKER_03Aaron Powell Okay, what are they?
SPEAKER_00You've got a physical barrier dysfunction, an immune dysregulation, and a microbiome imbalance. So if we look at the physical barrier first, your skin's outer layer is supposed to be an impenetrable shield. But in AD, there's a fundamental structural breakdown, mostly from genetics.
SPEAKER_03And the sources mentioned a specific mutation, right? FLG.
SPEAKER_00Yes, mutations in the FLG gene, which produces a protein called filigrin.
SPEAKER_03Filigrin. Okay, what is its job? Because I never heard of that before.
SPEAKER_00Aaron Powell It's the ultimate structural binding agent. Its primary job is to bind keratin fibers together to give skin cells their tough shape. And as those cells mature and reach the surface, the filigrin breaks down into natural moisturizing factors.
SPEAKER_03Wait, turns into moisturizer.
SPEAKER_00Essentially, yeah. Amino acids that literally grab onto water and hold it inside the skin tissue. But when that gene is mutated or when chronic inflammation basically turns the gene off, the skin loses its architecture. Water evaporates rapidly, leaving the tissue incredibly dry.
SPEAKER_03And gaps open up, right? Like I was thinking about this. Think of the skin as a brick wall. The skin cells are the bricks, and the filigrin is the mortar holding everything tight.
SPEAKER_00That's a great way to picture it.
SPEAKER_03So when the mortar crumbles, the wall gets incredibly leaky. And it's a two-way street of disaster. The essential moisture leaks out, and environmental invaders like pollen, pet dander, pollutants, they slip right in through the cracks.
SPEAKER_00Exactly. And when those invaders slip through that crumbled mortar, they immediately encounter the immune system's guards. In an AD patient, those guards are heavily biased toward what's called a TH2 dominant immune pathway.
SPEAKER_03The hypervigilant ones from the hygiene hypothesis.
SPEAKER_00Right. So instead of assessing the invader calmly, they panic. They flood the tissue with these chemical messenger molecules called cytokines. The heavy hitters here are interleukin 4 and intraleukin 13, which cause the redness and swelling, and crucially, intraleuin-31.
SPEAKER_03Ah, IL-31, the source material called that the specific itch cytokine. That sounds like a really highly specialized chemical.
SPEAKER_00It is incredibly specialized. And what's fascinating here is that it bypasses the normal inflammatory process. IL-31 directly binds to the sensory neurons embedded in the skin.
SPEAKER_03Wait, really? It goes straight to the nerve.
SPEAKER_00Straight to the nervous system. It wires an emergency signal directly to the brain saying you need to scratch this area immediately. It creates an intense, relentless itch that drives the classic itch-scratch cycle. And obviously, the more you scratch, the more the physical barrier you destroy.
SPEAKER_03Aaron Powell So we have a leaky wall and we have a panicked immune system sending nervous system alarms. But you mentioned a third piece to this microscopic storm, the microbiome.
SPEAKER_00Right, the microbiome.
SPEAKER_03Our skin is covered in bacteria, which I mean is usually a good thing, right? We want a diverse rainforest of microbes. But the research says in AD that diversity just plummets.
SPEAKER_00It drops off a cliff. The altered pH and the lack of natural antimicrobial peptides from that breaking barrier create a paradise for one specific bad actor, Staphylococcus aurais.
SPEAKER_01Staph.
SPEAKER_00Yeah, staph race. Yeah. The heavy bacteria die off, and staph heavily colonizes the skin. The real danger here is that it secretes specific toxins called superantigens.
SPEAKER_03And those get through the leaky wall.
SPEAKER_00Exactly. They penetrate the broken barrier and act as massive chemical accelerants. They force those TH2 immune cells to stay locked in the on position.
SPEAKER_03That is a terrifying feedback loop. The barrier breaks, the immune system overreacts, bacteria multiply and dump toxins, which causes more inflammation, which destroys more filigrin mortar.
SPEAKER_00And if we connect this to the bigger picture, the deeper issue is the systemic toll. This isn't just a local alarm going off on someone's arm. That persistent itch from IL 31 keeps the central nervous system in a constant state of arousal.
SPEAKER_03Oh, because the brain is constantly receiving that signal.
SPEAKER_00Right. We see severe sleep disruption in up to 80% of children with AD.
SPEAKER_0380%.
SPEAKER_00Up to 80%. They are spending their nights microawaking to scratch. And that chronic sleep deprivation leads to daytime fatigue, emotional dysregulation, profound anxiety. The psychological burden is just staggering.
SPEAKER_03Yeah, we are definitely not talking about a scratch on the paint anymore. We are talking about the car's entire wiring system melting down. So the logical first step in fixing this isn't necessarily to attack the immune system, right?
SPEAKER_00Yeah.
SPEAKER_03We have to rebuild the wall, patch the mortar.
SPEAKER_00Exactly. Prevent the leaks first.
SPEAKER_03Which brings us to daily maintenance and moisturization. And I have to say, I was completely floored by this number in our source. For an adult with moderate to severe AD, the clinical recommendation is 250 to 500 grams of moisturizer every single week.
SPEAKER_00It's a massive amount.
SPEAKER_03That is a giant tub of cream used in its entirety every seven days.
SPEAKER_00Aaron Powell Well, moisturizer in this clinical context isn't, you know, a cosmetic luxury just to make your skin feel soft. It's an active therapeutic intervention. You are literally providing artificial mortar for that broken brick wall. Right. The guidelines emphasize a highly specific technique called soak and seal. A patient bathes in lukewarm water to physically push hydration into the skin. But when they get out, they have a strict three-minute window to apply that heavy moisturizer.
SPEAKER_03A three-minute race against the clock?
SPEAKER_00Sure.
SPEAKER_03Just to trap the bathwater?
SPEAKER_00Yes, to physically lock that moisture inside the tissue before the ambient air evaporates it.
SPEAKER_03Wow. And I'm guessing you can't just use any cheap watered-down lotion from the drugstore for this.
SPEAKER_00Definitely not. A scientifically formulated AD moisturizer relies on three distinct mechanical elements. First, you have humectins like glycerin or hyaluronic acid, which actively draw water molecules from the deeper layers of skin up to the surface.
SPEAKER_03Okay, humectins pull the water up.
SPEAKER_00Right. Second, emollients like ceramides. These act as the spackle, physically filling in the microscopic gaps between the skin cells to repair the barrier. And third, occlusives like petrolatom, which create a heavy physical seal on top to lock everything in.
SPEAKER_03So it's pulling water in, patching the holes, and sealing the top.
SPEAKER_00Exactly. And ointments with a really high oil to water ratio work best for that occlusive seal, even if patients sometimes complain that they feel a bit greasy.
SPEAKER_03And there's also a minefield of ingredients you have to actively avoid putting on that fragile wall, right? Like alcohols, which just evaporate water and burn.
SPEAKER_00Oh, absolutely. Alcohols, fragrances, essential oils.
SPEAKER_03Yeah. The essential oils thing is wild. You see natural lavender oil on a fancy lotion label, and you naturally think, oh, this must be healing. But for an AD patient, it's just a raw chemical irritant slipping directly through a compromised barrier.
SPEAKER_00Because the skin barrier is wide open. Introducing known contact allergens like botanical fragrances directly into raw tissue will only provoke those hypervigilant TH2 guards even further.
SPEAKER_03Okay, well, let me push back on this whole approach for a second. If my immune system is overreacting and causing all this systemic inflammation, shouldn't I just look at what I'm putting into my body?
SPEAKER_00Ah, the diet question.
SPEAKER_03Yeah. Because the very first piece of unsolicited advice anyone with a skin condition gets is oh, you need to cut out dairy or stop eating gluten. Does changing my diet fix the structural wall?
SPEAKER_00No. And this is honestly one of the most pervasive, damaging myths in dermatology. The latest guidelines from the leading allergy and immunology academies emphatically debunk it. Routine elimination diets are absolutely not recommended for managing atopic dermatitis. No at all. Not unless the patient has a confirmed IgE-mediated food allergy.
SPEAKER_03Wait, what does IgE mediated mean in plain English?
SPEAKER_00It means the immune system produces a specific antibody, immunoglobulin E, that triggers an immediate systemic reaction when a specific food is eaten. We're talking about sudden hives, lip swelling, or anaphylaxis.
SPEAKER_03So a traditional immediate allergic reaction.
SPEAKER_00Right. If you do not have that specific immediate reaction, cutting out milk, wheat, or eggs is not going to clear up your eczema.
SPEAKER_03So no guessing games, no starving yourself of bread for six months just to see if the skin clears up.
SPEAKER_00Please don't. Doing that can actually be incredibly harmful. The research now clearly demonstrates that unnecessarily delaying a child's exposure to common allergenic foods can actually cause new food allergies to develop.
SPEAKER_03Wait, really? By avoiding the food you create the allergy?
SPEAKER_00Yes. Yeah. Because think about it, if an infant is kept away from peanuts, but peanut dust is in the household environment.
SPEAKER_03Which it always is.
SPEAKER_00Right. That dust settles onto their broken inflamed skin. So the immune system's very first encounter with the peanut protein is through a wound, surrounded by active alarm signals. The body registers the peanut as a dangerous invader and creates a lifelong allergy. Wow. So we must focus on repairing the skin barrier, not starving the patient of essential nutrients and driving caregivers crazy with impossible dietary restrictions.
SPEAKER_03Patch the wall, don't restrict the food, that makes total sense. But uh patching the wall is preventative, it's daily maintenance. What do you do when a localized fire has already broken out? Because when someone is in the middle of a massive, agonizing flare, a tub of moisturizer isn't going to cut it.
SPEAKER_00No, it won't. You have to move from prevention to active flare control. And for 60 years, the backbone of acute flare control has been topical corticosteroids or TCS.
SPEAKER_03The steroid cream?
SPEAKER_00Right. They're applied directly to the active lesions, and they work by broadly suppressing the inflammatory pathways at that specific site. They range from class one, which are incredibly potent, super high strength steroids, all the way down to class seven, which includes low potency over-the-counter options like hydrocortisone.
SPEAKER_03But the source outlines some pretty serious risks here. Like you can't just slather a high potency steroid on your eyelids or the inside of your elbows for months at a time, right?
SPEAKER_00No, you absolutely cannot. The primary risk of overusing topical steroids is skin atrophy, which is a permanent thinning of the skin tissue and the development of straya, deep stretch marks.
SPEAKER_03Because it stops the cells from growing.
SPEAKER_00Exactly. The steroid halts the inflammation, but it also halts the normal cellular turnover required to keep the skin thick and resilient. And if they're abused over massive areas of the body, they can even be absorbed into the bloodstream and disrupt the body's natural adrenal glands.
SPEAKER_02Yikes.
SPEAKER_00So the clinical mandate is strict. Use the lowest effective potency for the shortest duration necessary to put the fire out.
SPEAKER_03But if the skin on the face or the neck is too delicate for steroids, how do you stop the inflammation without thinning the skin?
SPEAKER_00Well, this is where steroid sparing agents come into play. The first class is topical calcinerin inhibitors, or TCIs. These medications penetrate the cell and bind to a specific protein, which prevents the activation of NFAT.
SPEAKER_03NFAT.
SPEAKER_00Yeah, NFAT is essentially a cellular switch that tells the cell to produce inflammatory cytokines.
SPEAKER_03Uh-huh.
SPEAKER_00By blocking that switch, the inflammation stops, but the cellular turnover isn't affected at all, meaning zero risk of skin thinning.
SPEAKER_02Oh, that's clever.
SPEAKER_00And another newer option is PDE4 inhibitors. These work by blocking an enzyme that normally breaks down a calming molecule called CMP. So by blocking the enzyme, CMP levels rise inside the cell, which actively dials down the inflammatory response.
SPEAKER_03Aaron Powell Okay, I love that. So think of the inflammation like a stereo blasting at maximum volume, right? The steroids take a sledgehammer to the stereo. It definitely stops the noise, but it damages the equipment. Right. The TCIs unplug the speaker wire, and the PDE4 inhibitors just reach over and smoothly turn the volume knob down.
SPEAKER_00Aaron Ross Powell That is a brilliant way to visualize it. And you know, for flares that are so severe they don't respond to any of those standard topicals, clinicians will turn to wet wrap therapy.
SPEAKER_03Oh, I read this section. It sounds intense. Like you apply the steroid medication, then you tightly wrap the skin in a layer of warm, damp cotton or gauze, and then you put a dry layer over that. You're basically marinating the skin.
SPEAKER_02You really are.
SPEAKER_03You force the hydration in, you force the medicine to penetrate deeper, and you create this physical cage so the patient literally cannot scratch their own skin in their sleep.
SPEAKER_00Aaron Powell It is intensive and it's usually performed for only a few days under medical supervision, but it rapidly breaks that maddening itch-scratch cycle and forces the localized ecosystem to just calm down.
SPEAKER_03Okay, but here's where I really need you to explain something because it sounds completely unhinged. The clinical guidelines mention bleach baths.
SPEAKER_00Uh yes.
SPEAKER_03Taking a child with raw, broken, agonizingly inflamed skin and putting them into a tub of bleach. How is that not chemical warfare on their already compromised burial?
SPEAKER_00Aaron Powell I know it sounds horrifying until you look at the actual math. We are not pouring pure concentrated bleach over a patient. The guidelines recommend a highly dilute.0005% sodium hypochlorite solution. Okay, what does that mean in practical terms? In practical terms, that is about a quarter cup of regular household bleach mixed into a standard 40-gallon bathtub full of water. The concentration is practically identical to a municipal swimming pool.
SPEAKER_03Oh. Okay, pool water. That sounds much less terrifying, but why do it at all?
SPEAKER_00Think back to our discussion about the microbiome. Remember the staphylococcus aureus bacteria that colonizes the skin and secretes toxins?
SPEAKER_03Right. The staph.
SPEAKER_00The dilute bleach acts as a highly targeted, broad-spectrum antiseptic strike against that specific bacteria. It reduces the microbial load on the skin.
SPEAKER_03Why not just give them antibiotics?
SPEAKER_00Aaron Powell Because the guidelines explicitly warn against routine oral antibiotics. They breed antibiotic resistance and wipe out the healthy gut bacteria without actually curing the eczema. So the bleach bath is just a safe topical maintenance strategy to keep the staph aureus from overrunning the wall.
SPEAKER_03Okay, so topicals, wet wraps, and pool water to put out local fires. But what if the entire forest is burning from the inside out? Like for the most severe refractory cases, creams and baths aren't going to reach the core of the problem.
SPEAKER_00No, they won't.
SPEAKER_03If those TH2 immune commanders are stationed deep inside the body, constantly sending out attack orders, we have to change the internal weather of the entire system.
SPEAKER_00Which brings us to the modern era of systemic therapies. And this has completely revolutionized dermatology. Historically, severe cases were treated with blunt immunosuppressants like oral steroids or cyclosporine.
SPEAKER_03The sledgehammer approach again?
SPEAKER_00Exactly. These drugs carpet bomb the entire immune system. They shut everything down, which leaves the patient vulnerable to serious infections, kidney toxicity, and massive rebound flares the literal moment the drug is stopped. Today, though, the focus is entirely on targeted therapies, biologics, and JK inhibitors.
SPEAKER_03Let's start with biologics, like dupalumab. These are subcutaneous injections, and instead of carpet bombing, they act more like a molecular sniper fire.
SPEAKER_00That's exactly what they are.
SPEAKER_03They are engineered antibodies that selectively hunt down and block just the IL-4 and IL-13 cytokines. They take out the specific messengers ordering the attack without shutting down the rest of the immune system. And they are incredibly safe, requiring no root turn lab monitoring, but they come with a staggering price tag of$30,000 to$40,000 a year.
SPEAKER_00Yeah, the cost is an immense barrier, but the clinical outcomes justify it for severe cases. To understand just how transformative this targeted approach is, the source highlighted a case series involving pediatric patients with a rare genetic disorder called hyper-IgE syndrome.
SPEAKER_03Right, I saw that. These kids have genetic mutations that give them severe early onset eczema, massive allergic responses, and recurrent life-threatening pneumonias. Like their immune systems are just completely unbalanced.
SPEAKER_00Their immune profile is so heavily skewed toward the TH2 allergic pathway that they literally lack the proper defenses in other areas to fight off basic bacteria. So researchers administered dupalumab to block the IL-4 and IL-13 signals.
SPEAKER_02And what happened?
SPEAKER_00Over several years, not only did their severe skin lesions achieve near complete clearance, but their massive recurrent infections. The pneumonias, the severe ear infections, they dropped drastically.
SPEAKER_02Wait, really?
SPEAKER_00Yes. By chemically balancing the TH2 scale, they restored enough overall immune function to allow the body to properly fight off external infections again.
SPEAKER_03So a drug designed to stop eczema actually helped their immune system stop getting pneumonia just because it brought the entire systemic weather pattern back into equilibrium. That is remarkable.
SPEAKER_00It's life-changing.
SPEAKER_03But biologics aren't the only option. We also have JK inhibitors like upadacetinib. These are oral pills that work inside the cell to block multiple cytokine signals simultaneously. But I was looking at the safety profiles in the source, and I'm a bit confused. Biologics seem incredibly safe. Meanwhile, the FDA mandates boxed warnings on J-Kane inhibitors for severe cardiovascular events, thrombosis, and even malignancies.
SPEAKER_00Yes, the black box warnings.
SPEAKER_03So if biologics are so safe, why would a doctor ever prescribe a drug with a black box warning?
SPEAKER_00It really comes down to the clinical mechanism and the agonizing reality of pruritus, the severe unrelenting itch. What's fascinating here is that biologics are large proteins. They take weeks, sometimes months to build up in the system and reach their maximum efficacy. But JK inhibitors block the Janus kinese enzymes inside the cell. Those enzymes transmit the itch signals, but they also transmit signals that regulate blood clotting and heart function. That broader blocking effect is exactly why those cardiovascular warnings exist.
SPEAKER_03So they carry a higher risk because they are blocking pathways that do multiple jobs in the body.
SPEAKER_00Exactly. But the trade-off is unparalleled speed. Because they are small molecules taken orally, JK inhibitors can shut down severe maddening paritis in literally two to three days.
SPEAKER_03Wow. Days instead of months.
SPEAKER_00Yes. If you have a patient who hasn't slept in a week, who is suicidal from the relentless sensation of their skin crawling, they simply cannot wait a month for a biologic to kick in. The choice is a highly calculated, shared decision between doctor and patient, balancing the immediate catastrophic distress of the disease against the specific cardiovascular risk factors of that individual.
SPEAKER_03That makes total sense when you frame it like that. Well, we have covered a staggering amount of ground today. We started at the microscopic crumbling mortar of the filigrin gene. We watched the invaders slip in, setting off the TH2 immune alarm and that specialized IL-31 itch cytokine.
SPEAKER_00We mapped out the race to patch the wall with a three-minute soak and seal moisturization technique.
SPEAKER_03Right. And we totally dismantled the myth that cutting out dairy will fix a genetic skin defect.
SPEAKER_00We also explored how to put out active fires with topical steroids and steroid sparing agents, and how dilute bleach bath strategically targets staphoresis.
SPEAKER_03Pool water. And finally, we saw how medical science is shifting the internal weather with targeted biologics and rapid acting JA inhibitors. It is an entirely new era of personalized medicine. Before we wrap up, I just keep thinking about our very first point, the hygiene hypothesis, the idea that our sanitized indoor lives are causing our immune systems to misfire in the first place.
SPEAKER_00It raises a profound philosophical question for the future of medicine, doesn't it? I mean, we just analyzed incredible$30,000 immune-blocking drugs. But if the root cause of this global rise in atopic dermatitis is our hyperclean environment, the ultimate preventative cure might not be found in a pharmacy. Right. What if the future involves deliberately rewilding our living spaces, exposing infants to dirt, to diverse environmental bacteria, and to farm-like environments right from birth to properly train their immune systems? We could theoretically stop the atopic march before the filigrin wall ever breaks.
SPEAKER_03Rewilding our homes to save our skin? Now there's a thought to chew on. So the next time you look at a patch of dry skin, remember you are looking at the check engine light for a beautifully intricate, deeply complex immune system. And maybe next time you are tempted to aggressively sanitize everything your child touches, you might want to think about their filigrin. Let them get a little dirty. We will see you next time on the Deep Dive.
SPEAKER_01Thank you for listening to the Nurse CE4 Less Continuing Education Podcast. To receive CE credit for this course and many others, please visit nursece.com. That's NurseCE, the number fourless.com. Use promo code Podcast15 to receive 15% off an unlimited CE plan. NurseCE4 Less, quality education at an affordable price.