B (3:29)

Was it?

C (3:29)

Yeah, I mean, was it.

A (3:30)

Was it double blinded that the. Did the patients know how often they were bathing?

B (3:34)

All right, they put them in the shower and just made noise.

C (3:37)

Exactly. They did point out that this was not a double blinded. They washed them with placebo water, which was actually like orange juice. It was tough, but no, there was no blinding. And so they were. So the baseline was that people, you know, you're like, how often do people shower? Apparently 4.3 times per week. So they had to do either more or less. And so people were actually, like, pretty good in terms of, when you ask them, like, you know, how adherent were you? Basically, like, the adherence was like 62% of people were adherent with it. So that would mean that, like, maybe they, you know, missed a shower or two or, you know, couldn't handle it and had to take an extra, you know, bath. Like, why did they do it? It was either like, my skin's too dry, I can't do this every day, or, gosh, my skin feels gross, or I worked out and I didn't want to wait five more days to shower. So kind of like the, you know, what you would expect. So what was the efficacy? So their primary outcome measure was the poem score. And so basically, you know, this was all sort of patient reported. There was no easy scoring or things like that. There was no difference. So weekly showering, daily showering, zero difference in the poem score. And it was a four week endpoint. This wasn't like 16 weeks. There was no, like, crossover arm or anything. There was no difference in itch. There was no Difference in quality of life. Basically shower however often you want to shower. There was no difference. So, you know, why was this kind of cool? Like, you know, it was basically an online shower. There were like six citizen science scientists. So the patients, you know, had input into the design of this study.

A (5:40)

And are you going to try and re. You're going to try and recruit some of those citizen scientists to be faculty in unc?

C (5:47)

Yes, because I don't have to pay them. I love faculty. I don't have to pay. That's my whole goal is a chair, is how many people can I get to do work for as little money. That's not true at all. I don't do that at all. I train my faculty well and advocate for them to be paid well because they work incredibly hard.

A (6:03)

So that's right.

C (6:05)

You know, basically kind of cool. Now we've got some data to guide us on how often people should bathe. And it doesn't matter. Do what you want.

A (6:13)

My favorite, My favorite part of this article was when you look at the, like, forest plot of where the, like, whatever. The people who thought that bathing daily was good for eczema, it worked amazingly for them. Amazingly, yes.

C (6:28)

And the people who thought that bathing weekly was better, we. They, they tended like they were in that arm of favors. Weekly bathing. Yes. So it just goes what patients think work tends to be what works better for them.

A (6:43)

And that, I will say that is honestly what I tell eczema patients, you know, when they're like, well, what moisturizer should I use? How? And I'm always like, if you think it helps, put it on. If you don't think it helps, it doesn't really matter. Tried, you know, different brands. It's. Everybody's different in terms of which one they like. Usually cerave works the best, but, you know, everybody's different, blah, blah, blah, because

C (7:06)

it truly a commercial for them. So there is that. That might be it.

A (7:11)

They only ran that commercial like three times. So I'm kind of mad about it.

C (7:14)

Mostly in, like, South America, I think.

B (7:16)

But yeah, yeah, they dubbed them, they overdubbed them. Hola, misiamo matruziris.

A (7:29)

But so the I, I, you know, because you, if you tell them like, you have to moisturize, you have to moisturize, that makes them less compliant with the stuff that really does help. Like, we know the more stuff you tell people to do, the less stuff that they actually end up doing. So that's the, you know, okay, all

C (7:46)

right, then it doesn't work. So it was a Good reminder of that. But yes. Doesn't matter how often you bathe. Do what you believe in and it will work the best for you.

A (7:57)

That's right. That's right. It's all relative. There's no truth.

C (8:01)

Exactly.

A (8:04)

All right, let's move on. Patton, what do you got? Let's give us some truth.

B (8:08)

My first six pack. Papers from the March 2026 JAMA Oncology and is titled Morbidity and mortality outcomes of Dupilumab for Cutaneous Immune Related Adverse Events by Block et al. So some background. There's a 2025 paper and journal of Immunotherapy of cancer retrospective study done at Mass Gen and Dana Farber. I compared patients with bad, I'm going to call it ICI immune checkpoint inhibitor rashes that got doopy to two other cohorts, patients that got bad ICI rashes and didn't get dupy and patients that didn't get bad ICI rashes. So the take home points from that previous study were that dupy worked like close to 90% of patients had complete or partial responses and there was no statistically significant difference in mortality between the groups. High dose steroids associated with worse outcomes, blah blah blah. So the current paper is a trinetics study. So not believable at all. We're thinking the authors took patients with ICI rashes that got dupy and compared them to two groups. They compared them to patients with ICI rashes that didn't get dupy and patients with ICI rashes that got systemic steroids. Propensity matched scoring done to match patients for a bunch of stuff. And the primary endpoint was all cause mortality at five years. And the results are represented in the figure. Just one figure, couple tables, one figure just kind of crazy, absurd hazard ratios. Right. 0.24 compared, you know, doopy compared to non dupy, 0.31 versus the steroid controls. So that's like, like close to 80%, 70% improved mortality if you got doopy for an ICI rash. They reran the data with the sensitivity analysis. Still kind of crazy hazard ratios for mortality. So yeah, I mean it's just, it's, it's not believable. I could see where doopie might help a little bit and I don't think it's really the fault of the authors. I think all the statistics probably check out. It's just that I like, I don't think trinetics is providing anyone with like realistic data.

A (10:18)

I've got an alternative explanation coming. Patent.

B (10:21)

Oh, let's hear it.

A (10:22)

Okay, so let's, let's. So we'll, we're, we're going to segue into my segment of, of the six pack. So this was a study which I had never really seen this before. The effect of pre existing atopic dermatitis on clinical outcomes of immune checkpoint therapy. And so having AD made immune checkpoint. Now this was also a trinetic study. So I gotta gotta be honest, it's Could Dolph still be baloney. But having preexisting AD dramatic made you much more responsive to immune checkpoint inhibitor therapy. So they had a much higher rate of getting the adverse events. So 5.93 hazard ratio of getting a cutaneous immune related event, increased rate of endocrine events, increased rate of GI events but they had better substantially overall survival. So let's see here. Pre existing AD had lower all cause mortality 0.56. So you were twice as likely or half as likely to die if you had AD and a got immune checkpoint inhibitor therapy. And they didn't really look at it in terms of like severity but it is meaningfully suspected that that is an important part of it. And so then I dug into this today because I was like that does not make any sense to me at all. Because I think of cancer as TH1 immunity and TH2 immunity like smushes down your TH1 immunity. And here's what I found out. It turns out eosinophils, they are learning have a very significant anti cancer activity. And so there now is, number one, eosinophils have anti cancer activity. And number two, IgE is much more potent as a oncolytic something or other than igg. And so now there are some reasons and across the board I guess it's been known for a while that people with AD tend to get less cancer than people without adult. But the immune checkpoint inhibitor thing, they think the other thing that's happening there is that the T regs are acting as sinks for IL2. And so when you've got a lot of Tregs because apparently your body upregulates T regs to try and control the ad. And I'm making all this up by the way in case anybody is like basic scientists out there. Like I could see Ferris twitching a little bit, so I didn't, but I did, I did read up on this today. So the, the Tregs act as a sync for illinois 2 and your. Whenever you do immune checkpoint therapy one of the things that happens is your Tregs go down. And when your Tregs go Down. If you've upregulated your IL2 because you had so many Tregs, now there's more IL2, which is also anti cancer. So it. It like there are multiple mechanisms by which being atopic might make you more responsive to immune checkpoint inhibitor. And it may be that the doopie is a just marker of. You have bad atopic dermatitis. So these mechanisms are even more operative in you.

B (13:43)

Yeah, I thought it was like, it wasn't exactly contradictory, but it was like if. If you looked at your paper and you said, okay, having a sort of Th2 hyperactive immune system helps you fight cancer. Doopy is anti th2. So you would think, okay, well, like, if we're going to be consistent between the two papers, it should show that doopie actually makes cancer treatments worse.

A (14:10)

But it was the opposite. Yes. And their takeaway was that or the takeaway that I found when I was digging into this, that the EOs are probably the best explanation because doopie is kind of pro eo. Like, we know that when you start on dupy, you get a transient eosinophilia because it. The particular, you know, IL5 is the eosinophil one. And so doopie doesn't block it at all. So it. It might be that it is almost stimulating your. The eosinophil part of your immune reaction.

B (14:47)

There are. And I. I was looking. There are a bunch of, like, pretty much looking at doopie in cancer treatments. Yeah, a fair number. There's like, five trials ongoing. They're like, we're just going to add doopie to standard immune checkpoint inhibitor. Right. I mean, we'll have the answer.

A (15:05)

Those companies need to send me some checks because like, a year ago, I was like, doopie needs to do these. In fact, Laura's husband, friend of our listeners, is, like, in charge of cancer at the University of North Carolina, and I told her to tell him. So if there are any trials going on at unc, I am taking full credit for that.

C (15:24)

You. You got senior author status on every single one of them. You're good.

A (15:29)

I. I don't even know.

C (15:30)

I don't know if I told them. I talked about you a lot, but I.

B (15:33)

You'll be acknowledged. You'll be an acknowledgment.

A (15:37)

That's more. That would make a lot more sense. I don't want to have to read the papers.

C (15:41)

So I do. I want to say, you know, dupy's used to treat copd, right? So what do people with copd, they smoke. They also get a Lot of lung cancer. I do believe that there's better survival and lung cancer patients on dupy. I. Or either that was a stud somebody was looking at or it's been shown. So, like, that will be a really interesting place to look at the doopy cancer thing. We have looked at this a couple times. Like, I think at the very least, we can feel pretty darn comfortable. Doopy does not increase cancer risk. If patients have cancer, we feel very safe having them on dupy, whether it is to treat their side effects of immunotherapy or for their underlying disease, since they have, like 11,386 indications for Dupy now.

A (16:27)

So I think that's just generally good for you, that's all.

C (16:31)

Yes.

A (16:32)

Right. All right, jump quickly to my other one. This one's just a fun one. Granuloma annulare. One of, you know, I like looking for, like, weird treatments for weird stuff. So ga, there was a paper, hyperthermia for granuloma annulare. And basically, and I reached out to these Chinese authors to find out, like, the specific regimen that they used. So they use local hyperthermia, 44 degrees centigrade, which I think is like 120 degrees Fahrenheit or 110, 120. Patent. Look that up for granuloma annulare. Pilot randomized controlled trial. So they did 30 minutes once a week on the most recently developed lesion. And they did like, randomized controlled trial. But there were like four people in each arm, so it, like, kind of counts. It was like, stunningly effective. Like, the pictures they have, it's like, wow. And so apparently heating up granuloma annulare makes it go away. And even some of the patients who had, like, widespread. One of them had widespread disease. And they got a lot of their widespread GA got better. It somehow affected the systemic immune response. So, Right. If this was like a $10,000 thing, no, I wouldn't be like, oh, we should all be doing this. But you get a heating pad, from what I could tell when I looked it up, was basically set the heating pad to medium, put it on your GA lesion for 30 minutes once a week, do that for three months. Usually they were better within like a month.

C (18:03)

It was a once a week heating pad. So maybe the full body. See, the problem is, I saw somebody with GA today. I was like, I guess I'm just gonna inject it because I had to work all day. You just sit and pick papers all day and you didn't have them uploaded for me to read. I'm the only Dermon drug who works on Mondays. I'm gonna put that out there.

A (18:24)

And so you need to get on some more drugs.

C (18:27)

It's got to be something.

B (18:29)

I have a heart problem. I would like to.

C (18:32)

That's true. You do have a heart problem.

B (18:34)

Thank you.

C (18:34)

You've got an excuse for now till you get surgery. Then I want.

A (18:37)

Well, he's always had a heart problem. Now there's a structural problem with his heart as well.

C (18:41)

Exactly. Okay, so then, like, I, you know, I think I remember seeing this paper. Like, I wonder if you put people in, you know, like those saunas, right? Like, full body sauna sauna, infrared sauna.

A (18:56)

Oh, my gosh. Fair said for, like, the people with widespread ga, that's genius. And you write them a script for it, and then they can use their HSA dollars to. To pay to go to the infrared sauna.

B (19:07)

It was an infrared device that they said they used in the study.

A (19:11)

Yeah, that's. That's actually more literature supported than the heating pad.

B (19:15)

And it's 112 degrees. And I do want to point out that one of the patients had a lesion on the penis. I don't know about that. I don't think I'd be like, yeah,

A (19:28)

yeah, maybe it was. It was that. It was the syphilitic variant, but. So that's it. Just so far. That's genius. The infrared sauna for widespread ga, because people are a pain in the butt to treat. And for localized ga, just, you know, do a heating pad at home, the back of their head, the top of their foot, whatever. They did just one lesion. They didn't do all of them, but it was. It was impressive. Like, it was impressive. Those pictures, easy, cheap.

C (19:56)

All right, everybody's got to try it. Now we're going to report back to see if it works.

A (20:00)

Okay? All right, we're in. All right, let's move on to our next paper. Dr. Fares, what do you got?

C (20:07)

Okay, I'm going on the kind of sort of ad theme, which is a paper in JAMA Dermatology, also out of, I believe, China's you et al. Safety and efficacy of ICP 332 for moderate to severe atopic dermatitis, phase 2 RCT. Okay, what's ICP 332? This is a tick 2 inhibitor. You're like, well, don't we have a bunch of tick 2 inhibitors? This one's different because it binds to the JH1 catalytic domain. So everybody who's been to, like, a Ducrabicitinib talk or anything from like Takeda. You're like, you know the word allosteric inhibitor? Like you know the back of your hand. So you know that those don't blind to where the ATP binds. It bind. But this one's different. It binds to the catalytic domain. What does that mean? It binds like the catalytic domain is not just in tick 2, it's in jak 1, 2 and 3. So this drug does have some jak 1 activity, unlike the tick. Typical tick 2s, but it's like 40 times more selective for tick 2 than jack 1. But the other ones will be like, we are 5,000 times more selective. So. So what's it doing? So it's kind of got like a tick to favored. It's like a tick to strong JAK inhibitor. And so this was a double blind placebo controlled phase two trial. 19 centers in China. So there it is. All Chinese people. Their eczema, their etopic derma is probably different, you know, than what you see in like sort of the broad spectrum US population. 75 patients total in the study, 25 per arm. So small study. Placebo, 80 milligrams or and 120 milligrams a day. Primary endpoint, four weeks. Okay, so this is also like a super short study. It is. So, you know, what does that mean? Like the single oddball event can throw off the results. Like the single oddball super responder, the weird, you know, whatever AE. So the efficacy part's kind of interesting. At week four, reduction in easy score was 78%. And with the 80 milligram dose and 72% with 120 milligram dose, like that's a pretty darn fast, significant easy response. Yeah.

A (22:33)

Wow.

C (22:35)

And so, and it was 16.7% with the placebo. So not nothing, but like that's a pretty, pretty big difference. Okay.

A (22:44)

That is the technical term, Dr. Ferris, is ginormous.

C (22:48)

Ginormous.

A (22:49)

Ginormous delta.

C (22:51)

Yes, ginormous delta. Okay, how about easy 75? The placebo adjusted easy 75 responses, 56%. And so if you look at like what that means, like easy 75 of drug minus placebo. And so like, what does that look like for a JAK inhibitor? It that's like kind of up there with like you had a sit nibs at 12 to 1612. I think their primary endpoints are 12 weeks. So, you know, that is, this is not a, you know, head to head comparison, blah, blah, blah, but like, it's pretty, you know, impressive. Common AES, the things that you would expect. The One weird standout AE was decreased fibrinogen levels which occurred in 24%. We never looked at that in our like jack inhibitor studies that I could see. So I don't really know. Like, so in theory I was like, what would decrease fibrinogen do? So you know, we worry about like clotting events, but really decreased fibrinogen would maybe be associated with increases in bleeding. So you know, but there wasn't like bleeding in here. It's just like that was like their thing, decreased fibrinogen levels. There was one case of rhabdo and the 120 milligram dose. Interestingly, the 80 milligram dose seemed to work better than the 120. But 25 patients, we don't know what that means for arm. So there was one case of Rhabdo. And like every single JAK inhibitor study, what did they say? Well, that person was really exercising a lot. So people in JACK inhibitor studies decide to take up exercising a lot. So that's really what it was. So you know, small study, early time point. You know, I just think it's going to be interesting to see where this goes, you know. And if you look at some of their other like BSA, like decrease in BSA was like, you know, from baseline, like 20. I'm trying to see what their, their baseline, I didn't, I didn't like look at what their baseline was. But like while the baseline was dec by the, the decrease from baseline in BSA at 4 weeks was like 5% in the placebo group. It was like 25 to 30% in the, in the active treatment in the, the tick 2 inhibitor group, you know, the patients get into like IgA01 was like 36%. It's pretty good.

A (25:35)

So mechanistically this is pretty similar to brepo. Brepocitinib is that, that's the dermatomyositis one.

C (25:43)

That's very impressive. It's like got Jack one, tick two, right?

A (25:46)

Yeah, right. And that drug has been like spectacularly effective for dermatomyositis. So I wonder if like that mix of JAK one and Tick two is like some magic. You know, you block those two and Woo.

C (26:04)

Yeah, it'd be interesting to see if they try that. I mean even just tick two, if you look at ducrabicitinib, it's probably better in like cutane, like connective tissue disease, like lupus, that or dermato than it maybe even is in psoriasis. So you know, I, I don't know. I think it's interesting. We got a bunch of tick twos coming out. Might they be the answer in atopic derm? Perhaps they will be. I will say that also in the study, they did like follow people after their four weeks. They withdrew the drug and then followed them. Itch went up, easy score went back up. BSA went back up. Like, they didn't. It wasn't a suspect sustained, you know, response. But it, but they did, you know, it wasn't. It also did what you would expect. So I just thought this was an interesting paper.

B (26:49)

Don't companies freak out with lab abnormalities? Like, isn't that enough to like, shut down a drug? I, I, There was a, a Brutons tyrosine kinase inhibitor. I think it was fenobrutinib for CSU and it worked great, but they were getting like these little bumps in LFTs and the company was like, yeah, forget it, we're not even going to try. So I don't know. The low fibrinogen sounded scary to me. And it was in both, it was in both arms. It was in the 80 and the 120 and it was up to a quarter of patients.

C (27:18)

Yeah, it's a high number. I guess I don't know enough about the clinical significance of that to know. And you know, I don't do all our tick to inhibitors do the same thing. We don't check it. And I've never seen, I went back like, you know, to look and see like, do we have this in the Ducravisit and of studies that wasn't monitored. It was specifically monitored here. I think it was based on data from another study.

A (27:41)

So, yeah, that's the thing is they had, there had to be a reason they're monitoring it because it's not like a normal thing anybody would be monitoring. Yeah, maybe it's measuring the synthetic capacity of your liver, something like that.

C (27:55)

Yeah, yeah, yeah. And they're all like, their liver function otherwise was normal. So, you know, it also made me. Yeah, again, because we've got all these other tick 2 inhibitors A around but not being really pushed for psoriasis or in development. Like, maybe atopic Durham will be the next, you know, frontier for them.

A (28:14)

This, this segment about fibrinogen is making me think like, if aliens were like listening to the podcast and we're like, these are the three dermatology experts in America. And we're like, oh, fibrin. I don't, it could be, I don't know, is it clinically Relevant What? Yeah, we're the experts. That's, that's, that's great.

C (28:34)

On our Spotify metrics as listeners, it's all good, but if they don't have LIKE accounts, it doesn't matter. We don't need them.

A (28:43)

All right, let's move on. Patton, what do you got?

B (28:45)

All right, my second six pack. British Journal of Dermatology, March 2026, titled Bath April Blockade with Teletasecept and Pemphigus Foliaceous, two cases by Wang et al. So what are BAFF in April? Bath is B cell activating. Like I guess it's F factor. There's two F's, but it's called B cell activating factor. So

C (29:09)

activating effing factor.

B (29:10)

That's good, we'll go with that. It's also known as B lymphocyte stimulator, so it's sometimes abbreviated as bliss B, L, Y, S. April is a proliferation inducing ligand and BAFF and April are cytokines that bind to B cells, influencing their activity and survival. One of the receptors to which they both bind is known as tasi T, A, C I. So teletasept is a fusion protein FC portion of an IgG and the Tassie receptor. And it so sort of kind of sucks up BAF and April, the two cytokines, theoretically not allowing them to bind to B cells. So the paper reviews two case Pemphigus foliaceous, 22 year old female, 44 year old female, both refused systemic corticosteroids like man pemphigus. Like I don't know how you could ever get a patient better not using systemic corticosteroids. So this is kind of monotherapy. They were both on minocycline. I don't really think the tetracycline antibiotics do much for pemphigus. One was also on some weird like Chinese medicine thing. Both patients were given Teletasept 160mg weekly by sub Q injection and both patients improved. So PD PDAI PDI measure of pemphigus severity dropped to zero in both patients. One by week eight, one by week 10. That's pretty quick. And the anti desmogline 1 antibody titers dropped. One patient, they went from 596 down to 2 and the other one, it was 209 down to 2. So maybe a promising drug. I mean it was kind of a dumb paper. I'm known for this. It's not FDA approved to treat anything. It is actually approved in China to treat sle, rheumatoid arthritis and generalized myasthenia gravis. So it's being studied for some autoimmune conditions. I think it got fast tracked here for Sjogren's and so maybe a promising future pemphigus treatment. I mean it's almost like you do have to hit B cells, right? You look at rituximab, you get, you hit B cells. This is kind of like a softer hit on the B cells, but maybe an effective therapy. So nothing that's clinically useful for anyone outside of China. So you're welcome and good night.

A (31:22)

It's like a B salt for somebody who's looking to do a little medical tourism. You know, just get on that 14 hour flight to China and you get there. Get your Tepalac little nib.

B (31:36)

That's exactly what it's called. Good. I'd like someone to go to China and ask for that. They'd be like, no, go back, we don't have that. There is no such thing. But Dr. Zyrus said,

A (31:53)

I think I'm banned in China. To be honest, it's likely China and Iran. Those are my two. All right, we're moving on to my last two. So first one, just interesting. So this was a study out of I believe Indonesia where they were looking at scabies and then people who after they got treated for scabies, how long their itch persisted. So relatively small study, you know, reasonable chance that these people had like co other stuff going on, whatever. But the, I mean I'm pretty fascinated by this. So the main takeaway, people who had a long term post kibetic itch universally, well, not really universally, but had really high IGE at baseline. So you could measure IGE at baseline and then that predicted very effectively that you were going to have a prolonged post kinetic itch. And that's very plausible to me. So like I think of it as being that, you know, scabies mites were allergic to them. It certainly is possible that people who are atopic are driving more allergy to them and it's going to take longer for the inflammation and the itch to like resolve. If this was like a super hard test to get, yeah, I'd be like, meh, I don't know. Or if it was expensive or you got to send it off or whatever. But like this is easy. You do, you know, an IGE test. If it's, if their ige level is super elevated, you then you tell them, oh, this might take a while. Like don't worry, you know, so just thought it was interesting then the other one that was even probably more interesting to me, but it's mostly mechanistic, was about sort of a different approach to food allergy and atopic dermatitis. So the idea is that with chronic skin inflammation, high alarmins, so IL33TSLP, you drive. And this, I think Ferris has talked about this a little bit, you drive th2 sensitization to weak allergens, especially in the gut. And so essentially you become cutaneously and maybe via gut routes sensitized to things like propylene glycol or propolis or whatever. And then that's driving a systemic TH2 inflammatory state that you could in theory get better via dietary avoidance. And this would go to some extent against my frequently repeated, like, thing. Look, just put people on the IL13 inhibitor and if they get better, you know, it was atopic derm. Well, no, if it's because, right, because contact Derm is a TH1 disease. Well, but if there's this other type of TH2 contact Dermot associated specifically with systemic contact derm, that then doopie would work for that. And maybe those are people we could get better with a avoidance diet. However, my final take on the whole thing is if avoidance diets worked, we would not need statins and we would not need blood pressure meds. We would just say avoid, you know, foods that are bad for you and people wouldn't die of heart attacks. But instead we have all those drugs and we have cabbages and we have cats and the whole thing. So I'm still, if I, if, if you told me like, we could do all of this testing, you do all of these avoidance diets and be super careful with what you eat for the rest of your life and you won't need to whatever. And it's going to take a year to figure out if you're one of those people. I would be like, just give me the doopie. Don't care. Like, I'd give myself a shot every two weeks. And if my insurance stops paying for it, then we can come back and try and figure this shit out. Like, that would still be my take on it, but might not be everybody's take. Just an interesting thing. I'm not sure what to do because kind of what they recommend is atopy patch testing, which is like sort of a modified normal patch test. It's mostly they're patch testing people to different stuff and you're reading the patch test a little bit differently, but like, nobody does this. There's probably like 10 people in the country who do it. So, like, unless other people start doing it, even if this is real, it's hard to. It's hard to, like, figure out other than doing empiric food avoidance.

B (36:30)

Yeah.

C (36:32)

No, like, ordering a test to the food. Right. Like, you know, so hard when people come in like, oh, look at this. I got the. I saw the allergist, and I'm allergic to these 18 foods. They're like, yes.

A (36:45)

Oh. Or even better if they went to this.

C (36:47)

Okay, yes.

A (36:48)

Or they went to the functional medicine doctor and got food IgG testing. And like, any allergist you talk to is like, IGG literally means you are not allergic to it when you get igg. That is specific. Like, we test that to prove, like, you're not allergic. But, like, since it's a positive test, people get, Whoa. Positive test to the, you know, corn. Yeah. But so just mechanistically interesting, these guys. I've had a strongly held belief about this TH2 skewing stuff is baloney. They convinced me that it's. It's at least, like, possibly not baloney. I now, I now give it real credibility that. That we could have this as another contributing factor to the rise in atopic dermatitis over the last 40 years.

C (37:39)

So, yeah, I mean, it does, like, also, like, kind of back up. Like the. We've had Peter Leo on and talk about the Gutskin accent axis. And I, you know, I was like, oh, the gut skin axis. But, like, maybe it's real. Right? Like, there are some now explanations that there may be. I don't. Still don't know what I think about leaky guts, but, you know, maybe there is something to all of this.

A (38:02)

Oh, it's. I. I still think of the microbiome as the, you know, intestinal microbiome is the best, but that's maybe the. Yeah, it's. It's. It's complicated. It's complicated. It's. It's like our kids. No, not my kids. Probably not you guys kids either. It's normal kids dating lives. It's complicated. That's what we'll go with. All right, we're ending the episode there. I want to thank everybody for joining us this week. I hope you learned a few things. Hope you laughed once or twice. But mostly, we hope you're planning to join us again next week. And until then, I'm Matt Zyrus.

B (38:38)

I'm Tim Patton.

C (38:40)

And I'm Laura Farris. And we are Derms on Drugs.