Sunscreen Heresy & Other Hot Takes

Summary

---

Podcast Summary: Derms on Drugs

Episode: Sunscreen Heresy & Other Hot Takes
Date: May 15, 2026
Hosts: Dr. Matt Zirwas, Dr. Laura Ferris, Dr. Tim Patton
Theme:
A rapid-fire “six-pack” of recent dermatology research, hot takes on practice, evidence updates, and thought-provoking clinical questions—all with the usual playful banter among three experienced dermatologists.

---

Main Topics & Key Insights

1. Novel CTCL Therapy: Brentuximab Vedotin + Ultra Low Dose Total Skin Electron Beam

• Paper Discussed: Small study combining brentuximab vedotin (anti-CD30 ADC) with ultra-low dose total skin electron beam therapy for tumor-stage Mycosis Fungoides (MF) (stage 2B+).
• Key Points:
  • Patient Cohort: 14 advanced, CD30+ MF patients with median 3 prior systemic treatments.
  • Treatment Protocol: Two fractions of 4 Gray (total 8 Gy) with brentuximab vedotin (1.8 mg/kg). Median of 9 cycles + methotrexate maintenance (79%).
  • Results: 100% response rate—64% complete remission, 36% partial. Median SWAT score dropped from 49 to 3. Median time to response 12 days.
  • Tolerance: Mostly mild toxicities; lower grade 1–2 neuropathy vs. larger trials.
  • Significance: Supports radioimmunotherapy paradigms (targeted antibody + radiation). Not practice-changing yet, but a sign of future therapeutic strategies.
• Quote:

  “The overall response rate here was 100%. So 64% of these patients had a complete remission ... median SWAT score ... dropped from 49 at baseline to 3 at 3 months.” — Laura Ferris [06:11]

2. Biologics and Cancer Risk in Psoriasis

• Paper: Large trinetics study (>60,000 patients per group) on malignancy risk with IL-17/IL-23/IL-12/23 inhibitors in psoriasis.
• Key Points:
  • Findings: No increased cancer risk—odds ratios for many cancers, including melanoma, were slightly decreased in biologic users.
  • Interpretation: Lowers concern for oncologic adverse effects of these agents. Risk reductions are minor on an individual basis but may be substantial at a population level.
  • Caveats: Baseline differences could include healthcare utilization, cancer screening frequency, and demographics.
  • Patient Messaging: “A study that looked at over 60,000 patients on biologics didn’t detect higher rates of cancer ... just take the biologic. Damn it.”
• Quote:

  “[T]he biologic patients had lower odds ratios for ... lots of different cancers... It reassures us on the safety ... in patients who are maybe concerned about developing cancer.” — Tim Patton [12:00]

3. Oral Photoprotection: Beyond Sunscreen

• Topic: Review of supplements shown to decrease sunburn risk.
• Key Points:
  • Evidence-based Options:
    • Polypodium leucotomos (Heliocare): Substantial evidence for reducing sunburn; mechanisms via antioxidant, not pigment absorption.
    • Carotenoids (lutein, beta-carotene, lycopene) and Omega-3 FAs: Good support, additive benefits.
  • Practice Note: Stacking carotenoids is more effective; pigment change is not an issue at recommended doses.
  • Other Points: Unknown if these prevent skin cancer; absence of evidence, not evidence of absence.
• Light-Hearted Moment:

  “When I go out in the sun, I take… I’m now up to… I take 16 Heliocare before I go on vacation, whenever I head out to the beach.” — Matt Zirwas [22:33]
  “This does not constitute formal medical advice.” — Laura Ferris [22:38]

4. Fungal Acne: Is It Really That Itchy?

• Key Points:
  • “Fungal acne” = Pityrosporum (Malassezia) folliculitis; search interest up 119%.
  • May be indolent or itchy; monomorphic lesions common, often on trunk/hairline.
  • Usual “acne” agents (BPO, sal acid, zinc) helpful; anti-fungals (itraconazole) often used.
  • Debate: Is itch a reliable distinguishing feature?
• Playful Banter:

  “Ascertainment bias. I don’t know if I’m using that term correctly.” — Matt Zirwas [26:10]
  “It sounds really smart. I go with it.” — Tim Patton [26:18]

5. Environmental Clusters in HS (Hidradenitis Suppurativa)

• Paper: Boston academic center geocoding study of HS “hotspots.”
• Key Points:
  • Clear HS clusters exist at sub-zip code level.
  • Strongest factors: Obesity, higher afternoon temp, air pollution, greater % Black residents.
  • Implication: Social determinants, not just individual risk, may drive disease prevalence.
  • Opens exploration of environmental/structural racism/urban planning on disease.
• Quote:

  “...there is sort of data that heat and pollution can promote ... air quality can influence like skin barrier and potentially microbiome. So there might be something there.” — Laura Ferris [30:32]

6. Epigenetic Skin Aging: Dihydromyricetin Serum

• Paper: Prospective use of facial serum with dihydromyricetin (“bioflavonoid” from Japanese raisin tree).
• Key Points:
  • Epigenetic “tape stripping clock” used to measure skin age.
  • 8 weeks of twice-daily application yielded mean 2-year reduction in epigenetic age; 40% >5 years.
  • Modest but significant improvements in wrinkles, texture, density (though photos unimpressive).
  • Debate: Could you take it orally for full-body effect? Safety vs. cancer risk? Product not yet FDA approved; is available in Europe.
• Memorable Exchange:

  “If the patient came in and was like, ‘Am I better?’ I’d be like, I’ve noticed. But I think the cosmetic dermatologists are like, ‘Oh, My gosh, you are glowing.’” — Tim Patton [36:45]
  “Couldn’t I just take this as a pill… and then like, not just… demethylate the epigenetic changes in my skin, but anywhere, right?” — Laura Ferris [38:08]

7. Azithromycin for Acne: Meta-analysis & Practice Shift

• Key Points:
  • Recent meta-analysis: Once-weekly azithromycin (500mg) at least as effective as daily doxycycline (100mg), with better tolerance and less photosensitivity.
  • Good alternative for those who don’t tolerate tetracyclines or want to limit resistance.
  • European guidelines currently discourage its use due to limited efficacy evidence and resistance risk, but hosts argue that for acne and related conditions, it’s an underused option.
• Quote:

  “Azithromycin stopped working for staph forever ago. So if we’re going to use something like this makes a lot of sense to me.” — Matt Zirwas [41:43]
  “I’m switching everybody.” — Laura Ferris [42:21]

8. Steroid Inhalers & Perioral Dermatitis in Kids

• Study: TriNetX retrospective—kids using inhaled or nasal steroids ~3x higher risk of perioral dermatitis.
• Clinical Note:
  • Advice: Rinse/wash face after inhaler to reduce risk.
  • Possible: Clindamycin wipes after use.
• Claim Confirmed:

  “I think… women who get peroderm who are, like, not using topical steroids on their face… ask them if they’re using inhaled steroids at all.” — Matt Zirwas [45:52]

---

Notable Quotes & Moments

• On Changing Standards:

  “Take the biologic. Damn it. To hell with shared decision making. Take the drug, make them take it…” — Tim Patton [14:13]

• On Social Determinants:

  “I think we’re going to find that there are a lot of things that are related to sort of chronic, ubiquitous exposures that are just kind of part of living in America…” — Matt Zirwas [32:00]

• On Epigenetic Serums:

  “I’m like too lazy to turn my age back two years by to put a cream on my face twice a day.” — Laura Ferris [37:45]

• On Evidence & Practice:

  “European guidelines discourage azithromycin due to limited efficacy evidence, negative benefit/risk… I always use azithro for CARP!” — Tim Patton [43:13]

• On Fungal Acne “Itch”:

  “Maybe acne vulgaris is just as itchy. Ascertainment bias. I don’t know if I’m using that term correctly.” — Matt Zirwas [26:10]

---

Timestamps for Key Segments

• CTCL therapy (Brentuximab + radiation): [01:10]-[10:05]
• Biologics & Cancer Risk: [10:56]-[17:09]
• Full-Body MRI, Overdiagnosis in Cancer: [17:10]-[19:20]
• Oral Photoprotection, Carotenoids, Heliocare: [21:50]-[23:24]
• Fungal Acne/Folliculitis, Diagnostic Uncertainty: [24:24]-[27:03]
• HS Environmental Clusters (Boston study): [27:06]-[33:42]
• Epigenetic Skin Aging, Dihydromyricetin Serum: [33:46]-[40:16]
• Azithromycin for Acne: [40:16]-[43:13]
• Inhaled Steroids & Perioral Dermatitis: [45:06]-[46:51]

---

Takeaways

• Cutting-edge research is increasingly spotlighting combination cancer therapies (e.g., radioimmunotherapy), social and environmental determinants of disease, and the fine print behind population data.
• Practical pearls—from stacking oral antioxidants for photoprotection to once-weekly azithromycin for acne—emerged throughout.
• The hosts combine rigorous evidence review with candid critique, humor, and real-world clinical wisdom, offering both science and practical take-home points.
• Throughout, the trio challenge received wisdom—on sun protection, overdiagnosis, biologic safety, and more—encouraging listeners to continually re-examine standards of care.

---

Funniest Banter:

“If you get on there and start trolling me, Ferris, that’s it.” — Matt Zirwas [26:51]

Memorable Advice:

“Just wash their face like 30 seconds after they do the inhaler.” — Matt Zirwas [46:47]

---

Transcript

[A]

Welcome to season three of Derms on Drugs, a video podcast brought to you by Scholars in Medicine, the best educational platform in dermatology and provided a no cost to medical providers. Derms on Drugs is where cutting edge derm meets hit or miss comedy. I'm Dr. Matt Zyrus from Docs Dermatology and each week I'm joined by residency buddies Dr. Laura Ferris from the University of North Carolina and Dr. Tim Patton from the University of Pittsburgh. And we use our 60 years of combined derm experience to discuss, debate and dissect the hottest topics in dermatology. It is everything you need to know to be on a cutting edge of derm and you'll actually have some fun listening. New episodes drop every Friday on Scholars of Medicine, Apple Podcasts, Spotify and other major podcast platforms. And I highly recommend that you download the Scholars of Medicine app to access the full podcast video archive. Explore the best derm educational content out there. Real pharma independent coverage of all of Derm, supported by an amazing clinical consultant called Ask Simon. So, so this week we've got one of our patented six pack episodes where we are going to go over the latest, greatest stuff that we have seen in the literature. Basically journal club on steroids and let's kick it off. Dr. Farris, what do you got?

[B]

All right, so today I thought I would go outside my comfort zone and I am going to talk about the treatment of ctcl, something I do not do at all. I always have worked with smarter people and referred it to them, but this was such an interesting paper that I thought that I would talk about it. So this is a study in which patients. Is a small study in which patients with cutaneous T cell lymphoma were actually treated with a drug called brentuximab Vedotant plus ultra low dose total skin electron beam therapy. Okay, so what was this? So patients with tumor stage MF, this is stage 2B or above. These guys have a pretty bad prognosis as we know. One of the treatments out there is a drug called rituximab vedotin and this is. It's an antibody drug conjugate or an ADC. So the antibody targets CD30 and then it has what's called a cytotoxic payload, which is mmae, which sounds kind of like mma, but it's mma. So I also like that part of it. So it's mono metal. What's up?

[A]

Somehow I doubt you're a big MMA fan, Ferris. Or you.

[B]

I'm not really. I dabble.

[A]

I'M almost, I'm a little, I'm surprised you can know what it is, but that you always surprise me.

[B]

You I aim to surprise.

[A]

Yes.

[B]

Mono methyl or a statin E. So what is that? That's it. So like basically the drug binds to the CD 30 positive cell and it gets, you know, taken in and then it releases sort of its weapon, which is the cytotoxic payload. This is sort of a mechanism, newer mechanism for chemotherapy drugs. And so this MMAE is an antimitotic agent that binds to tubulin, so it blocks tubulin, microtubule polymerization. It makes you know, cells go become apoptotic. And so, you know, it's so toxic that you couldn't just give this free floating. You gotta like micro, you know, dose it into the exact cell. So kind of just like an interesting mechanism of action. And so, so what they did. And so radiotherapy, like total, total beam electron therapy is also sort of, you know, one of these treatments that is done for CTCL patients. So normally you, you know, do that in this like 36, 30 to 36 gray range over several weeks. But then there's some studies that show that, you know, low dose schedules, maybe 12 gray over multiple fractions can be done.

[A]

Okay, so Pat, Pat and I almost killed one of our patients with this once.

[B]

Oh, way to go.

[A]

Let's hear about total skin electron beam was the lady who had bad, terrible Darier's disease. Disease was getting repeated just over and over and over. MRSA infections that were only susceptible to Vanco and they were getting less susceptible to Vanco. So somewhere in the literature there was something about electron beam for full body dairies. And so we sent her over to Allegheny General. Wasn't she like in the ICU for like a month or something? Because it like I don't think it was that long.

[C]

I think it was a week. But she did get better and we published it.

[A]

Yeah, yeah, she. Have you ever seen her back like in the last was 20 years ago.

[C]

So I don't, you know, she died of metastatic ovarian cancer. Not related to anything that we do.

[A]

Man, I really liked her too.

[C]

Yeah, she was good. Yeah, she was a good sport.

[A]

So she stayed, but she stayed like long term was good.

[C]

Yeah, her Dari really never became a sign significant problem. Okay. Yeah, she was happy overall. I mean, yeah, she went through a rough patch there, but overall she was happy with the response.

[A]

Yeah. Yeah. Okay. All right, all right, Ferris, go ahead.

[B]

Okay, so what they did basically was this was. So this was published in bjd, British Journal of Dermatology. For those of you who aren't MMA aficionados. Actually, it doesn't have anything to do with it. And they. So what they. This is a retrospective study where they looked at 14 patients with stage 2B MF, all of which were, you know, CD30 positive on average, had about 5% expression. And these were people who had already had at least like about on median three to, you know, three prior systemic treatments. And so they treated them with this Brantuximab vedotin in addition to just two fractions of four gray each. So total of eight gray, very low dose, total body electron beam. So wait, like therapy? Yeah.

[A]

So they just like went in twice, like literally two times.

[B]

Wow, two times for the total, you know, electron beam.

[A]

Yeah.

[B]

And then they gave that concurrently with standard dose Brantuximabin 1.8 makes per kg. And so then they, and then they, and then they look, they follow these patients and again they received like a median cycle, a median of nine cycles of brentuximab, but basically. And then 79% of them went on maintenance therapy, which was, you know, methotrexate. Methotrexate, mostly clinically. So the, the overall response rate here was 100%. So 64% of these patients had a complete remission and 36% had a partial remission. And the median SWAT score, which is like the PAZI of CTCL, is, I like to think about it, it is dropped from 49 at baseline to 3 at 3 months. The median time to response, 12 days. Now what's interesting is Brentoximabedotin was there was this large trial called Alcanza. And so in that where they gave, you know, systemic Brentuximab, the mean time to response in that study was 83 days versus 12 here. So and then they did follow these patients for on average about a year. Nobody had a tumor stage. Recurrent recurrence toxicity was pretty modest. Like 29% had a mild rash, 14% had grade one to two neuropathy. There were no grade. There were no like grade three or higher toxicities. Brentuximab vedotin, which I did not know had, you know, one of their, you know, biggest toxicities is actually neuropathy. So about 2/3 of patients in the Alanza study had neuropathy. So, you know, I thought that this was just really interesting. It was, you know, combining two therapies, low dose of, you know, of the total electron beam radiation, and, you know, what was what, like a really quick response and a really Good response. So, you know, I thought this was cool. It's not like, oh, we can go out and do this, or people like me should start treating ctcl. We should not. But, you know, maybe this will, you know, be developed into, you know, know, a more of a, you know, a. A clinical trial. So, you know, this is like this. The. This sort of paradigm of radio immunotherapy, which is that you basically, you know, biologically prime a tumor. So you've got an antibody that targets that tumor that, you know, puts like a radio sensitizing or, you know, some sort of cytotoxic payload. Then you hit those cells with radiation, and it's just like very targeted therapy. I. You know, I know that this is being done in, you know, prostate cancer, for example. You know, like, when you see that drug PLU Victo advertised that that's being done. So I just thought that this was interesting. This seems like this could really be kind of like the next generation of how we treat these diseases. Don't ask me any hard CTCL questions.

[A]

Well, I looked it up while you were talking because I couldn't remember what phase 2B meant or stage 2B. I mean, these are people with real CTCL. This is not patch black disease. These are tumors. Like, no, no.

[B]

And they failed three treatments on average. So.

[A]

Yeah. Wow. Wow.

[B]

Yeah, I thought it was really interesting.

[A]

So that's a bad disease. It's like, I get. I. Yes. Send all of them immediate. Ohio State's got a really good CTCL program that's co run between ONC and Derm. So I send all of them immediately over to. Over there. But, yeah, it's a bad disease. It's one of the ones.

[B]

As you should and as you should continue to do. But, yeah, it'll be cool if this will be the next phase of where we go.

[A]

Yeah.

[B]

Yeah.

[A]

All right.

[C]

Cool.

[B]

All right.

[C]

Can send them over and be really obnoxious and say if I were you. I really strongly think they will really appreciate that. I'm sure.

[A]

I bet they will. I'll discuss it with the patient first. I'll be like, yeah, if they're gonna take good care of you, this is what they will do. Anything else say no. No. Then they might send them back to me, and I don't want that, so I can't.

[C]

Yeah, then you'd be stuck.

[A]

Yeah, then I know.

[C]

Okay.

[A]

All right.

[B]

Testing them. Maybe this is really dermatitis. We're going to try to patch test, reverse.

[A]

It's what I did because I did diagnose a fair amount of ctcl. It wasn't rare that they would get sent for patch testing because, you know, in that pre diagnostic phase, it doesn't really look like atopic derm. And it, you know, I, I diagnosed a fair number of cases of it.

[B]

Yeah.

[A]

Yeah. All right, Patton, what do you got?

[C]

All right, my first six pack is from the March 2026 edition of Cutis and is titled Malignancy risk among psoriasis patients treated with interleukin inhibitors. A retrospective matched cohort study by Zariab, Alam et al. So we recently just looked at that paper, dupilumab use in patients on immune checkpoint inhibitor therapy. And it affected cancer mortality, like in a good way. And it made it look like patients taking dupy had better outcomes in terms of cancer. I think we all came to the conclusion, we don't know if it's true, but at least we can feel better about prescribing it. And from a safety standpoint. So one of the theories proposed by us crackpots was blocking Th2 inflammation. You push patients down a Th17 pathway, and that fights cancer. So one could reasonably ask, what if you blocked th17 or if you blocked il23, which influences the th17, would that people, would that make people more likely to develop cancer? A reasonable question, right?

[A]

Yes.

[C]

All right, well, this paper maybe helps answer that. Maybe it was a trinetic study. So they took psoriasis patients placed on anti IL17, anti IL1223 and anti IL23 therapies and matched them up with psoriasis patients who were not on those therapies. Propensity mass scoring was done on sex, age, race and ethnicity. 60,000 patients, like over 60,000 patients in each group. So you had 60,000 patients who got those biologics and 60,000 psoriasis patients that did not. And so after an average follow up of just under four years, the biologic patients had lower odds ratios for lots of different cancers, lower odds ratios for skin cancers, Hodgkin and non Hodgkin cancers, bunch of other solid malignancies. So, you know, it's, it's another trinetic study, but I think it's another one where it reassures us on the safety of these medications in patients who are maybe concerned about developing cancer. I doubt, I mean, again, I doubt that it actually significantly prevents cancer, but I think we can say now we have more data giving us that these are safe medications.

[A]

Yeah.

[C]

So, yeah, limitations, retrospective nature. Patients weren't matched on things that, like, would matter. UV exposure Ethanol consumption, HPV status, smoking, family history. Right. I mean, would that have made a difference? You know, if you have somebody with a family member that had cancer, they're probably extra cautious about using a biologic, so they won't do it. And then if they got cancer like that would count against the control group. Yeah. I think most of the data supports the biologic medications, particularly those affecting 1723 pathways don't predispose to malignancy. And now we have a larger trial, albeit a trinetic study. And you can insert your own trinetics study disclaimer here that shows the same thing. I don't think I'll tell patients that they protect them from cancer, but I will say that a study that looked at over 60,000 patients on biologics didn't detect higher rates of cancer compared to psoriasis patients not taking biologics. So just take the biologic. Damn it. To hell with shared decision making. Take the drug, make them take it so it's in.

[A]

Did they. So the thing I always forget about with articles like this, did they compare them to people who were on other biologics or just people who had never been on an I. They could have been on something else. They could have been on a tnf. They could have been. Or just they were people who'd never been on any biologic.

[C]

No biologics.

[A]

Huh. So.

[B]

So then that means like they don't have the same baseline diseases either. Yeah.

[C]

I mean, against that it seems like it would make it better, but.

[A]

Yeah, well, it's in part of. It could also be the idea that if you've got, if you're competent to get and stay on a biologic, you were also the kind of person who keeps up with your cancer screenings and sees your primary care doctor and all of that kind of baloney.

[C]

Yeah, there's that. I mean, that's always a confounding factor in these retrospective studies, just. But like use of the healthcare system.

[A]

Yes.

[C]

If you're a biologic patient, you're just a more savvy sort of healthcare consumer. And so all of those things are going to be better. And you know, they have these odds ratios numbers which like look amazing. Like for melanoma it was whatever, 36 reduction in odds ratio. But like odds ratio are funny things. And I just kind of went through a little bit of the statistics, but that's basically saying for if you had a thousand patients not on a biologic, a thousand psoriasis patients not on a biologic, you would see four cases of melanoma. And if you had a thousand patients on a 17, 23 or 2312 inhibitors, then you saw three cases of melanoma per 1,000. Like that. That gives you that odds ratio of 36% reduction, but it is a teeny, teeny difference. So again, this is not like these are protective against melanoma, but I think it's very, very reassuring that you could say they do not seem to increase. Like you, you, you see very close to the same number of these sorts of cancers, whether the patient's on a biologic or not. And so that's, I think, reassuring and hopefully reassuring to patients.

[B]

Yeah. Although I would argue so interestingly, like, you know, a 36% reduction in cancer is massive. Like at a population level, that would be a massive reduction. Even though, you know, at our. How would we see that in terms of how often we see melanoma? I get it. That would not feel massive to us. But at a population level it is, I would also say utilization. The healthcare system is generally associated the higher incidence of cancer because we detect more like we know we detect lots of indolent cancers. That's like what we do. So the fact that you saw less than people who we knew were high utilizers. Well, who we assume are higher utilizers, we don't know. To get into trinetics, you had to be in epic somewhere. So everybody was. There was no non utilizers of the healthcare system and there are no non utilizers and trinetics.

[A]

So that's the screening thing reminds me, I saw like a kind of an opinion piece today about all of these full body MRI clinics that are coming that are showing up and how much it's driving a increased diagnosis of incidentalomas that like, you may end up getting chemo or surgery for something that never would have actually turned into cancer. It's a really fascinating like, challenge because you, you think like, oh my God, I would want to know, like early. But like maybe, maybe 9 out of 10 cancers that you get, you know, that you don't know about go away. Like, we don't know. We don't know that number. We don't know.

[B]

That's a huge. That's like my whole, you know, right. Melanoma academic interest is like, yeah. Or a lot of it is like, what is, you know, what are the really like the relevant ones and what are we doing by. I mean, this is what we do. We are like the full body mri, people of dermatology. We are screening and screening and screening and finding and biopsying stuff without having the study. Right. And if you look at like all of the studies of you know, like mammography, they were done, you know, breast cancer. It was like, you know, mammograms done in a very defined population and there was a, of, you know, women at a certain age and there was a certain frequency and you know, this like kind of free for all of anybody can go out and get their whole body mri. You know, we don't know the, we don't know. So we know like the mortality of most cancers when they are detected in the normal way. We don't know what number when they are detected in ways that we never studied in the past. Right. Like who knows? Like, you know, they say, you know, if you, you know, like in Korea when they started doing thyroid ultrasounds on everybody as a screening test, like their incidence went way up. The mortality per population stayed the same, the case based mortality plummeted because you just found a bunch of cancers that weren't going to, weren't going to be.

[A]

That's right. In this piece I read today that was one of their like primary things that they discussed was that Korean thing where they just. Yeah. Ultrasounded everybody's thyroid or something.

[B]

Yeah, yeah.

[A]

Okay. All right, let's move on to our next. So I've got a couple. So first, so for any of our listeners, I've now gotten into being on X. My handle is Matt Zyrus. And it turns out if you, if you only engage with medical content, like nothing, you never look at anything political even once. Like it's actually pretty great. Like there's a lot of like smart doctors on there posting all kinds of stuff. I don't know if I'm one of them. But anyway, yeah, I had a coat. One of my posts went viral. Close to a million views. That was about that. I think the world of dermatology recommend, the AAD in particular recommends too aggressive of sun protection, which we've talked about on here before, that you know, there's good evidence that sun reduces your risk of heart attacks and strokes by 20 to 30% and that that far outweighs the, you know, the increased risk of dying from skin cancer. But the, as part of kind of doing research for that post, I came across an article that was recently, I think it was in Jet in JAD about oral photo protection. And it just is pretty cool. So the idea with these oral photo protection things is that there's, they probably don't reduce the risk of skin cancer to any significant extent, but they definitely have good evidence for reducing the risk of sunburn. And we've got really good evidence around this. So in particular, the ones we've got good evidence for, the polypodium leukotomas extract, AKA Heliocare, that's got very strong evidence. And then a bunch of keratinoids. So lutein, beta carotene and lycopene all have good evidence. And I was like, well, do you have to take so much that you, like, turn yellow and orange like the little kids do who eat nothing but squash? And no, it's not that the pigment is absorbing the light. It is that they are highly potent to antioxidants. And a big part of the inflammation from sun is via reactive oxidative species. And then the third one was Omega 3s. So, you know, Omega 3s that have been studied for cardiovascular and all that other stuff. And so take all those together and it probably can have a meaningful effect on reducing your susceptibility to burns. Might have some benefits with reducing photo aging. So just interesting. And you can stack them. So meaning the lutein, the lycopene and the beta carotene, they all kind of are doing somewhat different things. So even though they're all carotenoids, they taking all three of them is Nutri squelches more antioxidants than taking just one of them. So just interesting stuff. And the other thing, as you guys know, when I go out in the sun, I take. I'm now up to. I take 16 heliocare before I. When I go on vacation, whenever I head out to the beach.

[B]

And that I think 16 all at once.

[A]

16 all at once. And it gives me you.

[B]

This does not constitute formal medical advice. Zero evidence to do any of that. I. I love Polypodium. I'm going to say there is. Heliocare is one brand. There is one called Inner Glow that is actually made by a dermatologist. Not one who I know, but I like it because it comes as a gummy. So it feels like a treat and sun protection together. Okay, so there are more than one. But, you know, I guess I would say that there's not. Like, when you say that doesn't prevent skin cancer. We don't have evidence that it doesn't prevent it. We just don't have evidence that it does. Right. Like that's too.

[A]

Okay, correct.

[B]

But my, like, oh, it's helping with photo aging, but it's doing nothing for skin cancer. We don't have that. Okay.

[A]

My understanding is that the. That it'd be relatively Unlikely that there, there isn't enough of it like in the nucleus or something because, right, you get the reactive octave species in the nucleus or what's like getting your DNA. But when I look, when I kind of tried to dig into. Is it because I want it to prevent skin cancer, right? So I looked like, oh, can I say this prevents skin cancer? And it was. The main takeaway I got was like, probably not, but not a. Like there was a lot of like, we don't know, a lot of we don't know to go with it. And then the other one that I looked at this week was about fungal acne, which we all hear about all the time. 119% increase in the number of Google searches around fungal acne. And the interesting take here, right? So fungal acne is pitter spore and folliculitis. Oftentimes it is non inflammatory, in which case they can look a lot like closed comedones, but they also can be inflammatory, in which case they look more like papular acne. The biggest things that people talk about with it trunk more so than face. When it is face, it tends to be more like hairline. And people often talk about it being very itchy. That has not been my personal experience. Like whenever I see it in people, I. It's not been like super itchy itchy, it's just been like, hey, your acne is going too far down your back has always been kind of my takeaway. And then that most of the stuff that we use for acne, a lot of it at least kind of works for this too. So benzoyl peroxide is pretty good anti malassezia. Salicylic acid is pretty good anti melassesia. But then you also can use, you know, zinc. You can use dandruff shampoo as body wash and face wash. You can do weekly fluconazole or itraconazole, which is usually what I end up doing for these people is just long term here, once a week take a dose of itraconazole. And that like works really, really well for them. But what's, what is you guys take on fungal acne? Do you think it's like, I have, I've never seen it be itchy, but I always read that it's itchy.

[B]

Like what I don't, I have not seen it be. I don't think of it as being itchy. I don't know, it looks like to me it's like, it's monomorphic and it's seems to be People who sweat more and don't necessarily like, rinse off or wash after exercise. But maybe I've created that narrative, but

[C]

I think I've had itchy. But the thing is, when I thought it was malasses, I ask him if it's itchy and when I think it's acne vulgaris, I don't even ask. Maybe acne vulgaris is just as itchy.

[A]

Ascertainment bias. That's the. I don't know if I'm using that term correctly.

[C]

It sounds really smart. I go with it.

[A]

It's. What was the term that Ferris used the other week, that scope? What the hell does that mean again?

[C]

That is mostly used in. Yeah, radiation.

[A]

What's it mean?

[B]

It means that you treat one tumor and then treat tumors that you didn't treat. Go away.

[A]

Okay. Okay, Abscopal. I got it. That's the word of the month.

[B]

I'll keep people who know a lot about cancer so much that they can have viral X rays all know what the AB scope will effect is just

[A]

gonna say that, Ferris, if you get. If you get on there and start trolling me, Ferris, that's it.

[B]

I'd have to. Yeah, make an ex account somehow.

[A]

All right, let's move on. Ferris, what do you got? What's your next one?

[B]

Okay, so my next one is about HS and it's not about treatment, but I saw this paper and I was hoping it would give me more information, but I like this idea. So I moved from Pittsburgh where everybody is obese, but, you know, there's some hs, but it wasn't like mad hs, down to North Carolina, where, you know, people are also obese. I don't think it more obese than in Pittsburgh. And I'm like, everybody has HS in North Carolina, so I'm like, there's got to be something environmental and, you know, hs. And so this was a study that looked at this. So basically what they did was the four major academic centers in Boston, you know, which. And they, between 2017 and 23, they basically pooled their HS patients, about 3,000 of them. And then they like geocoded their, the patient's home address and they got to the census tract. So census tracts are like your zip, like the plus four of your zip. And so that is a way to kind of locate not just like you're in, you know, the five digit zip code, which could have like, you know, really wealthy and really poor people and, you know, but it does kind of get you down to a more narrow area. You can Correlate that with certain factors like, you know, what is the average income, what's the average education, what's the, you know, any like food instability, all those kind of things. So they did that and, and so then they said like, are there HS clusters? And so they did find that there were actually even within Boston clusters of hs. So there are hotspots in south and central Boston, meaning like those, those census tracts had more than other areas. And so they postulated, you know, it seems like there is sort of location or place based factors, you know, or neighborhood features that are associated or potentially drive, you know, hs. And so then they could compare hotspots with non hotspots. And so the four things that came out as factors that were more common in the hotspot areas were higher average afternoon temperatures, higher obesity prevalence, higher fine particulate air pollution, and then a higher percentage of black residents in that tract. So you know, interesting. So you know, the obesity thing, not super surprising. We know that that is associated. But you know, they, they reflect that. You know, potentially this means these are areas that have poor access to healthy food or it's, you know, harder to have like safe outdoor exercise areas or green space. You know, air pollution and heat is kind of interesting. So, so I guess like North Carolina versus Pittsburgh or Boston, like it is warmer. Does like a couple degrees matter? I don't know but I thought that that was sort of interesting. Or you could argue areas of poverty have more obese people and they've got more like cement and fewer green spaces. And that's what's associating, you know, the, the temperature. But you know, there is sort of data that like heat and pollution can promote. Right. Like we've talked about this when we talked about catalytic converters being associated with the increased incidence of atopic dermatitis. So certainly air quality can influence like skin barrier and potentially microbiome. So there might be something there. And then you know, racially there's probably, you know, issues of again like different socioeconomic factors, you know, structural racism, all the, you know, certain like, you know, areas that I don't know, like there's probably all kinds of things that could be going on. So I wasn't. Now if you looked at like what was the strongest of those four factors, the strongest association was with obesity in the areas of the highest interest, of the highest incidence and the lowest was the temperature. So does it really change anything for how we're going to practice? No, but I really think like there's got to be some environmental factor that is Driving HS in certain areas that kind of confirm this idea that there's hot spots. And, you know, maybe in addition to obesity, there are other modifiable factors. So I thought that this was just sort of interesting. And, you know, you could only look at whatever is measured for each census tract. So, you know, maybe this means we should be looking at other environmental factors. I don't know. Do you guys think there's anything to the, like, HS hotspots?

[A]

Oh, yeah.

[B]

Yeah. Okay.

[A]

Yeah, 100%. I. I saw this because I'm very right into the ad being driven by air pollution. Right. The effect, I don't think is as strong for hs, but I think we're going to find that there are a lot of things that are related to sort of chronic, ubiquitous exposures that are just kind of part of living in America. Air, clothes, you know, chemicals and clothing, blah, blah, blah. But, yeah, I bought. I. I absolutely buy this. Absolutely buy it. Patton, what do you think?

[C]

Yes, I buy it as well.

[A]

No, it's. Yeah, it's. It's going to be interesting as this data gets out there more. I need to send this on to Ian Miles, the guy at the NIH who figured out the atopic derm and catalytic converter thing to just give him, hey, here's another disease you need to look at.

[B]

Yeah. And there's like, you know, this whole field of, like, metabolomics. Right. Where you look at, you know, things like microplastics or micronutrients or, you know, you can sort of look for these things now in individual people instead of trying to look at it at sort of a census tract or population level. So, you know, obviously not everybody in that area gets hs, so what's different between them? So I don't know. I thought it was just kind of cool. And I hope that this is maybe a direction that will, as we can do more interesting, you know, like, individualized studies. Maybe we'll learn some of the things we could do.

[A]

Yep. All right, Patton, what do you got next?

[C]

All right, my second six pack article was published online April 2026 Dermatologic Therapy and was titled Epigenetic Skin Aging and its Reversal to Improve Skin Longevity. This is long across ethnicities and phototypes using a dihydromyrocetin containing serum results from a prospective single cohort study by Key et al. So my.

[A]

My interest is peaked. I am a. I'm a believer that this is how the air pollution is causing the.

[C]

I would have you at hypomethylation. It's not Even in there. But you know where it's heading.

[A]

Yeah, yeah. Because I mean, I'm.

[B]

DNA methylation. Yeah.

[A]

Can you just apply it once and you're like.

[C]

Because it's.

[A]

It like, do you got to keep it? Like, what's the deal here? Okay, go ahead, Batten.

[C]

Yeah. So fair number of the authors were from Beersdorf ag, so suggests maybe some commercial interest going on.

[B]

It was are in people for those of you.

[A]

You certain. Aquaphore.

[B]

Yeah.

[C]

This was a two part study. So the first part of the study looked at epigenetic changes to see if those changes were preserved across different ethnicities. And then the authors looked at the effects on the skin of a natural epigenetic inhibitor, dihydromyrocetin. So the first part of the study was just to show that the method that the authors wanted to use to test the effect of their topical cream was valid. And I suppose it was. I couldn't really explain what the hell the first part of the paper was about other than to say they validated their measurement tool that they used in the second part of the study. That's all you need to know. Second part of the study was taking a serum that contained dihydromyr setin and having 60 volunteers apply it twice a day to the face and neck along with an SPF 50 plus sunscreen. Different measurements were performed. The epigenetic tape stripping clock showed a mean reduced epigenetic age of two years, which that's like for eight weeks. I think they. They did that. You. You're. Yeah. And 40% of patients showing a reduction of more than five years on the. That eight week, twice a day. A bunch of other measures, both objective and subjective. It's complicated paper for what might be some silly serum we all add to our skincare regimens. But the takeaway is that the serum seemed to improve a lot of stuff. The hypomethylating activity interested me, you know. What sort of things did they measure? Let's see, you know, periorbital wrinkles, improved skin surface roughness, improved dermal density up 10.4%. Expert grading showed better firmness, elasticity, texture, radiance, and even neck wrinkles. They have some clinical photos. I gotta be honest, I don't know how these cosmetic dermatologists do it. Like, I don't see a damn difference,

[B]

but whatever looks like mildly better.

[C]

You know, it just.

[A]

I.

[C]

If the patient came in and was like, am I better? I'd be like, I've noticed. But I think the cosmetic dermatologists are like, oh, My gosh, you are glowing. I can barely see your wrinkles. Like, I just couldn't do that to the patient. It's a neat mechanism of action, right? It's, it's specifically looking at that, you know, methylation being a part of what we see with epigenetic changes and having a drug that specifically targets that, that, that, that ingredient dihydromyro setin falls under like the bioflavonoid sort of family.

[A]

Oh, I. So, so I knew I recognized it from somewhere. It is from the Japanese raisin tree and it. There is some belief that it blocks. Speeds up alcohol metabolism. It helps with hangovers.

[B]

It's the anti hangover supplement. I've heard you can buy it on Amazon even as a pill. I'm. You know what? I. Because like, okay, so here's the thing. I actually went out to like buyers DORF in Hamburg and I like saw their, all their data. I actually have that stuff sitting. I'm like too lazy to turn my age back two years by like to put a cream on my face twice a day. But I haven't. And now I want to go back. I'll go back and use it, but I have it sitting in my drawer because they like gave some to me. It's not available in the US yet because the regulatory oversight here is greater than it is in Europe. So I think it's either available or soon to be available there. So there is all that. But I kept wondering like, you know, the real reason why I have it as I was like, couldn't I just take this as a pill then and get it systemically and then like, not just, you know, demethylate the epigenetic changes in my skin, but like anywhere, right? So like, I mean, I could maybe get myself to put this on my face twice a day, but like, I'm not going to put it on my body twice a day. But then all my skin could look better. I've also been too lazy to take the pillow to see if that is true. But that was my big question. Why couldn't you just take this orally? It's a cheap supplement.

[C]

You're ready to go. When the good data comes out, you'll be way ahead.

[B]

I'll be ready. I'll be stockpiled.

[C]

Yeah, so it'll be in your survival trailer that's buried in your backyard.

[B]

Exactly.

[A]

Well, now there, there is date. So cancer cells are also hypomethylated. Now it's, I think it's believed that, that the hypomethylation Is a marker of cancer cel not a cause of cancer cellness. But Ferris, you could look younger at the cost of increasing your risk of skin cancer.

[B]

Possible. Maybe if I'm just lazy enough I'll just take a little bit of it and I'll get the good effect. But not too fair and hypomethylate. But yeah, I'd love to see the study done with oral, you know, dihydromyrcitin too.

[A]

Yeah.

[B]

Sorry to the people at Usrin who invested millions of dollars in this and I've given away my hack will be the oral reflumelast of anti aging.

[A]

Oral flumelast will make you smarter too.

[B]

Exactly.

[A]

All right, let's. Let's move on to my last ones. So first one was a meta analysis of azithromycin for acne. And basically the takeaway is we've got really good data now that azithromycin is at least as safe as doxy. It's way safer than doxy. Sorry, way safer than doxy. Way better tolerated and just as effective like the. And part of the benefit here. Right. And I'm not a big antibiotics for acne person. I'm like put everybody on Accutane. But if I'm going to use an antibiotic for acne at this point it's going to be azithromycin. It's cheaper and there's less concern about resistance. Right. So if we keep using doxy and minnow, we're going to start to eventually we're going to start to see staff community acquired staff stop responding to doxy and minnow. Azithromycin stopped working for staff forever ago. So if we're going to use something like this makes a lot of sense to me. The regimens that are out there, 500 milligrams three times a week. But there was a more recent article that just looked at 500 milligrams once a week. So like just literally like once a week you take a dose of azithromycin and it was just as effective as doxy 100 milligrams once a day. I haven't seen any studies comparing it to doxy 200 milligrams a day. But doxy 100 milligrams a day. Is ithromycin just as good?

[B]

500 milligrams once a week.

[A]

Once a week, just as good as doxy. Right.

[B]

What's the downside? Besides the dreaded Z pack resistance there.

[A]

There really isn't like there's no the gi up GI side because I, you know, I, I think of azithromycin as causing like diarrhea kind of stuff to some extent. But the GI side effects were much lower. The photosensitivity was much like it was much better tolerated and just as effective.

[B]

500 milligrams once a week. All right, I'm start, I'm switching everybody.

[A]

Starting tomorrow it'd be now there's only one study looking at that dosing. Most of the studies were 503 times a week. What I'm probably going to be doing is 500 milligrams for like three days in a row and then 500 once

[B]

a week after that trying based on no study. Just sort of a gestalt.

[A]

Just a gestalt.

[B]

Okay. Just wanted to make sure I wasn't missing a study there.

[C]

But yeah, so that's funny because I swear just today this headline came across about the European, like a consensus acne update statement coming out of the Europeans published in the Journal of the European. And they actually kind of discourage the azithromycin. The guideline states should not be used routinely.

[A]

Why?

[C]

Insufficient evidence of efficacy, negative benefit, risk balance, mainly due to concerns over promoting antimicrobial resistance. Which I was surprised because I'm right.

[A]

I just think, yeah, it already doesn't work for anything. What, so they, they are pro doxy and minnow?

[C]

Yeah, pro that whole tetracycline. What's that other one? Limacycline. Yeah, they're pro those and discourage the use of either azithromycin, which I was surprised. I always use azithromycin for carp. No, I always read like nano doxy azithromycin. 250 every other day for eight weeks. Absolutely. Wipes it out, way better tolerated. They don't have to take it as frequently. So yeah, I, I, I, it's just a nicer drug to give. I, you do get more drug interactions. Okay, so if they're on lots of meds, I mean, young kids, acne, that's usually not a problem. But that is one thing where azithromycin interacts with a lot.

[A]

And that's okay.

[C]

Probably the only drawback I use, I

[A]

use it for perioral derm and rosacea at, at times again instead of doxy or minnow. My favorite rosacea treatment though is the combination oral ivermectin with oral metronidazole. I think that is by far the most effective thing for papulo pustular rosacea. It's like miraculous. And it's got a pretty good study showing that it's, it is the most effective thing you can do to get rid of Demodex is the big take with it. I, and I'm a big believer that Demodex is the big problem with rosacea, which not everybody agrees with me on that, but I'm, I, I'm with you.

[B]

I think it's a big driver.

[A]

I'm sticking with it. All right. And then my last one after that was a perioral dermatitis article and it was just interesting. So this was another trinetic study, so, you know, questionable how accurate it is, but this one seemed pretty well done. It was basically looking at kids who get inhaled steroids. So either NAS nose spray or for asthma and they have a three times increased risk of getting perioral dermatitis compared to kids who get non steroid nose sprays and non steroid asthma inhalers.

[B]

So know that. Didn't we kind of have that sense?

[A]

Yeah, I think, yes. I've always said that, that like, I think that it's a thing in adults, like women who get peroderm who are like not using topical steroids on their face. I'm always like, oh, we need to ask them if they're using inhaled steroids at all. But I don't know that I've seen data for it. It's been more of a like, yeah, that makes seems, seems obvious. Falls into the category of seems obvious. But now, now we've got data to back it up. And I said if you're, but if your kid needs the inhaled steroid, you can basically do the inhaler and then like 30 seconds later, like wash their face and that because most of the exposure happens literally right after the dose, whenever they're kind of breathing it in and out on their face. So if you need to use it and you're worried about this or your kid gets it, just wash their face like 30 seconds after they do the

[B]

inhaler or do those clindamycin wipes. Wipe it down.

[A]

That probably would work as well. That's not bad. That's not bad. It would get it off of there. Okay. All right, that's it for this week. You know, good, good mix of practical stuff and challenging stuff. Fair is bringing the real medicine in, making us talk about ctcl. I like it. And so I want to thank everybody for joining us this week. We hope you learned a few things. We hope you laughed once or twice. Mostly though, we're hoping you're planning to join us again next week. And until then, I'm Matt Zyrus.

[C]

I'm Tim Patton.

[B]

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