The Best Central Centrifugal Scarring Alopecia Discussion You've Ever Heard

Welcome to season two of Derms on Drugs, a video podcast brought to you by scholars and medicine, the best educational platform of dermatology and provided a no-cussed medical providers. Derms on Drugs is where cutting edge derm meets hitter miscomedy. I'm Matt Zyres from Dr. dermatology in each week. I'm joined by my 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 the cutting edge of derm and you actually have some fun listening. New episode of Drop Every Friday on Scholars and Medicine, Apple Podcasts, Spotify and other major podcasts, platforms. In a reminder, there is a video component to the podcast that has to keep figures and tables from the articles we talk about. So we are so excited to have a special guest this week. We've got Dr. Agu from, I believe John Hopkins, although I probably should have confirmed that before we started the podcast. And we are going to be talking about CCCA, which is something that we all see all the time. It is a really difficult thing to manage. And Dr. Agu has done some credibly interesting work that is super clinically relevant. So so excited to have you on Dr. Agu. Thank you so much for having me. You already scored one point because he said John's Hopkins and not John Hopkins. Okay, that's pretty good. That's pretty good. I did interview at Hopkins for my pre-lim year way, way back in the day. But I didn't get into Hopkins Durham. So I didn't didn't go there. But all right, let's let's get into we're going to start. We're going to start with an article from Dr. Patton. Dr. Patton, and this is I believe one of Dr. Agu's articles. Dr. Patton, why don't you go ahead and get us started. Yeah. So my deep dive paper was titled using disease symptomatology to guide treatment and patients with central centrifugal, sick attritional alopecia introduction of C cat scoring tool by cadre at all. Dr. Agu was a senior author. And this was in the February 2025 edition of skin appendage disorders. What is the C cat? It's the CCCA clinical assessment tool. And it's pretty straightforward tool to you. Just just by the way, that is a very sad journal. I hear it again. And the end is orders. SAD. All right, go ahead, Patton. Sorry. That was the level of comedy that you can expect for the rest of the show. That's a bit of a comedy part. Yeah. That's a big part. Yeah. Figure one outlines of the scoring system. You evaluate patients based on disease progression, pain, pruridous, erythema, scalp resistance. The scalp resistance can only be done if you perform injections at the visit. So if you don't do any injections, you have to leave the score out. So disease progression is either zero or two. Initial visit always gets a two. And the rest of the symptoms are graded on a zero or one or two scale. So the high score is either a 10 or an eight. If you don't do the injection, you can't do the resistance. So it can only be an eight. I will confess, I don't think I've ever appreciated differing scalp resistance to attack injections. I think I treat a fair amount of CCCA, at least for a white boy. And I've never appreciated a difference between patients or in the same patient on different visits and how hard or easy it is to inject attack. That is definitely something I'm going to keep in the back of my mind when I when I'm treating these patients now. The authors applied the scale retrospectively to 82 patients with CCCA over a period of one year. Here's my first question here. So when you're doing this score, if you don't inject on a given day, say they don't want an injection today or for whatever reason, do you change the way that you interpret the scores? That's a great question. So it's not meant to be used like a salt score where you add up all the parts and come up with a final score because the goal is to get to zero, right? So have no symptoms. And so really what we do from visit to visit is we're looking to see if you have any activity. Now, if we don't do the injections, we just have less information. So we can't tell you, okay, you got a perfect score because we just don't know how much resistance we see in your scalp. But if you still have itching, then you're still active. And the idea behind this score is twofold. So one, can we now that we have all these options on the table, can we use your disease symptoms to go to guide which treatment we use? And two, do you really have to get injections forever and ever and ever until the end of time when in every other form of hair loss, we generally say, look, like you look good, we don't have to do anything. You know what, let's start peeling away your anti-inflammatories, your immunosuppressant CCCA is kind of like the one disease where we're like, well, because it's never really angry, we just keep going. Right. And so this is way to peel patients off of treatment. So we kind of look at it differently than we look at other disease activity skills. And we're like, how high can it go? Because if you're this high, then we can put you on to Pilyamab. Or if you're this high, then you can get, you know, an anti-IL17 with CCCA, we're like, how low can you go? So I'm gonna treat you, but at some point we'd like to know if we could just give you, if we could step away because you probably can for most patients as long as you're playing close enough detail to their symptoms. So the initial question is just zero or not zero. And if it's not zero, you're doing something. And if it's zero, you're probably, if they're not, you're keeping using their topicals or their systemics or whatever, probably. Okay. So that's why at the initial visit, you get a two. If this is the first time you've been assessed by dermatologist for CCCA, well, then you're worse than your baseline. And we're gonna treat. And we want all zeros for three consecutive visits. So that's about 12 months. And then we start to space out your treatments. And we start to pull off some things. Okay. How easy, how coachable are, if you're working with residents, for instance, are they in judging that resistance? Like do you question? Yeah. All of the almost everything on the scale is somewhat subjective, but that's the most subjective. Now I will tell you, CCCA is really the only condition that I've experienced a bent needle with injections. I mean, truly, like, we're out to toss the needle. And I'm like, we just can't get into your scalp. Okay. It's that I brought it. And that is just like, it just is what it is, right? Like if you're bending a needle, so that's what we give a score to that high scores. If you're really like using a ton of force and you're bending your needle, you need to toss that to two. And over time, my residents are like, okay, and you have to start from, I treat alopecia, I'm giving injections to non-scarred scalp all the time. I know that it should go in fairly easily. And what you have to do is you have to insert the needle before you push, right? Because if you're just like, then you don't get to assess, but when you're trying to assess the resistance and you're just starting to notice the force that it requires to get the needle in, you start to notice it really quickly. And so I'll let my residents start to inject and they'll say, Dr. August, it's hard right here. And I'll inject as well. And I'm like, yeah, you're right. Like that's a one. See, there's, I bet there's huge inter-observer variability patterns. Got such weak little girl hands. When I say little girl, I'm talking like a three year old, not like women have weaker hands in men, but like little, probably to him, it's probably, I have a two handed syringe device because it's really difficult. So it's okay, right? If there's inter-rater variability there, I think the biggest thing that comes from this scale, when you're dealing with scarring alopecia, that hardly ever re-grows. When patients are coming in and seeing you religiously, they need to know that it's worth it, right? And for germs, you know, like when there's red, we're like, it looks so much better and the patient has all this P.I. age and they're like, what? And like, not knowing you understand, like, right? And with the scale, I mean, you, you know, now we implement it for every CCCA patient. You really see the patient. You're like, wow, you're getting better. You're itching has decreased your scalp pain. And then you see the patients who aren't responding to therapies now. And you can really like quantify it and say, gosh, you've had this same itch score. You have the same erythema score for three visits. Like, we need to add in something else. But patients, when you say, hey, your scores are going down, they're like, that's awesome, right? And so so much of it is just trying to turn a visit that is mostly qualitative, a little bit quantitative so you can give patients just better feedback that this is, this treatment is working because the other thing we did in that paper is we looked at standard therapies. We're like, okay, well, we're doing this doxie and chlobetis. All did they change? And those work, right? Standard therapy. Let's let's go back to our capat and hear for a second. So Dr. Pat and tell us, yeah, keep going about the article. Uh, yes. So let's see, uh, table one, um, oh, wait, no. So they, they followed these patients and over the course of treatment, most patients, 88% had an improvement in the C cat score, 12% of the patients either had no change or worsening in the C cat score. So, you know, some numbers you could say like look to your patient. Most patients have some improvement. I think you have to coach them a lot on that. It seems to me like, hair loss improvement means my hair is coming back and that's not really the point of this scale. Right? You're not going to get hair growth. So, you know, coaching patients at the beginning, like, here's what our goal is, here's where we expect to see improvement. Here's where we're probably not going to see improvement. I really like Table 1 because it really just broke down. What percentage of patients are given what particular therapies? Because like for me, I'll do tack like five megs per mil and I do oral monocetyl if they don't want to take a pill then I throw in topical monocetyl. Maybe a topical steroid. I kind of stop doing doxia. I've never done that form and except for one time because the resident suggested it. I think I'm probably going to do that more routinely. But if you look at the numbers, so tack 96% of patients receive dial tack. So, you know, I'm getting not to most my patients, I think I'm in line there. 96 also either topical or oral monocetyl. 56 got topical, 40% got oral. 68% of patients were treated with topical clavitas all. And then there were lower percentages of patients treated with metformin or doxia. I was kind of surprised at doxia, especially given the table you have later where you're like that central box. This is my first treatment, tack, topical steroids and doxia. Doxia was only given to like 17% of patients, at least when you looked at responders. Was that a low number when you were going through that? It is more number. But I will tell you, implementing this disease activity scale has led me to doing doxia more. Right? Because what we did with those recommendations, that was based off of literature data. Doxia is a dual anti-inflammatory and anti-fibrotic treatment. So, what we're doing is we're kind of just looking at cases in our institution and saying, let's see how people were treated. But when you start to understand like where the activity occurs, right, the path of physiology, now when I do this scale and I see perifilicular hyperpigmentation, which is a one, perifilicular erythema is a two because CCCA is posse inflammatory. So, if you're seeing any bit of erythema, like that's a lot, right? And now when I see persistently elevated inflammation, I'm like, oh, you have a one-year doxia and it works great, right? So, I feel like if I were to rerun this, I would have a higher proportion and that and that spiel that you mentioned critical. I think anyone who runs an alopecia clinic, you have to, you see scarring alopecia, you have to have your spiel down, right? And the spiel is, look, this is scarring. We don't measure success by hair regrowth. We measure success by disease stability, but then also we measure success by decreased inflammation. And so, you're actually getting better and that's why we are giving you oral doxia cyclin. That way, they're not like, I took this, but my hair looks the same. You see, no, that you actually had a little bit of inflammation that was visible and that's now gone away. And so, I think it makes the visit easier because patients don't have to harp on hair regrowth as the only like measure of success, which they did like 15, 20 years ago, patients with doctor shop and they're like, I saw this Durham, they were great, but my hair looked the same. And it's like, actually, that's, that's the goal, right? And if you don't explain that to them up front, they leave very dissatisfied. So, if a patient comes in and they don't have any, let's say on the puritis and erythema and pain, I guess you haven't done injections yet, so you couldn't grade that. Everything's a zero. I mean, you would give them a two because it's their first visit there. But with those patients without the symptoms, without the puritis, erythema, do you kind of say like we're at the end stage and I'm sorry, it's scarring, but I don't know that there's anything we can do at this point that we've proven. I think one of the things that's important to patients is like being honest with them when you feel like there's not a lot that's going to change your quality of life. So, let's say someone has like 60, 70% scalp involvement in there in a wig. For those patients, I often choose not to treat. I think that scalp injections are just far too painful and that even when you look at a patient and tell them this is not meant to regrow hair, they think well maybe there's just a chance. But if reliably you cannot get them out of a wig, those patients, I say as of 2025, we just don't have treatments that are going to be able to reliably reverse the extent of disease that you have. And I think it's just important to say that it's a hard conversation. There are very few tough conversations in Durham, but this is one of them and we just have to have them. I think if I have someone who has very limited disease and maybe it's their first time seeing me, but they've seen a dermatologist for years and they're like, look, I was seeing so-and-so 15 years ago, I stopped going because I felt like the treatments weren't working. I'm coming to you for a second opinion to see if there's anything new, but it hasn't changed. I won't give them a two. I give them a zero. If they're reporting that it is, I can tell you definitively, I've gotten this diagnosis before, I was getting treatment before and it hasn't changed. I'll give them a zero. But if they came from their bedroom and they're like, God, I really should see a dermatologist. I give them a two. If they've never been assessed by dermatologists before, never received treatment, then they are by definition worse in their baseline. I want them to treat for at least 12 months. If they have mild to moderate scalp involvement, again, if they have widespread involvement, I just talk to them about like, you know, we try to see if we can write a letter for a week, but I try to be upfront with them and let them know that I don't want them to torture themselves to keep things the same. So we had reviewed a paper, gosh, maybe a couple months ago that was at a Mount Sinai retrospective study of Lodos, Doxy Cycling. And their like take home message was, this is important to do early on in the course of CCCA. And so, you know, one would you, it sounds like you would probably agree with that. And then do I guess like, but yeah. The other message was we should be using a low dose that we don't use 100 B.I.G. That was my other question is, you agreed to have a doxy or do you think here's the, you know, here's the dose that I would do. I've transitioned to Lodos doxy for scarring alopecia as well, just based on that data. And the patients that I put on Lodos doxy are doing well. Again, I use the the C cat to guide me. So if they don't have any inflammation, like let's say someone comes in there early and they don't have any inflammation, they don't have any itch, maybe they just have scalp resistance and they're insulin resistant. Then maybe I'll start with topical metformin, right? I want us to do doxy. We kind of play around with things, right? But if I feel like doxy is a great option for them, then I will do Lodos. If this is someone who's responded to 100 milliliters, maybe in the past. Wait, what's what's what what does Lodos doxy mean to you is that 51 today, 20 B.I.D. What's I've started at 50 B.I.D. Okay. Right? I've started at 50 B.I.D. But I do think you can go lower than that. But you're 50 Q.D. Why not 50 Q.D. Well, immediate release has a short half life, right? And so that's the thing is I think if you're trying to get full day coverage, just doing it once a day is tough, extended release, it's just would be ideal, but it's very difficult to get covered. Do you ever do the 20 because you can get the 20 cheap. Do you ever do 20 B.I.D. instead of 50 B.I.D.? I do from my rosacea patients for my scar. I have not gone down to 20. I should, right? These are things that it's like, you know, I could probably go down even lower. But when I do it, these are really symptomatic patients. I'm like, let's do 50 and see if it works. Okay. You're from, you may catch me. I'm like, I'm down to 20. Yeah. Yeah. Fair. Okay. Pat, what else you got from this paper? That was pretty much it. The last figure that just, it's that nice algorithm center box. And then like Dr. Agu said, maybe it's a patient with a high insulin resistance. And so you start thinking about metformin in those patients. If they're itchy, adding a systemic anti-histamine, just kind of a really nice like, you know, easy how I'm going to approach my CCCA patients. I thought it was a really helpful article. Thank you. My guide was helpful. I mean, you know, we do we we talked a little bit about how dermis so nice because there aren't that many algorithms. But I think scarring albisha is so hard. I just think it's such a hard visit, right? It's really emotional. We don't have great restorative treatments. And so I think it's just nice to get a little bit of a guidance because there are these options. It's kind of like, well, where do I start? And then that's really the take home of the paper. If you start really asking patients just systematically, how many times a week are you itching? How many times a week do you feel pain in the central scalp? And just starting to grade them and then just saying, okay, well, this person's good except they're really itching. I'm going to try really high dosatyrzine and see if we can knock that out. What's really high dose means means mean to you. Yeah, like twice daily zirtec instead of or satirzine instead of once a day. You can say zirtecline here where allowed to do brand. So, so twice daily zirtec is what I'll do. Okay, and it works. It's just compliance is tough, right? For these patients who don't have like allergic right now it is right those patients are taking it every day they know big deal. It works very well for that. I'll try doxycycline it can be tough and there is a very rare subtype of CCCA called like form thrust CCCA where patients will just instead of like smooth scalp they'll just have like a tough to hear that keeps breaking right in the middle those patients tend to be very symptomatic. They tend to be more symptomatic than your average CCCA patients and those patients you got to try you got to cycle through all types of things to to really get that itching to calm down but once you do then that hair starts to grow back. Now one one other question I have for you from the from this article in the algorithm you talk about Placquinoe, Hydrocycloroquine but it's not in the table which made me think that you don't use it all that much. Wow. Yeah. Never use it. Okay. I put that in there for buddies of mine like use it. I don't I don't need to because look doxycycline again the data is there right we a lot of that literature on its anti-fibotic effects and it down regulates CDF beta that's from the acne literature it can remodel it can do collagen remodeling so like I need a little bit of like I have to understand the pathophysal a little bit before I just like yep. The patient's asked her like well what's this doing and I'm like yeah yeah you heard some T cell needed inflammation which we don't know for sure as part of CCCA at all but you know so that's not for me okay but I'm glad I I'm glad I asked because I was like I don't use that actually chloroquine in these people in the middle of me. I know that that was very deductive you're like what you did it's on the table so like yeah I'm not there we go all right let's let's move on Dr. Ferris what do you got? All right so I have actually two papers they're both case series from JAD case reports and so they both are talking about using topical metformin for CCCCA just too many season there okay so the first one is adjuvant use of topical metformin with standard therapies and recalcitrant central centrifugal sycotritional alopecia a case series this is from Williams at all from Georgetown and then the second one is also out of Hopkins and this is Dr. Aguiz Piper it's a Royay et al hair regrowth and two so this is actually I was like thinking this is interesting you actually say hair regrowth and two patients with recalcitrant CCCA after use of topical metformin so you know this is really getting at the fact that like we're talking a lot about you know inflammation and I think you know my go-to is usually like how do I stop the inflammation is it doxie is it steroids is it topical blah blah blah but like fibrosis is really it's like such a prominent aspect of this so yeah so in the first one Williams at all three cases all had histologically confirmed CCCA and they were all treated with doxie topical steroids one with tack relimus and then all with topical menoxidil with inadequate response and then they all were given compounded 10% metformin at night and then they said that they all showed visible hair regrowth in six to ten months and then in your paper crystal that was two a case of two women who basically had had like years of unsuccessful treatment with eye-al-tack topical steroids one patient viviscal which reminds me I'm going to ask you about supplements but then they both got 10% metformin and so you know and both and then both of your patients also improved so you know it was interesting because I think that like the hair regrowth thing is a little subjective looking you know you look at the photos and it's not we don't have a salt score we don't have a great way to do it it's like and I like I was like wow you're really getting regrowth because I'm like stabilization that's my goal um I would say they both lean in both papers the cases were kind of maybe modest regrowth but definitely not worsening um I don't know what do you think when you yeah yeah so I think most hair specialists who over time have come to accept that there are going to be a subset of patients with scarring alopecia who if they're really lucky do get regrowth ccc a I think of the like big three let's call the big three ccc a like implant up high lyrus and frontal fur bursting alopecia right of the big three ccc a is probably most likely to grow ff a's probably second and then lpp's really tough okay lp will like really like just cinch like bird it's like it's the scalp has been burned okay but regrowth is difficult to achieve in any form of scarring alopecia and when you talk to patients they say well what's the chance I'm gonna get my hair back I tell them there no chance that's visit one we can I tell them 10 percent that's all they hear right and then when when I'm like oh my god your scores are going down you've less inflammation they're like yeah but what about that regrowth you promised wise me look this is a scarring alopecia we can't reverse the damage it's been done but we can at least make sure that the next five years look better than the last five years okay now we series that first one I published in 2018 and we had previously written a microarray we had done a microarray study where we just tried to define ccc a like what is ccc a what does it look like and I wanted to see if it looked like diseases of abnormal scarring right so these are things like keyloids focal segmental lamerialiscal roses systemic sclerosis where fibrosis outpaces inflammation right you get a little bit of inflammation but anti-inflammatories aren't super helpful because really the big issues fibrosis right and ccc had a lot of disease overlap with these classes of diseases and metformin has been used in many of them and been shown to have anti-fibratic effects so it was like okay well let's compound it put it on the scalp these are patients they didn't fail treatment they were on standard treatment they weren't inflamed but they were like please please please can I regrow my hair i was like well we can try this and they got better now one one of those patients used metformin for about 12 months did better and once she stopped she lost that progress last year we published an RNA we published a sequencing study on the use of oral meth right we're gonna get to that one right and so because that's the thing with case reports right is that like you're like okay like we think it looks better but if the general takeaway is like should I promise regarance to patients at ccc a no are there enough patients that improve with metformin that it should be considered a reliable option yes especially because it like has almost no side effects when we talk about the paper the other paper i'll talk to you about some more research that we're doing but there is a way to I think identify who are going to be the best candidates for topical metformin versus all the other adjuncts that we can do as well well that's great that'll be interesting yeah well hang on i got it you know me i got to come up with like the the resident take home what's like the nugget of basic science you can take out of here or you know noteworthy facts so i thought you know important to know there is an increased incidence of uterine fibroids among women with ccc a so those that's fibropaliferative so that all fits mechanistically like you said that we want to know metformin has been shown to be helpful in other fibiotic things like pulmonary fibrosis and then the you know the gene to know or the the enzyme so metformin activates AMP car AMPK which is a denocene monofosvate activated protein kinase and we know that that's actually under expressed in about a third of patients with ccc a so mechanistically it makes sense the science makes sense i know we're going to get to hear a ton more about it but i thought that was really good stuff and now we can hear about it with oral metformin you know yeah so let's just so the oral metformin paper this i'm a big metformin fan got interested in it back whenever the first information was coming out about it might make people live longer right metformin's got reasonable data for acne what's that so longevity medicine right longevity medicine's got good data for HS good data for acne okay data for i so when your article came out i was like oh okay so now we should be putting everybody on so my my biggest question so this was a 12 patient series it was like eight of them it did significantly better on the oral metformin when do you so at this point is essentially everybody that you see with ccc a on metformin of some form and if so or whether or not how do you pick between topical and oral do you think what works better than the other like what's the how do you differentiate very question probably everybody could be on top of old metformin because you're good and i compounded with clovate is all okay so that's at this point what i do in the case series it was just the metformin but i compound with clovate is all and i'm just like look you have both if i think Thank you. and primarily is an anti-fibrotic that does have anti-inflammatory activity. And a compound with a clubaid is also, sure. - Do you have a bespoke compounded pharmacy that does this or is there somewhere that our listeners can be like, 'cause I send my 10% topical metformin to Medrock, which is like 35, 40 bucks, is there somewhere that does metformin, or do you just do that and then have them pour some clubaid is all in? Or what do you do? - No, I send it to custom scripts in Florida. So you can call them, they pick up the phone every time, you can send it to them, they're making it for hundreds of patients, I can guarantee that. So I send them a lot of my hair compounds. - And what's a cost? About $35. - Oh, so the clubaid is all metformin combo is still only about 35 bucks? - Yes. - Are they, are you sure you're not using Emma since you're an academic practitioner, probably an epic or something? So yeah, I guess the other thing is, I don't know if they're an Emma or not. Well, that's a great question 'cause I kind of just type it out and send it to them and they just get it electronically. - Okay. - That's a great question, but I know a lot of people who use their pharmacy and they're very straightforward. So that's where I send my compounds to. Now, how do I decide who, so when we did that case series, we did 12 patients, four of them, we did pre and post biopsies for both RNA sequencing. And with the pre and post biopsies, the minimum time between sampling was six weeks, but to assess clinical regrowth, we waited six months. Okay, because like clinical regrowth takes time, but from a molecular standpoint, you can start to see those changes quickly. And when we had defined CCCA in microarray study back in 2017, we were like, these are all the pathways that are up and these are all the ones that are down. And in these patients, it's all the same gene ontology program. So you're just like, oh, well, let's see the pathways that are up and the pathways that are down and it was literally all of them flipped. It was crazy. Low dose metformin, 500 milligrams, one today literally, it just flipped everything. The fibronic processes went down. Hair cycling went up. We saw pathways implicated and wound associated hair regrowth. So metformin was really doing what it was supposed to do. Now, and at that time, I was putting patients on it, and I'm doing this study because I don't know if it works. - Yeah. - Right? That came out of giving talks about topical metformin and at the end of every talk, people will say, what about oral? And they say, I don't know. I've never tried it. I'm a dermatologist. I like creams. And then finally, I was like, you know what? I'll put people on oral. I don't know if it's gonna work. And it did. Now, we'll be publishing a paper soon. It seems to work better in patients with insulin resistance than in patients with insulin resistance. Right? And that sounds intuitive, but it's a little bit of a bummer too. Like I would love it because it's so safe. It is a longevity medication. Decreases your risk of dementia, getting cancer, all these great things. But for CCCA, it probably is not gonna work that well in patients who don't have insulin resistance. I do wanna share if there are residents listening. This should be on the board, by the way. What I'm about to say, whoever's in from the ABD, I hope you're listening to. So I think in medicine, when we talk about insulin resistance, 'cause this is gonna be relevance for psoriasis, hydrodynamitis, acanthosis, nigricans, CCCA, plethora of other diseases, dermatologists, we in the entire house of medicine, we are uniquely positioned to identify patients with hyperinsulinemia. No other specialty is gonna see it. And what ends up happening is that when people think about insulin resistance, they think, oh, high glucose levels, I'm gonna check your A1C and I'm gonna see if it's abnormal. If it is, then I'm gonna do whatever. But the problem is when you have young patients under 40, they are very, very efficient at producing insulin, like their pancreas, it's just like every organ's more efficient. They're pumping out a ton of insulin. So if you have two patients, you have a glucose of 100 every day. Over three months, those A1Cs are gonna be identical. But if one person needs an insulin of 10 to maintain that glucose, and the other person needs an insulin of 50, we would all be like, oh, well, that person's more resistant to insulin. But all we do right now is check A1C. So that's why when we see these 20-year-olds with acanthosis nigric hands, and we're like, (clears throat) well, this is associated with prediabetes. And they're like, stop right there. My A1Cs 5.3, I don't have prediabetes. And we're like, gosh, why do we always say that and their A1Cs are normal? It's because they're 20. And if you check their insulin levels, they are through the roof. And an insulin that's driving that epidermal thickening and dispigmentation, it's not glucose. And so we check a HOMA IR. So we check an A1C and we check a HOMA IR. A HOMA IR is just a calculation that puts an erasio between of your, of your instant, you're fasting insulin to your fasting glucose. These are $10 tests, right? They're cheaper than a CBC. You get both values, you plug it into Google and it gives you a HOMA IR score. If it's greater than two, that's abnormal. So I send these patients, I've seen HS patients, they have a fasting insulin of 100. And even when I try to put in the calculation, I get an error of some. I'm sending them to Indicrant and they're like, what is going on in Durham? How are you finding all of these people with elevated insulin? Because they don't make it to Indicrant until they're 40, their pancreas tires out and their A1Cs now 12. - So wait, so you just literally you order insulin level and glucose level. - You can plug in. - Tell the patient, you gotta be fasting, go first thing in the morning. And then you get those two back and just Google, what's it called a HOMA? - A HOMA, - How do you say? - Dash IR. - What's a HOMA stand for? - HOMA is static of metabolic, I can't remember the A, insulin resistance. So this is the thing, so I tell this to my patients, I'm prediabetic, I'm a very slim, prediabetic. I've checked my own HOMA, I make almost no insulin. And I'll have patients who have an A1C that it's identical to mine or lower and they have skin tags and acent those is Niagara cans and boils. And we're getting the same like counseling and it makes no sense, right? And they're like, well, your A1C's only 5.7 but those patients, their A1C's like 5.7, then it's 5.8, then it's 6.1, then it's 10. And it's because eventually when their insulin tires out and all of that goes away, they spiral into very uncontrolled type 2 diabetes very quickly and it's all an evolutionary advantage, right? If your body high levels insulin and you hold onto a ton of fat, in a period of famine, I'm dead, right? If you have evolved to hold onto fat, so that's why people have trouble losing weight. So that's why GLP ones are like magic, right? But Durham is the only specialty that's going to see hyper-insulinemia manifests. - All right, so let me see here. So what I hear you saying is, kind of at this point, you do a HOMA IR, if they are insulin resistant, you then do oral metformin. And I assume that means that if their HOMA IR is normal, you do topical metformin, or do you do not metformin at all? - Yes, I'll do topical metformin with clobatusol. - Okay. - And yeah, and that's it. And sometimes I'll do like clobatusol alone, but usually I'll put them together. - Okay, and I did, by the way, while we were, I looked it up in custom scripts, is in Emma. - Great. - So for all of our listeners, it's easy to send scripts there. And you might want to call them and set it up before you just to make sure some of this, you know, like custom scripts, pharmacy in somewhere in Florida, well-springs Florida, I think. So they are doing it. So you have people just use, clobatusol metformin, QHS, pretty much indefinitely. Well, until their scores hit zero, right? So because I think committing someone to indefinite treatment, especially because I do think CCC is the word. But yes, for the foreseeable future, for sure. - And so you have them, they gotta get to zero for like a year before, then you'll start tapered, weaning things off. - Yes. - And all right, let's. - So I hold on real quick. I, I, I, I, this home IR homeostatic model assessment of insulin resistance. And the, the ranges they give, I'm just curious if this is kind of your understanding of the home IR less than one, you're good, greater than three, that's your high risk. And then you kind of have between one and three, where it's like early insulin resistance, significant insulin resistance. Is it like anything above one, you start having that conversation or what happened? - Two, they can get a GLP one, right? So anything about, they can get a GLP one. But, but in practice, above three is really where you're gonna start to see issues. So like if someone's like a 2.5, I'm like, if you wanna just stick it through topical metform, and that's fine, right? Because it's equivalent of probably having an A1C of like 5.7 and 5.8, right? It's not like, you know, have to run. to do something, but I would encourage you to try it for all your ac anthosis and aggregate patients. They're almost always going to have normal A1Cs because they're young and it's their insulin. That's also, you know, I asked, when I give lectures, I say, do we ever wonder why we call it a disease of pre-diabetes and not a disease of diabetes? It's because their insulin levels are high because by the time you have diabetes, your insulin levels are coming down. Even if you have type 2, they're just not enough to control your glucose. So that's why we see it in young people with pre-diabetes. It just means that your insulin, your pumping out insulin efficiently enough to change your skin. So then would you anticipate, because I think we don't have enough sort of long term, you know, use of GLP1s, but would you anticipate that they will be associated with the lower incidence of CCCA? Great question. I think I haven't gotten that question before and I would love to believe yes, because now I'll get to my theory. I think I published this in chat, actually, Dr. Elson was very kind to let me just publish my thoughts. And I actually think that CCCA is a fibrotic pattern hair loss, okay? And one of the things about CCCA is we've tried to figure out why is it much more common in black women, right? And that's why hair practices were like the initial place to look, right? I think very reasonable. You're like, okay, well, this is the first thing. But, you know, Elise Olson years and years ago was just like, I think a lot of scarring alopecia might be fibrotic pattern, but like, you know, who knows? We published a study just a couple of years ago looking at ethnic variation in female pattern hair loss. And we were really trying to identify South Asian patients because these patients are definitely disproportionately impacted with pattern hair loss, right? And we saw that it was appearing 20 years sooner in South Asian patients. But the other thing that we found that was really interesting is that so black women and white women present with pattern hair loss similarly, by temporal recessions in most common areas, some people get part widening. But black women uniquely will get pattern hair loss in the vertex in isolation, right? And absence of other areas of involvement, so a primary vertex predominant pattern hair loss of the patients who had that 95% of them were black women. We had one white woman who had that. And so now pattern hair loss in the vertex responds more favorably to any treatment, oral minoxidil, propitian men. So it's a good area to have pattern hair loss. But that discrepancy alone can account for so much of the discrepancy we see in CCCA and black women compared to in other races. And so then it's like, well, then what would make someone develop scarring pattern hair loss or CCCA versus just regular pattern? And it could just be like metabolic disturbances, right? Because metabolic disturbances, hyperinsulinemia and hyperglycemia will increase fibrosis in organ tissues, right? That's why diabetes is terrible. Look what it does to your nerves. Look what it does to your kidneys, right? It just, this is how it damages that. Yeah. I thought a few years ago there was like some gene that they discovered that like everybody with CCCA had this mutation. Yeah. Yeah, you're talking about the PADI3 mutation. They found it in about a quarter to a third of patients and it was a heterozygous mutation that didn't stop protein. And that would be okay, but we already know of diseases where you get a complete knockout of the PADI3 and that's uncumble hair syndrome, right? Which is a pediatric genoderm that improves naturally with age. And so one of the things about PADI3, I think multiple things are true. One, we don't understand how like a partial mutation would only lead to scarring alopecia in older black women when a full mutation leads to nonscarring or reversible hair loss in predominantly non-black kids. So it might be a true, true unrelated. We also, with Dr. Roya, actually we did a scanning electron micrograph study where we took the hairs of patients and we were like, well, maybe some of these patients do have, you know, peeli trianguli at cannulaculai, right? Which is like the finding that you see in this process, a cumble hair syndrome. And out of 21 did, you know, one patient. So it's like, I think it exists, right? But like maybe there are a whole host of risk factors, but probably PADI3 is not enough to explain 100%. But maybe there are various risks that someone could be born with that would make it such that when they start to develop age-related hair thinning, which starts when women are in their late 20s, just like CCCA, right, that just sends them down a fibrotic pathway. And so maybe, you know, GLP1s and all these things, right, could help decrease the incidence of that. So that's my current theory. You have its paper. When I was trying to read up on this, I think that said that, you know, the theory was perhaps CCCA, and maybe it was data. CCCA is more associated with poverty than race and ethnicity. Was that your paper or was that somebody else who published that? That is such an interesting paper. That is an inversion of my paper. I actually published an FFA is associated with affluence and not race. So I'm in the DMV area where we have a lot of well to do black patients. So I'm happened to be in the one place, I think the best place in America to ask this question. And all of my patients with FFA for years have been educated professional women. And I see hair loss in people from all walks of life. I accept Medicaid and my FFA patients are always no matter what their race is. And so we finally did looked at the data. We pulled census data. And we looked and we, you know, we did logistic regressions. We controlled for so many variables and the best predictor, but such as being a woman, the best predictor of getting FFA was being in the highest income. There's like four different brackets in the census data. And rates completely fell out. There's nothing to do with race, all to do with affluence, which we don't need medicine. Well, I'm going to jump in and give you some now my unfounded theory on FFA. So here is what I believe in. And this goes completely with the affluence concept. What is unique about your frontal scalp, like right here? What is most unique about it? Environmentally, because we know FFA's got to be an environmental disease because it didn't exist in a meaningful way when we, when the three of us were residents. This gets this gets more exposure to chemicals than any other spot on your body. So everything you put on your face gets here, everything you put on your hair gets here. The rest of your face, the rest of your scalp only get half the exposure as your frontal scalp. I think we're barking up the wrong tree because we're looking for like one chemical. I think it is the cumulative, all of the chemicals you put on your face, all the chemicals you put on your scalp, they add up to like a toxic, we're going to kill those guys right there. It's possible. And certainly like with the affluence, like you have, you can afford the far more stuff. It was first described in Australia and I think we have to pay attention to that. The sunscreeny stuff. They're not in this in Korea, okay? And in, you know, the dorm research in Korea is huge, right? And so is the alopecia research community and there was, there are few papers where they published like the burden of alopecia, FFA is almost nonexistent there. And they've got lots of skincare products, right? So it's not just there. Yeah. So that's the thing, right? And so, and then when I was training too, when I'd see FFA, they'd bring in residents. Hey, come and take a look. We got some frontal far bursting alopecia. For the listeners, I've finished residency in 2015, okay? And during my training, we were still pulling in people. FFA is everywhere. Everywhere. Everywhere. Everywhere, right? It has already become, we used to, when I was training and when I first started we used to call, we would say, frontal far bursting alopecia is a subtype of like in Plano Pilaris. No. You see 10x FFA over L.P., right? It's totally environmental. I have my own theories. I do think, you know, I'm cutting it off right there because we're going to have you back on to talk about FFA. That's going to be a whole new episode because this is, yeah, we totally should. That would be great. Oh, we, there's more should. We're going to differentiate FFA and L.P.P. we got, yeah, we learned really. FFA, we're going to do all kinds of stuff. You are the, I don't want to say anything that's giving trouble to other people. This is so much fun. That's so much fun. That's so much fun. Oh, good, good. I'm hoping it's helpful. I'm just trying to give at least one clinical nugget, you know? Oh, you gave, you gave lots of them. That was fantastic. All right. Let's jump over to, I guess last, quite last thing here. So do we, do you talk to black women about hair care practices at all with CCCA or do you like, is that just unnecessary burden to be like? I think it's a great, I mean, that's a phenomenal question, right? Because when I was training, that was the counseling. Hotcoma LaPisha. Right. And now, if I mention it, it's in a different way, right? You're already dealing with one form of hair loss. Let's not add a second. Let's not add traction alopecia. Let's not add really bad breakage. Because I will tell you, with these patients with CCCA, you start treating them for two or three years, the CCCA will start to get better. And then the reason they're in a wig is because they have no hairline, and they've pulled it all out. You can camouflage hair loss in the middle. You can camouflage a decent amount of hair loss in the middle. You can't camouflage frontal alopecia. And so that's why I talk to them about hair care practice. I can't wait to have you come back on to talk about traction alopecia in front of my brosing alopecia. Oh, I forgot a lot to say. I told you. All right. Let's move on to what is generally everyone's favorite section of the podcast. Dr. Patton, you got any good trivia for us? Well, I think it's great trivia. It's black hair and entertainment. Oh. [LAUGHTER] We try and do-- Yeah. What was a-- yeah, pop culture, because a lot of times the scientific stuff we talk about, we don't know what we're talking about, but pop culture we're strong with. All right. Ready? This 2002 movie. We're also old. So I feel bad for all these young people that come on, because they're like, I wasn't born yet. This 2002 movie starred Ice Cube as Calvin Palmer, who inherits his father's business and looks to sell it to make some quick cash. Is it Friday? Next Friday? No. It has to do with hair. Like, I kept the thing-- Oh, oh, he's a barber. Oh, I got on. I can't-- Barbershop. Barbershop. Barbershop. Oh, that was the fun one. Oh, me and-- I don't watch enough movies, so I'm not going to get-- I knew. Yeah, barely there was sequel. I never saw it. I've seen clips of it, because there's some pretty fun grants that-- I saw it. --in some of the scenes. So yeah, pretty funny clips, never seen the whole thing. And it actually did well enough that there were one or two sequels, I think, too. Yeah. I wouldn't watch the sequels, though. What is the name of the 2009 documentary, produced by Chris Rock detailing many of the hair care practices of black women? Good hair. Good hair. That's tight. Nice job. I got it, all right. Never saw that either. Is that worth watching? Have you seen it? It was really good. I think it was good, because I think it was really a conversation started. But since 2009, hair-selling practices have changed so dramatically that it's already-- it would be obsolete. Like it would not be cool. Oh, wow. OK. Yeah. All right. One of the members-- And just because you and I have been doing our hair the same since 2009-- I don't know. 89. I can't-- I'm sure it might be in the hair every day. I moved my part over like a little bit. Maybe it was a good-- A comb over? We call that a cut. That's not moving apart. That's a comb over. Just a little while. OK, it's made a tomato, but I'm going to-- OK. All right. Number three, final question. One of the members of this famous female rap duo developed her iconic half-shaved hairstyle as a result of a burn that occurred from a hair styling mishap. Salt and pepper. Salt and pepper. Yeah. Salt and pepper. Nice job. That was iris. Oh, what's my-- Apparently, your sister just got her cosmologist license and applied like a perm or like a relaxer. And did it incorrectly burned off the side of her hair. And so she just kind of shaved it and then went with this look that a lot of people wound up imitating. Yeah. Pretty funny. That's cool. Good question. Push it. One of the greatest songs ever made. Oh, yeah. It really is. I'm sure. I remember that could be our new theme song. We'll take about that. All right, would Dr. Aguth thank you so much for coming on today. This was a fantastic, fantastic discussion. Really kind of appreciate your expertise and what you're doing out there in the world. And I want to thank all of our listeners for joining us this week. And we hope you learned a few things. We hope to laugh once or twice. And mostly we're open. You're planning to join us next week. Until then, I'm Matt Zyrus. I'm Tim Patton. And I'm Laura Ferris, and we are Derms on Drugs.