Practical Dermatology® partnered with Adam Friedman, MD for a new video series. He answered questions—some anonymous—about skincare, skin health, and more. You can watch the series online at PracticalDermatology.com/AskDrF or explore the pages ahead to learn from Dr. Friedman about skin cleansing and moisturizing, managing the microbiome, addressing hair loss, and more.

I’m confused by some topical product claims. Should I recommend products that say they are formulated with probiotics?

I really like the idea of symbiotics, meaning pre- and pro- and maybe even postbiotics.

Postbiotics refer to elements of a living organism—this could be dead or something that the organism makes—that can have a biological impact. A great example of that is the heat-killed bacteria V. filiformis. When it interacts with our local innate immune system in the skin, it can induce an immunoregulatory function, increasing T-regs and balancing the immune system.

I don’t think we should pick one or the other. I think we should be employing all of them, because they can work synergistically and have the greatest outcome.

We should push industry to further evaluate these different products, give us head-to-head data, so we can make an educated decision when we’re guiding patient choices whether it be oral probiotics or even topical probiotics.

We’re used to hearing about skincare products for eczema and acne but may not think so much about conditions like psoriasis. Any suggestions?



I think we’ve talked a lot about atopic dermatitis or even the eczemas in general with respect to barrier dysfunction, even mentioned acne and rosacea as diseases of dysbiosis. What I find so often, and it goes to the question that came in, is that many of our products are geared toward these three disease states in terms of formulations that are meant for acne-prone skin, sensitive skin of rosacea, or dry cracked skin of eczema. What about psoriasis? I feel like there’s almost a complete flip when it comes to the therapeutic armaments. We almost have too many treatments for psoriasis these days. The question isn’t do we have a biologic, but rather which biologic do we use?

Products formulated for psoriasis can be found over the counter. A lot of these are keratolytics given that with that chronic, persistent Th1 and Th17 inflammation, we get retention hyperkeratosis. We get this retained micaceous scale with a lot of these patients, which can be very disabling, especially if it cracks; with that cracking, you get Auspitz sign, that little bit of pinpoint bleeding.

So I think that utilization of keratolytics such as urea or ammonium lactate can be very effective, and we are seeing the emergence of some of these products. That said, I think restoring the microbiota is important. We do have some evidence that there is dysbiosis in patients with psoriasis, specifically that reduction in microbial diversity, which is true across the spectrum of all these inflammatory diseases.

Also of note, there does seem to be some role for the gut microbiota in dysbiosis, so could there be a role for oral probiotics? Maybe. We just don’t know yet.

In line with some of the studies we’re seeing with atopic dermatitis, in psoriasis we’re seeing that some of our standard of care, such as topical steroids, can help restore that baseline microbiota. A recent study in the Journal of Investigative Dermatology followed the microbiota and diversity of said microbiota in patients with psoriasis who were receiving ustekinumab.

Our treatments are impacting dysbiosis, but I think, truth be told, there are things we can do to help further that along with possibly prebiotic-containing moisturizers, as well as products that contain keratolytics to help break down that retained hyperkeratotic scale. Note that these keratolytics also function as humectants. They actually helped pull water in to help restore that water balance in the stratum corneum that allows for proper turnover of the stratum corneum and prevent that really painful and frustrating retention hyperkeratosis and micaceous scale.

We have to think about psoriasis with respect to restoring the microbiota—using moisturizers that can really help do that—and also using ingredients like urea or ammonium lactate, that really can help facilitate the proper turnover and prevent that painful fissuring that results from that very rigid stratum corneum.

Wearing face masks is causing irritation for many people. Do you have any advice for helping to reduce irritation and treat it?

Individuals are experiencing an inflammatory response or an exacerbation of primary diseases affecting the face secondary to friction from face masks; injury to the stratum corneum enables the inflammatory response.

The best approach to manage this irritation and inflammation is to follow the advice we offer for many chronic dermatoses: Wash the face either with a gentle facial cleanser or plain water, then to damp skin, you want to apply in this case a facial moisturizer, meaning it’s oil free and non-comedogenic.

Some patients develop milia and even some Demodex dermatitis from chronically wearing a face mask during the day. What I’ve been doing is throughout the day is go into an empty patient room or the lab and my mask off, pat a little water on my skin, and put on a facial moisturizer. I’ll try and do this multiple times a day, and I’ve found that to be quite effective at not just helping to mitigate some of that irritation but actually preventing it in the first place, and we know prevention is the best medicine.

We continue to learn that a balanced microbiome is essential and that dysbiosis can help drive disease. Is there evidence that topical formulations can help support a healthy microbiome?

Is there evidence that certain things we do can improve the diversity of the microbiota? The answer is “Yes!” I think the leaders probably in this research would be La Roche-Posay, through their own research and through investigator-initiated studies, followed by Aveeno. Leaders in this area include individuals like Elizabeth Grice, MD at University of Pennsylvania; Heidi Kong, MD at NIH; and Richard Gallo, MD at UCSD. Over time, research has shown that utilizing certain ingredients, specifically prebiotics, can actually restore someone’s proper balance of all of the different organisms on the skin.

It’s important to clarify terminology. So the microbiome refers to the genetic makeup of all the organisms on our skin. If we think about our skin as a planet to all these microorganisms, we start to think about different ecosystems. Face, groin, underarms, the back, the hands and feet, all these are like different ecosystems on planet Earth. We have dry areas, we have wet areas, we have oily areas, we have dark areas, occluded areas, and so the populations that live in these locations certainly vary.

The problems emerge when the different players don’t “play nice.” You may start to get increased growth of certain organisms, and these few foci or these few players overpower the community. As diversity goes down, we start to run into some trouble with respect to immunoregulatory properties and barrier properties that these populations, when in harmony, really impart on our skin. And it is really important to think about the microbiota as part of our skin barrier. Separate from just the stratum corneum and all its functionalities, this is an added layer of protection to the outside world.

We learn a lot about dysbiosis from primary skin diseases, atopic dermatitis probably being the poster child for this, and that’s where a lot of the people I mentioned have made their mark in this area. However, we also know that acne, rosacea, even psoriasis are diseases of dysbiosis. So how do we get the balance back?

Certainly a lot of the treatments that we use to treat these different conditions all influence the microbiota. These vary from topical steroids, topical retinoids, and antibiotics. With regard to atopic dermatitis, there was a nice study several years ago that showed that standard of care for flares of atopic dermatitis, such as topical steroids and bleach baths, restored individuals to their normal microbiota. Note that any atopic dermatitis patient is going to be abnormal compared to someone who doesn’t have atopic dermatitis.

Already our treatment algorithms are influencing the microbiota, but there’s certainly more we can do, and what we’re seeing is that moisturizers in general are prebiotics. They really offer the sustenance of life—carbohydrates, water, proteins, fats—to facilitate the growth of proper populations, but certain ingredients actually do more.

And that’s where the work from La Roche-Posay, looking at thermal spring waters from that location, La Roche-Posay being an area in France, can really help facilitate the balance of those populations and helps certain players, specifically a gram negative organism called Xanthomonas, grow to its full capacity. That can help really regulate what’s growing where and when.

We have multiple clinical trials looking at balneotherapy or high pressure showers with thermal spring waters in the hospital in France, replicating this data with moisturizers that contain these prebiotics, both in just patients with dry skin but also atopic dermatitis patients, and looking at various metrics, such as using sequencing of RNA to actually look at what organisms are there to even quality of life measures.

Other companies are participating in this space, such as Aveeno. It’s also looking at how colloidal oatmeal can play a role as a prebiotic.

On the flip side, there are things that we’re doing that can make things worse. Hand-washing or washing with traditional soap will do that. When we wash with soaps that have high pH or have surfactants in them, they will kill a lot of organisms. Altering the skin’s pH affects certain organisms. If you look at the skin of individuals with atopic dermatitis at baseline, they have a higher pH. They’re more basic than they are acidic. But using various soaps, we can actually increase that pH to create an atopic dermatitis-like picture that facilitates the overgrowth of Staph, leading to dysbiosis and then to ultimately a phenotype of dry, flaky, cracked, painful, itchy, red skin.

So be purposeful and meaningful when using soaps. Make sure to supplement by applying not only a moisturizer to wet skin. Also, evaluate any product based on the evidence. Show me the science. Prove to me that your claims mean something and I’ll recommend your product. I’ll use it myself. I’ll use it on my kids. So the good news is with the age of PubMed and the internet, it is easy to find that data, look to the data, choose the right products, and make sure you keep the microbiota happy.

So, to recap: the probiotics are the key players—the living organisms that are beneficial on the skin. The Prebiotics provide needed support or can be likened to being the infrastructure those probiotics need to thrive.

Two or three years ago, there was a really nice study in JAMA Dermatology that was well formulated and well-controlled. It looked at an oral probiotic in combination with standard of care for atopic dermatitis using validated tools to measure metrics of success. They found that a tri-combination of probiotics had a significant impact on reduction of disease severity using SCORAD and other tools in a population of atopic dermatitis patients.

That study, plus however many studies we have before it, provide sufficient evidence to say that probiotics could be useful.

The next question is which ones? And that’s the real question of what we should be recommending to our patient. We sadly do not know. There probably is no downside to recommending probiotics, but we’d prefer to have better data to support specific recommendations. Right now, we don’t have enough evidence to support one product over the other. However, if you really want to use one, I don’t think it would be bad and maybe can offer some help.

What we really need are head-to-head studies, and hopefully they are forthcoming.

What is your complete approach to hair loss in females?

—Kristine Kucera PA-C, MPAS, DHS, Dallas, TX

This sounds like a simple question; certainly anyone who takes care of these patients know this is not such a simple thing to do. There’s no perfect way to do this. However, I will relay my approach, which is manifold.

First and foremost, when a patient—especially a new patient—presents for assessment of hair loss, it is important to prepare yourself to be empathetic. Prepare yourself to spend a good amount of time with the patient because this can be a very disabling disease. One of my former residents, Misty Eleryan, MD, comments that, “Hair is someone’s crown.” Losing one’s hair can be exceedingly disabling and impact daily quality of life.

The next step is to ascertain what type of hair loss this person is suffering from. There are three typical features I assess.

Is the hair breaking?

Is the hair shedding?

Is the hair thinning?

These are not mutually exclusive. Actually, someone could have all three or two or one, but I think each one confers some information and insight in terms of what may be causing that overall hair loss.

Next step is to assess the scalp. Is it picture perfect and are there patent follicular ostia? Is there erythema? Is there scaling? Is there pain, itching, or burning? All these things are very important, but I think most important is scarring, because that will really distinguish between multiple forms of hair loss.

Next comes the physical exam. It’s really important to lay your hands on the patient, because even if it doesn’t give you any information, it really engenders goodwill and establishes that patient-practitioner relationship. I typically do a hair pull; try to grab 40 to 50 hairs from multiple sites and you want to tease the hair out. If you get more than two or three hairs per pull, that is a positive test. However, it’s very important to always ask if the patient has washed their hair that morning, because that will give a false negative. Any of the hair that would’ve shed at that point probably came out in the shower.

I also like to look at the scalp. I use my dermatoscope, which patients really like because they sense that I’m using technology to get to the bottom of their problem. Published studies show that there are unique dermatoscopic features for several hair loss conditions, such as alopecia areata, lichen planopilaris, and even CCCA.

Discussion of specific treatments is beyond the scope of this discussion. I would recommend if you have the opportunity, whether virtually or live, to hear either Jerry Shapiro, MD; Amy McMichael, MD; Wilma Bergfeld, MD; or Crystal Aguh, MD talk about treatment for hair loss. These are the masters and certainly can offer a lot of insight and advice.

However, here are some practical pearls. First: provide realistic expectations. Even if you do everything right, it’s going to be months to even years before the patient’s going to notice any difference. This is because hair only grows about a centimeter a month on average, and that will vary from person-to-person. I tell patients our first goal is to stop progression. We are the secret service of hair. We want to protect what they have. If we get increased density, if we get some regrowth, that is the cherry on top. We are aiming for that, but it’s not always possible. Our real goal is to stop progression, and if you provide that realistic expectation, you’re not going to get a call in three weeks saying, “I don’t see any improvement with my hair growth or my hair density,” because that would be pretty much impossible.

So regardless of what you’re going to do to treat these patients, I recommend you give practical, realistic expectations, a lot of handholding, and really dive in to figure out the different features of that unique form of hair loss, because every patient is unique and every hair loss experience is unique.

How do you treat alopecia areata of the eyebrows? I have a patient who had been treated with intralesional Kenalog 5mg/cc every six weeks. Initially, she had a good response, but then she went through a massive shed, and almost all of her hairs fell out. One of my colleagues suggested Latisse. Any other suggestions?  

—Danielle Mishkin  | Quincy, MA


I agree that first line should be intralesional Kenalog. I tend to go a little lower with concentration, because I am concerned about potential diveting from steroid atrophy, especially on the face. I usually use between 2.5-3.33mgs/cc with aliquots of 0.05-0.1cc per injection site. I typically do this a little more frequently, usually every four weeks versus every six weeks. However, there’s more you can do, and I always like to give patients something to do at home.

First you can use a topical. I like pimecrolimus because patients can use it every day, twice a day, ongoing, and I’ve had some success with it. Sometimes I’ll alternate between a topical steroid, such as hydrocortisone valerate or a desonide lotion, because the vehicle is easy to apply to this area, being a hair bearing area and a facial area.

I absolutely like to use bimatoprost, but I add that in later. If there’s still ongoing inflammation—that swarm of bees around those hair follicles—bimatoprost is going to be wasted because those hairs are still going to fall out. It’s going to be somewhat delayed. However, after treating for maybe a month or two, I will employ bimatoprost. The practical pearl here is how you use it and get the most for your money.

The rate limiting factor with bimatoprost is not the liquid in the bottle but actually the applicators, because there’s only enough, one for each side, for 30 days. Now that recommendation is probably related to ensuring safety with respect to bacterial colonization or even cleanliness of the actual brushes, so what I’m suggesting is off-label. I think that you could use one brush for both sides and get the most out of that bottle, the volume in that bottle, which I think could easily last someone about a month and a half if you use it this way. So I incorporate that usually a month or two after I start treating the inflammatory component. Always we should take a combination approach for everything we do, and that does seem to work pretty well for the eyebrows.

How do you keep your skin from drying out when cleansing with soap? Can it help to use a “facial cleanser” with aloe and vitamin E after as a moisturizer? Can I use a facial cleanser to wash my hands? Is it sufficiently hygienic?

Soap’s purpose is to remove debris; “debris” can be a loaded term. Debris could be dirt, dead skin cells, fats and oils, or organisms, whether it be pathogens or microbial flora. The way soap works in general for all these things is through surfactants in these soaps; these surfactants are charged molecules. They have two different ends: one is lipophilic, one is hydrophilic.

The lipophilic end will bind to all of these types of debris and will engulf or encompass it, whether it’s dirt or fat. Now as it engulfs it, it forms a little micelle, almost like a little bubble, where the inside part is lipophilic and the outside part is hydrophilic, which then enables you to easily wash this stuff off your skin.

This is why it’s so important when thinking about handwashing in the era of COVID that we really spend a lot of time doing all of this, because we want to create those micelles all over the skin so we can physically wash off that organism, that virus, or bacteria, or fungi, whatever you’re talking about. Yes, those surfactants, and even if you take a step further with antimicrobial washes, those ingredients can physically disrupt the cell membrane or cell wall of these organisms and physically kill and have a cidal effect, but the most important part is really removing it.

The problem is that these surfactants aren’t smart. They can’t delineate between the things we want in our stratum corneum versus what we don’t want there. Surfactants can sometimes be irritating, because they can disrupt the stratum corneum, creating microfissures or breaks in our barrier. Even worse, they can weasel their way through those breaks and get into the viable epidermis and create a local inflammatory response.

This is where gentle cleansers come in, many of which do not have surfactants, many of which do not have a charge or are non-ionic. These typically are soaps that are labeled as “sensitive” or meant for eczema-prone skin

The other part is acidity. Historically soaps are basic, meaning they have a high pH. Our skin likes to be acidic. In fact, many of the enzymatic proteins in our stratum corneum that are needed to convert the precursors of whether it be filaggrin or ceramides to their active forms or to even cleave elements of the stratum corneum require an acidic pH.

The other bad news is that at basic pH, the kallikreins start to break the corneodesmosomes, the connecting portion that really bring the corneocytes together. Their functionality actually increases at a higher pH. So you start breaking the stratum corneum apart, creating those little breaks and allowing things to get in that shouldn’t belong, but then you’re not kicking off those cells, so that’s where you see the clinical phenotype of that dry retained skin.

I think it’s okay to use a mild hand wash or—to the point of the question— a face wash on the hands. It’s about the motion, the physical motion of rubbing that soap in for 20 seconds and then washing it off to remove those offenders on the skin.

I have a patient with chronic blushing or “Idiopathic craniofacial erythema.” Can you comment on the best way to communicate to the patient about management alternatives?


—Stuart Shear, MD, Mission Hills, CA


I don’t have great answers, but I’ll share with you what I do to both educate patients about this and how I approach management.

I explain that this is signaling gone awry. There is miscommunication, usually in the neurovasculature. There may be inappropriate signals being sent or received that modulate vessel tone, leading to vasodilation and increased blood flow. This can be persistent or it can be sporadic. If the signaling itself is not increased, there could be increased sensitivity to those signals.

It’s important to home in on the specific concern. Is this the persistent facial erythema of rosacea? Is this persistent erythema that is also associated with hyperhidrosis? Is this persistent erythema that also has bouts of blushing with or without hyperhidrosis or is it just sporadic blushing? The association with or absence of hyperhidrosis is a key factor in my treatment approach.

Some underlying medical issues can certainly be associated with facial flushing or with focal hyperhidrosis. You want to rule out metabolic disorders, endocrine disorders, and even malignancy, like carcinoid. Once you’ve done that and you’re sure that this is simply idiopathic (which I always love to tell patients it’s our fancy way of saying we have no idea what this is), I like to go after those vessels.

Topical options are limited. Oxymetazoline can be very helpful for persistent erythema, though it is not so effective for flushing. I don’t tend to see so much rebounding associated with chronic use of this topical agent; if anything, I feel like it does work better as it is used over time.

Working from the inside out to target the flushing response, my first line is clonidine. I start really low. I prescribe the 0.1mg pills and I have patients split it in half to start at a dose of 0.05mg/day. I assess their response. Do they feel dizzy or lightheaded? Are they getting any response? We then go up to 0.05 twice a day, and I typically will work up to as high as 0.3 milligrams a day, sometimes a little higher.

Now, if this patient is also suffering from craniofacial hyperhidrosis, there are a couple of options. These certainly can include off label botulinum injections to the forehead or to the scalp. If you’re feeling a little feisty and want to try something, with caution, you could certainly use the glycopyrronium cloth. Just make sure you don’t get any in the eye, as that can cause mydriasis or chronic pupil dilation. I recommend caution combining anticholinergics with an antihypertensive.

If clonidine is not sufficient or the patient doesn’t tolerate it, I do use carvedilol. The dosing is 12.5mg twice a day, and there is some evidence in the literature supporting its use for chronic flushing or repeated flushing. Once again, we have to consider if there is also hyperhidrosis and you may want to employ some of those approaches to manage hyperhidrosis in addition to that flushing.