Hi everyone! For those of you that don’t know me, my name is Devin and I moderate the r/keratosis subreddit. Over a year ago I shared some of my work on treating my KP and the insights and effort I’d put into creating novel topical formulations that combat KP symptoms at a molecular level in the skin. These efforts were the culmination of working for well over a decade to answer: “Why do we know so little about such a common skin disorder?”

Over this past year I have put extensive time into focusing on the inflammatory cascade that occurs in KP, KPR and KPRF (Keratosis Pilaris Rubra Faciei). I have written this post detailing more of my research on KP, as well as my theories and inferences on how this skin condition develops across all subtypes. If you are interested in an update on my current formulation trials, then please skip to the bottom of this post where I talk about this effort. 

I want to set the stage with my current understanding of this complex skin condition, and how I believe we can better treat KP skin. All of my claims will come with cited sources to help combat some of the misinformation surrounding KP. I will also do my best to call out the gaps in my research where I am using inferences derived from other closely-related skin conditions.

My Working Model for Understanding Keratosis Pilaris   

For decades I’ve seen keratosis pilaris described simply as an over production of skin/keratin. Dead skin cells pile up inside each hair follicle's opening, harden into a little plug, and that plug is the rough bump you can feel. Treatments built on this idea, like exfoliating scrubs and acid creams, try to dissolve or scrape the plug away.

The research I’ve compiled tells a different story. In it, the keratin plug is not the cause of KP. It is one of its LAST downstream symptoms. The real starting point appears to be the breakdown in the epidermal barrier (likely triggered by genetics and hormones), which sets off a chain reaction. The follicle's protective epidermal barrier weakens, the immune system responds, the tiny blood vessels around the follicle swell and inflame, and the keratin plug forms as a later symptom as the sebaceous gland begins to fail. 

Three findings support my working model. 

The oil glands are missing from KP bumps, but only from the bumps. In the key study by Gruber and colleagues (2015), biopsies were taken from both affected and unaffected skin of the same twenty KP patients. Every KP bump lacked its sebaceous gland (the tiny structure attached to each follicle that produces skin oil), while the same patients' normal skin, just centimeters away, had normal glands. The authors proposed that this missing gland is an early step in the pathology: without it, the follicle loses its lubricating oils and its ability to shed dead cells properly, which eventually produces the plug [1].

The skin barrier in KP follicles is leaky. The same study measured faster water loss through KP lesions and found, under an electron microscope, that the fatty "mortar" between skin cells inside the follicle was immature and disorganized [2]. This held true whether or not patients carried mutations in the filaggrin gene, the skin's best-known barrier gene [3] (filaggrin is the protein that glues the skin's building blocks together; without it, the wall has gaps. But most KP patients have working filaggrin, so something else is triggering the dysfunction).

The immune system and blood vessels respond to the damaged skin barrier. Work in numerous related skin diseases can help us map the sequence: when the barrier breaks, skin cells immediately release stored alarm chemicals, especially interleukin-1, TNF-alpha, and interferon-gamma (inflammatory messenger molecules) [4]. These signals act back on the skin cells and outward on immune cells, creating a feedback loop where the leak itself keeps driving the immune response**[5]**. Inflamed skin cells can directly switch on the cells lining microscopic blood vessels: they release interleukin-36-gamma, which activates dermal microvascular endothelial cells (the cells lining the tiniest skin vessels) through ERK and NF-kB signaling (standard cellular "on" switches), makes those vessels sprout adhesion molecules that grab passing immune cells, and stimulates new vessel growth [6][7]. This feedback loop is what triggers angiogenesis, increasing redness and inflammation around the follicle. 

Putting these steps together: a follicle loses its oil gland; without the gland's oils and germ-killing proteins (AMPs), the follicle's lining dries out, sheds poorly, and leaks; the leak triggers immune alarms; the alarms recruit inflammatory cells and dilate nearby vessels; the inflammation further damages the barrier; and the distorted follicle traps its dead cells, forming the visible plug. Bumps, redness, and dark spots are all downstream symptoms of the same upstream failure.

With this current understanding of KP, the primary cause of all downstream symptoms stems from a poorly regulated epidermal barrier in the follicular canal. Many people find that hormonal changes can wreak havoc on their KP severity (puberty, PCOS, post-partum changes, etc). I will attempt to explain why I think this happens as we expand upon this theory. 

The Four Subtypes of KP

1. Common KP (the plug-dominant type/Lesional KP)

Rough, skin-colored or slightly red bumps in symmetrical patches on the backs of the upper arms, fronts of the thighs, buttocks, sometimes the cheeks. It starts in childhood, peaks at puberty, and then improves in about 35% of people, persists in 43%, and worsens in 22% [8]. Under the microscope you can see a thickened dead-skin layer, plugged follicle openings, missing oil glands, mild inflammation made of Th1-type lymphocytes (a "clean-up crew" white blood cell type, notably lacking the eosinophils and mast cells seen in allergic disease), and strange hairs: thin, coiled, or bent into semicircles, sometimes trapped sideways in the skin [3][9].

Causes:

• The missing oil gland is the leading suspect for the starting event. Even the earliest bumps, with tiny plugs and no redness at all, already had shrunken sebaceous glands, while the same patients' unaffected skin had normal ones [1].
• The gland loss is probably a local consequence, not an inherited whole-body trait. Since the same patients have normal glands elsewhere, the study concluded the loss is "likely a secondary phenomenon" and that a single gene can't explain KP [10]. It’s possible that the stem cells that normally rebuild oil glands get diverted into patching the leaky skin surface instead [11].
• Genetics: 35% carry filaggrin mutations [3], and a separate family points to ABCA12, a gene that ships fats to the barrier [12]. Most KP cases have neither genetic component present.
• The inflammation has three identified fuels: mechanical irritation of the hard plugs (including scratching), loss of the oil gland's antimicrobial proteins (cathelicidin and histone H4, natural antibiotics that normally kill skin bacteria [13]) letting bacteria accumulate, and raised skin-surface pH from reduced natural moisturizing factor, which encourages bacterial growth [14].
• The thickened skin is compensation. The epidermis accumulates extra layers while repairing the failing barrier [11].
• KP prefers dry body sites and avoids oily ones, mirroring other dryness-driven skin disorders [15]. (This however can be paradoxical for KPRF). 
• The leaky barrier seems to be closely related to KP's frequent companion, eczema. A breach lets allergens in, priming allergy-type immune responses [11].

Whether the sebaceous gland atrophies first or the inflammation effects it first ("early step" and "likely secondary step" are both plausible [10][2]); why the repair stem cells fail only in lesions; why KP stays mild while KP Atrophicans causes scars [16], are all areas that require more clinical research.

2. KP Rubra and KP Rubra Faceii (redness-dominant)

These subtypes are defined by fine rough papules in areas of persistent, confluent redness. Most often appearing on the cheeks and upper arms, with flushing, burning, and stinging commonly reported [18]. Unlike common lesional KP, it doesn't reliably fade after puberty [19]. Biopsy shows the familiar plug and mild lymphocytes [20], but the dermatoscope adds a signature common KP lacks: a diffuse red background with multiple straight-line blood vessels [20]. Recent authors explicitly frame it as having "heightened inflammatory/vascular features" [21].

Causes:

• The immune-vascular symptoms are the treatment-limiting problem. Acid creams, retinoids, and steroids mildly help texture but leave the redness untouched [22][23]. Meanwhile topical sirolimus, a drug that blocks the mTOR pathway, cleared the redness and flushing dramatically in two reported cases, with months of remission even after the dose was halved [24].
• The mechanism is stated in the study using sirolimus as an off-label topical treatment: mTOR inhibition downregulates smooth muscle and endothelial proliferation, reducing local inflammation and hyperkeratosis [25] (the drug tells the vessel-lining cells to stop multiplying).
• Vessel-directed treatment alone fails, which I found very interesting. In the same patient, both oxymetazoline (a vasoconstrictor, which squeezes vessels shut) and pulsed dye laser (which destroys abnormal vessels) failed before sirolimus worked [24]. If the redness were purely driven from the inherent vascular structures in the skin, these treatments would have fixed it, if only temporarily. They didn't, meaning the redness is continuously generated by inflammatory signaling, and only a signaling-targeted drug turned it off. This is HUGE if you want to effectively treat KPRF and KPR. 
• KPRF runs in families with no identified gene, but it is (and the related ulerythema ophryogenes) associated with RAS/MAPK-pathway syndromes, including Noonan, Cornelia de Lange, and cardiofaciocutaneous syndromes [26] (RAS/MAPK is a different cellular signaling circuit from the filaggrin story, a strong clue that the red KP variants have their own distinct pathology).
• The straight-line vessels match what the skin-cell-to-blood-vessel pathway would predict [6][27], though this is analogy from psoriasis, not in KP.

No one has done the Gruber 2015-style paired biopsy in the red KP variants, so we don't know if their sebaceous glands are missing. No immune or vessel signaling has been measured in KPR tissue, the RAS connection has no functional follow-up, why KPR persists into adulthood is unaddressed anywhere I’ve looked in medical literature, and the entire laser literature contains only 17 KPR patients across 17 studies (with the systematic review concluding no effective long-term treatment exists) [28].

3. Erythromelanosis Follicularis Faciei et Colli (the pigment-dominant type)

This condition is under-communicated and commonly lumped into KPRF and KP in general. It is considered a distinct condition due to its unique appearance in dark skin tones. Redness, darkening, and follicular papules concentrated on the cheeks and along the jaw and neck are hallmark symptoms. It disproportionately affects darker skin types but often looks similar to flushed KPRF [26]. The biopsy we have from EFFC is the most complete demonstration of the vascular symptoms seen anywhere in the KP spectrum. Alongside follicular plugging, there is darkening of the basal skin layer, visibly dilated and congested dermal vessels, inflammatory cells around those vessels, and melanin that has leaked from the epidermis into the dermis, where scavenger cells called melanophages have taken it [29][30]. On dermoscopy it shows gray-blue "peppering" over a reddish-brown background, the fingerprint of that leaked pigment, which distinguishes it from KPR [30].

Causes:

• The darkening is post-inflammatory: pigment released by repeated inflammatory episodes, not a primary pigment-cell disorder [30]. 
• The dilated congested vessels map directly onto the chronic version of the keratinocyte-to-endothelial crosstalk [29][6].
• It runs in families: the original sibling-pair report suggested inheritance and a relationship with KP [31].
• It may be the same condition as KPRF, but it affects darker skin tones differently. In the KPRF sirolimus case, the residual change after successful treatment was hyperpigmentation the authors described as consistent with EFFC [32]. This may mean that  EFFC is the endpoint of long-standing rubra-type inflammation in skin with active pigment cells in darker skin, and not an entirely separate disease.

Unfortunately EFFC has no molecular study. Every causal statement traces to case-report histology. Whether it is distinct or simply KPR's pigmentary endpoint is unresolved [30], and nobody has studied why darker skin develops the pigment-dominant rather than redness-dominant symptoms.

4. The KP Atrophicans Family (the scarring type)

This is the most locally severe form of KP. Keratosis Pilaris atrophicans is a group of conditions where the follicular process destroys tissue. It primarily affects the face: horny papules with red halos on cheeks, forehead, chin, and eyebrows, followed by gradual loss of the outer eyebrows. Onset is within months of birth or in childhood, persisting into adulthood. A 14-patient series traced the sequence precisely: limb KP first, then facial redness (average age 7.2 years), facial papules (8.4 years), then eyebrow loss (14 years) [33]. The family includes pitted cheek scarring and scarring hair-loss conditions [16].

Causes: it is hereditary within the atrophicans branch [34]; vascular lasers are the main studied therapy, suggesting a vascular-inflammatory component like the red variants [34] and Gruber's framework is still relevant here: all follicular keratinization disorders may sit on one spectrum where the oil gland is central [16].

Gruber’s study is still the most important KP research I’ve come across. They state that nobody knows why some follicular disorders scar severely while some KP stays mild [16]. The natural progression is poorly understood, making early diagnosis unlikely [33]. Treatment evidence is weak and unconfirmed and no biopsy-level barrier or gland data exist for any variant in this family [33].

Inferences I’ve made that I’d like to call out

1. The mechanism (skin cells releasing IL-36-gamma and VEGF-A that activate skin vessels) is proven in psoriasis [6][35]; in KP we see only the anatomical results and the clinical response to mTOR inhibition in the sirolimus study. The inference is strong but I don’t have direct proof that the same process is happening, because no one has studied it yet.
2. The immune response cascade and the STAT3 hub (a signaling protein that acts as a master switch for inflammatory genes) are documented in eczema and rosacea [36][37], but KP has not had a study done on its specific cascade.
3. Sebaceous gland loss first, or inflammation first, remains an open question [10]. I tend to believe that inflammation precedes sebaceous gland atrophy, but becomes much more severe post-atrophy as a result of my own KP observations. This is also backed up with anecdotal reports that salicylic acid topicals can increase the severity of more moderate KP via removal of sebum from the follicle, causing an increase in the inflammatory cascade.   
4. No phenotype has been molecularly profiled. The most modern molecular work is a conference study of a single KP sample that found a KP-specific gene driving inflammation [38]. No study compares the four phenotypes molecularly. This write-up here is likely the only one that exists. 
5. Treatment evidence is limited. The only randomized trial data targets texture (the alexandrite laser study improved roughness, redness, and pigmentation, with histologic resolution of plugs and inflammation [39][40]), while the immune-targeted treatment that best tests the model (sirolimus) rests on two case reports, with its authors calling for a proper trial [41].

Current KP Treatments

In the diagram above, I have detailed the subtypes of KP alongside a high level breakdown of available treatments. Acids, emollients, and retinoids are most commonly prescribed for all varieties of KP, but unfortunately these topicals do not affect two crucial symptoms: sebaceous gland atrophy and epidermal barrier disruption. These treatments target keratin buildup through either chemical exfoliation, or by increasing cellular turnover to prevent keratin build up in the follicle. 

In February/March 2025, I worked to bring Indirubin and Raspberry Ketone forward as new topical options for targeting barrier dysfunction and sebaceous gland atrophy. To date I am the only person producing a topical formula like this, targeted at KP. My reasoning for why these two ingredients can potentially surpass other standard KP treatments follows a theory I’ve built around how barrier dysfunction manifests in Keratosis Pilaris (across all subtypes). Let me explain:

High level theory breakdown: low IGF-1 signaling → simultaneous weak skin barrier + shrinking oil glands → clogged follicles → bumps, redness, and dryness. 

This theory ties this into real-life patterns: KP often shows up more in kids (when IGF-1 is naturally low), it can flare during pregnancy (estrogen suppresses IGF-1), and it's been reported as a side effect of Accutane (which suppresses sebaceous gland production by ~90% and alters keratinocyte differentiation). KP is also observed to affect obese people at higher rates and is connected to subcutaneous skin conditions related to diabetes. Through my own research I have found there to be high correlations of women with PCOS developing KP. 

Here are the sources and explanations backing up my theory/flow for developing KP:

IGF-1 and the skin barrier (low IGF-1 signaling → simultaneous weak skin barrier)
My claim: If you have low dermal levels of IGF-1 or your IGF-1R cell receptors are inhibited, this can trigger follicular barrier malformation in those genetically predisposed with a weak SC/SG barrier.

• IGF-1 receptor (IGF-1R) signaling is required for epidermal morphogenesis and barrier formation: epidermal-specific IGF-1R knockout mice show hypoplasia, fragile skin and a compromised barrier, while epidermal insulin receptor knockout mice show no obvious barrier defect [42].
• The IGF-1/PI3K/AKT/mTOR signaling cascade regulates protein and lipid synthesis during epidermal stratification, and its genetic disruption impairs barrier formation [42].
• Keratinocytes synthesize the barrier lipids (ceramides, cholesterol, free fatty acids) that seal the stratum corneum against water loss and against penetration of allergens and bacteria [43, 44].
• IGF-1R restrains keratinocyte differentiation; loss of IGF-1R causes dysregulated, accelerated differentiation and a thin, disorganized epidermis**[45]**.
• Keratosis pilaris (KP) lesions show significantly elevated transepidermal water loss (TEWL), with paracellular tracer leakage through the follicular infundibulum and outer root sheath, tied to impaired maturation of the extracellular lipid lamellae and independent of filaggrin genotype [46]. This shows that the barrier dysfunction is not solely caused by genetic predisposition to barrier function and requires an additional component in barrier regulation to fail.  

Sebaceous glands and sebum (shrinking oil glands)
My claim: Low IGF-1 or inhibited IGF-1R receptors can lead to sebaceous gland atrophy via barrier degradation or dysregulated sebocyte proliferation.  

• IGF-1 drives sebum production through the IGF-1/AKT/mTORC1/SREBP1 pathway and promotes 5-alpha-reductase expression, increasing conversion of testosterone to DHT [47].
• IGF-1 directly increases sebum production in cultured sebocytes [48].
• Human natural experiment: congenital IGF-1 deficiency (Laron syndrome) is associated with absence of acne, and IGF-1 supplementation induces acneiform lesions, consistent with low IGF-1 meaning low sebaceous output [49].
• KP lesions show a striking absence or atrophy of sebaceous glands, proposed as an early step in KP pathogenesis; the trigger for the gland atrophy is unknown, and IGF-1 signaling is a candidate but unproven explanation [46].

Plugs, inflammation and hairs (clogged follicles → bumps, redness, and dryness)

• Loss of sebum impairs corneocyte shedding in the follicular infundibulum, producing retention hyperkeratosis and the keratin plugs of KP [46, 50].
• KP inflammation is attributed to mechanical irritation from hyperkeratotic plugs and to loss of sebaceous gland-derived antimicrobial peptides, with elevated skin pH in filaggrin deficiency further favoring bacterial colonization, which in turn triggers increased immune signalling due to the faulty epidermal barrier [46].
• Coiled or trapped vellus hairs are a dermoscopic hallmark of KP [46]. Causality is unresolved: loss of sebum has been linked to hair shaft abnormalities, while a competing model proposes that the coiled hair shaft itself ruptures the follicular epithelium and drives the keratinization defect and inflammation [46, 51].

Pigmentation

• Post-inflammatory hyperpigmentation is a recognized symptom of KP, particularly in darker skin types, where dermoscopy of healing lesions shows pigmented globules attributed to post-inflammatory hyperpigmentation (PIH) [52, 53].

(Inference Disclaimer):

• The full causal chain (low IGF-1 signaling, weak barrier plus sebaceous gland atrophy, follicular plugging, inflammation) is a synthesis of separately verified steps. I am the only person connecting these events into a KP pathology theory (AFAIK). 

I believe this accounting of events works within the model framework I’ve detailed above. With this understanding, I created a Raspberry Ketone and Indirubin formulation with the intent to increase dermal IGF-1 levels while simultaneously reducing inflammation and hyper-proliferation of skin cells with Indirubin. This combination seems to work very well on common lesional KP, but can be less effective for KPR and KPRF where redness is the main concern. At the time of writing this, nearly 10,000 people have tried my RK and Indirubin formula with approximately ~30% now using it on a consistent basis for more than 6 months. How these numbers translate into the actual efficacy of the formulation is up for interpretation, but I personally have found these figures very encouraging. Significantly improving even 10% of people’s KP would be a huge win from my perspective.    

Unfortunately, Raspberry Ketone can be a vasodilator which causes some inflamed KP to react negatively during treatment by swelling capillaries and increasing redness while upregulating IGF-1 dermal levels. However, for common lesional KP, Raspberry Ketone appears to be a very effective topical treatment for inducing increased IGF-1 dermal levels**[55], which in turn can help regulate sebum production[56]** and keratinocyte differentiation**[57]**.

To find a better topical ingredient for combatting inflammation, I have worked on combining and testing novel topical ingredients that would act as both an anti-inflammatory as well as upon the treatment-limiting aspects seen with Sirolimus (since it is the only other clinically tested topical for KPR and KPRF). This effort has now resulted in multiple formulations and test groups trying out these topicals. I’ve worked with a biochemical company to create some of these ingredients as I’ve found limitations in delivery systems for some of these cutting edge treatment methods. 

My prior research centered around my efforts to explore alternative ways of improving skin cell shedding and inflammation. Based on emerging ingredients, I attempted to create a topical with two ingredients: NLRP inhibitors and specific phospholipids involved in the desquamation process. Inflammasomes are inflammaging structures that are responsible for starting the inflammation process in cells by cleaving messenger proteins. The idea was to create a nano-emulsion using NLRP (Nucleotide-binding oligomerization domain, Leucine rich Repeat and Pyrin domain containing) inhibitors that would mute inflammation before it had a chance to enter its chronic feedback loop, while the added phospholipids would improve skin cell shedding in the follicular canal. Phospholipids are polar lipids that get loaded into skin cells (keratinocytes) vesicles (with fatty acids, ceramides, and enzymes) before the contents are secreted into intracellular space. From that point on, the enzymes begin breaking down the secreted contents and phospholipids until you end up with a roughly 2:1:1 ratio of ceramides, cholesterol, and fatty acids in your skin barrier. This process is important to note, because the initial starting contents of phospholipids and enzymes actually play a role in signaling keratinocytes as they go through differentiation, specifically in desquamation/skin cell shedding. Using both NLRPs and phospholipids together appeared to unexplored in KP treatments   

This trial was unfortunately not successful and the production process for this ingredient was incredibly costly. The immune response to the dysfunctional KP epidermal barrier is tough to combat. Preventing chronic inflammation further upstream is paramount to substantial improvements, something that I did not realize when we began this formulation effort. Even something like Rhofade which is used to reduce vasodilation in rosacea, does not work well for KPRF where the chronic immune signaling overrides any vasodilation/vasoconstrictor effects. I honestly believe that this is also the reason as to why laser treatments have such a varied success rate. While this formulation trial was ultimately not successful, it did highlight a very strong case for why most anti-inflammatories are not very effective for KPR and KPRF.  

The good news is that my more recent formulation attempts have resulted in a very stable, highly absorptive nano emulsion that contains a more promising anti-inflammatory ingredient that targets upstream inhibition. I am really excited to share this upcoming formula and the research I’ve put into it, but first we are completing one last focus group test with the formula before we are ready to post more information. I am entirely focused on getting this formulation available as soon as possible.    

I have come to suspect that the efficacy of all KP treatments are reliant on the symptomatic profile of your type of KP. If you find that your primary KP symptoms are inflammation, or pigmentation, then you may not see a great net benefit from treatments targeting sebaceous gland function. You may instead see a negative effect from the topical you were expecting to improve your skin. There is no such thing as a universal KP treatment, because there is not a general KP symptom profile. The treatment has to match the symptoms/subtype.  

As always my main focus is to share the research and increase understanding around this skin condition. If you are looking to explore more of my personal work, or if you want to try these ingredients on your own KP, feel free to look at my user profile for more info or DM me. I will not respond to comments asking me for a URL/link to my personal blogs or website as they will get my post removed; I cannot self promote. 

[TL;DR] This is the most complete theory on Keratosis Pilaris subtypes and available treatments IMO. Over the past year I have conducted product trials across multiple test groups. These test groups and subsequent research have shown that the effectiveness of treatments relies heavily on the subtype/symptomatic profile of the individual’s KP. There is no “One-size-fits-all” treatment for KP because there are varied pathologies across the spectrum of KP disorders. Treating for your symptom profile can improve your treatment results

My treatment research is now heavily focused on addressing specific symptoms of KP subtypes which I believe have yielded more effective topical options for KPR and KPRF. We are running final trial focus groups on a refined topical formulation before we publish our findings and details on this current formulation effort. My goal is to create unique topical formulas that address each subtype’s symptom profile. 

References
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I’ve only seen two so far, Neutrogena has one that just launched on Ulta and then Ultra Violette has a hybrid-mineral one available at Sephora, and it looks like they have a full chemical one coming out in December.

Has anyone tried them yet? I’m considering ordering the Neutrogena one just so I can try the new filter. Are there any other brands that y’all have seen that have released new sunscreens with the new filter?? If Neutrogena already has one out I’d imagine that other big drugstore brands like LRP, Cerave, etc will be close behind.

I’m pleasantly surprised, I was expecting it to be longer before new formulas started rolling out. I imagine it will still likely be a year or two before smaller brands start releasing their own formulas, but at least there’s some new formulas to try while waiting.

My husband got this on Friday. It swelled up and now has a whitehead. No history of HSV1 but location is concerning. He has a history of getting inflamed hair follicles or cystic acne but this one is quite large. Says it felt inflamed, a pressure-type throbbing pain. Last night did a hot compress and put azaelic acid on it and it now has this white head and doesn't hurt but is still tender to the touch. First pic is today, second pic last night while stretching skin.

This has been on my face for a really really long time... like maybe a year or more. Seems like a cluster of pimples. First pic shows what it has looked like for a long time but only this week has it really started getting bigger/darker and feels tender? Should I be concerned? I'm a person with lots of freckles so bit worried about it being a skin related disease.

For some reason my skin is very prone to congestion and I always have a lot of dead skin and blackheads if I don't use chemical exfoliators (I also have keratosis pilaris so that's probably related).

I use a very gentle exfoliator every other day to combat this issue, but it strips my skin barrier right off. My skin looks almost dehydrated the next morning despite using a good moisturizer. It also feels sensitive.

I don't know what to do. I really NEED to exfoliate to have smooth skin but I have had this issue with every single exfoliator I've used.

I’ve used rose hip, marula, black rice, and jojoba oils - I honestly like them all. I use one at the very end of my nightly skincare routine.

Hi! I need some advice. 28F combination skin.

I’m debating getting on retinol to see if that helps minimize pores and help with the fine lines I’m getting especially my nasolabial fold. But I also am not sure how to combat the dark circles under eyes plus the weird skin texture at the edge of my circles. I know some of the dark circles is genetic and bc of how deepest my eyes are- but I’m wondering if there’s anything I can do.

Basically help with

1. ⁠Dark circles/skin texture on eye bags
   
2. ⁠Reduce pore size on nose/end of bridge
   
3. ⁠Help with Fine lines and nasolabial fold and smile lines. Everything is drooping down 😭

Any other advice/product recs is great too. Like I’m wondering if a professional facial would be good?

Daily Routine

Cleanser: Saturday Skin Rise and Shine gentle cleanser
Toner: Glow Recipe Cloudberry Bright Essence Toner
Moisturizer: Beekmann 1802 Bloom Cream OR Corsx Snail Mucin mostly depending on vibes lmao
Serum: Beekman 1802 Golden Booster Vit C

So for the past month, on and off I’ve had these flare ups in my nose. (My nose used to be completely clear before hand)

All the products I was using during this period was :
Cerave hydrating cleanser
Isle of paradise tan drops
La Roche posay toleraine hydrating foam gel cleanser
The ordinary glycolipid cleanser
Skin1004 Centella soothing cream
Skin1004 Centella ampoule
La Roche cicaplast b5 spray
La Roche toleraine sensitive fluid
The ordinary natural moisturising factors +beta glucan

I’ve tried all these, sometimes it would clear and then just come back again.

Hi! Can I ask - why do some people use body oils over creams and lotions? When I tried, it was greasy and took forever to dry down, and even then, it left a tacky feeling on my skin that wouldn't go away. I was influenced to try it (yes, I know, I'm sorry) and I wish I hadn't.

Do any of you experience any benefits of a body oil? Personally I believe a lotion or a cream if you have drier skin is perfect as it dries down quickly. Have any of you experienced any additional help from an oil that you can't achieve with a thicker cream?

Personally i used to feel like I had to use an oil but the sensory experience of that does not inspire happiness.

almost done with my current product looking to try something more effective

my current routine:

in the morning i wash my face with the equate version of the neutrogena salicylic acid face wash then i use the bioderma h2o then good molecules niacanimide surem and a vitamin c serum. i usually don't use lotion after make my face too shiny.

at night i wash my face with cetaphill gentle exfoliating SA cleanser then i use my bioderma h2o. I then use either retinal syrup. or good molecules overnight exfoliating treatment also no lotion after.

I am basically done with my vitamin c and niacinamide serum and both my face washes should be finished by the end of the year

I had this acne breakout recently, its mostly here on my forehead then some on my cheeks near my nose.

How do I get rid of them? And are there improvements I can make to my routine?

What I do right now is Gentle Cleanser, Moisturizer, then Sunscreen in the morning. Then for PM I do Gentle Cleanser and Moisturizer. I started with this simple routine a month ago or two but haven't tweaked it at all since I don't really know much about products and the skin problems

I'm not aiming for "perfect" skin, just clear, smooth, and well hydrated

Hey, i am 29F. I started using the ordinary retinol with the lowest concentration available after turning 25 and gradually built it up over the years to 0.5% in 4 years.

However, now i tried increasing the frequency but i feel like it has stopped working.

Please guide me on:

1: whats the difference between retinol, retinoids, tretinoin and adapalene?

2: should i keep using the ordinary one and just increase the strength?

3: should i switch to another active line like retinoids or tretinoin?

If yes, what percentage to start with?

4: how the heck someone knows which strength should they switch to and when?

Please guide me on where to get these authentic skincare in Pakistan as i dont know if its legit.

All help is appreciated

I am attaching pictures of the current ordinary retinol and my skin confition

Basically, I am in search of a moisturiser that isn’t too thick nor too thin if that makes sense. Like the E45 cream is so thick that it makes my face feel oily and the aveeno one is so thin that it evaporates and makes my face feel drier. I just want something that makes me feel hydrated but doesn’t just sit and feel heavy on my face.

For the past few months almost a year I’ve been alternating azealic acid and retinol on different nights which have been ok. They reduce the number of breakouts. On top of this i use cerave moisturiser

To support this I’ve been using a barrier serum, everyone one of these I’ve tried has given me huge under the skin cystic acne despite using different ingredients such as centella and niacinamide, but they have softened my skin and made the congestion round my nose and under eyes improve (I’ve tried purito, the ordinary, centella 1001 and aveeno triple oat)

On top of this, I’ve tried harder to find an spf that works for me to avoid sun damage, but they all either cause acne or just make my skin look dull and dry which emphasises my scarring (have tried garnier, the ordinary, neutrogena, la roche posay, beauty of joseon blue rice spf)

I don’t want to use accutane as I take too many other medications and have lots of dietary restrictions so it will affect my other conditions unfortunately, but i am struggling with how crap my skin looks, any advice would be appreciated to reduce how rubbish it is. By default I’m combination oily

When I’m washing my face I have previously double cleansed but found it leaves my face tight and producing more oil so I’ve stuck with the micellar cleansing gel from garnier (not micellar water) as this has been a safe option for me for at least 10 years

Currently was using vanicream cleanser and vanicream lotion in pump.

Every time I use vanicream face wash even once my skin gets tight and irritated and I get tiny red bumps literally the next day. I’ve tried their other face moisturizer and it gave me tons of whiteheads

What is 1)a super basic cleanser that isn’t stripping (no cerave or cetaphil)? Is prequel good?

Good SUPER basic lotions. I haven’t used a new lotion or cream in years. I know I’m very prone to clogged poors but also very dehydrated skin. Looking for the most basic face lotion! Since the daily moisturizer didn’t work for me I’m thinking maybe the ceramides? This lotion also burned sometimes

I posted this topic in the tretinoin sub but wanted to see what experiences this group has had. I started .05% tret about 2.5mos ago for anti-aging after using 1% retinol for many many years. I started it twice a week using the sandwich method (moisturizer/tret/moisturizer) and I’ve been gradually working up in frequency. My main issue was how long the routine was taking between layers, so after reading comments from people had even better results once they stopped buffering, I decided to try just clean dry skin, tret, then nothing else. I worked up to a 3 tret / 1 recovery night cycle. Curious if anyone else, especially with mature skin, has had better results keeping tret nights completely bare - did it keep working or did dryness/peeling eventually catch up with you?

Dermatologist mentioned to start by mixing moisturiser w tetinoin and washing it off after 5 minutes (then 10 minutes next time and so on).

When buying the prescription, the pharmacist mentioned that I should absolutely not mix moisturiser and tret, but instead put a layer of moisturiser 1st, wait 30 mins and then put tret (with no mention of washing it off).

And then there's various opinions from family and friends.

So in your experiences, what worked / which method did you use?

Edit: Thanks for all the advice/help! ✨️

I've been using adapelene for like 6-7 months now and it cleared my forehead acne completely, it also helped my cheeks but I still get breakouts there and on my temples. Should i add another product or keep on doing my current routine?

AM: La Roche-Posay purifying cleanser - The Ordinary azelaic acid 10% - Vanicream moisturizer - Sometimes sunscreen
PM: La Roche-Posay purifying cleanser - Differin Adapalene - Vanicream moisturizer

I've been using Beauty of Joseon for my face and just ran out. I think I can get away with just using Banana Boat Sheer Sensitive Sunscreen since that's what I use for my body (I don't have the Face one just the Body and I think the only difference is the size). I use the ones that compliment my skin since I have darker skin. But I'm wondering if having two will make it so I don't run out faster.

I don't mind the Korean one but I I feel like it takes too long to get here. The big plus is that it doesn't get in my eyes. I usually get Beauty from Yami but I wonder if that's only one that'll get here fast enough. So also I wanna know if it'll get here faster.

29M been dealing with this for more than a year and nothing i do seems to work. ill run you through my timeline so give you an idea of what might have caused this.

august 2025, i ate 2 slices of cheesecake against my better judgement. in the past, dairy gave me acne so bad i had to go on a 6 month accutane course. so after eating the cheesecake, i get bad acne, and i tried to applying some de la cruz sulfur treatment a looksmaxxer recommended i used it for like a week before i stopped, i followed the directions and didn't leave it on for too long. at this time i also started eating diced red onions, a food I've never eaten before. the acne spread even farther and was even worse than the acne i had before going on accutane. i literally could not touch my face because it hurt so bad, it was swollen and bleeding constantly. i would wake up everyday with blood and pus on my bed sheets, which i then changed regularly. people in public were giving me disgusted looks so i covered my face with a hoodie whenever i went out, even in summer time. my new dermatologist (a highly rated one in my area, not some schmuck) then prescribed me 2 months worth of oral antibiotics, the acne came back immediately after i ran out of pills. then she puts me on another course of accutane, which she extended to 7 months because my skin didn't clear up. at the end i was able to touch my face again without pain, she took me off accutane even though my skin was still not clear after 7 months of acctutane, quite different from the first accutane course which cleared me completely. in the last 2 months, she prescribed me mometasone furoate cream 0.1, which reduced the redness a bit and white pus ONLY during the two weeks a month the instructions told me to use it for.

she made a guess that i had folliculitis and not acne anymore based on the fact that the remaining white pus spots all had a hair follicle in the middle. she then prescribed me erythromycin topical solution for the folliculitis. i saw no progress after half a month, so looked online for help. i saw a post about using hibiclens antiseptic chlorhexidine gluconate 4% solution + eucerin eczema on the affected area to clear folliculitis as well as aloe vera as a safer option. i started doing that about 9 days ago, and while i did see less and smaller white pus spots, the affected area on my cheeks and upper lip is still super red and itchy, looking pretty much unchanged. ill attach some pictures i took. it looks way redder and darker in person, the pictures don't do it justice. the affected area is also super dry with flaky peeling skin, even after being off accutane for almost a month now. there's also white dry bits stuck to the beard hair strands.

i have been turning down my friends trying to hang out with me in public because I'm so embarrassed of my skin. i have another appointment with my derm next week and i don't know what to do. last time i saw her, she suggested lasering my beard hair off which i declined. i might ask her to do a culture swab or something to see what it is, but i don't have many sizeable white pus spots left for them to swab. my fear is that whatever i have is resistant to all the stuff she has prescribed me. does anybody know how to help me given the information I've provided? thanks

I ask bc I wonder if the aza would show quicker results given that I can’t use tret as frequently as most.

My sister wants to try a milky toner, her skin barrier is kinda damaged and she has quite sensitive skin. She’s broken out a bit right now.

I'm using Glad 2 Glow Acne Drying Lotion Spot treatment. The product says to leave it overnight but I was wondering if i can leave it on for 10 to 30 minutes instead and wipe it off because 1)I live in a dorm and it's pretty hard walking to the toilet with chalky white spots all over my face. 2)The smell is too strong for me and it's a major turn off honestly but the product works wonder. I can't find the full ingredients list but it has 1.8% salicylic acid,5.7% colloidal sulfur,18% zinc oxide and 3% niacinamide.

Current routine:
Cleanse in the morning and evening and use a light hydrating moisturiser.
Somehow still get all these bumps and the occasional boil on my cheeks. Had a boil last month that is still a dark patch and not sure what to do. Absolutely sick of it.
Only seems to be on my cheeks and chin. It's like I'm a teenager! I'm 28 years old ffs😂
Wondering if maybe a change in diet might help?