It happens at roughly the same point every year.
The mornings turn colder. The heating comes on. And within a fortnight your skin feels tight after washing, the moisturiser that worked all summer stops being enough, and the patches you had forgotten about are back on your shins, your hands, the sides of your face.
Most people assume their skin has become more sensitive. It usually has not. Your skin is built exactly the same way it was in July. What changed is the air it lives in, and the effect of that change lands almost entirely in one place: the outermost layer of your skin, the skin barrier.
I spent over twenty years in NHS cellular pathology looking at skin under a microscope before I ever formulated anything. What follows is the version I would give a colleague, written for someone who has never read a paper in their life.
What the skin barrier actually is
The outer layer of your skin is called the stratum corneum. It is about as thick as a sheet of cling film, and it is the only thing standing between your living cells and the rest of the world.
The easiest way to picture it is a brick wall.
The bricks are dead, flattened skin cells, packed tightly in overlapping layers. The mortar between them is a mixture of fats: ceramides, cholesterol and fatty acids, laid down in ordered sheets. It is the mortar that does the sealing. It holds water in and keeps irritants, allergens and microbes out.
That is the whole job. Water in, trouble out.
When the mortar is intact, skin feels comfortable and behaves predictably. When the mortar thins, gaps open. Water escapes faster than your skin can replace it, and things that should have stayed on the surface start getting through. That is a damaged skin barrier, and almost every seasonal skin complaint I get asked about traces back to it.
What the cold actually does
Cold air is dry air. It physically cannot hold much water vapour. Then you walk indoors into central heating, which warms that same dry air and makes it thirstier still. Your skin sits between the two all day, and water leaves it faster in both.
Add the things that come with the season. Hotter showers. Longer showers. Wind on your face. Wool against your neck. Washing your hands more often because everyone around you has a cold.
None of that is dramatic on its own. Together, over six weeks, it is enough to measurably change the structure of your skin barrier. This has been measured repeatedly.
The mortar genuinely thins in winter. A study that sampled the stratum corneum of the same women in winter and again in summer found that total ceramides, individual ceramides, cholesterol and free fatty acids were all significantly lower in winter than in summer. Water loss through the skin was higher, hydration was lower, visible dryness scored worse, and the surface held together less well (Wei et al., Journal of Cosmetic Science, 2016).
So it is not your imagination. Less mortar, measured in a laboratory, in the same people, in the same skin, a season apart.
It happens in healthy skin too. A year long study measuring all four seasons found water loss through the skin peaked in winter and fell to its lowest in summer, with hydration doing the exact opposite (Yang et al., Skin Research and Technology, 2020).
And sensitive skin feels it more. A study of 140 people compared healthy skin with three subtypes of sensitive skin across winter and summer. Water loss, skin pH and blood flow all differed significantly between seasons in every group, and the strength of people's stinging and burning tracked closely with how much water their skin was losing (Jiang et al., Journal of Cosmetic Dermatology, 2021).
That finding is worth sitting with. The stinging is not a separate problem from the dryness. It is the same problem, measured a different way.
Signs of a damaged skin barrier
From the outside, a compromised barrier looks like this:
- Skin feels tight, especially in the ten minutes after washing
- Products that never bothered you suddenly sting or tingle
- Redness that comes and goes without an obvious cause
- Flaking, rough patches, or a texture you can feel with your fingertips before you can see it
- Moisturiser that seems to vanish within the hour
- Itch, particularly at night or when you get into a warm bed
If you recognise three or more of those, the question is not which new product to buy. It is why your skin is losing water faster than it is holding it.
The part most people never hear about
Here is where it gets interesting, and where I think most skincare writing stops short.
Your DNA does not change when the weather turns. The instruction manual is fixed. But which instructions get read, how loudly, and which stay quietly shut, changes constantly. That layer of control sitting on top of your genes is called epigenetics.
Think of your genome as a very long cookbook. Epigenetics decides which recipes are bookmarked this week and which are stuck together. Same book, different meal.
Environment is one of the things holding the bookmarks. And your skin is the organ most exposed to environment there is.
This matters for the barrier because the genes that build it sit clustered together in a region called the epidermal differentiation complex, which holds many of the genes encoding the structural proteins your outer layer is made from, filaggrin among them. How those genes get switched on as a skin cell matures is controlled epigenetically, through DNA methylation and changes to the proteins DNA is wrapped around (Leśniak, Epigenomes, 2024).
And in skin conditions where the barrier fails, that pattern is measurably different from healthy skin. Reviews of atopic dermatitis describe altered methylation across genes governing both the structure of the epidermis and the immune response beneath it, alongside changes in the small regulatory RNAs that fine tune how much of each protein gets made (Nedoszytko et al., International Journal of Molecular Sciences, 2020; Bin and Leung, Allergy, Asthma and Clinical Immunology, 2016).
I want to be careful here, because this is where skincare marketing tends to overreach. Nobody has shown that a moisturiser rewrites your epigenome, and I am not going to tell you that one does. What the science supports is simpler: your skin cells are constantly reading their environment and adjusting their output accordingly. A barrier under stress is a barrier sending different signals.
From a gap in the wall to a flare on your face
This is the chain, and it explains why so many different looking problems share one root.
The barrier thins. Water escapes. The cells underneath detect that they are drying out and they respond the way cells respond to any injury signal, by releasing inflammatory messengers. One of the best studied is interleukin 1, which sits ready made in the outer layer of your skin waiting to be released.
You can actually measure this. In that same winter and summer study, the balance between interleukin 1 and its natural counterpart, the interleukin 1 receptor antagonist, sat significantly further towards the pattern associated with skin inflammation in winter than in summer (Wei et al., 2016). Earlier work on how the environment affects the stratum corneum found the same marker shifted in inflamed skin, and still detectable long after the visible redness had gone (Tagami et al., Journal of Investigative Dermatology Symposium Proceedings, 2001).
Read that last part again. The signal outlasts the symptom. Your skin can look settled and still be running hot underneath.
Once inflammation is running, what you see on the surface depends largely on what your skin is prone to:
- Eczema prone skin flares. The barrier defect and the immune response drive each other in a loop, which is exactly how the genetic and epigenetic literature describes atopic dermatitis developing.
- Rosacea prone skin goes red and reacts to temperature swings, hot drinks, wind.
- Skin with no diagnosis at all simply becomes dry, tight, itchy and intolerant of products it used to like.
Different names. Same starting point. A wall that is letting water out and irritants in.
There is a third element too. The mix of microbes living on your skin, the skin microbiome, shifts when the surface it lives on changes, because the pH, the moisture and the available fats all change with it. That shift is part of the picture, not a separate story.
Why you protect the barrier before the weather turns, not after
If a compromised barrier is what starts the inflammatory signalling, then the most effective thing you can do sits earlier in the chain than most people put it.
Waiting until your skin is already cracked and angry means trying to settle a process that is already running. Supporting the barrier now, while the weather is still turning, means the water stays where it should be and the signal is never sent with the same force.
This is the logic behind one of the most consistent findings in dermatology. Reviews of moisturiser use in atopic dermatitis show that regular daily moisturising measurably improves the skin barrier, and that longer term studies find it reduces how often flares happen and lengthens the gaps between them (Hebert et al., American Journal of Clinical Dermatology, 2020).
Consistency beats intensity. Every time.
What I would do this month
- Change your cleanser before you change your moisturiser. Foaming cleansers strip lipids. If your face feels tight after washing, that is the cleanser talking.
- Turn the shower down. Hot water dissolves the mortar. Warm, and shorter.
- Moisturise onto damp skin, within three minutes of getting out. You are trapping water that is already there.
- Go heavier at night. Bedtime is the longest uninterrupted stretch your skin gets, with nothing rubbing it off and no make up over it. A richer product does more work there than the same product at breakfast.
- Stop introducing new actives. Autumn is a bad time to start an exfoliating acid or a retinoid. Get the barrier stable first.
- Start now, not in December. You are getting ahead of the change, not reacting to it.
How I formulate for this
Everything above is why both of my barrier balms are waterless.
A conventional cream is mostly water, which needs emulsifiers to hold it together and preservatives to keep it safe, and that water evaporates within minutes of application. An anhydrous balm contains no water at all, so it has nothing in it to evaporate and needs neither emulsifier nor preservative. What you put on is still there hours later.
Calm is the lighter one, for daytime and for skin that reacts to everything. It is built around ucuuba butter, sea buckthorn and tamanu oil, with blue chamomile for its alpha bisabolol content. Sea buckthorn is one of very few plant oils containing palmitoleic acid, a fatty acid that also occurs in human skin.
Restore is the heavier one, for overnight and for the patches that have gone past dry. It contains oat, hemp seed oil, shea and cocoa butter, and turmeric.
The oat in Restore is there for a specific reason, and it is the ingredient in my range with the strongest clinical file behind it.
Colloidal oatmeal is finely milled whole oat, listed on an ingredients label as Avena sativa kernel flour. It has been used on uncomfortable skin for centuries, which on its own would not persuade me. What persuades me is the mechanism.
Laboratory work found that oat extracts increased the expression of genes involved in epidermal differentiation, tight junctions and lipid regulation in skin, and helped the barrier recover in a laboratory model of atopic dermatitis. In the accompanying study of fifty women with moderate to severe dry skin on the legs, an oat lotion significantly improved dryness, moisturisation and barrier measures (Ilnytska et al., Journal of Drugs in Dermatology, 2016).
That first finding connects to everything above. Oat is not simply sitting on the surface being soothing. It is influencing which barrier building genes get read, which is precisely the layer of control this article has been about.
A randomised trial in people with mild to moderate eczema then compared a 1% colloidal oat cream with a standard moisturiser over fourteen days. The oat cream significantly improved skin pH, barrier function and hydration, and was associated with a trend towards greater microbiome diversity and lower prevalence of Staphylococcus species at lesion sites. The standard moisturiser improved hydration alone (Capone et al., Journal of Drugs in Dermatology, 2020).
Two honest caveats, because you deserve them. Those studies tested their own formulations, not mine, and a finding about one oat product is not automatically a finding about every oat product. And Calm and Restore are cosmetic products that moisturise and support the skin barrier. They are not medicines and they are not treatments for eczema, psoriasis or dermatitis.
If you want to try both, the Starter Duo gives you each in 10ml, which is enough to patch test properly and then use long enough to actually know.
When to see a doctor instead
Please do not use any of this as a reason to avoid getting help. See your GP or a pharmacist if your skin is broken, weeping, bleeding or looks infected, if an itch is keeping you awake, if a patch is spreading or changing, or if you have been managing something on your own for weeks without improvement.
Eczema, psoriasis, rosacea and dermatitis are medical conditions. Barrier care sits alongside medical treatment. It does not replace it.
The short version
Your skin has not turned against you. The air around it got drier, your barrier lost some of the fats that hold water in, the cells underneath noticed and started signalling, and the surface is now showing you the result.
Which means the fix is not a stronger product. It is a better protected barrier, started before the worst of the weather rather than after it.
Nature provides the idea. I add the science.
Hana
Founder and Scientific Director, Born of Necessity
HCPC registered Specialist Biomedical Scientist
References
- Wei KS, Stella C, Wehmeyer KR, et al. Effects of season stratum corneum barrier function and skin biomarkers. J Cosmet Sci. 2016;67(3):185-203. https://pubmed.ncbi.nlm.nih.gov/29394019/
- Yang J, Tu Y, Man MQ, et al. Seasonal variations of epidermal biophysical properties in Kunming, China: A self-controlled cohort study. Skin Res Technol. 2020;26(5):702-707. https://doi.org/10.1111/srt.12857
- Jiang W, Wang J, Zhang H, et al. Seasonal changes in the physiological features of healthy and sensitive skin. J Cosmet Dermatol. 2021;21(6):2581-2589. https://doi.org/10.1111/jocd.14476
- Tagami H, Kobayashi H, Zhen XS, Kikuchi K. Environmental effects on the functions of the stratum corneum. J Investig Dermatol Symp Proc. 2001;6(1):87-94. https://doi.org/10.1046/j.0022-202x.2001.00016.x
- Leśniak W. Dynamics and Epigenetics of the Epidermal Differentiation Complex. Epigenomes. 2024;8(1):9. https://doi.org/10.3390/epigenomes8010009
- Nedoszytko B, Reszka E, Gutowska-Owsiak D, et al. Genetic and Epigenetic Aspects of Atopic Dermatitis. Int J Mol Sci. 2020;21(18):6484. https://doi.org/10.3390/ijms21186484
- Bin L, Leung DYM. Genetic and epigenetic studies of atopic dermatitis. Allergy Asthma Clin Immunol. 2016;12:52. https://doi.org/10.1186/s13223-016-0158-5
- Hebert AA, Rippke F, Weber TM, Nicol NH. Efficacy of Nonprescription Moisturizers for Atopic Dermatitis: An Updated Review of Clinical Evidence. Am J Clin Dermatol. 2020;21(5):641-655. https://doi.org/10.1007/s40257-020-00529-9
- Ilnytska O, Kaur S, Chon S, et al. Colloidal Oatmeal (Avena Sativa) Improves Skin Barrier Through Multi-Therapy Activity. J Drugs Dermatol. 2016;15(6):684-690. https://pubmed.ncbi.nlm.nih.gov/27272074/
- Capone K, Kirchner F, Klein SL, Tierney NK. Effects of Colloidal Oatmeal Topical Atopic Dermatitis Cream on Skin Microbiome and Skin Barrier Properties. J Drugs Dermatol. 2020;19(5):524-531. https://pubmed.ncbi.nlm.nih.gov/32484623/
- Lisante TA, Nunez C, Zhang P, Mathes BM. A 1% Colloidal Oatmeal Cream Alone is Effective in Reducing Symptoms of Mild to Moderate Atopic Dermatitis. J Drugs Dermatol. 2017;16(7):671-676. https://pubmed.ncbi.nlm.nih.gov/28697218/
Literature retrieved via PubMed.
