By Alice Henshaw, RN, NMP | Founder of SKIN|CYCLES & Harley Street Injectables

May 2026 · Approx. 5 min read

The Conversation That Keeps Happening in My Clinic

I want to start with something that has been bothering me for a long time. Not a scientific question. A communication failure.

Almost every week at Harley Street Injectables, a woman in her mid-forties or early fifties will sit across from me and describe the same experience. She'll say something like: "My skin just... changed. Over a few months. I don't know what happened." And then she'll look at me as though she's done something wrong. As though she missed a step. Forgot a product. Let herself down somehow.

She hasn't. What happened is biology, and nobody bothered to explain it to her before it started.

That gap, the one between what the science tells us about menopausal skin changes and what women are actually told, is one of the reasons I built SKIN|CYCLES in the first place. Not as a "menopause brand." I find that label reductive, honestly. I built it as a clinical range that targets specific biological mechanisms. Mechanisms that happen to accelerate sharply during hormonal transition. Collagen degradation. Barrier failure. The collapse of dermal hydration from the inside out.

So this article is my attempt to close that gap. I want to walk through what is physically happening in your skin during perimenopause^{1PerimenopauseThe transitional years before menopause when oestrogen fluctuates irregularly.} and menopause, why it is happening, and what a genuinely thoughtful topical protocol can (and cannot) do about it. No hand-waving. No ingredient lists without context. I want to be specific, because specificity is what this conversation has been missing.

Oestrogen Was Running Everything. Then It Stopped.

Here is the thing most skincare articles about menopause get completely wrong. They treat oestrogen^{2OestrogenA steroid hormone that regulates collagen synthesis, hydration and barrier function in skin.} as though it were just a reproductive hormone that happens to affect the skin a little bit on the side. It is not a side effect. Oestrogen was, to put it bluntly, the single most important regulator of your skin's structural integrity. Collagen production, hyaluronic acid levels, barrier lipid composition, sebum output, wound healing speed. All of it, regulated by oestrogen. All of it, at least partially.

I sometimes describe it to patients this way: imagine someone was secretly doing maintenance on your house every night while you slept. Fixing the roof tiles, repainting the woodwork, replacing worn pipes. You never noticed because everything just... worked. Then one day, they stopped coming. You wouldn't notice for a week, maybe two. But within a few months, the cracks would start showing everywhere at once.

That is what oestrogen withdrawal does to skin. The cracks show everywhere at once because the hormone was holding everything together at once.

Let me get more specific. Oestrogen directly stimulates fibroblasts^{4FibroblastsCells in the dermis that produce collagen, elastin and hyaluronic acid.} in the dermis^{3DermisThe middle skin layer containing collagen, elastin and blood vessels.}. These are the cells that manufacture collagen, elastin and hyaluronic acid. Oestrogen upregulates procollagen I production (the precursor to Type I collagen, which accounts for about 80% of your skin's collagen structure) and also boosts tropoelastin and fibrillin, the elastic fibre components. At the same time, and this is the part people miss, oestrogen suppresses the matrix metalloproteinases^{5Matrix metalloproteinases (MMPs)Enzymes that break down collagen and other structural proteins in the dermis.}, the enzymes that chew through existing collagen. So it was simultaneously building new structure and protecting old structure. Both jobs, gone at once.

Thornton published a thorough review of this in Dermatoendocrinology back in 2013, documenting that oestrogen receptors sit on keratinocytes, fibroblasts, melanocytes^{10MelanocytesCells in the epidermis that produce melanin, the pigment responsible for skin colour.}, hair follicles and sebaceous glands. The hormone's reach across skin biology is not incidental. It is foundational. That paper is worth reading if you want the full mechanistic picture.

Thirty Percent in Five Years

I need to talk about the Brincat data, because it is still the most cited finding in this entire field and it deserves to be understood properly.

Mark Brincat and his team at King's College Hospital in London published a study in Obstetrics & Gynecology in 1987 that measured skin collagen content, skin thickness and bone mass in postmenopausal women. The central finding: women lose roughly 30% of their dermal collagen in the first five years after menopause. After that, the decline continues at about 2% per year for the next fifteen years or so.

I want to sit with that number for a moment. Thirty percent. Five years. The amount of collagen your skin loses in half a decade of early post-menopause is greater than the cumulative loss from the previous two decades of adult life. And, this is the part I find most clinically interesting, Brincat showed that the decline tracks menopausal age rather than chronological age. Meaning if you enter menopause at 45, you may have significantly less dermal collagen at 50 than a woman of the same age whose menopause didn't begin until 52. The clock doesn't start at your birthday. It starts at the hormonal shift.

Affinito and colleagues confirmed this in 1999, publishing in Maturitas. Their study measured skin collagen directly in postmenopausal versus premenopausal women and concluded that the decline is an oestrogen-related phenomenon. They also found that oestrogen supplementation partially reversed the losses. Partially. That word matters, and I'll come back to it.

In my clinic, this data translates to real faces. The woman who tells me her jawline changed shape seemingly overnight. The woman whose moisturiser "stopped working" even though she is using the same one she has used for five years. Her moisturiser did not change. Her skin did. The infrastructure underneath it eroded, and the same product can no longer compensate for what has been lost structurally.

Why Perimenopause Feels Worse Than the Thing It Is Leading To

This is something I wish more women were told. Perimenopause is often harder on skin than actual menopause.

I know that sounds backwards. You'd think the worst phase would be after menopause, when oestrogen is at its lowest sustained level. But here's the thing: during perimenopause, oestrogen doesn't decline in a nice smooth curve. It spikes. It crashes. It spikes again. It drops lower than before, then surges unpredictably. This can go on for years. And your skin, which has oestrogen receptors on almost every major cell type, is responding to every single fluctuation with impeccable biological accuracy.

What does that look like in practice? Chaos. Genuinely. A breakout appears on skin that has been clear for twenty years, then vanishes, then comes back on the other cheek. Patches of oil and patches of dryness on the same face at the same time. A product works beautifully for three weeks, then suddenly triggers redness for no apparent reason. The woman is not imagining things and the product did not change. Her hormonal signal did, and her skin followed it.

This is why I am wary of the phrase "menopausal skin." It implies one stable condition with one stable set of needs. The reality is three distinct phases, and each one asks something different of your skincare.

Early perimenopause (your late 30s into early 40s, typically)

Oestrogen starts to wobble. Most women don't notice much on the surface yet. But barrier function is already shifting. Transepidermal water loss^{6Transepidermal water loss (TEWL)The rate at which water evaporates through the skin's outer layer.} ticks up. If you've always been on the sensitive side, this is often when it gets noticeably worse. Products that were perfectly fine six months ago might start stinging for reasons you can't explain.

Late perimenopause (mid-40s into early 50s)

The fluctuations intensify and the collagen decline accelerates. Ceramide^{7CeramidesLipid molecules in the stratum corneum that form the skin barrier's waterproof seal.} production drops because oestrogen was supporting it in the keratinocytes, and the skin barrier gets measurably weaker. Dryness becomes a daily problem rather than a seasonal one. This is the phase people describe as their skin "ageing overnight."

Post-menopause (twelve months without a period)

The wild fluctuations stop. Oestrogen settles at a lower, stable baseline. In a strange way, some women find this easier to manage than the volatility of perimenopause, because at least the skin's behaviour becomes predictable again, even if it's predictably more fragile. Collagen keeps declining, roughly 2% a year. The focus shifts from riding out the chaos to rebuilding what was lost.

Understanding which phase you're in changes the strategy. What I suggest to a woman in early perimenopause is different from what I suggest to someone five years post-menopause. The concentrations, the frequency of actives, the layering order. It all needs to evolve with the hormonal landscape. I went into the biology of this cyclical approach in my skin cycle article, and honestly, everything in that piece becomes doubly relevant once hormonal transition begins.

The Five Changes That Actually Drive Women Into My Clinic

I could list two dozen skin symptoms associated with oestrogen decline. I won't, because most of them aren't what brings women through the door. These five are.

1. Firmness disappearing, sagging appearing

Collagen decline made visible. The scaffolding that was holding everything taut against the bone structure underneath is literally thinning. Jawline softens. Cheeks lose their projection. Nasolabial folds carve deeper. People sometimes assume it's fat loss or muscle wasting. Sometimes those contribute, sure. But mostly it's the dermis itself losing density.

What actually helps here: procollagen-stimulating ingredients. Retinoids remain the gold standard, and I covered the evidence in my retinol vs peptides piece. But peptides, specifically collagen-signalling types like Palmitoyl Hexapeptide-12, work through a different mechanism and complement retinoid activity rather than duplicating it. The Collagen Renewal Complex was my attempt to provide that peptide-driven stimulus in a way that works alongside, not instead of, a retinoid protocol.

2. Dryness that no moisturiser can fix

This one frustrates people enormously. They buy a richer cream. They layer more on. They still feel tight two hours later. The problem is not at the surface. It's structural. When oestrogen drops, hyaluronic acid production in the dermis decreases. At the same time, ceramide levels in the stratum corneum^{8Stratum corneumThe outermost layer of the epidermis, forming the skin's physical barrier.} decline, so the barrier can't hold onto water the way it used to. You're putting moisture on top of a surface that can't retain it.

This is exactly why I built the 5D HA with five different molecular weights of hyaluronic acid. Ultra-low weight penetrates down to the intercellular matrix. Low weight reaches the deeper dermis. Medium weight sits in the mid-epidermis. High weight forms a surface film. And cross-linked HA provides extended-release surface moisture. Menopausal skin needs hydration at every single level because it's losing water at every single level.

3. Sensitivity that appeared from nowhere

Oestrogen is anti-inflammatory. People don't talk about this enough. When it declines, your inflammatory threshold drops. Things your skin tolerated perfectly well for years, a particular cleanser, the wind, certain active ingredients, can suddenly provoke stinging, redness, a feeling of heat. The skin isn't weaker. It's lost a buffer. The hormonal buffer that was dampening those inflammatory cascades.

Bio-Balance was built for this moment. Ectoin^{9EctoinA naturally occurring amino acid derivative that stabilises cell membranes and protects against inflammation.} for membrane stabilisation under stress, niacinamide for barrier reinforcement, squalane for lipid replenishment. I wrote about the broader science of barrier support in the city skin article, and the principles there apply doubly when the barrier is under hormonal pressure.

4. Dark spots and uneven tone

Melanocyte behaviour becomes erratic. Oestrogen was helping to regulate melanin production, and when it declines, you start to see patchy pigmentation, especially in areas with accumulated UV exposure. The skin is also thinner and more translucent now, which makes underlying pigmentation more visible than it would have been a few years ago.

Daily SPF becomes absolutely critical. Not optional. Not seasonal. The DNA Defence Sun Shield is the protection layer, and I struggle to overstate how much more important UV protection becomes when oestrogen is declining. UV on oestrogen-depleted skin accelerates damage through every mechanism simultaneously. I covered this in my daily DNA defence article.

5. Everything heals slower

Ashcroft's team published a genuinely important study in Nature Medicine in 1997 showing that oestrogen accelerates wound healing through TGF-beta1 upregulation. Without it, cuts take longer to close. Irritation lingers. Post-procedure recovery extends. Bruising happens more easily because the collagen-depleted dermis offers less cushioning for the capillary network.

An overnight repair strategy becomes the highest-leverage intervention here. The ExoYouth Sleep Mask creates an occlusive, peptide-rich environment during the hours when your skin's circadian repair activity peaks. I talked about this in the skin in your 30s, 40s and 50s article.

Why I Keep Coming Back to Peptides

I realise I talk about peptides a lot. I should probably explain why, because it isn't brand loyalty. It's pharmacology.

The standard menopause skincare advice is: retinol, vitamin C, hyaluronic acid, SPF. Done. And look, that's not bad advice. Those are good ingredients. But the recommendation treats menopause as though it were generic ageing, just slightly accelerated. It isn't. It's a specific hormonal withdrawal causing specific cellular consequences. And some of those consequences can be addressed more precisely with peptide chemistry than with the standard four ingredients alone.

The TGHA4®^{11TGHA4®SKIN|CYCLES' proprietary peptide complex of Argireline, Acetyl Tetrapeptide-5, Palmitoyl Hexapeptide-12 and Glutathione.} complex that runs through the SKIN|CYCLES range wasn't designed as a marketing concept. It was designed as a clinical response to a set of problems I was seeing in clinic every single day. Let me explain what each piece does in the context of menopausal skin, because the context changes things.

Argireline. A neurotransmitter-modulating peptide. Reduces the force of muscle contractions behind expression lines. During menopause, the collagen layer beneath those expression areas has thinned, so the same muscle movements create deeper, longer-lasting creases. Argireline doesn't stop movement. It softens the mechanical impact on a surface that can no longer absorb it as well.

Acetyl Tetrapeptide-5. This one targets the fluid dynamics around the eyes, reducing oedema and puffiness. Periorbital concerns get worse during menopause because microvascular integrity declines along with everything else. It's an area most skincare ranges don't address specifically enough.

Palmitoyl Hexapeptide-12. The most directly relevant component for what we're discussing here. It's a collagen-signalling peptide that stimulates fibroblast activity. Think of it as a workaround: the oestrogen signal that used to tell your fibroblasts to produce collagen has weakened, and this peptide provides an alternative instruction. Not a replacement for the hormone. An alternative route to a similar outcome.

Glutathione^{12GlutathioneThe body's primary intracellular antioxidant, protecting cells from oxidative damage.}. The body's own master antioxidant. I included it because oestrogen itself has antioxidant properties, and when it declines, the skin's oxidative defence takes a hit that gets less attention than it should. Glutathione addresses that gap at the cellular level.

I went deep on all of this in the Inside TGHA4® article, and if you've read this far, I'd genuinely suggest going back to that piece with the menopausal context fresh in your mind. It reads differently when you understand why these specific peptides were chosen.

The Delivery Problem Nobody Talks About

I need to raise something that sounds technical but has enormous practical implications. Peptides are large molecules. They don't waltz through the stratum corneum unaided. And during menopause, you've got a frustrating paradox: the skin that most needs these actives is simultaneously the skin that is least equipped to absorb them. The barrier is thinner (less collagen underneath) but the lipid matrix is also disordered (compromised ceramide composition), which creates unpredictable permeation pathways.

This is why liposomal encapsulation^{13Liposomal encapsulationA delivery technology that wraps actives in lipid vesicles to improve skin penetration.} is not an add-on feature in the SKIN|CYCLES range. Every product wraps its active peptides in phospholipid vesicles that are structurally similar to the skin's own lipid layers. Two things happen: the active gets deeper than it would in a conventional serum, and the release is controlled, so you don't get the kind of concentration spike at receptor sites that triggers irritation. For menopausal skin, which is already more reactive, that controlled-release profile is often the difference between a product the skin can tolerate and one it cannot.

The Actual Protocol I Recommend

People always want the routine, so here it is. This is what I tell women in my clinic who are navigating perimenopause or post-menopause and want a topical protocol they can follow at home.

Morning

Cleanse gently. Squalane Cream Cleanser. No foaming cleansers, no "deep clean" promises. Your barrier is compromised. Treat it accordingly. The temptation is to cleanse harder because the skin looks dull. Resist that. Stripping a weakened barrier makes every product you apply after it less effective, not more.

Serum. 5D HA on damp skin. The hyaluronic acid is hygroscopic, meaning it pulls water from its surroundings. If you apply it to dry skin, it pulls moisture from the dermis. On damp skin, it pulls from the water film you've just created. This matters more than people realise.

Moisturise. Bio-Balance. Every day. This isn't optional on menopausal skin. The barrier needs structural lipid support daily.

SPF. DNA Defence Sun Shield. Every single day. I'm not being dramatic. UV on oestrogen-depleted skin is exponentially more damaging because the repair mechanisms that used to fix UV-induced DNA damage were themselves oestrogen-dependent.

Evening

Double cleanse. You wore SPF all day (you did, right?). You need an oil-phase cleanse to dissolve it. ExoYouth Cleansing Balm first, then Squalane Cream Cleanser second.

Active treatment. Here's where it gets nuanced. I don't suggest retinol every night during menopause. The skin's tolerance is reduced. What I recommend instead: alternate nights. Retinol Youth Serum on some nights, Collagen Renewal Complex on others. You get the collagen benefit of both classes of ingredient without overwhelming a barrier that's already under stress. I wrote about this alternation approach in the retinol vs peptides piece.

Hydration layer. 5D HA again, damp skin again.

Overnight repair. ExoYouth Sleep Mask two or three nights a week as a final occlusive layer. Other nights, ExoYouth Radiance Cream. The occlusive matters because transepidermal water loss actually increases at night, and the barrier that's supposed to prevent it isn't doing its job fully.

What I Will Not Pretend Skincare Can Do

I would be lying to you if I said topical skincare can replace oestrogen. It cannot. No peptide, no retinoid, no serum of any kind can replicate what a systemic hormone was doing across dozens of cellular processes in every organ of the body. HRT has real, documented effects on skin collagen and thickness, and for women who are candidates for it, the dermatological benefits are meaningful alongside the cardiovascular, bone density and neurological benefits that get discussed more often.

But. And this is a big but. There is a wide, clinically useful space between "HRT fixes everything" and "nothing else matters." Topical retinoids, peptides, niacinamide and multi-weight hyaluronic acid, used consistently in well-formulated products, produce measurable improvements in skin thickness, elasticity, hydration and collagen density. Even in oestrogen-depleted skin. The published data supports this.

The critical word is "protocol." One product in isolation will do something modest. A coordinated system, where collagen stimulation, barrier support, hydration, antioxidant defence and UV protection are all addressed simultaneously, creates a compound effect that genuinely exceeds the sum of its parts. That's the operating principle behind the skin cycle concept that the brand is built on. Work with the biology, not against it.

When Should You Start? (The Answer Is Annoyingly Simple)

Earlier than you think you need to.

If you're in your late 30s and haven't noticed skin changes yet, good. That's the perfect time to build your foundation. Collagen was already declining at about 1% a year since your mid-twenties. Perimenopause is going to accelerate that. Starting a peptide and retinoid protocol now means you'll enter the hormonal transition with a stronger baseline.

If you're already in perimenopause and feeling it, starting now still matters enormously. That 30% figure from Brincat is a population average. It is not a fixed destination. Women who use effective collagen-stimulating regimens during this window demonstrably retain more collagen than those who don't. You can't prevent the hormonal shift. But you can change the rate at which its consequences accumulate.

And if you're post-menopausal, I want to be clear: it is not too late. Fibroblasts retain the capacity to respond to peptide and retinoid signals at any age. The results may take longer to become visible, and the ceiling of improvement may be lower. But improvement is achievable. I see it in clinic regularly. I wrote about the full decade-by-decade picture in the skin in your 30s, 40s and 50s article.

A Quick Word About HRT and Topical Skincare Together

If you're on HRT, brilliant. It is doing things for your skin that topical products cannot. But topical skincare isn't redundant. HRT addresses the systemic deficit. Your skin still needs products applied directly to it: SPF, barrier support, hydration, exfoliation. Those needs don't evaporate because you're on systemic therapy. If anything, you're in a fortunate position because the topical protocol and the HRT work synergistically.

If you're not on HRT, by choice or because of contraindications, the topical protocol carries even more weight. It's the most effective non-systemic intervention available, and it is entirely in your hands.

What I Actually Want You to Remember

Your skin is not failing you. I want to be really clear about this. It is doing exactly what the biology predicts it will do when oestrogen withdraws. The collagen loss, the dryness, the sensitivity. None of it is random. All of it is mechanistically explainable. And that is not depressing. That is useful. Because if you know the mechanisms, you know what to target.

Collagen stimulation. Barrier repair. Deep hydration. UV protection. Antioxidant defence. Five pillars. Five specific responses to five specific consequences of the hormonal shift. Not five marketing categories. Five biological necessities.

That is what SKIN|CYCLES was built around. Not to reverse menopause, because nothing does that. Not to replace hormones, because nothing topical can. To give your skin the targeted support it needs at the exact moment when the biology demands it most.

Alice Henshaw

RN · NMP · Founder of SKIN|CYCLES & Harley Street Injectables

Alice is the founder of SKIN|CYCLES, a cosmeceutical skincare range formulated around the proprietary TGHA4® peptide complex and sold at Harrods, Liberty and Harvey Nichols. She is also the founder and medical director of Harley Street Injectables, the largest clinic on Harley Street dedicated exclusively to non-surgical aesthetic treatments.

A qualified nurse prescriber registered in the UK, Australia and New Zealand, Alice is a Key Opinion Leader for Allergan Aesthetics, was named Best Aesthetic Injector in London by the GHP Awards, and has been featured in Vogue, Tatler, Vanity Fair, and the Tatler Cosmetic Surgery Guide.

LinkedIn @skincycles @harley_st_injectables

To explore the SKIN|CYCLES range, visit skincycles.com. To book a consultation at Harley Street Injectables, visit harleystreetinjectables.com or call +44(0) 3455 485 658.

Disclaimer: The information in this article is intended for educational purposes only and does not constitute medical advice. Hormonal changes during perimenopause and menopause affect individuals differently, and outcomes from topical skincare vary based on individual biology, health history and lifestyle factors. If you are experiencing menopausal symptoms, please consult a qualified healthcare professional for personalised guidance. Hormone replacement therapy (HRT) decisions should be made in consultation with a GP or menopause specialist. SKIN|CYCLES products are cosmeceutical formulations and are not medicines.

Sources

1. Thornton MJ. Estrogens and aging skin. Dermatoendocrinology. 2013;5(2):264-270. doi:10.4161/derm.23872. PMC3772914. Full text
2. Brincat M, Kabalan S, Studd JWW, Moniz CF, de Trafford J, Montgomery J. A study of the decrease of skin collagen content, skin thickness, and bone mass in the postmenopausal woman. Obstetrics & Gynecology. 1987;70(6):840-845. PMID: 3120067. PubMed
3. Affinito P, Palomba S, Sorrentino C, Di Carlo C, Bifulco G, Arienzo MP, Nappi C. Effects of postmenopausal hypoestrogenism on skin collagen. Maturitas. 1999;33(3):239-247. doi:10.1016/s0378-5122(99)00077-8. PMID: 10656502. PubMed
4. Hall G, Phillips TJ. Estrogen and skin: the effects of estrogen, menopause, and hormone replacement therapy on the skin. Journal of the American Academy of Dermatology. 2005;53(4):555-568. doi:10.1016/j.jaad.2004.08.039. PMID: 16198774. PubMed
5. Shu YY, Maibach HI. Estrogen and skin: therapeutic options. American Journal of Clinical Dermatology. 2011;12(5):297-311. doi:10.2165/11589180-000000000-00000. PMID: 21714580. PubMed
6. Emmerson E, Hardman MJ. The role of estrogen deficiency in skin ageing and wound healing. Biogerontology. 2012;13(1):3-20. doi:10.1007/s10522-011-9322-y. PMID: 21369728. PubMed
7. Ashcroft GS, Dodsworth J, van Boxtel E, Tarnuzzer RW, Horan MA, Schultz GS, Ferguson MWJ. Estrogen accelerates cutaneous wound healing associated with an increase in TGF-beta1 levels. Nature Medicine. 1997;3(11):1209-1215. doi:10.1038/nm1197-1209. PMID: 9359694.
8. Duarte GV, Trigo AC, Paim de Oliveira MF. Skin disorders during menopause. Cutis. 2016;97(2):E16-E23. PMID: 27023099.
9. Lephart ED, Naftolin F. Menopause and the skin: old favorites and new innovations in cosmeceuticals for estrogen-deficient skin. Dermatology and Therapy. 2021;11(1):53-69. doi:10.1007/s13555-020-00468-7. PMID: 33230672. PubMed
10. Viscomi L, Muniz M, Sattler S. Managing menopausal skin changes: a narrative review of skin quality changes, their aesthetic impact, and the actual role of hormone replacement therapy in improvement. Journal of Cosmetic Dermatology. 2025. doi:10.1111/jocd.70393. Full text

This article is intended for informational purposes. It does not constitute medical advice. For personalised treatment recommendations, please book a consultation.