There was a time when hitting your 50s meant quietly accepting that your skin would become drier, thinner and generally more unpredictable, a sort of unspoken truce with time and hormones. Thankfully, those days are behind us. We now understand the physiology of skin in perimenopause and menopause far better than we once did, how falling oestrogen changes collagen turnover, how hyaluronic acid production slows and how shifts in sebum and barrier lipids affect hydration and texture. In essence, your skin is responding logically to a new hormonal landscape, not ‘ageing badly'.
In your 50s, especially if you’ve moved through or are moving through the perimenopausal years, you’re not just contending with ageing skin in the generic sense. There’s a combination of the interplay of hormonal shifts, cumulative sun damage, changing facial architecture and altered skin physiology all going on at the same time. In this article I will attempt to detangle what’s changed and how to respond efficiently. The clever bit is knowing how to support it with a few targeted, scientifically sound products that protect, restore and coax the skin back to equilibrium rather than a dozen complicated steps. At this stage of life, skincare can help your skin behave as well as it possibly can, given what it’s navigating.
Why Skin Changes in Your 50s: The Hormone Connection
Perimenopause and menopause mark one of the most profound biological shifts in the body and the skin feels every bit of it. Oestrogen, long your silent skincare ally, regulates the fibroblasts that make collagen and elastin, the lipids that keep the barrier supple and even the enzymes that maintain hydration. As levels fall, collagen production can decrease by up to 30 per cent in the first five years post-menopause. The result is skin that feels drier, thinner and less resilient, often more reactive than before.
Hyaluronic acid and ceramide production also declines in the skin, leading to that parched, tight sensation many women describe. Alongside this, sebum output drops, which can mean you suddenly feel as though you’ve switched skin types. Since oestrogen helps regulate melanocyte activity, pigmentation and uneven tone often appear at this stage. None of this is failure; it’s biology doing its work. The aim with skincare is to adapt intelligently, supporting the skin with ingredients that replace what’s been left, reinforce what’s there and protect against further issues.
Why your skin behaves differently around the perimenopause and menopause
Around the perimenopause, the sneaky transition before the menopause proper, your skin enters a unique chapter. Hormone levels begin to swing and dip rather than decline in a straight line and this has ripple effects throughout the skin’s biology. Here’s what the science shows:
Decline in oestrogen and collagen/structural integrity:
- In the perimenopausal and post-menopausal period, the decline in oestrogen ripples through the skin’s architecture. Oestrogen receptors (ER-α and ER-β) are present on dermal fibroblasts, the cells responsible for producing collagen and elastin (the main proteins that give the dermis its strength), thickness and resilience. When oestrogen levels fall, the stimulation of these fibroblasts declines. At the same time, the balance between matrix synthesis and matrix breakdown changes: the expression of matrix metalloproteinases (MMPs), enzymes that degrade structural proteins such as collagen type I and III and elastin, increases. The combined effect is a net loss of collagen, thinning of the dermis and weakening of the skin’s structural scaffold. This in turn contributes to increased laxity, deeper wrinkles and diminished firmness. There is robust evidence that oestrogen supplementation (in the form of topical 17β-estradiol can significantly improve the situation (i.e. it’s not all bad news!) (Philips N et al., 2003). Indeed, from a quantitative standpoint, one meta-analysis found that women not receiving hormone replacement therapy may lose approximately 2% of dermal collagen per year after menopause, compounded by the reduced dermal thickness (~1.1 % per year) observed in the same studies (Lephart & Naftolin, 2022).
- The clinical significance of this is clear: thinner dermis, fewer collagen fibres, more MMP-mediated degradation results in skin that is less plump, less springy and more susceptible to the mechanical forces of gravity, facial expression and volume change.
- In short, the structural integrity of the skin is compromised, which explains much of the visible ‘loosening’ and textural change seen in the 50s, especially for women in the peri- and post-menopausal phase.
Reduced hyaluronic acid and sebum production resulting in a weaker barrier and increased water loss:
- In the decline of oestrogen that accompanies the perimenopause and menopause, several less-frequently discussed changes begin to undermine the skin’s capacity to retain moisture and maintain a robust barrier. Aside from collagen and elastin, oestrogen has been shown to stimulate the production of glycosaminoglycans (including hyaluronic acid) in the dermis and support oil and ceramide production in the epidermis. Research indicates that oestrogen deprivation leads to diminished fat synthesis in the stratum corneum (particularly ceramides of longer chain length) and a rise in transepidermal water loss (TEWL), evidence of weakened barrier integrity (Kendall et al., 2022; Winston et al., 2002).
- As the barrier lipids fall, especially ceramides, and sebaceous output declines, the skin gradually becomes more vulnerable to desiccation, roughness and sensitivity. Specifically, a recent study observed that post-menopausal women had significantly lower ceramide levels, shorter average chain length of ceramides, and higher TEWL compared to pre-menopausal controls; importantly, these changes were less apparent in women on hormone replacement therapy (HRT), suggesting a direct role of oestrogen in maintaining barrier homeostasis (Kendall et al., 2022). Clinically, this barrier compromise manifests as the sensation of tightness, flaking, increased roughness or sensitivity common complaints in women in their 50s and beyond.
- From a treatment perspective, recognising that the skin’s moisture-retaining and lipid-sealing systems are hormonally influenced provides a sound rationale for recommending barrier-supportive skincare: products rich in ceramides, humectants (such as hyaluronic acid) and gentle, anti-inflammatory formulations suitable for more reactive skin rather than aggressive exfoliants.
Pigmentation and flare-ups:
- The fluctuating hormone levels of the perimenopause can also disrupt the behaviours of melanocytes, the skin’s pigment-producing cells. This can render you more vulnerable to persistent
hyper-pigmentation, such as sunspots (solar lentigines) and worsening of Melasma. It is now well established that oestrogens can directly increase production of melanin (via increased expression of melanocortin receptors and microphthalmia-associated transcription factor (MITF) pathways) while progesterone may exert a dampening effect.
- In the peri- and post-menopausal phase, the decline in oestrogen combined with cumulative UV exposure and diminished repair capacity appears to amplify the risk of pigmented lesions. For example, studies demonstrate increased expression of oestrogen receptors in the epidermis and upper dermis of melasma-affected skin, supporting the notion that hormonal changes can exacerbate melanocyte activation and pigment deposition.
- From a practical standpoint, this means that skin in its 50s is less forgiving when it comes to uneven colour: fewer hormonal buffers, slower turnover and a thinner epidermis can all conspire to make pigmentation appear more stubborn. The aim in skincare thus shifts to pigment prevention and regulation (
daily broad-spectrum SPF, consistent
antioxidant use, and gentle yet effective
tone-correcting actives.

Structural fatigue and support loss:
- The architecture of the face, much like that of a grand old building, relies on a complex interplay of scaffolding and filler: bone, deep and superficial fat pads, muscle tone, connective ligaments and the overlying skin envelope. With time, each of these elements undergoes subtle but measurable change and the harmony between them begins to shift. From the late forties onward, the superficial and deep fat compartments of the face - particularly those of the midface, temples and periorbital region - begin to atrophy and descend under gravity. The effect is twofold: volume loss where you want it least (under the eyes, in the cheeks) and heaviness where you don’t (along the jawline and lower face).
- At the same time, the bony foundations themselves are not static. Menopause and oestrogen decline accelerate skeletal remodelling, particularly in the maxilla (the bone supporting the upper teeth) and the mandible (the jawbone). Imaging studies have demonstrated resorption along these areas, leading to reduced midfacel projection and widening of the lower face. These subtle changes alter the tension and anchoring of the overlying soft tissues, compounding the visual effects of sagging and hollowing as the fat pads descend towards the middle of the face. In women, declining oestrogen also influences the metabolism of osteoblasts and osteoclasts (the bones involved in bone build up and bone resorption, respectively) further contributing to facial bone demineralisation and contour loss (Shaw and Kahn, 2007; Mendelson and Wong, 2015).
- Finally, as the supporting collagen and elastin matrix degrades, and as mimetic muscle tone relaxes, the connective ‘retaining’ ligaments that tether the skin to the deeper structures begin to stretch. The once-sharp transition from cheek to jawline blurs, nasolabial and marionette folds form and progressively deepen and the face takes on a subtly ‘tired’ geometry. It’s a cumulative, structural fatigue resulting from each of these elements: slow, inevitable and highly individual. This is why treatments targeting volume, lift and collagen support must always consider anatomy as a dynamic whole rather than a two-dimensional surface.
In plain English: your skin isn’t simply ‘getting older’. It’s negotiating a new hormonal environment, managing accumulated damage and losing volume, bounce and resilience in incremental but perceptible ways. While your favourite serum may still feel familiar, your skin no longer responds with the same gusto. Hence the need for a recalibrated routine.
A streamlined ‘core’ routine for your 50-something skin
So now we’ve established that menopausal and perimenopausal skin behaves differently it’s time to decipher how we can deal with the key issues to optimise the way your skin functions around this time Collagen loss, barrier fragility and reduced lipid synthesis are no longer mysteries but measurable biological events. The good news is that we now understand these mechanisms far better than even a decade ago. Skin science has become more sophisticated, allowing us to address hormonal and structural changes with a level of nuance that once belonged only in academic papers.
Where older advice might have focused simply on ‘hydration’ or ‘anti-ageing’, we now talk about more targeted molecular repair: replacing lost ceramides to strengthen the barrier, supplying antioxidants that modulate melanocyte activity, supporting mitochondrial function to improve cellular energy and using advanced retinoids that stimulate fibroblasts without overwhelming sensitive skin. Modern skincare for women in their fifties is all about fine-tuning the system and supporting the natural changes as they happen.
I designed my formulations with that philosophy in mind: products that work with the skin’s evolving physiology rather than against it. Each one corresponds to a biological need: cleansing that replenishes rather than strips; antioxidant serums that actively prevent oxidative and pigmentary stress; sunscreens that double as barrier support; and night treatments that encourage collagen renewal while also restoring lipids and helping DNA repair itself. What follows is a practical sequence grounded in how skin at this age truly functions and how science can now support it with intelligence and restraint.
Cleansing with respect for the barrier
Cleansing in your fifties requires consideration of the barrier and protecting what remains. As I mentioned, the skin’s lipid barrier naturally depletes with hormonal change, making it prone to dryness and sensitivity. Using harsh foaming agents or acids can worsen trans-epidermal water loss (TEWL) and micro-inflammation, both of which accelerate visible ageing. The answer lies in lipid replenishment rather than removal. Ceramides the waxy lipids that account for nearly half of the skin barrier’s composition — are crucial here. They help form the protective matrix that keeps moisture in and irritants out.
Step in
Afterglow, my ceramide-rich cleansing balm. This advanced balm cleanser is designed to dissolve impurities without stripping, and to deposit barrier-building lipids back into the skin. It also includes emollients that mimic the skin’s natural sebum composition, a subtle but important point, since sebum levels drop significantly after menopause. The formulation includes ceramide NP, AP and EOP, cholesterol and phytosphingosine (key barrier lipids), alongside hyaluronic acid (a potent humectant) and a mild exfoliant blend of fruit enzymes and azelaic acid.

In practical terms this means that for menopausal skin which is more fragile, more sensitive and more prone to dehydration, Afterglow offers a double benefit: it cleanses (removing makeup, SPF and daily debris) without stripping the barrier and it replenishes lipids and hydration simultaneously. Moreover, the gentle exfoliation via fruit enzymes and the powerful anti-inflammatory azelaic acid helps maintain texture and brightness at a time when cellular turnover is slowing and skin tone can become uneven. The exfoliation is mild enough not to provoke barrier disturbance, which is key when skin is less resilient. In short: Afterglow respects the ageing barrier, supports it and adds light renewal. The goal is to leave skin clean, calm and ready for active ingredients rather than tight and depleted. You can also use it for longer than it says on the tin: leave it on for 15-20 minutes as a mask every few days and your skin will really benefit.
Antioxidant protection and brightening in the morning
One of the biggest challenges in menopausal skin is the rise in oxidative stress and decline of the mechanisms designed to deal with it. Declining oestrogen correlates with an increase in reactive oxygen species (ROS) molecules that damage collagen, DNA and cell membranes. As I discussed above, combined with UV exposure and pollution this creates a daily oxidative burden that accelerates pigment production and collagen loss. To counter this, antioxidants like vitamin C, azelaic acid and niacinamide become indispensable.
My daily serum
Good Morning was formulated as a simple but potent morning step: a multi-antioxidant serum that addresses both oxidative damage and pigmentation and sets your skin up for the day ahead. 10% vitamin C, in a highly stabilised form, helps neutralise free radicals while also stimulating collagen synthesis by activating pro-collagen gene expression. Azelaic acid and niacinamide work in tandem to regulate uneven tone: azelaic acid by inhibiting tyrosinase (the enzyme responsible for melanin production, also inhibited by vitamin C) and niacinamide by interrupting the transfer of pigment to surrounding keratinocytes. The combination brightens dullness, strengthens barrier function and improves elasticity over time.
Daily sunscreen in the perimenopause and menopause: a skincare non-negotiable
If there’s a single step that outperforms all others in preserving skin health, it’s daily sun protection. UV exposure remains the principal driver of premature ageing, responsible for up to 80% of visible skin changes. By the time you’re in your fifties, your cumulative sun exposure is substantial and the skin’s ability to repair UV-induced DNA damage is diminished, meaning consistent SPF protection becomes not just helpful but essential.
All Day Long, my SPF 50 + daily moisturiser, was formulated to simplify this habit. A moisturiser and SPF in one, it combines broad-spectrum UV and blue light filters with niacinamide and vitamin E, the latter of which enhances the antioxidant effect of the Vitamin C in Good Morning. Vitamin E also nourishes the lipid barrier, counteracting some of the dryness that SPF formulations can cause. The inclusion of niacinamide further reduces redness and blotchiness while supporting ceramide synthesis, a quiet but critical contribution to overall resilience.
Retinoids for menopausal skin: Repairing damaged skin overnight
Evening is when the skin’s natural repair processes peak, collagen synthesis, cellular turnover and barrier restoration are most active overnight. In your fifties, this rhythm slows. A well-formulated night product should therefore encourage cell renewal without irritation, support collagen production and replenish lipids simultaneously.
I developed
Good Night to meet these criteria. It features a granactive retinoid, a next-generation vitamin A derivative that converts to retinoic acid in the skin without the dryness or flaking typical of older formulations. Retinoids remain the gold standard for collagen induction but in mature or hormonally sensitive skin, tolerance is key - hence the choice of this retinoid over more traditional retinol based formulas. In Good Night, I paired it with gentle polyhydroxy acids (PHAs) hydrating, calming acids which help to refine the skin’s texture and peptides that act as molecular ‘messengers’, which work alongside the retinoid to stimulate fibroblast activity and enhance elasticity. Together, these active ingredients help rebuild what time and hormones have gradually worn down resulting in smoothing, firming and strengthening of the skin.
Deep nourishment and mitochondrial repair
During menopause, another process accelerates quietly beneath the surface: mitochondrial decline. These are the energy generators of our cells and when their efficiency wanes, skin repair, hydration and barrier renewal all suffer. Oxidative damage also accumulates faster. One of the most promising ingredients for this is resveratrol, a polyphenol found in grapes and Japanese knotweed which has been shown to activate SIRT1 pathways and improve mitochondrial resilience.
My new reparative barrier cream
Skin Cushion was designed to replenish depleted ceramides and essential fatty acids from the skin’s barrier while delivering a dose of resveratrol to help restore the skin’s energetic capacity. The effect is visibly stronger, healthier skin: the kind that holds hydration, reflects light more evenly and responds better to everything else you do.
Why this system works
I designed this routine to reflect what ageing skin truly needs rather than what marketing trends dictate. The routine is based on the physiology of mature skin I’ve discussed here including reduced lipid synthesis, collagen decline, increased TEWL and oxidative stress. The products work together to provides targeted answers including rebuilding the barrier, protecting collagen and elastin, stimulating renewal and restoring cellular energy production and hence repair. Whilst it’s not a ‘miracle’ system (no products truly are); it’s a pragmatic, biological one, designed to work with your skin as it changes. It’s also in a simple format that is easy to stick to. Far too often when there are too many complex steps, people get tired of this an end up not sustaining use over the longer term. The simplicity of the steps allow users to adhere for longer and get the maximal benefits as a result.
Final thoughts
Your skin at 50-plus isn’t giving up; it’s simply evolving. The changes you see: dryness, uneven tone, softer contours, are part of a new biological rhythm on multiple fronts rather than a straightforward decline. In this decade and beyond your skin needs different support. When you answer this need with simplicity and science: a routine that restores lipids, defends against oxidative stress and gently stimulates renewal and repair, your skin responds in kind. This stage relies on investing in long-term skin health and resilience.
If you’re ready to build a skincare routine tailored to how your skin behaves now, explore the Dr.
David Jack Skin Health Systems, clinically designed for skin in its 40s, 50s and beyond. Discover the range
here or
book a consultation to create your personalised skin plan in clinic.
References
Kendall, A.C., Pilkington, S.M., Wray, J.R., Newton, V.L., Griffiths, C.E.M., Bell, M., Watson, R.E.B. & Nicolaou, A. (2022) ‘Menopause induces changes to the stratum corneum ceramide profile, which are prevented by hormone replacement therapy’, Scientific Reports, 12, 21715. Available at:
https://pubmed.ncbi.nlm.nih.gov/36522440/ [Accessed 7 November 2025]
Mendelson, B. and Wong, C-H. (2012). Changes in the facial skeleton with aging: implications and clinical applications in facial rejuvenation [Journal Article] in Aesthetic Plastic Surgery, 36(4), pp. 753–760. Available at:
https://pubmed.ncbi.nlm.nih.gov/22580543/ [Accessed 8 November 2025]
Natale, C.A., Duperret, E.K., Zhang, J., Sadeghi, R., Dahal, A., O’Brien, K.T., Cookson, R., Winkler, J.D. and Ridky, T.W. (2016). Sex steroids regulate skin pigmentation through nonclassical membrane-bound receptors [Journal Article] in eLife, 5:e15104. Available at:
https://elifesciences.org/articles/15104[Accessed 8 November 2025]
Shah, M.G. and Maibach, H.I. (2001). Estrogen and skin: an overview [Journal Article] in American Journal of Clinical Dermatology, 2(3), pp.143–150. Available at:
https://pubmed.ncbi.nlm.nih.g ov/11705091/ [Accessed 7 November 2025]
Shaw, R.B. Jr and Kahn, D.M. (2007). Aging of the midface bony elements: a three-dimensional computed tomographic study [Journal Article] in Plastic and Reconstructive Surgery, 119(2), pp. 675–681. Available at:
https://pubmed.ncbi.nlm.nih.gov/17230106/ [Accessed 8 November 2025]
Stevenson, S. and Thornton, M.J. (2007). Effect of estrogens on skin ageing and the potential role of selective estrogen receptor modulators (SERMs) [Journal Article] in Clinical Interventions in Aging, 2(3), pp.283–297. Available at:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2685269/[Accessed 8 November 2025]