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as a key mediator of metabolism and stress via the hypothalamic pituitary adrenal axis, and female sex hormones jointly orchestrate tissue repair, inflammatory balance, extracellular matrix homeostasis and barrier integrity. Of particular note, cutaneous biology appears
to depend not only on hormone levels but also on the rhythmicity and coherence of endocrine signals. Regular profiles support balanced adaptation, whereas dysregulated states increase vulnerability and alter ageing trajectories, most markedly during phases of hormonal variability such as the menstrual cycle and the peri to post- menopausal transition. This framework justifies a shift from symptom
oriented anti-ageing towards a biologically informed well ageing model, structured around molecular networks such as barrier function, dermal remodelling, inflammatory cascades, pigmentation pathways, sebaceous activity and microbiome dynamics, rather than around a single target or ingredient.
Staging the menopausal transition: from premenopause to postmenopause The menopausal transition is scientifically described according to the STRAW+10 system, the reference framework in reproductive endocrinology, based on menstrual cycle characteristics and hormonal markers (FSH, AMH, inhibin B). Premenopause corresponds to the full
reproductive period: regular cycles, followed by a slight, discreet decline in AMH and antral follicle count towards the end of this period, without perceptible change. Perimenopause begins with marked cycle
variability, elevated but fluctuating FSH, and subsequently progresses to skipped cycles or amenorrhea, with unpredictable residual ovarian activity. FSH, or follicle-stimulating hormone, is
secreted by the anterior pituitary gland and constitutes the key marker of ovarian ageing and the menopausal transition. This late stage, lasting one to three years, accounts for the majority of hot flushes and night sweats. It ends 12 months after the final menstrual period.2 Postmenopause begins retrospectively
from this point. Its early phase (five to eight years) is characterised by rapid changes in FSH and estradiol before stabilisation; vasomotor symptoms frequently persist during this period. The late phase marks a definitive hormonal stabilisation, in which overall somatic ageing becomes the dominant factor.
Menopausal skin: an active steroidogenic organ Skin is not merely a passive target of circulating steroid hormones, it is itself a peripheral steroidogenic organ, capable of locally synthesizing its own steroids, a phenomenon known as cutaneous ‘intracrinology’.3 The cell types involved are keratinocytes,
dermal fibroblasts, hair follicle cells and, most notably, sebocytes, the most steroidogenically active, a point worth considering when selecting
PERSONAL CARE MAGAZINE October 2026
models and skin sites for efficacy testing. The mechanism relies on cutaneous uptake
of adrenal DHEA/DHEA-S, locally converted by cutaneous enzymes (3β-HSD, 17β-HSD, 5α-reductase, aromatase). This produces active androgens (testosterone, DHT, linked to sebum production, hormonal acne and androgenetic alopecia), oestrogens (estradiol, estrone) and corticosteroids.4
This mechanism helps explain the diversity
of manifestations observed in peri- and postmenopause: as ovarian oestrogen production declines, adrenal DHEA, still taken up by the skin, allows residual local synthesis of estradiol or DHT, depending on the enzymatic balance specific to each skin site and each woman. This locally produced androgen/oestrogen
ratio contributes to the relative hyperandrogenism characteristic of perimenopause, while also modulating dryness, loss of firmness and sensitivity. For dermocosmetics, this dimension supports
an evaluation approach that also targets the enzymatic pathways and biomarkers of this local metabolism, guiding the development of actives that modulate cutaneous 5α-reductase or aromatase, closer to the skin’s actual physiology than to systemic hormonal status alone.
Cutaneous signs of menopause The sustained decline in oestrogen results in intrinsic cutaneous ageing comparable to age related ageing, yet accelerated and accentuated. Its manifestations are progressive and highly variable between individuals. Dryness is among the earliest signs of oestrogen deficiency; in perimenopause, it is compounded by relative
hyperandrogenism such as acne, hirsutism and hair loss, arising from the loss of balance between androgens, oestrogens and progesterone. These signs may be categorized along several
axes: ■ Colour and pigmentation: redness, senescent age spots, loss of radiance and complexion homogeneity. ■ Skin topography: crow’s feet, furrows, forehead lines, fine lines of the upper lip and periorbital area, roughness. ■ Hydration: drier epidermis and dermis, reduction in natural moisturizing factors. ■ Skin structure: loss of density and thickness, alteration of the dermo epidermal junction and barrier function. ■ Volume: slackening of the face and neck, loss of facial contour, eye bags, eyelids. ■ Biomechanical properties: loss of firmness, tone and elasticity. These signs are frequently accompanied by
alopecia and nail alterations, as well as hot flushes and vascular disorders.
Histological changes The structural changes observed at menopause are now well documented. At the epidermal level, a decrease in the number of cell layers, a slowing of cell renewal and a loss of adhesion at the epidermal junction are observed. At the dermal level: a decline in cellular activity and number; a reduction in collagen content of approximately 30% within the five years following menopause; a modification of the collagen III/I ratio; an increase in metalloproteinases (MMP 1 and MMP 3, degrading enzymes); a rarefaction and horizontalization of collagen fibres; a
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