Understanding skin at different ages.

A child’s skin is not a miniature version of an adult’s: it is an organ in full development, whose structures and functions are progressively established over the years. From birth until roughly six years of age, the skin barrier strengthens, cells renew at a rapid rate and the microbiome gradually stabilises. These transformations, both microscopic and visible, shape the skin to prepare it for its mission: protecting the body from the external environment.

In the newborn, the skin is thin, permeable and particularly vulnerable to environmental insults. The stratum corneum consists of loosely packed lipids and small corneocytes, which makes the skin barrier less effective than in adulthood. Water loss through the skin is thus higher, which explains infants’ tendency to exhibit dry skin. As growth continues, the skin becomes thicker and more resilient. By the age of six, stratum corneum thickness, water loss and corneocyte size reach levels comparable to those of adults.

Moreover, during early childhood, cellular metabolism is sustained by the high proliferation of keratinocytes. Similarly, melanocyte activity, the cells that produce melanin, gradually increases. Children’s complexions become slightly darker, while the skin thickens and gains resistance to UV radiation. However, this developing skin remains highly sensitive to the sun. The melanogenesis is not yet optimal and the defence mechanisms against free radicals are immature. This is why it is very important not to expose the children to the sun.

Finally, the skin microbial ecosystem undergoes a gradual progression as well. In infants and young children, bacteria of the phylum Firmicutesdominate the skin flora, whereas in adults it is primarily the Proteobacteriaand the Actinobacteriathat predominate. Microbial diversity increases and gradually stabilises, allowing immunity to strengthen.

The skin continues to develop between childhood and adulthood. Puberty marks the onset of an intense hormonal stimulation, notably of androgens (testosterone and dihydrotestosterone). These hormones activate the sebaceous glands, leading to increased sebum production. Sebum contributes to the hydrolipidic film, a barrier that limits water loss and protects the skin from external aggressors. However, during adolescence, sebum production is often excessive and tends to clog pores. Combined with hyperkeratinisation, this process promotes the formation of comedones and microcysts.

This imbalance is exacerbated by an evolving skin flora. The proliferation of Cutibacterium acnes, a bacterium naturally present in hair follicles, intensifies in sebum-rich environments. This microbiological imbalance triggers inflammation and the onset of the first acne lesions. Sebaceous activity is generally at its highest during adolescence: it often peaks around 16–18 years of age before stabilising.

Moreover, the pigmentary system continues to self-regulate during adolescence. Melanocyte activity, stimulated by hormones and sun exposure, increases slightly, which can alter the complexion. In certain cases, post-inflammatory hyperpigmentations appear following acne lesions, as the skin overreacts to inflammation by producing more melanin. Furthermore, excessive unprotected sun exposure during adolescence can cause lasting damage, notably premature degradation of collagen and elastin fibres, which will promote premature skin ageing in adulthood.

Between the ages of 20 and 30, the skin attains a physiological equilibrium: the skin barrier functions effectively, microcirculation is well regulated and sebum production continues to maintain a good level of hydration. Cell turnover remains rapid, imparting a radiant appearance and a uniform texture to the complexion. Yet, from this decade onwards, the first biological signs of ageing begin to set in slowly, well before they become visible. The activity of fibroblasts, the cells responsible for producing collagen, elastin and glycosaminoglycans, begins to diminish. This decline results in a slight reduction in dermal density and cohesion, initiating a progressive loss of firmness and elasticity.

Concurrently, the synthesis of hyaluronic acid gradually diminishes, reducing the skin’s capacity to retain water in the extracellular matrix. This reduced hydration manifests as skin that can be more sensitive to temperature fluctuations or lifestyle factors and the appearance of the first dehydration lines, most often at the outer corners of the eyes. Oxidative stress, exacerbated by UV exposure, pollution or lack of sleep, also starts to impair dermal structures by promoting collagen breakdown through metalloproteinases. Although these changes may still be imperceptible to the naked eye for some, they set the stage for skin ageing to come.

Discover here evidence-based tips for maintaining healthy skin between the ages of 20 and 30.

Between the ages of 30 and 40, the skin enters a transition phase where the signs of ageing become truly apparent. Cellular renewal slows down: keratinocytes migrate more slowly towards the surface, which makes the complexion duller and the skin texture less even. Fibroblast activity continues to decline, reducing the synthesis of type I and III collagen, as well as elastin. At the same time, hyaluronic acid production keeps decreasing, impairing the dermis’s ability to retain water and leading to a loss of volume and suppleness. The dermo-epidermal junction, which maintains cohesion between the skin layers, becomes flatter and less efficient, resulting in a less uniform diffusion of nutrients and water towards the epidermis.

In addition, under the influence of external factors, such as UV rays or pollution, the fibres of collagen and elastin begin to fragment. This disruption of the dermal network promotes the appearance of the first expression lines, particularly around the eyes and mouth, where muscle movements are repeated. The skin tends to become thinner, sometimes drier, and its ability to regenerate after an insult decreases. In some individuals, cutaneous microcirculation becomes slightly impaired, which accentuates the loss of radiance and favours the formation of localized pigmented spots. This decade thereby marks the transition from still youthful skin to skin in which the signs of cutaneous ageing become perceptible.

Find here advice on caring for your skin between the ages of 30 and 40.

Between 40 and 50 years of age, the skin undergoes a clear acceleration in biological ageing. The gradual decline in hormonal activity, particularly that of oestrogens in women plays a major role in this process. These hormones normally stimulate the production of collagen, elastin and hyaluronic acid. Their decline during perimenopause, and then at menopause, leads to a marked decrease in dermal density and in the skin’s water‐retention capacity. The dermis consequently loses thickness and mechanical strength, intensifying skin laxity and deepening wrinkles. Fibroblast numbers and activity diminish, reducing the repair of damaged fibres. Meanwhile, the hydrolipidic film becomes impoverished, exacerbating dryness and weakening the skin barrier.

Furthermore, pigment spots become more frequent during this decade owing to disrupted melanocyte activity and a less homogeneous distribution of melanin. Microcirculation slows, reducing the delivery of oxygen and nutrients, hence a typically duller complexion and less radiant skin. At the same time, oxidative stress induced during metabolism and following UV exposure intensifies the degradation of structural proteins and the stiffening of elastin fibres, a phenomenon known as actinic elastosis.

Discover here science-backed advice on caring for your skin as you approach your fifties.

From the age of 50, the skin enters a phase of profound structural ageing. Hormonal changes, notably the drop in oestrogens after the menopause, accelerate alterations that had already begun in preceding decades. Fibroblast activity continues to decline, as does the synthesis of collagen, elastin and hyaluronic acid. The dermis thins and loses density: expression lines deepen, the skin envelope becomes less plump, and the skin loses firmness and elasticity. Blood circulation, increasingly reduced, limits the supply of nutrients and oxygen, giving the complexion a duller, more fatigued appearance.

In the epidermis, the reduction in Langerhans cells, immune cells, weakens the skin’s natural defences and increases the risk of cutaneous infections. Cellular turnover also slows, resulting in a rougher surface and a impairment of barrier function. Finally, in the hypodermis, the number and size of adipose cells decrease, leading to a loss of facial volume, hollowing of the cheeks, and the appearance of under-eye bags and deep wrinkles.

Discover here science-backed advice on caring for your skin after the age of 50.

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