Understanding the skin at different ages.

A child’s skin is not a miniature version of an adult’s: it is an organ in active development, whose structures and functions gradually take shape over the years. From birth to around age six, the skin barrier strengthens, cells renew rapidly, and the microbiome slowly stabilizes. These transformations, both microscopic and visible, mold the skin to prepare it for its role: 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 adults. As a result, water loss through the skin is higher, explaining infants’ tendency to have dry skin. As they grow, the skin becomes thicker and more resilient. By about six years of age, stratum corneum thickness, water loss, and corneocyte size reach levels comparable to those in adults.

Furthermore, during early childhood, cellular metabolism remains high due to the rapid proliferation of keratinocytes. Likewise, 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 sunlight. The process of melanogenesis is not yet optimal and the free radical defense mechanisms are immature. This is why it is very important not to expose the children to the sun.

Finally, theskin's microbial ecosystem also undergoes a gradual evolution. In infants and young children, bacteria of the phylum Firmicutes dominate the skin flora, whereas in adults, it is mainly the Proteobacteria and the Actinobacteria that predominate. Microbial diversity increases and gradually stabilizes, allowing immunity to strengthen.

The skin continues to evolve between childhood and adulthood. Puberty marks the starting point of a heightened hormonal stimulation, especially by androgens (testosterone and dihydrotestosterone). These hormones activate the sebaceous glands, resulting in an increased production of sebum. Sebum contributes to the hydrolipidic film, a protective layer that limits water loss and shields the skin from external aggressors. However, during adolescence, sebum production is often excessive and tends to lead to pore blockage. Combined with hyperkeratinization, this phenomenon promotes the formation of comedones and microcysts.

This imbalance is exacerbated by an evolving skin microbiota. The proliferation of Cutibacterium acnes, a bacterium naturally present in the 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 ages 16 to 18 before stabilizing.

Furthermore, the pigmentary system continues to regulate itself during adolescence. Melanocyte activity, stimulated by hormones and sun exposure, increases slightly, which can alter skin tone. In some cases, post-inflammatory hyperpigmentations can appear following acne lesions, as the skin overreacts to inflammation by producing more melanin. Additionally, excessive unprotected sun exposure during adolescence can lead to lasting damage, notably premature alteration of collagen and elastin fibers, which will promote apremature skin aging in adulthood.

Between the ages of 20 and 30, the skin reaches a physiological equilibrium: the barrier function is efficient, microcirculation is well regulated, and sebum production still maintains an adequate level of hydration. Cellular turnover remains rapid, giving the complexion a radiant appearance and an even texture. Yet, during this decade, the first biological signs of aging begin to set in slowly, long before they become visible. Fibroblast activity—the cells responsible for producing collagen, elastin, and glycosaminoglycans—starts to decline. This decrease leads to a slight reduction in dermal density and cohesion, initiating a gradual loss of firmness and elasticity.

Meanwhile, the synthesis of hyaluronic acid gradually decreases, reducing the skin’s ability to retain water in the extracellular matrix. This reduced skin hydration manifests as skin that can be more sensitive to changes in temperature or lifestyle and the appearance of the first dehydration fine lines, most often at the corners of the eyes. Oxidative stress, amplified by UV exposure, pollution, or lack of sleep, also begins to affect dermal structures, promoting collagen degradation by metalloproteinases. If these changes remain invisible to the naked eye for the luckiest among us, they lay the groundwork for skin aging to come.

Find here evidence-based recommendations for caring for your skin between the ages of 20 and 30.

Between the ages of 30 and 40, the skin enters a transition phase where signs of aging become truly noticeable. Cell turnover slows down: keratinocytes migrate more slowly to 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, which impairs the dermis’s ability to retain water and leads to a loss of volume and suppleness. The dermo-epidermal junction, which ensures cohesion between the skin layers, becomes flatter and less effective, resulting in a less uniform distribution of nutrients and water to the epidermis.

Moreover, under the influence of external factors, such as UV radiation or pollution, the fibers of collagen and elastin begin to fragment. This disorganization of the dermal network promotes the appearance of early expression lines, particularly around the eyes and mouth, where muscle movements are repeated. Skin tends to become thinner, sometimes drier, and its ability to regenerate after damage decreases. In some individuals, cutaneous microcirculation becomes slightly dysregulated, which accentuates the loss of radiance and promotes the formation of localized pigment spots. This decade thus marks the transition from still-youthful skin to skin where the signs of cutaneous aging become noticeable.

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

Between 40 and 50 years of age, the skin undergoes a marked acceleration of biological aging. The gradual decline in hormonal activity, especially that of estrogens in women, plays a major role in this evolution. These hormones typically stimulate the production of collagen, elastin, and hyaluronic acid. Their decline at the pre-menopause, then at menopause, brings about a marked decrease in dermal density and in the skin’s water retention capacity. The dermis then loses both thickness and mechanical strength, which intensifies skin laxity and deepens wrinkles. Fibroblasts become fewer and less active, limiting the repair of damaged fibers. Simultaneously, the hydrolipidic film becomes depleted, exacerbating dryness and compromising the skin barrier.

Moreover, pigmented spots become more frequent during this decade due to disrupted melanocyte activity and a less uniform distribution of melanin. Microcirculation slows, reducing the supply of oxygen and nutrients, resulting in a complexion that often appears duller and skin that is less radiant. At the same time, oxidative stress generated during metabolism and from UV exposure accelerates the degradation of structural proteins and the stiffening of elastin fibers, a phenomenon known as actinic elastosis.

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

From the age of 50, the skin enters a phase of deep structural aging. Hormonal changes, notably the drop in estrogen after menopause, accelerate the alterations already set in motion in preceding decades. Fibroblast activity continues to decline, and with it 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 delivery of nutrients and oxygen, giving the complexion a duller, more fatigued appearance.

In the epidermis, a decline in Langerhans cells, which are immune cells, weakens the skin’s natural defenses and increases the risk of skin infections. Cellular renewal also slows down, resulting in a rougher surface and a impairment of barrier function. Finally, in the hypodermis, a decrease in both the number and size of fat cells causes volume loss in the face, hollowed cheeks, the appearance of under-eye bags and deep wrinkles.

Find here scientifically based advice for caring for your skin after age 50.

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