Skin aging

Intrinsic aging affects all skin, including skin that is rarely exposed to light. The outer layer thins, the dermis (the deeper layer that gives skin its strength) produces less collagen and elastin, and fine wrinkles appear. Its pace depends on age and inherited factors.

Extrinsic aging is superimposed on this by external exposures, chiefly UV radiation and tobacco smoke. Photoaged skin shows coarse wrinkles, leathery texture, blotchy pigmentation and loss of elasticity, and it is concentrated on the face, neck, forearms and hands. In a study of 186 pairs of identical twins, who share the same genes, the twin with more sun exposure, more outdoor activity or less sunscreen use looked older, and the longer a twin had smoked, the older that twin appeared. Rhytids (wrinkles) and patchy discoloration were more common in twins who smoked. The relationship with body weight depended on age: a higher body mass index was associated with an older appearance before about age 40 and a younger appearance after it [4].

UV radiation damages DNA in skin cells and suppresses the immune response of the skin [1]. The International Agency for Research on Cancer classifies solar radiation and UV-emitting tanning devices as carcinogenic to humans (Group 1) [10].

The effect of sun protection on skin aging was tested directly in the Nambour trial in Queensland, Australia. Of 1,621 adults randomly selected from the community, 903 were younger than 55 and had the fine texture of their skin (microtopography) graded by assessors who did not know their group. Participants were assigned to daily application of broad-spectrum sunscreen or to use at their own discretion, and separately to beta-carotene or placebo, for 4.5 years. The daily-sunscreen group showed no detectable increase in skin aging, and aging from baseline to the end of the trial was 24% less than in the discretionary group (relative odds 0.76, 95% confidence interval 0.59 to 0.98). Beta-carotene supplements had no overall effect [2].

The World Health Organization estimated that excessive UV exposure caused about 1.2 million new cases of non-melanoma skin cancer (basal cell and squamous cell carcinoma) and 325,000 melanomas in 2020, together with 64,000 deaths from non-melanoma skin cancer and 57,000 from melanoma [1]. Melanoma, a cancer of the pigment cells, is the least common and most lethal of the three.

The same Nambour trial followed participants for 10 years after it ended. There were 11 new primary melanomas in the daily-sunscreen group and 22 in the discretionary group (hazard ratio, the rate of events in one group relative to another, 0.50; 95% confidence interval 0.24 to 1.02), a difference just short of statistical significance. The reduction in invasive melanomas was larger, 3 cases against 11 (hazard ratio 0.27, 0.08 to 0.97) [3]. The trial measured cancer incidence, not deaths.

Artificial UV carries similar risks. A meta-analysis (a study that pools the results of earlier studies) of 27 studies found that ever using sunbeds was associated with a 20% higher risk of melanoma, rising by about 1.8% with each additional session per year, and that first use before age 35 was associated with 87% higher risk (relative risk 1.87). The authors estimated that 3,438 melanoma cases in 2008 in 18 western European countries could be attributed to sunbed use [8]. Childhood appears to be a period of particular susceptibility: ecological studies consistently found lower melanoma risk among people who grew up in low-UV environments, although case-control studies of recalled childhood exposure were inconsistent [11].

Survival from melanoma depends strongly on how far it has spread at diagnosis. In US cancer registry data for 2016 to 2022, 77% of melanomas were found while still confined to the skin [9].

Full deep dive: skin health and lifespan.

Smoking accelerates facial aging independently of genes: in the identical-twin study, the longer a twin had smoked, the older that twin was judged to look [4]. Tobacco use and its other effects are described under smoking.

Advanced glycation end products (AGEs) are compounds formed when sugars bind to proteins such as collagen, stiffening them. Their accumulation in skin can be estimated without a biopsy by skin autofluorescence, the light the skin gives off under ultraviolet illumination. Among 109 patients on haemodialysis followed for 3 years, higher skin autofluorescence independently predicted death (odds ratio 3.9 for overall mortality) [12]. In 1,707 people with moderate (stage 3) chronic kidney disease followed for a median of 3.6 years, the highest quarter of autofluorescence carried a higher age- and sex-adjusted mortality (hazard ratio 1.84), but the association disappeared after adjustment for cardiovascular disease, diabetes, smoking and kidney function [13]. The evidence therefore comes from people with kidney disease, and skin AGEs have not been shown to predict mortality independently in the general population.

Collagen supplements are widely marketed for skin aging. A meta-analysis of 23 randomised trials with 1,474 participants found improvements in skin hydration, elasticity and wrinkles overall, but studies not funded by pharmaceutical companies, and high-quality studies, showed no significant effect; the authors concluded that there is no clinical evidence to support collagen supplements for preventing or treating skin aging [14].

How old a person looks is associated with how long that person lives. In a Danish study of 1,826 twins aged 70 or over, assessors estimated each twin's age from a facial photograph. By the end of follow-up 675 twins (37%) had died. Perceived age predicted survival after adjustment for chronological age, sex and rearing environment, and after further adjustment for physical and cognitive function. The larger the difference in perceived age within a twin pair, the more likely the older-looking twin was to die first. Perceived age also correlated with leucocyte telomere length, a molecular marker of aging, and twin analyses suggested that shared genetic factors influence both appearance and survival [5]. Telomeres are described under telomeres.

Bags and sagging around the eyes are mostly a matter of inherited anatomy and age. With age the tissue that holds the fat around the eye in place weakens and the fat bulges forward, and fluid can collect in the thin skin under the eyes [15]. In a study of the upper eyelids, 17.8% of 5,578 older adults in the Dutch Rotterdam Study had dermatochalasis (skin of the upper lid hanging over the lashes). Independent risk factors were older age, male sex, lighter skin colour and higher body mass index, with a borderline association for current smoking. Heritability (the share of differences between people explained by genes) was estimated at 61% in 1,052 twin pairs from the UK Adult Twin Registry, and a genetic variant near TGIF1, a gene already linked with skin aging, was associated with protection [6].

Short sleep changes the appearance of the eye area within a day. In an experiment at the Karolinska Institutet, 40 observers rated photographs of 10 people taken after normal sleep and after 31 hours of wakefulness; the sleep-deprived faces were rated as having more hanging eyelids, redder and more swollen eyes, darker circles under the eyes, paler skin and more wrinkles [16]. In a related study, 65 observers rated 23 sleep-deprived adults as less healthy, more tired and less attractive than after a normal night's sleep [17]. Sleep and its measurement are covered under sleep quality and sleep regulation and sleep stages.

A small number of eye-area signs point to other conditions. Floppy eyelid syndrome, in which the upper lids become lax and are easily turned inside out, is strongly associated with obstructive sleep apnoea, repeated collapse of the upper airway during sleep [18]. In a study of 1,651 men followed for a mean of 10.1 years, untreated severe sleep apnoea was associated with 2.87 times the odds of fatal and 3.17 times the odds of non-fatal cardiovascular events compared with healthy men, and treatment with continuous positive airway pressure (CPAP) reduced this risk [19]. Puffiness around the eyes can accompany an underactive thyroid [20] and allergic rhinitis, in which dark, swollen areas under the eyes are known as allergic shiners [21]. New, persistent swelling around the eyes can also accompany kidney disease, which often goes unrecognised in its early stages [22].

Xanthelasmata, flat yellowish deposits of cholesterol on the eyelids, are the eyelid sign most clearly linked to heart disease. In the Copenhagen City Heart Study, 12,745 adults were followed for up to 33 years; the 4.4% with xanthelasmata had a 48% higher risk of myocardial infarction (heart attack; hazard ratio 1.48), 39% higher risk of ischaemic heart disease and 14% higher risk of death, independent of cholesterol and triglyceride levels. Arcus corneae, a grey ring around the iris, was not an independent predictor [7]. For bags caused by fat, no topical treatment reverses the change; the definitive treatment is lower-eyelid surgery (blepharoplasty), which is cosmetic [15].

Full deep dive: eyebags and health.

Most evidence on skin aging is observational. The twin studies control for genes but rely on photographs, questionnaires and recalled exposures [4, 5]. The Nambour trials are the main randomised evidence; the skin-aging analysis had some missing outcome data and modest power to detect moderate effects [2], and the melanoma result rests on small numbers of cases [3]. Evidence that childhood sun exposure raises melanoma risk comes mainly from ecological comparisons of places rather than individuals [11]. The glycation findings come from people with kidney disease and did not hold after full adjustment in the larger study [13]. The eyelid and sleep apnoea studies found associations; eyebags themselves have not been shown to shorten life.