What are the effects of lack of sleep on the skin?

A study conducted by Eunjoo KIM assessed skin changes in 32 individuals in their forties who had their sleep limited to four hours per night for six nights. Several parameters, including elasticity, crow's feet wrinkles, and frown lines were measured. The parameter for analysing elasticity was R2, calculated using the following formula: R2 = Ua/Uf, where Uf is the maximum skin distension and Ua is the total skin distension. The closer the R2 value is to 1, the more elastic the skin is. The wrinkles at the corner of the eye and the frown line were measured based on their average depth (in mm).

The results show that skin elasticity gradually decreased after sleep reduction, moving from an R2 of 0.65 to 0.59 with a noticeable reduction between the fifth and sixth day. Moreover, after just one day of sleep deprivation, crow's feet and frown lines significantly increased by about 20 μm to 21.5 μm in depth.

Other studies have shown an association between lack of sleep and an increase in pro-inflammatory cytokines such as TNF-α. The latter binds to specific receptors on the surface of skin cells, thereby triggering intracellular signalling pathways, such as the NF-kB pathway. Indeed, the activation of these pathways leads to the expression of genes involved in inflammation, including those associated with the production of reactive oxygen species (ROS).

It can also increase the activity of certain enzymes, such as NADPH oxidase and xanthine oxidase, which are involved in the production of ROS. ROS are free radicals known to cause oxidative stress, and are supposedly involved in skin ageing through the destruction of collagen and the elastin network, responsible for the elasticity and integrity of the skin. Therefore, less sleep can accelerate skin ageing.

The aforementioned study also evaluated the impact of sleep deprivation on skin hydration, desquamation, and transepidermal water loss (TEWL). The researchers found that skin hydration significantly decreased after the first night and continued to decrease progressively. Skin desquamation significantly increased after a night of reduced sleep, and continued to increase throughout the period. Finally, the TEWL was higher than the value for normal sleep (eight hours of sleep per day) by the sixth day, rising from 16 g/m2h to 19 g/m2h. The skin then becomes less hydrated, and drier.

The circadian rhythm, or theinternal clock synchronised with the light-dark cycle of the environment, orchestrates numerous cellular functions. Sleep promotes a microenvironment conducive to cell proliferation, migration and differentiation. These effects are mediated either directly by the genes of the circadian clock (CLOCK), or indirectly by hormones, such as melatonin and cortisol. Thus, not getting enough sleep leads to poor cell regeneration and therefore an accumulation of dead cells on the skin's surface. This consequence may be linked to the observed skin dryness, in parallel with the increased TEWL.

Furthermore, recent studies have revealed that circadian rhythms would affect the metabolism of skin lipids, produce different lipid products, and in turn affect the TEWL (Transepidermal Water Loss). However, the exact mechanisms are not yet known.

When we do not get enough sleep, our complexion tends to turn a bit greyish, as shown in a study conducted by Damien LEGER and his team in 2019 (three hours of sleep per night for two consecutive nights). Changes in skin tone are widely perceived as a symptom of sleep deprivation. This change is particularly noticeable under the eyes with the dark circles.

In an experiment conducted by Hae-Kwang LEE, it was observed that skin blood circulation decreased after a night of sleep deprivation, alongside a more significant presence of dark circles. Indeed, the stagnation of blood flow contributes to the development of under-eye circles. The blood pigments that show through the thin skin are responsible for the dark colour of the circles. The blood capillaries are filled with blood and dilate, releasing the pigmented waste into the perivascular space. Similarly, the lymph, tasked with removing waste, struggles to circulate and therefore cannot eliminate the accumulated pigments.

Our complexion can also turn yellowish due to lack of sleep. Tomohiro HAKOZAKI and his team measured the effects of total sleep deprivation (0h) and repeated partial sleep deprivation, that is, four hours of sleep for five consecutive nights, on the dullness of facial skin. They then examined yellow chromophores, such as bilirubin and carotenoids, in the blood serum as potential causes of yellowing. Both protocols significantly exacerbated the yellowing of the facial skin. However, the absence of significant changes in circulating levels of yellow chromophores suggests that the increase in yellowing is likely regulated by epidermal keratinocytes, which are themselves capable of producing substantial amounts of bilirubin.

Recurring insomnia can lead to the onset of skin diseases. In an experiment conducted in 2019, Elma D. BARON and her colleagues sought to determine if there was a significant difference in the prevalence and severity of skin diseases between day workers and night workers. Due to their disrupted circadian rhythm, the latter were much more affected by skin conditions such as common acne and dermatitis, as well as enlarged pores.

Lack of sleep results in an increase in the production of glucocorticoids, which can impair the integrity of lamellar bodies and thus the integrity of the skin through a modification of the conformation of collagen molecules. Moreover, as previously mentioned, sleep deprivation leads to an increase in pro-inflammatory cytokines, such as TNF-α, which promote cellular differentiation, oncogenesis and the pathogenesis of inflammatory skin conditions like psoriasis. ROS will also be produced. In excess, oxidants can react with all cellular macromolecules, including lipids, proteins, nucleic acids and polyunsaturated fatty acids of cell membranes. A chain reaction is then triggered, leading to cellular damage.

It is important to understand that ROS (Reactive Oxygen Species) can also increase the levels of pro-inflammatory cytokines through the positive regulation of the genes that encode them.

Furthermore, lack of sleep results in a dysregulation of the immune system. It has been observed that the number of leukocytes reaches its peak during the night, such as T lymphocytes controlled by a direct activation of the IL-23 promoter by the circadian rhythm of the CLOCK protein. A lack of sleep therefore leads to a decrease in immune cells and thus an increased exposure to infections.

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