The Impact of Sleep Quality on Skin Color

Abstract

Sleep plays a crucial role in regulating immune, endocrine, and skin functions. Increasing evidence suggests that sleep deprivation and circadian rhythm disruption can impact skin pigmentation by influencing melanocyte biology, hormonal balance, and inflammatory pathways. Clinical observations and molecular studies have revealed links between poor sleep and various pigmentary disorders. However, the underlying mechanisms remain incompletely understood, and the causal relationships are still under debate due to physiological confounders such as psychological stress and metabolic dysregulation. This review summarizes recent findings from experimental, clinical, and epidemiological studies on the relationship between sleep quality and skin pigmentation. Relevant literature was retrieved through PubMed and cross-referenced sources, focusing on research involving melanocyte activity, circadian genes (e.g., PER1, BMAL1), hypothalamo-pituitary axis (HPA) activation, and pigmentation-related dermatological conditions. Both human and animal studies were included. Poor sleep has been shown to alter skin parameters including melanin, hemoglobin, hydration, and trans-epidermal water loss, often through keratinocyte barrier impairment and microbiome imbalance. Disruption of the HPA leads to elevated cortisol and proinflammatory cytokines, further affecting melanogenesis. Clinically, sleep disturbances are associated with pigmentary disorders such as melasma, rosacea, floppy eyelid syndrome, and acanthosis nigricans. Obstructive sleep apnea contributes to pigmentation changes via hypoxia-induced inflammation and vascular remodeling. A newly described disorder, maturational dyschromia, may also involve habitual sleep patterns. Future research integrating wearable technology and artificial intelligence-based skin imaging may enable real-time, individualized assessment of sleep-pigmentation interactions.

Introduction

In contemporary society, getting less sleep is becoming increasingly prevalent due to a variety of factors, including labor, education, personal obligations, medical conditions, and sleep disorders.[1] The transition between wakefulness and sleep results from a dynamic balance between the interactions of pertinent brain systems, and is controlled by circadian and sleep homeostasis processes. Lack of sleep can cause the disruption of circadian rhythm.[2]

Skin and Melanocytes

It appears that dysregulation of circadian rhythms is associated with alterations in skin function,[3] but the association between sleep and skin color has not been well investigated. Many factors determine skin color. Among them, melanin has a major impact.[4] Melanin is widely found in human skin, mucous membranes, retina, and can absorb ultraviolet (UV) rays and reduce the harm they do to the skin. However, they can cause irregular skin pigmentation.

Melanocytes, which are found on the dermal/epidermal boundary, employ elongated dendrites to deliver melanosomes carrying melanin to keratinocytes.[4,5] Keratinocytes in the basal layer then propel this towards the skin’s surface as new cells push it higher.[5,6] Fibroblasts in the dermis, which influence the overlying melanocytes and keratinocytes, hormones derived from the circulatory supply, neural factors, and inflammation-related factors are all intrinsic elements that help regulate skin color, while UV radiation is the extrinsic one.[6] Exploring how melanin is structured, formed, and accumulated, provides critical insights into the elucidation of several pigment-related skin diseases and are also valuable for the manufacture and application of various whitening products.

The enzymes tyrosinase, tyrosinase-related protein 1, and dopachrome tautomerase cooperate to synthesize two different kinds of melanin: yellow-reddish pheomelanin and black-brown eumelanin.[7] Both endogenous and external factors can affect the order of events required for melanogenesis. Keratinocyte-derived factors,[8] fibroblast-derived factors,[9,10] arachidonic acid-derived chemical mediators, neuronal cell-derived factors,[11] and UV light[11] all affect melanin production. The most widely recognized receptors for controlling melanocyte function are melanocyte-stimulating hormone and adrenocorticotropic hormone,[12] While melanocyte inducing transcription factor (MITF) is the most important transcription factor governing melanocyte activity, its expression is regulated by a variety of factors like fibroblasts, keratinocytes, and others.[12,13] Remarkably, there is a skin pigmentation mechanism independent to MITF.[14] Targeting nicotinamide nucleotide transhydrogenase, a mitochondrial redox-regulating enzyme, causes cellular redox alterations that impact tyrosinase breakdown. These modifications regulate eumelanin production and pigmentation by regulating melanosome maturation. It is important to note that most endogenous elements indicated above are elevated when UV light is present.[12]

Circadian Rhythms and Pigmentation

Circadian rhythms are irregularities in behavior and metabolic processes caused by organisms’ inherent ability to align with the environment’s 24-hour light/dark rhythm.[2] These are caused by an intrinsic biological clock that controls many elements of human biological functioning, including the sleep-wake cycle and daily fluctuations in body temperature, blood pressure, and cortisol. The suprachiasmatic nucleus of the anterior hypothalamus, which serves as the central regulator, controls and automatically integrates peripheral tissues’ circadian rhythms using neuronal and hormonal cues in response to environmental changes.[15,16,17] In a molecular setting, circadian rhythms in vertebrates are governed by a set of primary clock genes, namely CLOCK, BMAL1, the PER family (PER1, PER2, PER3), and cryptochromes (CRY1 and CRY2).[16] The identification of these genes facilitates a deep comprehension of how the circadian rhythm affects biological functions in humans. Several studies have demonstrated that malignant melanoma and human epidermal melanocytes both include clock genes.[18,19,20,21] Clock gene transcripts were found to be higher in uninvolved and lesional psoriatic areas than in healthy skin.[22] It has been proposed that detecting changes in clock genes in hair, combined with multi-dimensional data such as body temperature and blood samples, can provide a non-invasive and practical approach for tracking and assessing a variety of human circadian rhythm-related diseases, and help to understand any possible mechanisms underlying circadian rhythm-related disorders.[23]

Studies investigating the relationship between circadian rhythm and age-related pathologies[24,25,26,27,28] have shown that the clock genes are linked with Reactive Oxygen Species (ROS) homeostasis. Similarly, recent studies have implicated metabolism and mitochondria[29,30] in the age-related graying of melanocytes in hair.[17,29,31,32] More in-depth analyses of the genetic level have recently been conducted, but studies on how BMAL1 and PER1 affect the formation of melanin have produced conflicting results in various trials. Melanogenic activity was triggered in human epidermal melanocytes and hair follicles when PER1 and BMAL1 were silenced, indicating that the suppression of both fundamental clock genes obviously influence melanogenesis.[33,34] A later investigation by Assis et al., however, failed to replicate this finding.[35] Discrepancies among different studies could be caused by variations in the species and cell lines employed in these investigations. PER1 expression was downregulated in identical cell lines following triple cumulative UVA irradiation. Interestingly, overexpressing BMAL1 led to an increase in melanin levels under UVB irradiation, and corresponding to the surge in BMAL1, PER2 declined.[36] The explanation might be that the mechanism by which UVA and UVB influence the expression of the clock genes may differ. Even if the same species had received the same amount of UVA exposure, the varied times that the samples were examined may have affected the results. However, the research mentioned above can obviously show that disturbances in circadian rhythms can manifest in skin pigmentation, but the exact mechanism through which melatonin, a sleep-regulating hormone, modulates melanocyte activity via peripheral circadian mechanisms remains unclear. Yet, in cultured keratinocytes, exposure to melatonin and its metabolic products was found to trigger NRF2-regulated antioxidant mechanisms, as shown by multiple pathway analyses including Gene Set Enrichment Analysis (GSEA), Reactome Functional Interaction Visualization (Reactome FVIz), and Ingenuity Pathway Analysis (IPA),[21] while another planar surface immunoassay result shows that the modulation of BMAL1 protein triggers PI3K/AKT signaling pathway.[37] There may be a possible explanation for the mechanism. Melatonin may regulate the clock genes, like BMAL1, which in turn suppress enzymes involved in melanin synthesis,[33] by activating Nrf2, triggering the PI3K/AKT signaling pathway.

In addition to melanocytes, keratinocytes—the predominant cells in the epidermis—also demonstrate circadian control.[38,39] Their proliferation and differentiation are tightly regulated by core clock genes such as BMAL1, PER1, and CLOCK.[40,41] These genes synchronize keratinocyte turnover with the sleep-wake cycle, ensuring optimal barrier formation and skin renewal during nighttime. Disruption of circadian rhythms can impair keratinocyte differentiation and lipid synthesis, weaken the epidermal barrier, and increase transepidermal water loss (TEWL).[42,43] These changes may indirectly contribute to the visible skin pigmentation by altering light reflection, increasing inflammation, and facilitating abnormal pigment accumulation in the stratum corneum.

Moreover, keratinocytes are responsive to melatonin, a key hormonal regulator of circadian rhythm. These cells express melatonin receptors (MT1 and MT2) and utilize melatonin signaling to activate antioxidant and anti-inflammatory pathways, thereby contributing to epidermal homeostasis. Sleep loss reduces melatonin bioavailability, compromising this protective mechanism and increasing keratinocyte vulnerability to oxidative stress and inflammatory insults.[42] This weakened defense may further impair barrier function and promote pigmentary alterations.

Sleep and Skin Color

The long-term adverse impacts of poor sleep—including sleep deprivation (SD) and sleep restriction (SR)—on immunity, cognition, psychomotor function, mood, metabolism, and behavior have been well established in prior research.[43,44,45,46,47,48,49,50,51,52] A study[53] of 111 young Shanghai females between 18 and 25 years of age characterized the concept of “ideal skin” as oriental women as having lower sebum content, TEWL, melanin, hemoglobin, and roughness, while having higher hydration content and skin pH value. Nevertheless, a lack of sleep, which may be obvious from certain facial features, may easily have a detrimental effect on interpersonal communication.[54] Therefore, the study of sleep loss and facial changes has both biological and sociological significance. However, the literature does not provide a strong case for skin color changes caused by SD and/or SR. But TEWL can reflect impaired keratinocyte function and lipid synthesis, which compromises the skin barrier and predisposes to inflammation and pigmentation.

A recent study[55] analyzes the alterations and impact of regular late-night sleep on skin physiological parameters and the facial bacterial flora, and found that late sleep can significantly weaken the structural and functional integrity of the skin, while destabilizing its water–oil balance, and reducing the abundance and diversity of facial flora. Among these, Pseudomonas abundance was strongly adversely linked with skin hemoglobin, melanin, and skin water content, indicating that late sleep can lead to dark skin. After SR, there were substantial drops in facial brightness and saturation, leading to the change of skin color. Local in situ skin-derived factors, rather than systemic chromophore change, play a key role.[56,57] It is challenging to tell whether the observed changes in skin color are totally caused by poor sleep, because the SD approach not only throws off circadian rhythm but puts extra stress[47,58] on the individuals. For example, in a study of healthy adult women, TEWL significantly increased and stratum corneum hydration decreased during stressful periods, indicating epidermal barrier impairment[59] Furthermore, sleep deprivation-induced stress can activate the HPA, resulting in elevated secretion of cortisol and adreno- corticotrophic hormone, and elevated concentrations of inflammatory mediators, including interleukin-6 and tumor necrosis factor- α, and C-reactive protein. These changes can influence melanocyte and keratinocyte function, disrupting pigmentation homeostasis.[58]

These mechanisms are reflected in several skin diseases. Rosacea, for instance, shows a significant correlation with sleep disturbances. A case-control study reported that over half of rosacea patients experienced moderate to severe sleep problems, with sleep quality positively associated with the severity of erythema and papules.[60,61,62] Animal studies further revealed that SD exacerbated rosacea-like lesions and upregulated key inflammatory factors including matrix metalloproteinase-9 (MMP-9), toll-like receptor 2 (TLR2), cathelicidin antimicrobial peptide (CAMP), and vascular endothelial growth factor (VEGF)—molecules implicated in both skin structural damage and melanogenesis.[61]

Similarly, melasma, a hypermelanotic skin disorder, is susceptible to psychological–inflammatory–hormonal influences. Although direct studies linking melasma to sleep are limited, the elevated expression of CD4, IL-17, and COX-2 in melasma lesions parallels the systemic inflammatory states seen in chronic SD.[63] Melasma patients often suffer from a significant psychological burden and diminished quality of life, which in turn may impair sleep quality, forming a vicious cycle.[64]

More systemic sleep disorders, such as obstructive sleep apnea (OSA), affect skin pigmentation from another dimension. OSA involves recurrent hypoxia and sleep fragmentation that activate inflammatory pathways and provoke metabolic dysregulation. It is frequently comorbid with conditions such as diabetes, psoriasis, and acanthosis nigricans, all of which present with uneven pigmentation, dullness, or hyperkeratosis.[65,66,67] Its cutaneous manifestation, floppy eyelid syndrome (FES), is a typical skin adnexal disorder marked by upper eyelid laxity, corneal inflammation, and chronic conjunctival changes.[68,69,70] FES has been linked to OSA-related upregulation of matrix metalloproteinases, elastic fiber degradation, and vascular abnormalities,[69,71,72] thus providing a clinical illustration of the sleep–systemic disease–skin color axis.

Additionally, a newly described pigmentary disorder known as maturational dyschromia primarily affects middle-aged individuals with darker skin types. While its pathogenesis remains unclear, it has been associated with cumulative sun exposure, metabolic syndrome, and possibly habitual sleep behaviors.[73] This suggests a role for sleep patterns within the multifactorial etiology of pigmentation disorders.

In summary, sleep influences skin pigmentation through multiple mechanisms: directly impairing keratinocyte barrier function, altering hormonal and inflammatory pathways, and indirectly triggering pigmentary changes via metabolic and systemic disease comorbidities. Skin conditions such as rosacea, melasma, FES, and maturational dyschromia serve as clinical reflections of this multifaceted relationship. Future research on the interplay between sleep behavior and pigmentation should extend beyond individual diseases and incorporate multidimensional mechanistic exploration.

Health Impacts and Clinical Considerations

The interaction between sleep and skin pigmentation involves complex physiological, psychological, and metabolic mechanisms. The relationship between sleep quality and skin health, particularly skin pigmentation, aging, and pathological changes, has garnered significant attention in recent years. In clinical practice, the treatment of sleep disturbances and pigmentation issues often requires multifaceted, integrated interventions. For patients with OSA, continuous positive airway pressure (CPAP) therapy is the most used and effective treatment.[67] For individuals with insomnia, cognitive behavioral therapy for insomnia (CBT-I) has been proven to be an effective non-pharmacological approach.[74] By improving sleep habits and cognitive patterns, CBT-I helps restore regular sleep patterns, thereby indirectly enhancing skin health. In cases of severe insomnia or other specific sleep disorders, pharmacological treatments, such as benzodiazepines or non-benzodiazepine medications, may be considered, although their use requires strict monitoring to prevent dependence. For pigmentation caused by systemic diseases, the primary disease should be actively treated to control symptoms. Additionally, topical use of whitening agents or laser therapy can be employed to disrupt melanogenesis or inhibit melanin synthesis, promoting skin cell renewal. Most importantly, adopting a healthy lifestyle is essential- ensuring adequate sleep duration, managing stress levels, maintaining a balanced diet rich in antioxidants and nutrients beneficial for skin health (such as vitamins C and E), engaging in regular physical activity, and avoiding excessive sun exposure.[75]

Rosacea, a chronic inflammatory skin condition often exacerbated by stress and poor sleep, should also be managed with an integrative approach. Beyond standard dermatological treatments and intense pulse light, laser, and surgery,[76] clinicians should assess patients’ sleep quality and stress levels. Sleep hygiene education and stress reduction techniques may improve both systemic inflammation and skin symptoms.[77] Since rosacea flares have been associated with poor sleep, incorporating sleep assessment into rosacea management could yield better therapeutic outcomes.

Similarly, melasma- a hyperpigmentary disorder frequently observed in women- is influenced by hormonal, inflammatory, and psychological factors, including stress-induced sleep disturbances. While treatment often includes topical agents (e.g., hydroquinone, tranexamic acid) and laser-based therapies,[64] addressing sleep quality and mental well-being is increasingly recognized as an adjunct strategy.[78] Psychological support and behavioral sleep therapy may help to break the cycle of stress, poor sleep, and progression of hyperpigmentation.

Optimizing sleep health has substantial potential for improving pigmentation-related skin conditions. A comprehensive clinical strategy should integrate dermatological care, behavioral therapy, sleep medicine, and lifestyle interventions. Clinicians should consider sleep quality as both a diagnostic clue and a therapeutic target in patients presenting with pigmentation disorders or chronic dermatoses.

Future Research Directions

Although some studies have explored the relationship between sleep and skin pigmentation, most have been limited to macroscopic skin manifestations, lacking in-depth investigation into the cellular mechanisms involved. Future research should focus on how sleep quality affects melanin synthesis and distribution through pathways such as oxidative stress, immune responses, and metabolic regulation. For example, future research may explore how sleep deprivation or sleep-related disorders trigger signaling cascades—such as the NF-κB or MAPK pathways—to regulate the transcription of core clock genes like BMAL1 and PER1, leading to pigmentation or skin aging. Currently, research on the combined effects of sleep disorders and systemic diseases on skin pigmentation is relatively limited. Future studies should delve deeper into how metabolic diseases, such as diabetes and obesity, along with autoimmune conditions like systemic lupus erythematosus and psoriasis, interact with sleep disorders to affect skin health, particularly about pigmentation. Research should focus on how these diseases influence skin conditions through shared biomarkers, such as inflammatory cytokines and metabolic byproducts.

With ongoing technological advancements, new techniques and methods hold great potential in expanding our understanding of the interaction between sleep and skin pigmentation.

Emerging technologies such as wearable sensors and real-time monitoring systems are enhancing the ability to collect and analyze physiological data. These technologies track not only sleep metrics but also skin condition indicators, including moisture levels, elasticity, and temperature.[79] The integration of artificial intelligence (AI), particularly machine learning algorithms, enables the analysis of large volumes of sleep data, identifying patterns and anomalies that may impact overall well-being. By processing data from wearable devices, AI can track sleep quality, duration, and stages, providing insights into how sleep disruptions may affect skin health. Studies have shown that inadequate sleep can impair the skin’s ability to regenerate, leading to issues such as increased skin aging, acne, and reduced skin barrier function.[80] AI tools can not only correlate these sleep disturbances with specific skin conditions but also offer personalized recommendations for improving both sleep and skin health.[81]

Conclusion

Overall, the findings suggest that getting less sleep can be hazardous to a range of biological processes; however, there is insufficient evidence to pinpoint the precise link between poor sleep and skin color. One thing is for certain, though; SD or SR modifies an organism’s circadian rhythm, and a changed circadian rhythm can directly influence melanocyte activity and affect skin color by controlling the expression of molecular clock genes, such BMAL and PER1.

However, as SR and SD also cause significant stress when they alter the circadian rhythm, endocrine imbalance may result in a change in skin color. Therefore, further investigation is required to determine the impact of SD or SR on skin color, either by subjecting control groups to additional stressful situations or by keeping laboratory settings like those of habitual sleep. For patients with sleep disorders, active treatment will contribute to the improvement of skin symptoms and overall quality of life.

In the future, we will pay more attention to the discussion of sleep quality on the cellular level of skin, and further study how systemic diseases and sleep disorders work together to affect skin health. Wearable devices, AI, and big data analytics may become powerful tools for further research.

Conflicts of interest

There are no conflicts of interest.

Use of artificial intelligence (AI)

We acknowledge the use of ChatGPT-4o to summarize our initial notes and to proofread our final draft. We have referred to publisher’s policy of use of AI as depicted in information for authors and assume full responsibility for the content of our manuscript, even those parts produced by an AI tool, and are thus liable for any breach of publication ethics.

Funding Statement

The National Natural Science Foundation of China (81972931 and 82273548 to Hong Fang) supported this work.