Stress and cortisol: what are the effects on the skin?

The stress can be defined as a set of physiological responses triggered when the body perceives a threat (real or anticipated).

Whether acute (short-lived) or chronic (long-standing), it mobilizes a tightly coordinated network among the brain, the neuroendocrine system, and the immune system. At the center of this response, we find the activation of the hypothalamic-pituitary-adrenal (HPA) axis. First, the hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to secrete adrenocorticotropic hormone (ACTH), subsequently driving cortisol production by the adrenal glands. In parallel, the nervous system releases catecholamines such as norepinephrine. These circulating mediators orchestrate the stress response throughout the body, including at the level of the skin.

The skin is also regarded as a peripheral neuroendocrine organ capable of sensing, integrating, and responding to stress signals. Its cells—particularly the epidermal keratinocytes and the dermal fibroblasts—secrete mediators themselves and carry the receptors to react. Thus, there is a cutaneous equivalent of the HPA axis, with local production of CRH, peptides derived from proopiomelanocortin (POMC) such as ACTH, and, under certain conditions, local synthesis of corticosteroids. This arrangement allows the skin to finely tune its responses, but it can also lead to dysregulation when stress becomes too intense or prolonged.

At the immunological level, stress affects the skin in different ways depending on its duration and nature. Acute stress can transiently enhance certain aspects of innate immunity, whereas chronic stress tends to disrupt immune responses, notably by modulating the Th1/Th2 balance and by impairing specific cellular functions. Skin cells participate directly in this orchestration: activated keratinocytes can produce cytokines such as IL-1α, stored in large amounts in the stratum corneum, or mediators capable of recruiting and activating skin immune cells like Langerhans cells, T lymphocytes, and macrophages.

Finally, stress also acts through the neuro-immune pathway. Substance P is a key example: released by skin nerve endings and elevated under stress, it can influence local inflammation and interact with cells such as mast cells, which are involved in many stress-related skin symptoms (burning sensations or discomfort, itching…). The mast cells can then release cytokines and inflammatory mediators in turn, further amplifying the skin’s local responses.

Beyond its general effects on inflammation, immunity, or skin barrier, stress can also influence the onset, severity, or progression of certain skin diseases. This relationship is explained by the ongoing dialogue among the nervous system, stress hormones, and cutaneous immune responses, which can disrupt the physiological equilibrium of the skin when stress exposure becomes prolonged. Numerous clinical observations and experimental data thus suggest that stress functions as a triggering or exacerbating factor in several skin diseases, although it is not the sole cause of these dermatoses.

Stress and eczema.

The eczema is a chronic inflammatory disease characterized by a disruption of the skin barrier, significant dryness, and intense itching. It is notably due to an immune imbalance, often skewed toward a Th2-type response, as well as increased production of inflammatory cytokines. In this context, the stress can act as a major exacerbating factor: prolonged activation of the HPA axis, the release of neuropeptides, and mast cell stimulation promote skin inflammation and intensify itching. This connection explains why some individuals experience a flare-up of eczema linked to stress, particularly on the face or hands.

Several studies have focused on the specific role of stress in the progression of atopic eczema from the patients’ perspective. A study involving 28 individuals with this skin disorder examined the impact of psychological stress and emotional factors on disease exacerbation. All participants believed that stress could worsen eczema and its associated pruritus, even though it was sometimes difficult to distinguish its effect from that of other physiological triggers such as infections, climate, or allergens. Patients especially reported a more pronounced influence of chronic stress compared to acute stress, citing family or financial problems, work overload, exam periods, and unexpected events as frequent aggravating factors. Moreover, in addition to conventional treatments for eczema, such as topical corticosteroids, emollients and phototherapy, some participants noted possible benefits of physical activity and psychological support.

Stress and psoriasis.

The psoriasis is a chronic inflammatory dermatosis characterized by keratinocyte hyperproliferation associated with an immune activation dominated by Th1 and Th17 pathways. This inflammation leads to the emergence of well-demarcated erythematous-scaly plaques. The stress can act at multiple levels, as cortisol secretion may dysregulate inflammatory cytokine production and interact with the skin’s nerve receptors. These mechanisms can promote disease onset or trigger stress-induced psoriasis flare-ups.

A meta-analysis pooling 39 studies involving more than 32,000 patients examined this question and concluded that there was a statistically significant association between psoriasis and stress. The authors nonetheless remained cautious and noted numerous limitations in the studies. They therefore considered it difficult to assert a strong causal relationship, even though a moderate influence of stress on psoriasis remains plausible.

Stress and acne.

The acne is a multifactorial condition involving the overproduction of sebum, follicular hyperkeratinization, the proliferation of the bacterium Cutibacterium acnes and local inflammation. Stress can influence each of these mechanisms: elevated cortisol stimulates the activity of the sebaceous glands, while neuropeptides and proinflammatory cytokines modulate the cutaneous immune response. This interaction explains why some individuals report the onset of stress-induced breakouts or acne flare-ups related to stress.

One study, for example, was conducted among 144 sixth-year medical students to explore the relationship between perceived stress, measured by the Perceived Stress Scale (PSS), and acne severity, assessed using the Global Acne Grading System (GAGS). The results revealed a statistically significant positive correlation between stress level and acne intensity. Notably, in this population, 72.2% of the students had mild acne, 22.9% had moderate acne, and 2.8% had severe acne, while only 2.1% exhibited no lesions.

Stress and vitiligo.

The vitiligo is a pigmentary dermatosis characterized by autoimmune destruction of melanocytes, the cells that produce melanin, leading to depigmented macules. Its origin is complex and involves genetic, immune, and environmental factors. The stress may act as a trigger or aggravating factor. Studies have highlighted altered cortisol and dehydroepiandrosterone sulfate (DHEAS) levels, a hormone involved in stress resistance: healthy individuals generally have higher DHEAS concentrations than vitiligo patients, suggesting a reduced ability to cope with stress in the latter. Moreover, DHEAS’s antioxidant properties normally help limit oxidative stress, a mechanism involved in melanocyte destruction, which may contribute to the progression of vitiligo.

In this context, several studies have attempted to better understand whether stress might contribute to the onset of vitiligo. A questionnaire-based study of 1,541 adults with vitiligo assessed the impact of stressful events occurring in the two years before disease onset, as well as their influence on disease progression and the possible emergence of associated symptoms. The 77-item survey aimed to identify psychological factors present before diagnosis. The results indicate that a majority of participants reported experiencing at least one stressful event in the two years before the onset of vitiligo, which suggests a potential role of stress in its triggering.

Stress and rosacea.

The rosacea is a chronic inflammatory facial dermatosis characterized by persistent redness, flushing episodes, and telangiectasias, resulting from vascular and neuro-inflammatory dysregulation. The stress could act as a trigger or exacerbating factor by inducing flushing episodes: under the influence of adrenaline released by the autonomic nervous system, cutaneous vessels dilate, increasing facial blood flow and causing redness. Repeated episodes may result in a loss of vascular tone and permanent vessel dilation. Moreover, the concurrent activation of cutaneous mast cells and the release of vasoactive and pro-inflammatory mediators under the influence of stress hormones, such as corticotropin-releasing factor, may amplify local inflammation and contribute to telangiectasias that are persistent and characteristic of rosacea.

Building on this, a 2017 clinical study investigated whether psychological stress preceded symptom worsening in patients with rosacea. Sixteen participants rated their daily stress on a 0–10 scale via questionnaires while recording in a diary the presence of papules or pustules, the intensity of redness, and burning sensations. The results showed that 12 of the 16 patients exhibited a association between higher stress levels and increased severity of skin symptoms. To date, this study represents one of the few clinical investigations directly exploring the link between stress and rosacea. However, the very small sample size precludes drawing firm conclusions, and further research involving a larger number of participants remains necessary.

Stress and skin cancers.

The link between stress and skin cancers is now the focus of growing interest, even though the evidence remains partial. Experimental studies suggest that stress might promote tumor onset, progression, or spread, notably by modulating immunity and inflammation. For example, prolonged activation of the stress axis and the release of glucocorticoids can inhibit certain functions of cytotoxic T lymphocytes, essential for antitumor surveillance, and create a more permissive microenvironment for the development of tumors such as melanoma. Other proposed mechanisms include activation of molecular pathways related to hypoxia, angiogenesis, or epithelial-mesenchymal transition, which may increase the invasive and metastatic potential of tumor cells.

Stress may also play a more direct role in the metastatic cascade. Animal models show that chronic stress exposure is associated with a increase in pulmonary metastases and elevated levels of stress hormones, while certain catecholamines such as norepinephrine can stimulate tumor angiogenesis and the expression of pro-inflammatory mediators. Conversely, some findings occasionally suggest a slowdown in tumor growth depending on the timing and nature of the stress, highlighting a complex relationship that depends on the biological context rather than a single linear effect.

Finally, multiple lines of evidence suggest that stress could reduce the effectiveness of antitumor immune responses and certain immunotherapies, by decreasing the activity of T cells and dendritic cells or by altering the expression of immune regulatory molecules. Similar effects have been reported for basal cell and squamous cell carcinomas, where chronic stress may diminish the recruitment of protective lymphocytes and promote an immunosuppressive environment.

Despite these mechanistic insights, most findings derive from animal or experimental studies. In humans, the relationship between psychological stress and skin cancers remains to be clarified through large-scale clinical research.

Although some studies suggest links between stress and skin imbalances, it is important to remember that a single episode of stress alone is not sufficient to trigger a skin disease. The development of conditions such as acne, eczema, rosacea, or vitiligo depends on a complex interplay of genetic, immune, hormonal, and environmental factors. Stress can act as a triggering or exacerbating factor in predisposed individuals, but it is almost never the sole cause.

In other words, going through a stressful period in life does not automatically cause the skin to develop visible or lasting lesions.

That said, chronic and prolonged stress can have broader repercussions on the body and health, underscoring the importance of learning to manage it. Stepping back from difficult situations, maintaining regular physical activity, practicing meditation or breathing exercises, making time for leisure, and connecting with one’s social circle are simple strategies that can help limit the daily impact of stress. When anxiety becomes overwhelming, medical or psychological support can also be beneficial in restoring better balance.

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