Stress and cortisol: what effects do they have 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-term) or chronic (long-term), it engages a tightly coordinated network between the brain, the neuroendocrine system and the immune system. At the heart of this response is the activation of the hypothalamic-pituitary-adrenal (HPA) axis. Firstly, the hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to secrete adrenocorticotropic hormone (ACTH), subsequently leading to cortisol production by the adrenal glands. In parallel, the nervous system releases catecholamines, such as noradrenaline. These circulating mediators orchestrate the stress response throughout the organism, including at the level of the skin.

The skin is moreover considered a peripheral neuroendocrine organ capable of sensing, integrating and responding to stress signals. Its cells — in particular epidermal keratinocytes and dermal fibroblasts — secrete mediators themselves and possess the receptors to respond. 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 organisation enables the skin to finely tune its responses, but may also result in disturbances when stress becomes too intense or too prolonged.

From an immunological perspective, stress influences 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 altering certain cellular functions. Skin cells take an active part in this orchestration: activated keratinocytes can produce cytokines such as IL-1α, stored in large quantities in the stratum corneum, or mediators capable of attracting and activating skin immune cells, including Langerhans cells, T lymphocytes and macrophages.

Finally, stress also operates via the neuro-immune axis. 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 implicated in numerous stress-related skin symptoms (burning sensations or discomfort, itching...). Mast cells can then in turn release cytokines and inflammatory mediators, further amplifying local skin responses.

Beyond its general effects on inflammation, immunity or the skin barrier, stress can also influence the onset, severity or progression of certain skin conditions. This relationship is explained by the constant interplay among the nervous system, stress hormones and cutaneous immune responses, which can disrupt the physiological balance of the skin when stress exposure becomes prolonged. Numerous clinical observations and experimental data thus suggest that stress acts as a triggering or exacerbating factor in several skin conditions, without however being the sole cause of these dermatoses.

Stress and eczema.

The eczema is a chronic inflammatory condition characterised by a disruption of the skin barrier, significant dryness and intense itching. It is primarily due to an immune imbalance, often skewed towards a Th2-type response, and an increased production of inflammatory cytokines. In this context, the stress can act as a major aggravating 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 stress-related eczema flare-up, particularly on the face or hands.

Several studies have examined the concrete role of stress in the progression of atopic eczema from the patients’ point of view. A study of 28 individuals with this dermatosis investigated the impact of psychological stress and emotional factors on disease exacerbation. All participants considered that stress could exacerbate eczema and associated pruritus, although it was sometimes difficult to distinguish its effect from that of other physiological triggers such as infections, climate or allergens. Patients particularly reported a more pronounced influence of chronic stress compared to acute stress, citing family or financial problems, workload, examination periods or unexpected events as frequent exacerbating factors. Moreover, in addition to conventional treatments for eczema, such as topical corticosteroids, emollients and phototherapy, some participants mentioned a possible benefit from physical activity and psychological support.

Stress and psoriasis.

The psoriasis is a chronic inflammatory dermatosis characterised by hyperproliferation of keratinocytes associated with immune activation dominated by the Th1 and Th17 pathways. This inflammation leads to the appearance of well-defined erythematous scaly plaques. The stress can act at multiple levels, as cortisol secretion may deregulate inflammatory cytokine production and interact with the skin’s nerve receptors. These mechanisms can facilitate disease initiation or trigger stress-induced psoriasis flares.

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

Stress and acne.

The acne is a multifactorial condition involving excessive sebum production, follicular hyperkeratinisation, 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 pro-inflammatory cytokines modulate the cutaneous immune response. This interaction explains why some individuals report the appearance of stress-related pimples or acne flare-ups related to stress.

Notably, one study conducted among 144 sixth-year medical students analysed 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. It should be noted that 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% showed no lesions.

Stress and vitiligo.

The vitiligo is a pigmentary dermatosis characterised by the autoimmune destruction of melanocytes, the cells that produce melanin, leading to the appearance of depigmented macules. Its origin is complex, involving genetic, immunological and environmental factors. The stress could play a triggering or aggravating role. Studies have revealed altered cortisol and dehydroepiandrosterone (DHEAS) levels, a hormone involved in stress resilience: healthy individuals generally exhibit higher DHEAS concentrations than those with vitiligo, suggesting in the latter a reduced capacity to cope with stress. Furthermore, the antioxidant properties of DHEAS normally participate in the limitation of oxidative stress, a mechanism involved in melanocyte destruction, which may contribute to the progression of vitiligo.

In this context, several studies have sought a better understanding of whether stress may be involved in the development of vitiligo. A questionnaire‐based study of 1,541 adults with vitiligo thus assessed the impact of stressful events occurring in the two years preceding disease onset, as well as their influence on its progression and the possible occurrence of associated symptoms. The questionnaire, consisting of 77 questions, aimed to identify psychological factors prior to diagnosis. The results indicate that a majority of participants reported having experienced at least one stressful event in the two years preceding the onset of vitiligo, which suggests a potential role of stress in its triggering.

Stress and rosacea.

The rosacea is a chronic inflammatory skin disorder of the face, characterised by persistent redness, flushing episodes and telangiectasias, resulting from vascular and neuro-inflammatory dysregulation. The stress may act as a triggering or exacerbating factor by inducing flushing episodes: under the influence of adrenaline released by the autonomic nervous system, the cutaneous blood vessels dilate, increasing facial blood flow and resulting in redness. Repetition of these episodes can promote a loss of vascular tone and permanent vessel dilation. Furthermore, concomitant 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, could amplify local inflammation and contribute to telangiectasias that are long-lasting and characteristic of rosacea.

Following on from this, a clinical study conducted in 2017 sought to determine whether psychological stress preceded symptom exacerbation in patients with rosacea. 16 participants assessed their stress levels daily on a 0–10 scale using questionnaires, while recording in a diary the presence of papules or pustules, the intensity of redness and sensations of burning. The results showed that 12 out of 16 patients exhibited a association between higher stress levels and increased severity of skin symptoms. To date, this study remains one of the few clinical investigations directly exploring the link between stress and rosacea. However, its very small sample size precludes any firm conclusions, and further research involving a larger number of participants is still required.

Stress and skin cancers.

The link between stress and skin cancers is the subject of growing interest today, even though the data remain incomplete. Experimental studies suggest that stress could promote tumour onset, progression or dissemination, 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, which are essential for antitumour surveillance, and create a microenvironment more permissive to the development of tumours such as melanoma. Other proposed mechanisms include the activation of molecular pathways related to hypoxia, angiogenesis or epithelial–mesenchymal transition, which may increase the invasive and metastatic potential of tumour cells.

Stress could also play a more direct role in the metastatic cascade. Animal models show that chronic stress exposure is accompanied by a rise in pulmonary metastases and elevated stress hormone levels, while certain catecholamines, such as noradrenaline, can stimulate tumour angiogenesis and the expression of pro-inflammatory mediators. Conversely, some findings occasionally suggest a slowing of tumour growth depending on the timing and nature of the stress, emphasising a complex, context-dependent relationship rather than a single, linear effect.

Finally, various data suggest that stress may reduce the effectiveness of antitumour 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 noted in basal cell and squamous cell carcinomas, where chronic stress may impair the recruitment of protective lymphocytes and foster an immunosuppressive environment.

Despite these mechanistic leads, the majority of findings are derived from animal or experimental studies. In humans, the relationship between psychological stress and skin cancers remains to be clarified by large-scale clinical research.

Although certain studies suggest a link between stress and skin imbalances, it is important to emphasise that a single stressful episode on its own is not sufficient to provoke the onset of 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 may act as a triggering or exacerbating factor in predisposed individuals, but it almost never constitutes a sole cause.

In other words, undergoing a stressful period in one’s life does not automatically mean that the skin will develop visible or long-lasting lesions.

That said, chronic and prolonged stress can have wider repercussions on the body and on overall health, hence the importance of learning to manage it. Taking a step back in difficult situations, maintaining regular physical activity, practising meditation or breathing exercises, setting aside leisure time and engaging with one’s social circle are all simple strategies that can help limit the daily impact of stress. When anxiety becomes overwhelming, medical or psychological support may also be useful to restore a better balance.

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