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The Brain- Skin communication: the role of stress in cutaneous diseases.

El estrés en la piel

As we discussed in our previous post, the similarity in response processes and the communication between the brain and the skin explains how psychological stress can trigger or worsen the development of dermatological disorders. Some of the conditions that are more commonly affected by stress, also named psychodermatological disorders, are:

  • Psoriasis

Psoriasis is a chronic immune disease that affects 2% of the population, representing just over 125 million people worldwide (1). People with psoriasis have scaly patches commonly located on their elbows, knees, or scalp. Stress is both a consequence of living with psoriasis and one of the causes that contributes to its development. The uncomfortable symptoms of this disease (itching, stinging, irritation, eczema, burning…) lead patients to present sleep disturbances and scratching, which generates stress and anxiety that, in turn, contribute to worsening the symptoms of the disease.

Currently, psoriasis is considered to be a complex inflammatory, immune disease with a genetic component. That is, although it is a disease promoted by alterations in the immune system, it is also associated with the presence of some genes. Until the mid-20th century psoriasis was thought to be caused by excessive proliferation of keratinocytes resulting in the well-known psoriatic lesions. However, in 1970, it was discovered that a psoriasis patient who had been given an immunosuppressive drug to prevent transplant rejection showed a significant improvement in his skin lesions (2). This fact highlighted the autoimmune component of the disease and led to the discovery of the important role that T cells and other immune cells play in the development of psoriatic plaques. Recent scientific findings suggest that other components released by the peripheral nervous system, such as neuropeptides, and the skin microbiome could also mediate in this disease.

  • Ance

Acne vulgaris, commonly known as acne, is a well-known dermatological condition that affects much of the population at some point in its life, mainly during adolescence. It generally appears in regions of the skin that have a high density of sebaceous glands such as the face, upper trunk or back.

The development of acne is favored by an overcolonization of the bacterium C. acnes, an anaerobic bacterium that is part of the natural microbiota of our skin, and is characterized by the increase in sebum production by the sebaceous glands and by hyperkeratinization of the epidermis.

Although stress has been popularly linked to acne, it was not demonstrated by a controlled study until 2003, when a scientific publication showed that students under increased stress had greater severity of the disease (3). In addition, it has been observed that molecules synthesized as a result of stress, such as CRH, contribute to fat synthesis in dermal cells.

  • Atopic dermatitis

Atopic dermatitis is an inflammatory, chronic and recurrent skin disease associated with the onset of eczema and itching. Although in numerous occasions it is difficult to diagnose by the subjectivity of its symptoms it is thought to affect between 15-20% of the population in developed countries (4).

Atopic dermatitis is developed by a complex interaction between physiological imbalances (immunological, neuropathic) and environmental factors. In fact, environmental factors such as pollution, exposure to allergens or certain irritating chemical compounds can aggravate the course of the disease. However, imbalance in nociceptive receptors (sensory receptors) is known to play an essential triggering role in this condition. Numerous scientific studies suggest that an increase in the activation of the TRPV1 nociceptor, present in numerous skin cells, is related to the appearance of uncomfortable sensations typical of atopic dermatitis such as itching, stinging, burning or pain (5, 6).

As it occurs with psoriasis, the symptoms of atopic dermatitis are both cause and consequence of stress. For instance, stress can negatively affect skin permeability, which worsens its balance and natural barrier function, resulting in a higher rate of transepidermic water loss. As a result, the skin shows a dry appearance and greater sensitivity to the action of allergens or microorganisms. All these facts contribute to lowering the itching threshold and the frequent onset of discomfort.

There are other skin mechanisms that are severely affected by stress. For example: wound healing. The stratum corneum, the most superficial layer of the epidermis, has an important barrier function that prevents water loss by regulating skin permeability and that protects us from infections. A disruption in this system implies the vulnerability of internal skin layers and a scaly and dry appearance.

The wound healing process is a complex process involving skin cells, the extracellular matrix, and systemic factors, i.e. factors that travel through the blood such as platelets. For complete healing, the mechanoreceptive and sensitive nerve endings that re-populate the area giving it sensitivity and responsiveness are also involved. This complex healing process is divided into three stages: inflammation, proliferation and remodeling. There are numerous scientific publications showing that chronic release of corticosteroids, which are important mediators of stress, has a negative impact at all stages of this process, resulting in incomplete or not fully functional scarring (7).

A study carried out on mice showed that high levels of stress increased transepidermic water loss, lowered the proportion of fluid retention and damaged barrier function, which resulted in exfoliation and the appearance of wrinkles (8). Other work focused on the consequences of insomnia showed that stress can damage the proliferation and differentiation of epidermal cells and decrease lipid synthesis, essential elements for healing. However, the same study affirmed that topical application of fats, such as essential fatty acids and ceramides, can restore skin balance and dermal barrier (9).


  1. Martins AM, Ascenso A, Ribeiro HM, Marto J. The Brain-Skin Connection and the Pathogenesis of Psoriasis: A Review with a Focus on the Serotonergic System. Cells. 2020 Mar 26;9(4):796.
  2. Mueller W, Herrmann B. Cyclosporin A for psoriasis. N Engl J Med. 1979 Sep 6;301(10):555.
  3. Chiu A, Chon SY, Kimball AB. The response of skin disease to stress: changes in the severity of acne vulgaris as affected by examination stress. Arch Dermatol. 2003 Jul;139(7):897-900.
  4. Weidinger S, Beck LA, Bieber T, Kabashima K, Irvine AD. Atopic dermatitis. Nat Rev Dis Primers. 2018 Jun 21;4(1):1.
  5. Mollanazar NK, Smith PK, Yosipovitch G. Mediators of Chronic Pruritus in Atopic Dermatitis: Getting the Itch Out? Clin Rev Allergy Immunol. 2016 Dec;51(3):263-292.
  6. Caterina MJ, Leffler A, Malmberg AB, Martin WJ, Trafton J, Petersen-Zeitz KR, et al. Impaired nociception and pain sensation in mice lacking the capsaicin receptor. Science. 2000; 288(5464):306-13.
  7. Chen Y, Lyga J. Brain-skin connection: stress, inflammation and skin aging. Inflamm Allergy Drug Targets. 2014;13(3):177-90.
  8. Denda M, Tsuchiya T, Hosoi J, Koyama J. Immobilization-induced and crowded environment-induced stress delay barrier recovery in murine skin. Br J Dermatol. 1998 May;138(5):780-5.
  9. Choi EH, Brown BE, Crumrine D, Chang S, Man MQ, Elias PM, Feingold KR. Mechanisms by which psychologic stress alters cutaneous permeability barrier homeostasis and stratum corneum integrity. J Invest Dermatol. 2005 Mar;124(3):587-95.


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