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Stress is the way our body prepares for a imminent danger situation. Stress is not always negative, it serves to prepare ourselves for specific situations. However, when stress levels are high for a long time, health problems can occur.

In particular, prolonged high levels of stress can cause insomnia, headaches or digestive disturbances. But it also produces alterations in the skin, being able to cause permanent changes.

Stress increases the signs of skin aging

One of the most visible effects of stress is the increase in the most visible signs of aging, such as wrinkles, dark circles and blemishes on the skin.

Skin aging occurs by two mechanisms known as chronological aging and photoaging, both processes being cumulative [1]. However, while photoaging is due to sun exposure and pigmentation, chronological aging is mainly due to the passage of time [1].

In stressful situations, the human body reacts by activating a series of pathways:

  • The sympathetic adrenal medulla (SAM) pathway.
  • The renin-angiotensin system (RAS) pathway.
  • The hypothalamic-pituitary-adrenal (HPA) pathway.
  • The parasympathetic (cholinergic) pathway.

The body initially responds to stress by activating the autonomic nervous system to release catecholamines from the adrenal medulla. In addition, the pituitary gland releases adrenocorticotrophic hormone (ACTH), causing the adrenal cortex to release glucocorticoids (cortisol, known as the stress hormone ). All this together plus the increase in oxidative radicals and the damage produced to the DNA of dermal cells, promotes skin aging [2].

To slow down these signs of aging, different potentially effective strategies have been described, such as the topical use of beta-blockers, angiotensin receptor blockers, glucocorticoid blockers, and cholinergic modulators (including botulinum toxin) [2].

Immune response to stress

As we have seen in the previous section, stress influences the immune system, triggering the release of certain hormones such as cortisol. In addition to hormone release, immune cells regulate tissue inflammation via cytokine release (interleukin-6, interleukin-1, interferon-γ), and activating the system formed by peripheral corticotropin-releasing hormone (CRH), proopiomelanocortin (POMC), adrenocorticotropic hormone (ACTH) and corticosteroids [3].

The local secretion of these corticosteroids and other inflammatory mediators affect the integrity of the skin, causing its inflammation. All this can lead to dermal diseases such as psoriasis, atopic dermatitis or chronic urticaria, in addition to skin infections or acne [3]. Inflammation of the skin produces, in turn, neurogenic inflammation. This includes the sensory neurons of the skin, which can aggravate existing skin diseases and increase feelings of discomfort such as itching, tightness or even pain [4].

Stress worsens the signs of atopic skin

The barrier function plays a crucial role in maintaining the integrity, protection and moisturisation of the skin. In atopic skin, this layer is damaged what allows the entry of allergens and bacteria, and increases transepidermal water loss.

The effects of stress on the barrier function are manifested in alterations in the permeability [5] and integrity of the stratum corneum [6], and the reduction in the innate and adaptive immunity of the epidermis [7,8]. All this occurs due to the increase in cortisol levels by the enzyme 11β-hydroxysteroid dehydrogenase type I (11ß-HSD1) in peripheral tissues, such as the skin [9].

The disruption of the barrier function in atopic skin is induced, in part, to a reduction in the renewal of the epidermis due to less proliferation of keratinocytes [10]. In this sense, the enzyme 11ß-HSD1 is associated with this inhibition of the proliferation of keratinocytes, but also of fibroblasts [11]. Furthermore, the enzyme 11ß-HSD1 affects the barrier function after exposure to ultraviolet radiation, since it produces an increase in the expression of 11ß-HSD1, which translates into an increase in transepidermal water loss [12].

The role of the enzyme 11ß-HSD1 is not only limited to atopic skin, since its expression is increased in other dermal diseases, such as seborrheic keratosis and basal cell skin cancer [11].

In addition to the altered barrier function, the constant itching sensation is another of the most characteristic signs of atopic and sensitive skin. In this sense, it is evident that stress, acute and chronic, increases the sensation of itching both in healthy individuals and in those with atopic skin. Resulting in a vicious cycle in which stress exacerbates the itch and vice versa. Mechanisms by which stress induces or aggravates pruritus include central and peripheral activation of the hypothalamic-pituitary-adrenal axis and the sympathetic nervous system [13].

Increases the hair loss

Hair loss is another visible sign of the effects that stress can have on our skin. Among the most common causes of hair loss are alopecia aerata, caused by genetic predisposition and neurogenic inflammation, androgenic alopecia, due to increased androgens (testosterone, androsterone, and androstenedione), and telogen effluvium. The latter is the second most common type of alopecia, after androgenic alopecia, and is due to an abnormality in the hair growth cycle that results in excessive hair loss in the telogen phase [14].

Hair cycle

Telogen effluvium occurs mainly in women, due to a hormonal imbalance, but also to high levels of stress [15]. Stress causes a disruption of the normal hair growth cycle in which hair in the anagen stage prematurely enters the telogen stage. Thus, sudden, short episodes of hair loss begin with little or no hair growth [16].

A possible explanation for hair loss due to stress is the study by Nan Liu et al., who found that the hair cycle is altered in situations of chronic stress in mice. Thus, the telogen stage is prolonged, while the anagen and catagen stages are delayed [17]. This is due to increased expression of the SP protein in peripheral sensory neurons and mast cell activation, accompanied by increased oxidative stress.

To try to reverse this process, the effect of two molecules was determined in this same study. On the one hand, an antagonist of the SP receptor, compound RP67580, reduced mast cell activations and oxidative stress, normalizing the hair cycle. On the other hand, the antioxidant Tempol restored the hair cycle, reducing the expression of SP proteins and the activation of mast cells [17]. These two molecules could serve as potential therapies to delay or reverse hair loss due to stress.

How we can reduce the effects of the stress

Stress is a process by which the human body prepares itself to be able to respond quickly to dangerous situations. However, continued stress can lead to health problems, such as increased blood pressure, which can cause heart diseases, as well as digestive or skin conditions.

Nowadays, we constantly live with stressful situations. Therefore, it is important to prepare ourselves to reduce the effects of the stress. In this sense, it is convenient to rest well, have a good physical shape, follow a good diet, avoid coffee, alcohol and tobacco, among others [4]. In short, follow an adequate pace of life that allows us to take care of our body in the best possible way.


  1. Fisher GJ, Kang S, Varani J, Bata-Csorgo Z, Wan Y, Datta S, et al. Mechanisms of photoaging and chronological skin aging. Arch Dermatol. 2002;138[11]:1462-70.
  2. Dunn JH, Koo J. Psychological Stress and skin aging: a review of possible mechanisms and potential therapies. Dermatol Online J. 2013 Jun 15;19(6):18561.
  3. Pondeljak N, Lugović-Mihić L. Stress-induced Interaction of Skin Immune Cells, Hormones, and Neurotransmitters. Clin Ther. 2020 May;42(5):757-770.
  4. Peters EM. Stressed skin?–a molecular psychosomatic update on stress-causes and effects in dermatologic diseases. J Dtsch Dermatol Ges. 2016 Mar;14(3):233-52; quiz 253.
  5. Garg, A. et al. Psychological stress perturbs epidermal permeability barrier homeostasis: implications for the pathogenesis of stress-associated skin disorders. Arch Dermatol 137, 53–59 (2001).
  6. Choi, E. H. et al. Mechanisms by which psychologic stress alters cutaneous permeability barrier homeostasis and stratum corneum integrity. J Invest Dermatol 124, 587–595, (2005).
  7. Aberg, K. M. et al. Psychological stress downregulates epidermal antimicrobial peptide expression and increases severity of cutaneous infections in mice. J Clin Invest 117, 3339–3349, (2007).
  8. Kleyn, C. E. et al. The effects of acute social stress on epidermal Langerhans’ cell frequency and expression of cutaneous neuropeptides. J Invest Dermatol 128, 1273–1279, (2008).
  9. Choe, S.J., Kim, D., Kim, E.J. et al. Psychological Stress Deteriorates Skin Barrier Function by Activating 11β-Hydroxysteroid Dehydrogenase 1 and the HPA Axis. Sci Rep 8, 6334 (2018).
  10. Berroth A, Kühnl J, Kurschat N, Schwarz A, Stäb F, Schwarz T, Wenck H, Fölster-Holst R, Neufang G. Role of fibroblasts in the pathogenesis of atopic dermatitis. J Allergy Clin Immunol. 2013 Jun;131(6):1547-54.
  11. Terao, M., Itoi, S., Murota, H. & Katayama, I. Expression profiles of cortisol-inactivating enzyme, 11beta-hydroxysteroid dehydrogenase-2, in human epidermal tumors and its role in keratinocyte proliferation. Experimental dermatology 22, 98–101, (2013).
  12. Tiganescu, A. et al. UVB induces epidermal 11beta-hydroxysteroid dehydrogenase type 1 activity in vivo. Experimental dermatology 24, 370–376, (2015).
  13. Golpanian RS, Kim HS, Yosipovitch G. Effects of Stress on Itch. Clin Ther. 2020 May;42(5):745-756. Epub 2020 Mar 5.
  14. Alteraciones del cabello. Protocolos diagnósticos y terapéuticos en dermatología pediátrica. Pedragosa R.
  15. Thom E. Stress and the Hair Growth Cycle: Cortisol-Induced Hair Growth Disruption. J Drugs Dermatol. 2016 Aug 1;15(8):1001-4.
  16. Tosti A, Piraccini BM, Sisti A, Duque-Estrada B: Hair loss in women. Minerva Ginecol. 2009;61:445-52.
  17. Liu N, Wang LH, Guo LL, Wang GQ, Zhou XP, Jiang Y, Shang J, Murao K, Chen JW, Fu WQ, Zhang GX. Chronic restraint stress inhibits hair growth via substance P mediated by reactive oxygen species in mice. PLoS One. 2013 Apr 26;8(4):e61574.