It has been established in recent years that the skin is a direct target of psychological stress via a cascade of hormones, neuropeptides, and neurogenic signals (causing nerve hypersensitivity and inflammation). The skin has been shown to be capable of launching its own local response to stress as well by producing many of the same substances that the brain produces, further enhancing the local effect at the skin level when someone is under acute or prolonged stress. It is no surprise that the skin can perceive and respond to stress similar to the brain and nervous system, since the two systems have evolved from the same germ layer during embryonic development.
The main skin cells (keratinocytes), mast cells (involved in allergy type reactions and inflammation), immune cells, and peripheral nerve endings all will have an effect on various cell behaviour and processes within the skin under stress that can lead to skin disruption, premature ageing and disease development.
The skin is rich in nerve endings, so when an individual is stressed the peripheral nerve endings secrete numerous substances such as Substance P and Nerve growth factor that contribute to hypersensitivity, inflammation, and allergic reactions.
Due to the impact of stress related hormones and peptides, and growth factors on the skin, stress can play a role in the development and exacerbation of skin disorders such as Eczema, Acne, Psoriasis, and Rosacea.
Psychological stress activates the autonomic nervous system to trigger release of catecholamines [e.g. epinephrine and norepinephrine] from the adrenal glands, and in situations of chronic stress corticotrophin releasing hormone [CRH] and ACTH (adrenocorticotropic hormone), mediate a release of glucocorticoids (Cortisol) from the adrenal cortex.
Here is a brief outline of some key stress mediators and the effect that they have on the skin:
Excess levels can cause atrophy and impaired wound healing by interfering with keratinocyte and fibroblast function. Keratinocytes are the primary skin cells that form the epidermis of the skin, and fibroblasts are responsible for collagen and elastin formation.
This manifests as atrophy and thinning of the skin, increased trans-epidermal water loss related to disruption to the skin permeability barrier, and easy bruising with impaired wound healing.
The skin barrier is also negatively impacted by excess cortisol as this effects the lamellar bodies in the skin cells which are responsible for lipid synthesis; the lack of essential lipids weakens the barrier resulting in dry skin, allergies and sensitivity, delayed healing and infections.
Excess glucocorticoids stimulate Insulin production and lead to insulin excess and Insulin resistance. Elevated Insulin stimulates IGF2 (Insulin growth factor) which increases growth of keratinocytes, and stimulates abnormal keratinocyte growth, (exacerbates Psoriasis and Acne) and increases androgens and testosterone release.
This is neuropeptide released in times of stress. Substance P stimulates sebaceous germinative cells and proliferation of sebaceous glands which results in excess oil production and blockage of the oil ducts and the development of acne. Substance P also activates mast cells, increasing histamine release and itch sensation. Substance P induces vascular permeability and inflammation, which aggravates conditions like Eczema and Rosacea.
Corticotropin Releasing Hormone (CRH):
CRH stimulates release of MSH (melanocyte stimulating hormone) causing hyperpigmentation and blotchy skin.
Catecholamines (Adrenaline, Noradrenaline)
Decrease blood perfusion to skin reducing availability of oxygen and nutrients resulting in poor texture and sallow / pallor. Catecholamines have also been shown to cause immune suppression, interfere with DNA repair and contribute to ageing.
While the effects of stress on the skin are only briefly outlined above, it illustrates the significant impact this can have on individuals predisposed to skin conditions. It is therefore imperative to minimise stress where possible in order to avoid any exacerbation of skin disorders.
There are some straight forward tips to reduce stress such as getting a good night’s sleep, exercising and following some simple dietary guidelines (listed below).
Reduce salt intake
Avoid skipping meals
Avoid refined, processed foods.
Avoid high fat foods
Do eat high fibre, low glycaemic index diet
In the following blogs we will present some relaxation techniques that are easy to implement and will have a direct effect in reducing the side effects of stress.
- Dunn, Jeffrey HKoo, John; Psychological Stress and skin aging: A review of possible mechanisms and potential therapies; Dermatology Online Journal 19 (6): 1 University of Colorado, School of
- Medicine, 2 University of California, San Francisco, Department of Dermatology 2013 Permalink: http://escholarship.org/uc/item/3j0766hs
- Jessica M. F. Hall, desAnges Cruser, Alan Podawiltz, Diana I. Mummert, Harlan Jones, Mark E. Mummert; Psychological Stress and the Cutaneous Immune Response: Roles of the HPA Axis and the Sympathetic Nervous System in Atopic Dermatitis and Psoriasis; Dermatology Research and Practice Volume 2012, Article ID 403908, doi:10.1155/2012/403908
- Ying Chen, John Lyga; Brain – Skin Connection: Stress, Inflammation and Skin Aging; Inflammation & Allergy – Drug Targets, 2014, 13, 177-190
- Theoharis C. Theoharides, Jill M. Donelan, Nikoletta Papadopoulou, Jing Cao, Duraisamy Kempuraj, Pio Conti; Mast cells as targets of corticotropin releasing factor and related peptides; TRENDS in Pharmacological Sciences Vol.25 No.11 November 2004