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Stress and the skin: the brain-skin feedback loop

Stress and the Skin

The relationship between stress and disease has been well described with many conditions proven to be triggered or exacerbated by stress. Well known examples are hypertension, migraines and epileptic seizures. However, does stress worsen skin conditions? The answer is a resounding ‘Yes’.  In fact, this has been clearly demonstrated during the pandemic over the last 18 months, when mounting emotional stress has triggered some skin diseases and caused other stable skin conditions to flare up.

While from clinical experience we are certain that a relationship does exist, are there any clear underlying mechanisms to support this?

Indeed, there is…. in embryology the skin and brain are derived from the ectoderm layer. As a result, it doesn’t seem a stretch to believe that the same cells and pathways found in the central nervous system (CNS) are also found in the skin.

What is Stress?

Stress is the body’s natural response to physical, mental, or emotional pressure from events in our life. When the amount of stress we perceive overwhelms our coping mechanisms, hormones are produced to adapt our body to cope with the stress. In the short term these can cause changes to blood pressure, heart rate, blood sugar levels and mood. In the long term, with prolonged stress there may be more lasting changes impacting our overall health as well as skin health.  These hormones are sometimes called ‘stress hormones’ and there are various pathways between the brain and the endocrine system releasing these hormones. 

The main pathway is the HPA axis (hypothalamic- pituitary-adrenal axis). Stress causes the hypothalamus in the brain to produce CRH (corticotrophin releasing hormone) which in turn causes the pituitary gland in the brain to release ACTH (adrenocorticotrophic hormone). ACTH enters the blood and cause the adrenal gland to secrete cortisol and glucocorticoids. Cortisol is considered our main ‘stress hormone’ and remains elevated in those with chronic stress. Interestingly the skin also has a peripheral HPA axis and CRH, ACTH and cortisol are released by various cells in the skin. 

Other important stress hormones, adrenalin and noradrenalin, neurotrophins, substance P and prolactin are released by cells of the brain and endocrine system as well as the skin. The result is that the skin is both a producer and a target of these hormones that mediate a range of effects impacting the course of many skin conditions. 

Skin and Stress

What are the effects of these stress hormones and which skin conditions do they impact?

In a nutshell ‘Stress hormones’ impair the skin barrier function, immune function, wound healing and fibroblast function.  These hormones also increase inflammation, sebum production, melanogenesis (pigment production) and angiogenesis (blood vessel production). Most of these hormone mediators have more than one effect.

Inflammation in particular seems to feature as the major contributing factor in the exacerbation of disease in general in the body as well as the skin. Stress seems to worsen inflammation by various mechanisms. 

As a result of these hormonal effects stress can aggravate conditions like psoriasis, eczema, acne, urticaria and rosacea or trigger new onset of a skin condition. Chronic stress can even accelerate the ageing process!

Atopic eczema/ Atopic dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterised by a defect in skin barrier function and a faulty inflammatory response.  Stress exacerbates AD by impairing the integrity of the skin barrier leading to trans epidermal water loss (TEWL). Stress causes release of hormones in the skin that increase inflammation and worsen eczema. Impaired barrier function also means that more irritants can penetrate the skin and further worsen inflammation. Common scenarios demonstrating the effect of stress on eczema include worsening of eczema during exams, pregnancy and conditions affecting general health and wellbeing

Psoriasis

Psoriasis is a chronic skin condition in which there is overproduction of keratinocytes and inflammation which leads to itchy, red, thickened psoriatic plaques.  

It is well known that psoriasis is worsened by stress, though the exact mechanism is still not quite certain. One theory is that activation of the HPA axis by stress causes increased ACTH and cortisol promoting proliferation and inflammation. Another is that increased substance P released by nerve fibres in the skin of patients with psoriasis triggers an inflammatory response.  High levels of cortisol have also been found in the blood and in psoriatic plaques of patients with psoriasis. 

Rosacea

Rosacea is a skin condition characterised by vascular hyperreactivity and resultant dilated blood vessels and inflammation. Rosacea sufferers flush in response to various stimuli like hot drinks, spicy food and emotional stress. Stress hormones increase inflammation, and skin sensitivity. Histamine released from mast cells in stressful situations also causes flushing.

Urticaria

In more than 50 % of cases the cause of urticaria or hives can’t be identified, but psychological factors have consistently shown to trigger episodes of urticaria. The most likely mechanism is anxiety causing the release of cortisol and adrenalin leading to inflammation as well as release of histamine from unstable mast cells.

Over production of sebum and/ or Acne

Stress does not directly cause acne but can worsen it. Stress causes the adrenal glands to produce more adrenalin, cortisol and androgens that in turn stimulate the sebaceous glands to produce more sebum. The follicles become blocked with sebum and dead surface keratin. This blocked follicle is the perfect environment for acne bacteria in the follicle to proliferate and trigger inflammation around the follicle resulting in acne or breakouts on the skin. CRH receptors on sebocytes promote sebum production. In addition ‘picking of acne spots” during times of stress also worsens acne.

Skin barrier function

The stratum corneum which is the uppermost layer of the skin has a combination of proteins and lipids that create a ‘seal’ on the skin. The skin barrier functions to prevents bacteria and irritants from entering the skin and maintains hydration by preventing water loss (TEWL) from the skin. 

Though the exact mechanism in unknown, studies have shown that stress, including reduced sleep can alter the protein and lipid content of the stratum corneum. This leads to impaired barrier function with consequent dehydration and a dry flaky skin. Untreated, this can trigger an inflammatory response and dermatitis.

Impaired wound healing

Fibroblasts and keratinocytes (skin cells) are key players in the process of wound healing which is regulated by various chemical mediators. There is evidence to demonstrate that elevated levels of cortisol and epinephrine which occur during periods of stress impair wound healing by affecting the functions of these cells.  Psychiatric conditions like anxiety, depression and dementia have been associated with delayed wound healing, presumably due to psychological stress in these patients.  The risk of skin infection during wound healing is also increased during periods of stress due to impaired immune function in the skin. An infected wound is slower to heal.

Wrinkles and fine lines and hyperpigmentation(chronic stress)

We know that genetics, lifestyle and environmental factors affect the ageing process, but emotional and psychological stress can be a big contributor towards ageing. While short periods of stress can sometimes benefit us chronic stress leads to suppressed immune function with increased susceptibility to infections, inflammation and skin cancers. 

The skin immune function protects against both ultraviolet (UV) damage and infection and consequently protects from skin cancers. With suppressed skin immune function there is a greater chance for skin cancers to occur. 

As we age our DNA shortens with each cell division. This process is called telomere shortening.  Chronic stress has been shown to further reduce the length of our telomeres, accelerating ageing.

Stress reduces the production of healthy fibroblasts which synthesize collagen and elastin and the extracellular matrix. This results in thinning of the dermis, loss of elasticity and resultant fine lines and wrinkles.

CRH causes increase in Alpha MSH which promotes pigment production in melanocytes which explains why skin hyperpigmentation can increase during periods of chronic stress, severe illness and even lack of sleep. 

What is the way forward?

There is more than enough circumstantial evidence to support the connection between the skin and brain. It seems that stress management should be an integral part of management of most skin conditions

The first step is to be able to identify our triggers of stress, then to start managing them as best we can. This is a difficult task as stress shows up in many ways and does affect the body as a whole. Most people may not even perceive that they are experiencing emotional stress and find it difficult to accept as a reason for their worsening skin condition. Doctors and dermatologists take care to first exclude all possible explanations for exacerbation of disease before considering stress as a cause.

Make an appointment with Dermatologist Dr Kesiree Naidoo to assist you with any stress related skincare conditions or contact one of our medical skincare specialist to help you with a customized skincare routine. For a complimentary Skin Assessment, click here.

Dr Kesiree Naidoo: 021 531 1107 / [email protected] / www.kesireenaidoo.co.za

Medical Skincare Specialists : 021 023 2501 / [email protected] / www.skinsmart.co.za 

References

  • Inflammation & Allerfy – Drug Targets, 2014, 13, 177-190
  • Brain-skin Connection: Stress, Inflammation and Skin Ageing
  • Ying Chen* and John Lyga – Global R&D, avon products, 1 avon place, Sufferen, NY 10901, USA
  • 2014 Bentham Science Publishers
  • Experts explore the underlying mechanisms of the link between the brain and the skin, feature: By Allison Evans, assistant managing editor, December 1, 2020

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