Relax, Refresh, Rejuvenate
01 Feb 2021

Decoding the connection between stress and ageing

Navigating the stresses of 2020 felt like 10 years of ageing all in one.  On an emotional level, grappling with prolonged stress certainly feels aging, and the physical fatigue induced by stress is more than just a trick of the mind. Long-term stress generally impairs wellbeing: linked to weakened immunity, poor hormonal control and age-related illnesses such as Alzheimer’s.

Additionally, skin researchers are uncovering how stress dramatically impacts skin, exacerbating conditions and even increasing the risk of glycation in the skin: accelerating ageing processes.

Every aspect of our physical and mental health can be altered by stress, and the complex connections within the body result in a myriad of intertwined responses. The complex hormonal response triggered by stress impacts dramatically upon skin – both directly and indirectly – and an understanding of the all-encompassing impact of stress is crucial to tacking the problem.

Understanding precisely how stress impacts and ages skin is a useful tool for therapists, as clients experience greater degrees of longer-term chronic stress than ever before.

When good stress turns bad

“Stress hormones act directly on the skin to alter skin cell growth, increase sebum production, increase inflammation and impair immunity.”

Dr Gaby Prinsloo

“When we’re stressed the brain triggers the release of adrenaline and cortisol, two important stress hormones, into the body,” explains Dr Gaby Prinsloo, medical director at the iiaa. “Stress hormones act directly on the skin to alter skin cell growth, increase sebum production, increase inflammation and impair immunity,” she adds.

These are sometimes referred to as “fight or flight” hormones. They prime the body to respond to, and recover from, stressful situations: in the short term they can improve alertness, performance and memory.

Stress is only damaging when it is out of control. Chronic stress, caused by ongoing stressful situations, has a detrimental impact on the whole body: including on the skin. Cardiovascular irregularities, diabetes, obesity and Irritable Bowel Syndrome (IBS) can all be exacerbated or triggered by chronic stress, as can insomnia and mental health issues.

Glycation vulnerabilities

Dwindling, damaged supplies of collagen, are a well-known concern for ageing skin. Cortisol’s impact on collagen adds to other natural degrading factors such as UV damage, smoking and free radical damage, as it promotes the damaging phenomenon of glycation in the skin.

Glycation occurs when a sugar molecule bonds with a protein (for example collagen), creating a new, differently shaped molecule. As the number of these distorted molecules accumulates within the skin, skin structure is disrupted, resulting in a loss of elasticity and causing fine lines and wrinkles as collagen and elastin cease performing their typical functions.

The higher the amount of sugar in the blood, the more likely glycation is to occur. When cortisol is released, it inhibits insulin and releases sugar and fat into the blood for use as energy. In a short-term stress response, this energy is used up in response to a stressful situation and blood sugar levels return to normal. However, when cortisol levels remain consistently high due to chronic stress, so do levels of sugar within the blood, and there is less insulin available to reset the balance. As a result, the increased number of sugar molecules are vulnerable to, making the process more likely to occur in the skin.

In your DNA

Recent studies have illuminated the role DNA plays in ageing. Damage to DNA within cells alters how they renew, sometimes becoming “senescent”, or inactive. Senescence compromises skin cell functions and leads to signs of ageing . UV exposure can accelerate DNA damage, and researchers now believe stress is another degrading factor accelerating the shortening of telomeres in DNA. 

“Telomeres are DNA repeats at the ends of chromosomes [that] shorten with each cell division, eventually leading to replicative senescence and premature cellular ageing,” explain Ying Chen and John Lyga in a 2014 study. “Various chronic stress situations have been associated with shorter telomere length.”

Stressed on many levels

Oxidative stress is an imbalance between free radicals and antioxidants, and is notorious for its ageing impact. Research suggests our body’s inflammatory response to psychological stressors is one factor causing free radical damage, and therefore skin ageing. Environmental and lifestyle factors such as UV damage, pollution, smoking and poor diet also add to this.

Antioxidants are crucial for protecting against oxidative stress, and vitamin C is a particularly powerful option. The adrenal gland uses large volumes of vitamin C when triggered, so replenishing the body’s stocks via supplementation or topical care is vital to ensure stressed skin is protected.

 “Vitamin C plays a potent role in diminishing the effects of free-radical damage,” notes Dr Des Fernandes, founder of Environ®. “Because of its antioxidant activity we can expect that vitamin C will tend to slow down photo-ageing.”



Nicholas J. Justice, The relationship between stress and Alzheimer's disease, Neurobiology of Stress,Volume 8, 2018, Pages 127-133,

Campisi, J. “The role of cellular senescence in skin aging.” The journal of investigative dermatology. Symposium proceedings vol 3,1 (1998): 1-5.

Chen, Ying, and John Lyga. “Brain-skin connection: stress, inflammation and skin aging.” Inflammation & allergy drug targets vol. 13,3 (2014): 177-90. doi:10.2174/1871528113666140522104422

 Rinnerthaler, Mark et al. “Oxidative stress in aging human skin.” Biomolecules vol. 5,2 545-89. 21 Apr. 2015, doi:10.3390/biom5020545

Khansari, Nemat et al. “Chronic inflammation and oxidative stress as a major cause of age-related diseases and cancer.” Recent patents on inflammation & allergy drug discovery vol. 3,1 (2009): 73-80. doi:10.2174/187221309787158371

Chen, Ying, and John Lyga. “Brain-skin connection: stress, inflammation and skin aging.” Inflammation & allergy drug targets vol. 13,3 (2014): 177-90. doi:10.2174/1871528113666140522104422