Almost all of my clients have a stress response that is out of whack. Concurrently, almost all also have some kind of skin issue.
This post explains how stress causes a bunch of problems for your skin.
Psychological stress increases your stress response, but it is far from the only way to activate it. See the full list of ways that our stress response gets activated.
It is known that acne is made worse by emotional stress. (R) This post is going to dive into the mechanics of it.
CRH, ACTH, a-MSH, ß-endorphin and their receptors can be generated and secreted in various cells found on your skin (epidermal and hair follicle keratinocytes, sebocytes and mast cells). ACTH, a-MSH, ß-endorphin are products of CRH production. (R)
P acnes, the bacteria that causes acne, uses sebum as a fuel source. (R)
There are various theories as to why the stress response increases sebum production.
ACTH also increases sebum indirectly by increasing adrenal male hormones (DHEA, Androstenodione, Androstenodiol, Androsterone, DHT (R)). (R) DHT not only increases sebum production, but also proinflammatory cytokines in acne. (R)
CRH causes less VEGF in the skin. (R) VEGF promotes hair growth and can, therefore, result in reduced hair growth or baldness.
CRH inhibits the growth of hair cells and melanin producing cells (which cause you to tan). However, it also inhibits apoptosis of melanin cells and stimulates production of hair cells. (R)
Theoretically, this means that you will burn more easily. The melanin cells are there to protect you from sun (UV) being able to damage your DNA. (R)
Cortisol inhibits skin fat (lipid) synthesis and secretion in the skin, which is needed for an effective skin barrier. (R)
Also, in animal models, stress has shown to inhibit antimicrobial peptide production and increased susceptibility to severe skin infection. (R)
So less lipids and antimicrobial peptides in your skin will allow infections – including fungal – to fester. So if you have a skin condition caused by fungi (tinea, dandruff, etc…), activation of your stress response could be at cause. (R)
Inhibition of CRH and cortisol returned antimicrobial peptide level to normal and improved the severity of infection. (R)
With regard to inflammation, we see mixed effects from CRH and its downstream products. I’d say it’s overall for the worse, but genetics has a large role in how the stress response affect your skin.
CRH causes the release of IL-4, IL-6, IL-10, and IL-13 from skin cells and mast cells. All these have the effect of reducing the skin immune system and inflammation. (Serotonin can reduce mast cell activation in the skin.) (R)
By activating mast cells, you feel more flushy. Mast cell activation plays a central role in skin issues such as eczema, itching and hives. (R)
CRH decreases IL-18, the proinflammatory cytokine, while ACTH increases it. (R)
In people, CRH, ACTH, a-MSH were increased in the skin in Alopecia Areata. However, they had insufficient cortisol. So the first part of the stress pathway increased, but not the last part. The effect of CRH on mast cells contributes to less hair growth. (R)
In mice, vasopressin and POMC were increased. The mice showed a significantly weakened systemic HPA responsiveness to acute stress and exhibited an imperfect adaptation to chronic psychological stress. (R)
Stress suppressed the skin immune system overall and it can’t fight cancer as well. Also, CRH enhanced tumor cell growth and angiogenesis and can cause or contribute to melanoma. (R)
The increased stress levels of the modern era is one reason why skin cancer has been such a problem in this century, even though we’ve evolved with sun for billions of years. This is even though we bath ourselves with sunscreen and stay indoors mostly, as opposed to our evolutionary history.
CRH and mast cell activation from it play an important role in contact dermatitis, which is a rash you develop from a foreign substance. CRH increases the immune response to foreign substances and also increases inflammation (Nf-kB) in hair cells. (R)
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