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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 or Corticotropin-releasing hormone is the first part of your stress pathway.  It’s the most studied substance in the stress pathway with regard to skin health. (R)

CRH is believed to be an important cause of acne, psoriasis, eczema, alopecia areata, skin tumors and hives (urticaria). (R)

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)

The stress response pathway increases sebum production and this causes acne by making the skin more hospitable to acne producing bacteria and inflammation (from squalene). (R)

P acnes, the bacteria that causes acne, uses sebum as a fuel source. (R)

Indeed, sebum was 59% greater in people with acne (particularly squalene).  Increased sebum (particularly squalene) causes inflammation and blackheads. (R)

There are various theories as to why the stress response increases sebum production.

CRH increases sebum (oily secretion) production.  (R, R2)  One mechanism is by CRH increasing testosterone in the skin.  (R)  P. acnes also increases CRH in the skin.  (R)

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)

MSH and beta endorphins (increased by CRH) also increases sebum (MSH is controversial).   MSH synergizes with testosterone and progesterone to produce sebum secretion by an unknown mechanism. (R)

Substance P, increased by stress, also influences a bunch of events that lead to increased sebum. (R)  Substance P synergizes with a variety of inflammatory cytokines to increase 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)

Hypothalamus and skin disease.

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8 COMMENTS

  • myhealthandwellnessblogsite

    How do you increase VEGF and even out the CRH as well? How do these hormones become out of whack in the first place? I have alopecia as well as hashimotos thyroiditis, eczema, asthma, acne, allergies, chronic fatigue, etc. I would love to know the cause behind this and what I could do to finally heal. I know there is a reason.

  • Greg

    Any clue on how fish/cod liver oil (or dha/epa) supplementation could cause Acne? It’s caused quite a lot of regular and cystic acne for me and many others online, which is a shame because it’s valuable for anxiety and inflammation

    1. Shaun

      Cod liver oil is high in vitamin A which increases deman for zinc. You have zinc deficiency and hence skin issues after cod liver oil. I had such severe outburst of skin problem after cod liver oil that was very scary. Avoid vitamin A, add zinc. Be careful with vitamin C that it lowers zinc as well but not in such high amount.

  • SWarner

    Hi Joe, usually you mention how to correct things or make suggestions. Is there another article that follows or could you recommend what to do to correct it?

  • Lisa

    Hi Joseph. I’m really happy I stumbled onto your site. I read the post on how adrenal fatigue is bogus. At a gut level my intuition was that you were totally right. I found your explanation of what is really going with people who have those symptoms fascinating. It was a real aha moment and pretty annoying to think I had been focusing on fighting fires downstream of where the real problem is. So I decided to test it out. I have had subclinical low thyroid, adrenal female hormone imbalance symtoms for years and been on dessicated thyroid. I used to take around 90 mg and through supplementing various nutrients I was deficient in like iron iodine zinc selenium vitamin d etc had gotten it down to 15-30 mg but could never get below that. Interestingly the higher I went with vitamin d the more I had to lower the thyroid. I felt warm, energy and just pretty good all around up to about 15,000 iu but not at higher. However I didn’t want to keep taking at that high level indefinitely. It helped a lot but not completely it didn’t get me totally off the thyroid. I’m thinking based on your article it was because of anti inflammatory effects but that it just wasn’t enough to totally do it. So several days ago when I read your post I decided to try something else I have on hand to see what would happen. The only thing I could think of that I had on hand that I knew was very anti inflammatory is fish oil and black currant seed oil. The other kinds of anti inflammatories I have taken at higher doses like turmeric/curcumin, boswellia etc I never noticed an improvement in the low metabolism symptoms. I had noticed that for me it seemed that the black currant seed oil was more anti inflammatory than the fish oil. I mainly took it near my period and it would virtually halt mild cramps or at times if my gut was feeling inflamed I would use and it stopped that very quickly. I hadn’t taken it long enough ever or paid attention to metabolism effects. So I decided to take one soft gel of each at each meal for awhile and see what happened. It has been about 5 days and I’m feeling fine with no thyroid supplement. Normally by day two I would be feeling bad and not feel better til taking it.

    It seems like maybe these oils go into the brain better than some other things. Are there other things that would enter the brain especially well to work as anti inflammatory for the hypothallamus? I don’t know if I should take these oils all the time but don’t want what is happening to stop if I stop taking them. I am type 2 dominant according to your lists of symptoms.

    Thanks

    1. Joseph M. Cohen

      Thanks for your feedback! Take the recommended supplements for Th2 dominance then. Hard for me to help you more without a thorough case review.

  • Dylan

    Good compilation, bro.

    It all seems to go back to HPA-axis dysregulation. I would bet that most perceieved hypothyroid issues are really a consequence of high or low cortisol levels caused by HPA-axis dysregulation.

  • Daniel

    I’ve been thinking that stress is the roof cause of all evil. I seem to beseitigen to stress. I believe it was you who Posted the genes for a higher cortisol rdsponse and i have exactly that. Have psoriasis since forever. And since ms and psoriasis and gut problems offen Come together i think tbey all have something to do with stess….

    Thanks for the post…

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