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Stress and Eczema: How The Two Are Connected

About 73% of adults diagnosed with eczema report that stress triggers flares or exacerbates existing flares. Research has confirmed that there is a link between stress and atopic dermatitis flares. 


How does stress promote atopic dermatitis flares or worsen them? We are learning that several different body systems interact to respond to stress. Our skin, as it turns out, plays a role in helping these different systems communicate.  

 

Stress and Eczema: A Multisystem Interaction


In the 1970’s, psychology researcher Robert Ader and immunology researcher Nicholas Cohen conducted ground-breaking research into the long-suspected but poorly explained connection between psychological stress and immunosuppression. Working together, they established that psychological stress led to immune system dysfunction.


Around the same time, researchers in Switzerland discovered that the connection between psychological state and immune system function went both ways; not only could psychological stress inhibit the immune system–the immune response to antigens likewise affected neuronal activity in the hypothalamus. 


These discoveries represented a turning point in our understanding of the relationship between psychological state and physical illness, and they laid the foundation for research that continues into the present. Ader coined the term “psychoimmunoneurology” to describe the interplay between psychology, the immune system, and the nervous system. His unwieldy term is now an interdisciplinary field in its own right. A good deal of current research in this field is dedicated to how these interlocking systems affect skin disorders such as atopic dermatitis. A basic understanding of the body’s response to stress can give us a little insight into the effects stress has upon the skin.

 

stress and eczema


Fight or Flight


You’ve likely heard the phrase “Fight or flight.” It refers to an instinctive response to threats an individual perceives in their environment–in other words, stress. Neurotransmitters stimulate the production of hormones such as cortisol and norepinephrine, which act upon the blood vessels, heart, and other organs to assist a person in confronting a threat (fight) or fleeing from it (flight). While the process is much more complicated than the simple fight/flight dichotomy, the stress response begins with the body’s attempt to protect itself. 


Chemical Communicators


The fight/flight instinct is largely mediated by the hypothalamic-pituitary-adrenal axis (HPA). This system is responsible for maintaining the body’s internal stability while responding dynamically to external stimuli–a state called homeostasis.


The first part of the HPA axis, the hypothalamus, is located deep within the brain. It begins a cascading response to stressors by secreting higher concentrations of corticotropin-releasing hormone (CRH). This hormone is the MVP of the stress response. It acts upon the pituitary gland to increase secretion of other hormones, which in turn act upon the adrenal glands to increase their production of some hormones you’re probably somewhat familiar with–cortisol and epinephrine (adrenaline). 


Cortisol, the so-called stress hormone, signals for a greater availability of glycogen stores needed for energy, and it helps the brain use these stores more efficiently. Epinephrine increases heart rate and respiration rate. Its precursor, norepinephrine, causes vasoconstriction, or narrowing of the blood vessels, so that blood pressure rises. 

You can probably see how these changes could help us spring into action when we are threatened.


This is a rough, simplistic sketch of a very complex response that depends upon the coordination of several different systems. Several different biochemicals facilitate communication between these systems. 



The skin’s role in this complex response might not be obvious at first glance–but remember, the stress response is about maintaining internal stability while responding to external influences. Our skin is the first barrier between us and the outside world. It serves as a sentinel, a first alert to the body’s systems when we experience external stressors. Signals sent by this first alert system are part of what spurs the hypothalamus into action. 


Like your adrenal glands and the hypothalamus, your skin is responding to signals from neurotransmitters and is sending signals of its own all the time. In fact, the skin appears to facilitate communication between the endocrine, immune, and nervous systems, relying upon several different biochemical mediators (including some we’ve already mentioned) to do so.


Specialized cells in the skin produce their own neurotransmitters and neuropeptides, among them serotonin and prolactin (both of which are related to mood), as well as corticotropin-releasing hormone and a peptide called substance P. Stress can cause these biochemical mediators to become dysregulated, and this affects atopic dermatitis patients in several different ways. 


Excess corticotropin-stimulating hormone is associated with inflammation, which we know plays a role in eczema flares. Interestingly, stains of skin samples from people with active eczema flares tend to show either excess CRH or abnormally low levels–a similar phenomenon is noted with serotonin. 


Substance P is the most abundant peptide in the nervous system. It enhances nociception, or the perception of pain, during stressful events.Substance P also enhances the perception of itch. This has led some researchers to suggest that the higher levels of Substance P during stressful periods might kick off an itch-scratch cycle in people who are experiencing eczema flares; the skin is already compromised and itchy, and the increased sensitivity to itch leads to scratching. Scratching damages the inflamed skin even more, which in turn leads to more itching. This in itself is stressful, so the reaction is viciously reinforced. This could be part of the reason that stress worsens preexisting eczema flares.


In some studies, treatment with serotonergic drugs such as bupropion, normally used to treat depression, lessened the severity and shortened the length of eczema flares. In other studies, such treatments were associated with increased itching and worsening of symptoms. In either case, there is a link between serotonin and atopic dermatitis; stress can either stimulate overproduction or decreased production of serotonin, and it can also interfere with its receptors. 


Stress and Immunity


The dysregulation of CRH, serotonin, and other biochemicals is not the only factor at play in the stress-eczema relationship. The immune system is also affected by the endocrine response to stress. As outlined above, the HPA axis stimulates the production of cortisol when the body is exposed to stress. Cortisol acts as an anti-inflammatory–in fact, exacerbations of eczema are frequently treated with hydrocortisone, a synthetic cortisol. 


However, prolonged or excessive cortisol production, such as we experience during a traumatic event or prolonged stress, can disrupt the feedback loop and impair cortisol’s anti-inflammatory function. Normally, cortisol binds with glucocorticoid receptors, which signals the hypothalamus to slow its production of corticotropin-releasing hormone. Many think that excessive cortisol production can result in glucocorticoid receptors becoming resistant to cortisol. When that happens, the hypothalamus does not receive a signal to halt CRH production, so CRH surges continue. CRH stimulates proinflammatory mast cells, many of which are in the skin.  



Another theory is that excess cortisol binds with mineralocorticoid receptors instead of glucocorticoid receptors; when this happens, proinflammatory by-products are produced which could lead to heightened innate immune response. 


Stress also correlates with higher blood levels of both immunoglobulin e (IgE), an antibody responsible for defending the body against pathogens and irritants, and special disease-fighting white blood cells called eosinophils.  


Both IgE and eosinophils are associated with overactive innate immune responses, and they are both found in higher levels in people with atopic diseases such as eczema The connection between stress, higher IgE and eosinophil counts, and eczema was demonstrated in a 2009 study in Germany, in which sustained maternal stress during pregnancy correlated to an increased risk of eczema within a child’s first two years of life. Children whose parents experienced significant stress in the first two years after birth were also found to be more likely to develop atopic dermatitis. In both cases, the children with eczema were found to have higher-than-normal blood levels of both IgE and eosinophils.


The body’s response to stress is meant to protect us from threats to our well-being, including those posed by pathogens. When the feedback loop between the HPA axis and other systems works properly, the immune system protects us from disease-causing pathogens. When one component of this intricate process malfunctions, we either experience overactive immune responses that lead to inflammation, or we experience an impaired response to disease-causing pathogens. 


In either case, atopic dermatitis sufferers are at risk. Pathogens such as staph reproduce and endanger the skin’s barrier function when the immune response is diminished. Inflammation and oversensitivity to antigens occurs when the immune response is abnormally reactive. 



The more we learn about the intricate communications between various systems during times of stress, the blurrier the old mind-body dichotomy becomes. Stress and mood are not merely products of the brain; the entire body is enlisted in the stress response, and any of its systems or organs can suffer when the response fails in some way. As our body’s largest organ, the skin is both our first alert system in times of danger and the immune system’s first defense against pathogens. It is not so surprising that it would be affected deleteriously by stress. 


We cannot completely avoid stress. Fortunately, there are effective treatments for eczema flares triggered by that stress. SmartLotionⓇ brings relief and healing to stress-triggered eczema flares. Its prebiotic components foster a healthy microbiome, giving skin a better protection against pathogens associated with flares. The small amount of hydrocortisone it contains reduces inflammation and soothes itching. 


SmartLotionⓇ isn’t a cure for stress by any means–it can, however, relieve eczema symptoms that often add to the stress response. 

 

You can find more articles about eczema and atopic dermatitis management on our blog, along with news articles too. 

 

- Zula Elwood