Chronic skin conditions Flashcards
What are some primary considerations for chronic skin conditions?
Food sensitivites Disbiosis Elimination Immune function Stress
How are food sensitivities related to chronic skin conditions?
Food sensitivities can irritate the intestinal lining, setting up a cycle of inflammation that can trigger or worsen most skin conditions, including acne, eczema, rosacea, and psoriasis.
How is the function of elimination related to chronic skin conditions?
need to make sure that waste is leaving the body efficiently—which includes making sure that we urinate, defecate, and sweat when we need to! Chronic constipation is common, but many people may not realize that having a bowel movement less than once a day isn’t ideal, much less that it could be connected to the health of their skin.
Chronic constipation can alter the balance of bowel flora and contribute to intestinal permeability (Khalif et al., 2005; Zhu et al., 2014). In turn, microflora and intestinal health play a role in skin health, and intestinal dysbiosis may be associated with acne, psoriasis, and eczema (Salem et al., 2018)—which brings us back to the importance of maintaining healthy GI function and flora!
How is the immune system related to chronic skin conditions?
Both acute and chronic skin conditions may be related to dysregulation of immune function, either in the skin itself or in the organism as a whole. Of course, if the body can’t generate a sufficient immune response to manage pathogenic bacteria, we’re likely to experience more frequent infections and poor wound healing. But an excessive or “misdirected” immune response can result in the development of inflammatory skin disorders such as atopic dermatitis (eczema), psoriasis, and scleroderma. Though they vary significantly in severity and symptoms, these are all immune-inflammatory disorders that result when immune-active proteins cause an inflammatory response or directly target the cells and tissues of the skin (Eyerich & Eyerich, 2018).
What is the relationship between Stress and chronic skin conditions.
Acute stress can cause impaired barrier function in the epidermis, while chronic stress results in increased systemic and cutaneous expression of certain inflammatory compounds that are associated with atopic dermatitis, psoriasis, and other inflammatory skin conditions (Chen & Lyga, 2014). Stress has been correlated with worsening or flares of acne, atopic dermatitis, rosacea, and psoriasis, and with decreased rates of wound healing (Chen & Lyga, 2014; Ebrecht et al., 2004).
Stress and skin conditions may also feed off of each other in a nasty cycle. For one thing, shame, embarrassment, or other social stress we feel about our skin’s appearance is, itself, a stressor! Additionally, perception of stress can cause an increase in the neuropeptides released in the skin; while these neuropeptides are intended to act as part of the skin’s protective response, they can also worsen inflammatory skin conditions (Chapman & Moynihan, 2009).
Explain the gut-brain-skin axis
The “brain-skin axis” refers to bidirectional communication and influence between the central nervous system and the skin.
The sensory receptors of the skin transmit information about the external environment—such as temperature, pain, and pressure—to the brain through the nerves. Information from the central nervous system is then relayed back to the skin in order to mediate a response to physiological stressors. For example, thermoreceptors perceive cold air, and the central nervous system responds by sending signals to the skin (along with other parts of the body!) to help regulate temperature.
Temperature change is an example of a physical stressor, but psychological stressors trigger the same type of biological response (Chen & Lyga, 2014; Cohen et al. 2007). The stress response is mediated through the hypothalamic-pituitary-adrenal (HPA) pathway, in which a cascade of hormones from different regions of the brain and the adrenal glands trigger physiological and psychological coping mechanisms, such as changes in blood pressure, blood sugar, and mental alertness.
Importantly, the skin appears to function as a peripheral HPA system, in which multiple stress hormones are produced locally and bind to receptors within many types of skin cells, triggering changes in immune activity and skin function (Arck et al., 2006). Cortisol and other stress hormones produce different effects in different cell types, but their net effect in skin cells appears to be pro-inflammatory, including induction of mast cell granulation, increased vascular permeability, and an increase in inflammatory signaling proteins (Chen & Lyga, 2014).
In addition to this brain-skin axis, the established connection between the GI microbiome and the health of the skin creates a “gut-skin” axis. (See Unit 2, Lesson 3 for more on this topic.) These pathways intersect in a “gut-brain-skin” triangle mediated by the intestinal microflora. Evidence suggests that psychological stress, particularly when combined with a low-fiber diet, can cause alterations in gut function and balance of microflora; in turn, shifts in the microflora result in upregulation of cytokines (chemical messengers) that trigger inflammation in the skin (Bowe & Logan, 2011; Salem et al., 2018). At the same time, changes in the microflora may also influence expression of neurotransmitters and neuropeptides, either by intestinal cells or from the gut bacteria themselves (Salem et al., 2018). These changes in neurohormone levels can then increase feelings of depression or anxiety, creating a feedback loop that generates even more psychological stress. This pathway has been suggested as an underlying mechanism by which increased intestinal permeability may affect both the skin and the nervous system, resulting in changes to the skin as well as mood, cognition, and perception of stress (Bowe & Logan, 2011; Salem et al., 2018).
What are some common chronic skin conditions?
Acne
Atopic dermatitis(eczema)
PSORIASIS
Rosacea
Acne: Causes
The immediate cause of common acne, or acne vulgaris, is an accumulation of sebum and dead skin cells within the sebaceous follicles (oil pores) of the skin, leading to the development of comedones (blackheads or whiteheads). Bacteria on the skin contribute to inflammation of these comedones, which results in the development of papules (hard nodules) or pustules (pus-filled nodules). Hormonal shifts can trigger the release of additional sebum, which is why we’re more likely to experience acne during puberty and at certain points of the menstrual cycle.
Propionibacterium acnes bacteria feed off of skin sebum; in the presence of increased sebum, such as during adolescence, P. acnes may proliferate in the sebaceous follicles, where they produce a biofilm that adheres to corneocytes, initiating the development of comedones while simultaneously promoting the inflammatory response that causes acne (Beylot et al., 2014). These bacteria also create an optimal environment for their own survival by stimulating increased sebum production (Beylot et al., 2014), generating a perfect storm for further acne breakouts.
Alterations in GI flora and intestinal permeability are also associated with the development of acne, and the addition of oral probiotics to standard therapies for acne has been shown to improve treatment outcomes, possibly by shifting the expression of immune cytokines toward a less inflammatory pathway (Clark et al., 2017).
Acne:Dietry support
A high fiber, Low glycemic diet works best, while eliminating milk, chocolate and refined carbohydrates
Acne: Internal support
addressing hormonal balance is a prime factor, since hormone surges or excess can be a part of the etiology of acne. Although choosing appropriate herbs to specifically modulate hormones requires an individualized approach, hepatic alteratives can be used as overall hormone normalizers by most people, as they support the liver’s ability to conjugate and excrete steroid hormones. These include Oregon grape (Berberis aquifolium) root, dandelion (Taraxacum officinale) root, reishi (Ganoderma lucidum) mushroom, turmeric (Curcuma longa) rhizome, and sarsaparilla (Smilax ornata) root.
Interestingly, one of the key herbs often included in acne formulas is red clover (Trifolium pratense) aerial parts. In addition to its lymphatic and alterative activity, red clover contains phytoestrogens that selectively bind to certain estrogen receptors in human cells. Red clover is believed to have an estrogen-modulating effect, and in cases of relative estrogen deficiency, it may act as an estrogen analogue.
Acne: Topical support
Although high sebum production is part of the acne cycle, harsh or excessive cleansing that dries out the skin can actually encourage skin irritation and “rebound” production of sebum. Many dermatologists recommend that you clean skin no more than twice daily using a gentle cleanser, resist the temptation of overly drying toners and astringents, and avoid irritating the skin by scrubbing, rubbing, or vigorously exfoliating (American Academy of Dermatology [AAD], 2013).
Herbal preparations can soothe heat and inflammation and support microbial balance on the skin’s surface in order to more quickly resolve existing acne lesions. While you do want to avoid overly drying the skin, the use of astringent toners can help minimize skin irritation and restore normal pH. Witch hazel (Hamamelis virginiana) bark and agrimony (Agrimonia eupatoria) aerial parts make excellent toning astringents. Lavender (Lavandula spp.) flower bud, calendula (Calendula officinalis) flower, rosemary (Rosmarinus officinalis) leaf, and sage (Salvia officinalis) leaf are frequently suggested for acne-prone skin, as these are both astringent and antimicrobial.
Many over-the-counter acne treatments include salicylic acid, which helps regulate shedding of skin cells and resolve clogged pores. Herbs that contain salicylates, such as meadowsweet (Filipendula ulmaria) aerial parts, violet (Viola spp.) leaf, and willow (Salix spp.) bark may mimic this action; these generally also have anti-inflammatory and astringent properties that are appropriate for acne-prone skin.
Eczema: Causes
Atopic dermatitis (AD) is a form of non-allergic skin irritation that typically presents as an extremely itchy, red, and patchy rash, often with skin roughness and scaling; it may progress to include small fluid-filled vesicles (blisters) that produce weeping or oozing, or develop deep cracks or fissures than can be very painful. Chronic AD may also result in thickening of the skin. AD is most common among children and may resolve or persist into adulthood. Patches frequently appear in skin folds, such as between the fingers and inside elbows or knees, but can appear anywhere on the body.
While AD often flares as a result of triggers—such as certain soaps, cosmetics, and fabrics, or food sensitivities—it’s not the result of a “true” or immediate allergic reaction. However, AD is much more common among allergy sufferers, and eczema may worsen during allergy flares (Spergel, 2019). The association of allergies, asthma, and atopic dermatitis is so widespread that the constellation is often described as the “atopic triad”; all three conditions are linked by a common denominator of immune hyperreactivity, in which the immune system is primed to run on high alert, responding to otherwise benign substances as though they were disease-causing pathogens.
A major factor in the development of AD is disruption of both barrier function and immune response. Changes in the proteins of the stratum corneum trigger decreased barrier function, resulting in sensitization to environmental triggers, disruption of normal skin pH, and an inflammatory response within the skin (Arnold & Lio, 2018; Salem et al., 2018). However, the chronic hyperreactive immune profile may remain even once the immediate trigger is removed (Arnold & Lio, 2018).
Eczema: Internal Support
The microbiome has been implicated in the increase in prevalence of atopic disease (asthma, allergies, and AD) through the hygiene hypothesis, which suggests that allergies develop when sanitation and hygiene practices prevent the immune system from becoming familiarized with a range of bacteria and antigens early in life. More recently, the diet-microbe hypothesis has emerged, positing that the typical Western diet fundamentally changes the gut microbiome, ultimately resulting in decreased immune tolerance both in the GI tract and throughout the body (Salem et al., 2018).
Considering the frequency of association with both environmental and food allergies, a holistic response to AD needs to address any underlying allergies and sensitivities contributing to the inflammatory state that characterizes AD. If food allergy or sensitivity is present, supporting gut health with astringents and vulneraries, as discussed in Unit 2, Lesson 3, will be a key component of lasting improvement.
Herbal support often includes immunomodulants such as reishi (Ganoderma lucidum) mushroom and astragalus (Astragalus membranaceus) root in combination with anti-inflammatory herbs such as turmeric (Curcuma longa) rhizome and baikal skullcap (Scutellaria baicalensis) root. In children, milder anti-inflammatories such as chamomile (Matricaria chamomilla) flower and calendula (Calendula officinalis) flower are more appropriate; these can be administered transdermally as well as orally.
A dry tissue state is often seen in those with AD, which might be reflective of both altered barrier function in the skin and poor nutrient absorption due to compromised GI flora or function. In this case, moistening herbs such as licorice (Glycyrrhiza glabra) root and marshmallow (Althaea officinalis) root can be used both internally and topically. You’ll recall that in Unit 2 we discussed the role of omega-3 fatty acids in maintaining a healthy lipid barrier in the skin; omega-3 supplements can be of great benefit in improving the damaged barrier integrity and dry tissue state that often appears in AD.
Relaxing nervine herbs can also be helpful in AD; the extreme itching can be unbearably aggravating for some people and, as mentioned, psychological stress can have a pro-inflammatory effect on the skin. Anxiolytic herbs such as gotu kola (Centella asiatica) leaf and chamomile (Matricaria chamomilla) flower may be particularly good choices, since they both have inflammation-modulating properties as well.
Eczema: Topical support
mpaired barrier integrity appears to allow AD to take hold, and in turn AD continues to disturb barrier function, so restoring barrier integrity in the skin is an important intervention point. Topical use of cooling anti-inflammatory salves, creams, or lotions can ease itching and irritation, help promote tissue repair, and provide an occlusive barrier that prevents further transepidermal water loss. Essential oils may be included for antimicrobial and anti-inflammatory properties, but these can sometimes be irritating to inflamed skin.
We might be inclined, quite logically, to address weepy or oozing eczema with physically drying remedies such as clays and powders. Although it may seem counterintuitive, both wet and dry presentations of AD are likely to respond well to moist topical preparations such as washes and compresses. German phytotherapist Rudolf Weiss (Weiss in Yarnell & Meserole, 1996, p. 243) pulled no punches in outlining his approach:
The use of powder or pastes with a weeping eczema is wrong and will always lead to failure. Moist compresses are needed until the weeping stage and the acute inflammation have passed. After this a change may be made to pastes and finally to ointments.
All forms of AD will benefit from the use of anti-inflammatory and vulnerary herbs; wet or weepy AD may also do well with herbs that are both astringent and anti-inflammatory, such as willow (Salix spp.) bark, white oak (Quercus alba) bark, and rose (Rosa spp.) petal.
Psoriasis: causes
Like atopic dermatitis, psoriasis is an inflammatory condition resulting from an overactive immune response. However, psoriasis is a true autoimmune condition, in which the immune system directly attacks the body’s own cells and tissues. The most common type of psoriasis is plaque psoriasis, which appears as well-defined areas of red, thickened skin, often covered with white or silvery scale-like patches. The knees, elbows, scalp, and back are the most common sites for plaque psoriasis. Plaque psoriasis can sometimes also progress to affect the joints in psoriatic arthritis.
No clear cause of psoriasis has been established, though it is likely to result from a combination of genetic and environmental factors; it’s possible that a specific event, such as a physical injury, infection, or medication, may sometimes play a role in initially triggering the development of psoriasis (Ayala-Fontanez et al., 2016). At the onset of psoriasis, a large number of activated T cells are recruited to one or more areas of the skin; this causes hyperproliferation of keratinocytes and changes in the structure of the epithelium, followed by a significant inflammatory response that leads to the development of thickened plaques. Antigenic memory T cells remain in the body, leading to a chronic condition that usually moves through relapsing and remitting phases (Ayala-Fontánez et al., 2016).
Pain and fatigue are common symptoms of psoriasis. Inflammation in organ systems beyond the integumentary system is common, and the association with GI tract inflammation is especially strong. For example, up to 11% of inflammatory bowel disease (IBD) patients also have psoriasis (Takeshita et al., 2017). Individuals with psoriasis are more likely to develop other autoimmune disorders such as rheumatoid arthritis, celiac disease, and inflammatory bowel disease. There’s also a strong correlation between psoriasis and cardiometabolic diseases; individuals with psoriasis have a significantly higher risk of developing diabetes, hypertension, hyperlipidemia, heart disease, and/or heart attack. This is currently believed to be caused by shared inflammatory pathways, specifically the effects of cutaneous inflammation on blood vessels and the subsequent development of systemic vascular inflammation (Katta & Desai, 2014).
