How to manage eczema effectively

Living with eczema can feel like an uphill battle broken only with brief periods of remission. Skin feels tight, irritated and itchy; sores open and eczema scabs form. Humid summers become dreaded and the seasonal changes in pollen count fearfully anticipated. Traditionally treatment entails excessively rich emollient creams that barely feel absorbed within an hour of application. Loose cotton clothing is recommended and un-dyed natural fibre mittens can become a nightly necessity. While these treatment options work, there are many more to choose from. Understanding the cause of your eczema, the reason why your skin becomes itchy, red and irritated will help you to effectively manage it into remission.

What is eczema?

Eczema, medically defined as dermatitis is the malfunction of a person’s skin barrier function. When healthy, skin presents a strong, mostly impenetrable barrier to commonly met irritants, allergens, viruses, and bacteria. When affected by eczema this barrier becomes compromised, allergens and bacteria are allowed in, the immune system is activated and inflammation begins. There are 8 widely accepted presentations of eczema¹, ranging from forms mostly affecting pre-adolescents to those mostly affecting the elderly. These 8 dermatitis’s can be provoked by contact with an allergen e.g. fragrance² or by age e.g. cradle cap or by environmental factors e.g. hard water³.

Who does eczema effect and why?

Although the exact cause (e.g. gene vulnerability or mutation) of eczema is unknown, there are several, identified causing factors. When skin becomes eczematous, it looks likely that 2 co-factors have collided;

1. Genetic vulnerability – determined by a person’s DNA (hereditary)
2. Environmental or lifestyle aggravators – stress, hormones, diet, hard water etc.

People developing eczema will often find close family members suffer from the condition. While eczema is very common in pre-adolescents and can be outgrown, up to one-third of reported cases are made by the adult population⁴.

The suspected causes of eczema

There are 3 widely discussed and accepted models of eczema, ranging from skin specific to systemic;

1. Brick-and-mortar hypothesis
2. Atopic march hypothesis
3. Hygiene hypothesis

The brick and mortar hypothesis accounts for genetic mutation within a gene specific to the healthy function of normal skin. The filaggrin gene. Skin is often described by dermatologists as bricks and mortar because of its very similar structure. As skin cells mature, they migrate towards visible layers of skin, differentiating into ‘corneocytes’ – dead, tightly contained packages of keratin. These bricks are held together by a ‘mortar’ of free-fatty acids, ceramides, and cholesterol. In the classical presentation of eczema, skin’s lipid manufacturing mechanisms are impaired leading to a brick structure with too little mortar⁵. Conversely, the atopic march hypothesis treats eczema as an allergy triad linking its occurrence to the future development of allergic rhinitis and asthma⁶. The atopic march hypothesis implicates a miscommunication or malfunction of the body-wide immune function. Specific antibodies such as IgE (immunoglobulin E) are present in blood at much higher concentrations than in non-atopic individuals. These antibodies evoke hypersensitivity and inflammatory responses to triggers such as foods, dust mites, and pollen. The third widely discussed model of eczematous skin, the hygiene hypothesis is based upon a poorly developed immune function. Immune defence is continually developed throughout life as a person experiences new bacteria and viruses. This teaching process allows an individual to develop needed and defensive antibodies. The hygiene hypothesis plays heavily into the concept of good and bad bacteria with imbalances caused by modern lifestyle factors causing prolonged and negative shifts e.g. in gut microflora⁷.

How eczematous skin biologically differs from non-atopic skin

Understanding the differences between eczematous and non-atopic or healthy skin, helps individuals to select the best possible self-care practices. Below are 6 predominant ways in which eczema prone skin differs from the normal dermatological model of healthy skin;

1. Increased transepidermal water loss
2. Lipid compositional changes (e.g. reduction in ceramide manufacture)
3. Thickening and hardening of skin (lichenification)
4. Decreased linoleic and linolenic acid levels (types of fatty acids)
5. Hypersensitive immune reaction e.g. inflammation
6. Keratinocyte differentiation to tightly packed corneocytes is impaired

The marked, visible and noticeable difference of eczematous skin is its dryness, which often in isolation can lead to ichthyosis. This increase in transepidermal water loss is in turn connected to permutations in skins lipid profile including linoleic and linolenic acid deficiencies. A sub-optimal lipid composition is also often paired with and disordered epidermal skin cells (corneocytes). Acknowledging these changes helps an individual to choose appropriate methods of skincare, for example the thickening and hardening of skin can be counteracted for with softening actives such as lactic acid. Skins decreased linoleic and linolenic acid content can be compensated for through the use of natural, essential fatty acid high oils such as evening primrose.

How to treat and prevent eczematous flairs

As the primary cause of eczema remains to be identified, there is currently no known cure for the condition. Without knowing the target responsible for beginning eczematous cascades, a cure is unknowable. Even so, there are many effective management practises that can successfully tame eczema into remission. Below some of the most successful strategies are detailed;

• Investigate your diet for allergy and intolerance

All hypotheses of eczema involve an altered immune function, whether this is caused by genetics, excessive hygiene practises or the infiltration of allergens. Specifically the atopic march hypothesis links the development of eczema to an increased likelihood of other, similar atopic conditions. When an individual’s immune function is activated, anti-bodies such as IgE travel through blood to reach and effect the entire body.  Food allergies and intolerances can trigger similar effects. Several studies directly link specific foods to the worsening of eczematous symptoms and eczema flairs⁸. These include dairy, specifically cow’s milk and hen’s eggs alongside other common, allergy provoking food groups – nuts, wheat, soya and fish. To determine whether your eczema is reactive to specific food groups, trial 2 week eliminations and monitor your symptoms. If you see a beneficial effect, elimination diets such as the low-FODMAP or auto-immune paleo may provide a basis from which your eczema is able to heal. These diets are restrictive and should be undertaken with guidance from a medical professional.

• Trial the effect of taking a daily probiotic

Clearly, an individual’s immune function plays a very important part in the rearing of eczematous symptoms. Whenever immune function becomes over activated a flare-up of eczema is triggered. Over 70% of a person’s immune cells are located in the gut⁹. Poor gut health is more commonly becoming linked to several autoimmune conditions including eczema. Supplementation with Bifidobacterium lactis Bb-12 or Lactobacillus strain GG has been noted to help counteract the inflammatory responses associated with triggering an eczematous flare-up¹⁰. Alongside these findings, Lactobacillus rhamnosus has also been found to reduce the cumulative prevalence of eczema in infants¹¹. Trial the effect of taking a Lactobacillus based probiotic supplement daily for 2 weeks to a month and note the effects.

• Use an occlusive, emollient rich moisturiser

Moisturisers contain an array of different ingredients, however out of the hundreds available, all fall under one of three functions;

1. Humectant (attracts and locks-in water)
2. Emollient (soothes and softens skin)
3. Occlusive (reforms a protective barrier)

When choosing skincare appropriate for the care of eczematous skin, best results are achieved by using moisturisers that are rich in both emollient and occlusive ingredients. Both families help to tackle some of the commonly associated changes in eczematous skin types – reduced barrier function, thickening and hardening of skin, reduction in essential fatty acids. Examples of emollients include; Evening primrose oil, rosehip oil, jojoba oil and shea butter. Examples of occlusive moisturisers include; Beeswax, cocoa butter, lanolin and squalene.

• Consider investing in a water softener

Hard water contains a notably high amount of minerals such as calcium and magnesium carbonates. When washing in hard water, these mineral deposits can be left on the skin causing irritation and inflammation. Many studies have investigated and concluded a link between bathing in hard water and increased eczema risk¹². There are 2 proposed ways in which hard water can cause eczema to flare-up;

1. Through direct deposition of mineral deposits
2. By inactivation of surfactants e.g. SLS in shower gel

Calcium is naturally occurring within the skin. The levels at any given layer effect maturation of skin cells and their eventual desquamation (shedding). Hard water deposits left on the skin after washing may aggravate these processes, provoking eczematous flare-ups. Traditional cleansing actives such as sodium lauryl sulphate (SLS) are inactivated by hard water minerals. Usually foaming to help improve user experience and washout, when deactivated by hard water minerals, foam forming is impeded making wash-out harder to achieve. SLS is highly irritating to skin when left in contact for prolonged periods of time (+ 1 hour) encouraging a breakdown of the skin barrier and consequently an eczema flare-up.

• Use gently cleansing products

In addition to softening water, avoiding strongly cleansing body washes, irritating bubble baths and foaming face washes will help to protect the skin’s natural barrier function. Surfactants such as SLS work by removing both oil and water based impurities; however their strength also allows them to remove not only makeup and daily collected pollution impurities, but also part of the skins protectively acting ceramides, fatty acids and cholesterols. Specifically, products containing SLS are best avoided in self-care routines for eczema prone skin types. Consider replacing foaming washes for cleansing gels such as our griffin+row skin Cleanse.

Avoid skincare containing fragrance

Fragrances contain several known allergens, irritants and sensitizers. These ingredients are especially troublesome to skin because of their small molecular size, allowing them to slip through skins protective barrier easily. Once within the skin, they’re recognised by the immune system as foreign and an inflammatory response is triggered. Eczema flare-ups are inflammatory; therefore their arrival can be easily provoked by scented personal care products. Fragrance is one of the most common causes of dermatitis type reactions¹³.

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1. Types of Eczema “https://www.eczema.org/types-of-eczema”
2. Ortiz, K. J. and Yiannias, J. A. (2004), Contact dermatitis to cosmetics, fragrances, and botanicals. Dermatologic Therapy, 17: 264–271. doi:10.1111/j.1396-0296.2004.04027.x
3. Atopic eczema and domestic water hardness McNally N.J., Williams H.C., Phillips D.R., Smallman-Raynor M., Lewis S., Venn A., Britton J. (1998)  Lancet,  352  (9127), pp. 527-531.
4. Systematic review of treatments for atopic eczema. C Hoare, A Li Wan Po, H Williams Health Technol Assess. 2000; 4(37): 1–191.
5. Hon K-LE, Yong V, Leung T-F. Research statistics in Atopic Eczema: what disease is this? Italian Journal of Pediatrics. 2012;38:26. doi:10.1186/1824-7288-38-26.
6. Zheng T, Yu J, Oh MH, Zhu Z. The Atopic March: Progression from Atopic Dermatitis to Allergic Rhinitis and Asthma. Allergy, Asthma & Immunology Research. 2011;3(2):67-73. doi:10.4168/aair.2011.3.2.67.
7. Okada, H., Kuhn, C., Feillet, H. and Bach, J.-F. (2010), The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update. Clinical & Experimental Immunology, 160: 1–9. doi:10.1111/j.1365-2249.2010.04139.x
8. Werfel, T., Ballmer-Weber, B., Eigenmann, P. A., Niggemann, B., Rancé, F., Turjanmaa, K. and Worm, M. (2007), Eczematous reactions to food in atopic eczema: position paper of the EAACI and GA2LEN. Allergy, 62: 723–728. doi:10.1111/j.1398-9995.2007.01429.x
9. Vighi G, Marcucci F, Sensi L, Di Cara G, Frati F. Allergy and the gastrointestinal system. Clinical and Experimental Immunology. 2008;153(Suppl 1):3-6. doi:10.1111/j.1365-2249.2008.03713.x.
10. Isolauri, E., Arvola, T., SÜtas, Y., Moilanen, E. and Salminen, S. (2000), Probiotics in the management of atopic eczema. Clinical & Experimental Allergy, 30: 1605–1610. doi:10.1046/j.1365-2222.2000.00943.x
11. A differential effect of 2 probiotics in the prevention of eczema and atopy: A double-blind, randomized, placebo-controlled trial Wickens, Kristin et al. Journal of Allergy and Clinical Immunology , Volume 122 , Issue 4 , 788 – 794
12. Association between domestic water hardness, chlorine, and atopic dermatitis risk in early life: A population-based cross-sectional study Perkin, Michael R.Young, Louise et al. Journal of Allergy and Clinical Immunology , Volume 138 , Issue 2 , 509 – 516
13. Ortiz, K. J. and Yiannias, J. A. (2004), Contact dermatitis to cosmetics, fragrances, and botanicals. Dermatologic Therapy, 17: 264–271. doi:10.1111/j.1396-0296.2004.04027.x