Atopic eczema: causes, triggers and natural treatments

Atopic eczema (also known as atopic dermatitis) is a chronic inflammatory skin condition that can affect people of all ages, although most commonly presents in early childhood. It is one of the most common chronic skin diseases, thought to affect up to one-fifth of the population¹ and its prevalence is rising, particularly in developed and fast-growing countries.

Our latest blog looks at the underlying causes of this condition, what factors can trigger it and the natural treatments, including nutritional and lifestyle approaches, that may help.

Eczema is the most prevalent in early life, with symptoms typically presenting in the first five years of life and in adults, the condition has usually been present for decades². In the majority of cases eczema will improve or resolve with age; however approximately 10% of patients experience symptoms into adulthood³. The condition can affect people of all ethnicities and has a significant psychosocial impact on patients and their relatives.

The pathophysiology is complex and can involve a strong genetic predisposition, epidermal dysfunction and inflammation, and those with eczema are at an increased risk of comorbidities, including food allergy, asthma and allergic rhinitis⁴.

Atopic eczema

The word ‘atopic’ is defined as relating to, or caused by, a hereditary predisposition towards developing certain hypersensitivity reactions, where the immune system over-reacts such as asthma, hay fever and in this case, eczema. The “atopic march” is an epidemiological phenomenon which refers to the time progression which commonly occurs from eczema to asthma and allergic rhinitis, suggesting that eczema is an “entry point” for subsequent atopic disease⁵ although this theory has been questioned by some.

Common symptoms of eczema include:

• itching of the skin
• warm, tender skin
• skin that becomes scaly and raw
• burning sensation or pain on the skin
• red bumps on the skin that may weep and crust
• skin that becomes dry, red, or rough
• inflammation of the skin

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Common causes behind the onset of atopic eczema

Atopic eczema has a complex, multifactorial pathogenesis, including genetic, immunological and environmental factors that cause skin barrier abnormalities and immune dysfunction. These processes trigger dysbiosis of the cutaneous microbiome, which further aggravates skin barrier damage and immune imbalances and increases the risk of secondary infections, complicating the course of the condition⁶.

We’ll take a closer look at the most common factors that contribute to the development of atopic eczema and discuss how to support skin health in those affected by the condition.

Skin barrier function and formation 

It is important to briefly look at the structure and function of the skin, which provides an effective barrier between the internal and external environments of the body – acting as an interface between the inside/outside and therefore providing protection and support to the body.

The epidermal barrier serves three primary functions: limiting passive water loss, restricting environmental chemical absorption and preventing microbial infection. The epidermal barrier protects against mechanical, chemical and microbial injury through the formation of differentiated keratinocytes. This process is known as keratinization, where epidermal mature from basal epidermal cells to form the flattened cells of the stratum corneum; the outermost layer of skin⁷.

The stratum corneum is the primary mediator of the epidermal permeability barrier, accounting for over 90% of the functionality of the skin, therefore proper development and maintenance of this layer are essential for maintaining its ability to defend the body against both chemical and microbial attacks and dehydration.

Epidermal barrier dysfunction is increasingly recognised as a key determinant in the pathogenesis of eczema⁸ and epidermal permeability, predisposed by individual genetics and exacerbated by environmental exposures, is believed to contribute to the disease process in eczema as:

a weakened skin barrier is more susceptible to topical infections that also trigger an immune response⁹.

 Genetics – filaggrin 

A major genetic risk factor for eczema is loss-of-function mutations in the FLG gene, which encodes the skin protein filaggrin.  Filaggrin is essential for the alignment of keratin in the stratum corneum, and filaggrin breakdown products act as natural moisturizing factors, important for proper skin hydration¹⁰.

Natural moisturising factor components are essential for skin barrier integrity, i.e. for skin hydration, skin pH modulation, immunosuppressive properties, antimicrobial defence, photosensitivity and skin elasticity¹¹. Thus, we can see that filaggrin is important for maintaining a functional skin-barrier.

It is important to note, however, that FLG mutations are neither necessary nor sufficient to cause eczema; in fact, approximately 60% of sufferers do not have this genetic mutation¹² which again highlights the multifactorial aspect of eczema pathogenesis. 

Skin microbiome 

As mentioned, the skin is an important first-line defence against pathogenic microbial invasion, with tight connections between cells in the stratum corneum forming a physical barrier, while antimicrobial peptides and lipids secreted from keratinocytes and glands provide a chemical barrier¹³.

The skin microbiome represents an ecosystem composed of numerous microbial species interactive with each other, as well as with host epithelial and immune cells. This skin microbiome can support healthy skin function and inhibit the colonisation of pathogenic bacteria, but a disturbance of this microbial balance can result in dysbiosis and contribute to skin diseases such as eczema¹⁴.

The bacterium present in the highest percentage in atopic skin is Staphylococcus Aureus. It is able to produce toxins, enzymes and antigens capable of bypassing the immune system and the skin barrier. Its enterotoxins can initiate the production of pro-inflammatory cytokines, leading to inflammation and perturbation of the skin barrier as seen in eczema¹⁵.

S. aureus also causes displacement of other bacterial species, which disrupts the cutaneous homeostasis dependent on host-microbiome signallin¹⁶⁷.

Immune dysregulation 

Eczema results from a combination of a skin barrier deficit and an immune dysregulation, and different hypotheses have been reported; the first suggesting that dysfunctional immunity occurs first, affecting skin barrier function, and the second one stating that a compromised epidermal barrier primarily leads to the onset of eczema and secondarily to immune dysregulation¹⁷.

The immunological pathogenesis of atopic eczema is complicated because its development is orchestrated by both the adaptive and innate immune systems. Skin-resident cells such as keratinocytes, dendritic cells, mast cells, macrophages, and innate lymphoid cells contribute to skin inflammation in eczema patients, and additionally T cells, monocytes and granulocytes are recruited from blood circulation and contribute to the condition.

Although a complex interaction of immune cells mediates eczema skin lesions, its immunopathogenesis is characterised by the tendency toward Th2-skewed responses. The Th2-type cytokines include interleukins 4, 5, and 13, which are associated with the promotion of IgE and eosinophilic responses in atopy. Raised T regulatory cells have also been observed in the lesions and peripheral blood of eczema patients¹⁸.

Immunoglobulin E (IgE) plays a central role in atopy. IgE binds to various immune cells and acts as both an effector for chemical mediator release and a regulator for pro-inflammatory cytokine production.

Skin barrier disruption increases its permeability to external antigens/allergens and facilitates Th2 immune response through antigen-presenting cells such as Langerhans and dendritic cells. This leads to an increase in the production of IgE, which mediates subsequent hypersensitivity responses to antigen exposures.

Hence, IgE plays an important role in the pathogenesis of atopic eczema and is present at increased levels both in the serum and skin of patients.

There is a significant association between higher levels of IgE and the severity of eczema¹⁹.

It has been observed that adults with atopic eczema are more frequently diagnosed with autoimmune diseases compared to those without eczema.

Autoimmune disorders involving the skin, the gut (such as Crohn disease, coeliac disease and ulcerative colitis), or the connective tissue (such as bones, tendons or ligaments) were most commonly associated with eczema.

In patients with more than one autoimmune disease, the association grew stronger with each additional disease which may support the idea of an autoimmune component and/or shared immune pathways in atopic eczema²⁰.

Poor gut health 

Our gut microbiome is vital for immune system development and functioning, and an imbalance in microbial composition and function (dysbiosis) in both the skin and gut have recently been linked to alterations in immune responses and the development of atopic eczema²¹.

The increased prevalence of eczema, particularly in industrialised regions has been hypothesized to be due to excessive hygiene that accompanies the Western lifestyle and reduces exposure of the host’s immune system to a diverse range of microorganisms such as viruses, bacteria and fungi²².

Several recent findings in patients with atopic eczema reveal a dramatic change in microbial community structures compared to healthy volunteers²³.

Gut health in infancy and early childhood

This is an important and vulnerable period in the development of the gut microbiome, which in turn shapes an individual’s disposition to eczema²⁴. It was believed that infants were born sterile. This view is being challenged and it is now thought that the mother’s gut flora may start to populate the baby’s gut ‘in utero’²⁵.

The infant then receives a ‘mouthful’ of bacteria as it passes through the birth canal and will continue to receive bacteria from the mother via breastfeeding. A number of factors may compromise this early development of a healthy gut flora – e.g. where the mother has a dysbiotic flora herself, the use of antibiotics during and/or after birth and caesarean births²⁴.

Maternal prenatal nutrition and dietary diversity are crucial factors in a child’s development.

A growing body of literature points to how sufficient nutrition during the first 1000 days of a child’s life, from conception to their second birthday, is essential for proper brain development, healthy growth and immune system that impacts the entirety of the child’s life, and beyond. Indeed, it is proposed that the first 1000 days accounts for 70% of an individual’s future health²⁶.

The intestinal microbiome also develops within this period, and therefore, factors that influence the development of the microbiome and reduce the risk of allergy are strongly emphasised: natural birth, breastfeeding, contact with nature, having pets, appropriate diets (e.g., high-fibre food, fermented products, home-made food), as well as the consumption of probiotics and prebiotics²⁷.

For infants born by caesarean section, taking a swab of bacteria from the mother’s vagina and wiping these around the infant’s mouth is being used in some hospitals.

Leaky gut 

Dysbiotic bacteria, as well as detrimentally affecting immune function, can produce toxins that damage our gut lining, increasing gut permeability, known as “leaky gut”. Disruption to the intestinal barrier allows the penetration of poorly digested food, microbes, and toxins into the circulation to reach target tissue, including the skin, where they trigger Th2 immune responses resulting in further tissue damage²⁸.

Several studies have also demonstrated increased intestinal permeability in those afflicted with atopic eczema, as well as a range of atopic conditions²⁷.

Candida Albicans 

As discussed, the prominent colonisation of S. aureus in eczema lesions has meant that many of the studies have focussed on the analysis of the bacterial microbiome,

but emerging evidence suggests the involvement of a fungal microbiome (also known as the mycobiome)³²⁹.

A number of studies have identified higher rates of colonisation of Candida Albicans in those with eczema, when compared to healthy controls^30,31, and patients have demonstrated improvements in their symptoms when treated with antifungal drugs.

Environmental factors affecting atopic eczema 

There are a number of different environmental factors that can cause an exacerbation in atopic eczema such as:

• Increased hand hygiene – following the COVID-19 pandemic, hand hygiene using detergents has increased, which can affect the microbiome as well as the protective function of the skin barrier and increase the sensitivity of the skin to trigger substances in eczema.^32,33
• Indoor air pollutants such as formaldehyde and volatile organic compounds³⁴. Air pollutants can interact with the skin by binding to the stratum corneum, becoming metabolised and potentially penetrating the epidermis³⁵.
• High heat and/or humidity may aggravate eczema symptoms by provoking perspiration; one of the most common aggravants reported in children with eczema³⁵.
• Tobacco smoke exposure can have a detrimental effect on immunity, cause oxidative damage and diminished skin barrier function, as well as having an irritant effect on the skin³⁵.
• …plus several others, a few of which we touch on below. 

Allergens

If you have a genetic predisposition to atopic eczema, then exposure to certain environmental factors may cause the condition to flare up, such as certain allergens, including:

• Pets
• Pollen
• Moulds
• Dust mites

Irritants

These are very specific to the individual in terms of causing eczema to flare up however some of the most common ones include:

• Soaps and shampoos
• Detergents
• Disinfectants
• Wool and synthetic clothing

Food

It is believed that around one-third of children with eczema also have a food allergy. Some of the most common food allergies associated with eczema include:

• Eggs
• Nuts and seeds
• Wheat
• Dairy products
• Soy
• Citrus
• Food colouring
• Yeast containing foods

Stress

Sleep deprivation and stress are inflammatory and can also have a direct impact on the skin barrier function – which as we mentioned earlier is essential to preventing the onset of atopic eczema, or at least reducing its severity^36,37. 

Therapeutic approaches to treating eczema

Diet:

• An anti-inflammatory diet that is high in vegetables (6-8 portions per day) and good quality fats (nuts, seeds, avocado, oily fish, olive oil). Sugary foods and inflammatory fats such as trans fats, sunflower and corn oils should be avoided.

Trial elimination diet:

• If there are suspected food allergies and sensitivities a trial elimination diet removing eggs, nuts and seeds, gluten, dairy and soy can be considered to see if symptoms improve.

Support gut health:

• Diets high in fibre, vegetables, fruits, antioxidants and prebiotics help to create a healthy microbial balance, whereas diets low in fibre, fruits and vegetables and high in sugar, refined carbohydrates, and processed foods can create dysbiosis³⁸.
• Fermented foods such as kimchi, sauerkraut and fermented vegetables are rich in probiotics (friendly bacteria), which can positively influence the metabolic activity of the microbiome³⁹.
• Consider taking a multi-strain probiotic. A recent meta-analysis demonstrated a beneficial effect of Lactobacillus-containing probiotics on the severity of eczema symptoms in infants⁴⁰, and studies in adults have reported significant symptom improvements through the use of probiotic supplements including strains such as Lactobacillus Paracasei, L. acidophilus, L. salivaruys, Bifidobacterium animalis, B. breve⁴¹.
• If leaky gut is suspected, consider drinking bone broths – make a broth from meat carcass (ideally organic) – this is high in the amino acid glutamine which supports the repair of the digestive lining. Other nutrients to support gut integrity include zinc, copper, vitamin A and collagen peptides.

Essential Fatty Acids:

• Polyunsaturated fatty acids are divided into 2 families: omega-6 and omega-3. In the last several decades, dietary intake of omega-3 fatty acids has declined, while intake of omega-6 fatty acids has increased. In fact, omega 6-3 fatty acids are now consumed in a ratio of about 20–30:1 in the modern Western diet, relative to 1–2:1 traditionally. Research has suggested that this imbalance may result in increased mediators of inflammation⁴². Foods rich in omega-3 PUFAs include fatty fish, algae, flax seeds and oil, chia seeds, and walnuts, and studies looking at supplementing with omega-3 fatty acids have shown benefits to the severity of eczema⁴³.
• While some omega-6 fatty acids, such as linoleic and arachidonic acid, promote inflammation, gamma-linolenic acid (GLA) appears to reduce inflammation, and a deficiency in GLA in the skin may thus result in increased inflammation. It has been suggested that the enzyme responsible for converting linoleic acid to GLA may be deficient in patients with eczema⁴². Evening primrose oil is high in GLA and is an area of investigation in the management of eczema⁴³.

Vitamin D3:

• has immunomodulatory effects and there are many studies connecting vitamin D to allergic disease and describing a beneficial effect of vitamin D supplementation on eczema^45,46.

Vitamin C:

• Normal skin needs high concentrations of vitamin C, which plays many roles in the skin, including the formation of the skin barrier, the ability to counteract skin oxidation, and the modulation of cell signal pathways of cell growth and differentiation. However, vitamin C deficiency can cause or aggravate the occurrence and development of some skin diseases, such as eczema⁴⁷.

Vitamin E:

• may have therapeutic potential in eczema due to its antioxidant and anti-inflammatory properties⁴⁸.

Zinc:

• plays a number of roles in supporting skin health. A number of studies have demonstrated benefits in inflammatory skin conditions such as eczema⁴⁹, with low zinc levels shown to increase the risk of developing the condition⁵⁰.

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Last updated on 3rd January 2024 by cytoffice