Eczema is an inflammatory skin condition characterised by red itchy, scaly thickened skin which can also weep and ooze. It is a chronic condition which starts in childhood with intermittent flares and spontaneous remissions. Backs of knees, crooks of elbows are the most commonly affected areas – but it can be anywhere. It’s made worse by the itch-scratch cycle and can easily become infected. (Meneghin 2012)
85% of eczema begins before the age of 5. 15-30% of children and 2-10% of adults will be affected during their in life time. 40-60% of children with eczema will still have the disease as adults. Although, many ‘grow out’ of the condition by their teens, a further 40-60% will still suffer to some extent as adults. (Bieber 2008)
The cause of eczema is multifactoral and still not precisely understood but involves a complex immunological cascade, including epidermal barrier disturbances, IgE dysregulation, defects in cutaneous cell-mediated responses and the influence of environmental factors in genetically prone individuals. (Boguniewicz 2011)
Eczema is part of an ‘atopic march’ – with food allergies developing first, followed by eczema, asthma and then allergic rhinitis – a ‘progression from one epithelial lining to another’ (Spergel 2010) (Carlsten 2013).
Diet and lifestyle, food allergens, allergies to animals, dust mites, pollen, tobacco, air pollution and low humidity are considered risk factors (Williams 1995) (Schultz-Larsen 1993) (Stracken 1989.) The most common food allergens are milk, eggs, peanuts, fish, soy, wheat, citrus and chocolate. Soaps, shampoos, chlorine and washing powders are accepted as ‘irritants’ which worsen symptoms. (Williams 1995)
Along with all atopic disease it has nearly tripled in the last 30 years (Kay 1994). The ‘hygiene hypothesis’ is often put forward as an explanation.
Reduced early exposure to childhood and bacterial infections increases incidence. (Williams 2006) Children from smaller families, with higher educational and socioeconomic levels, who live in less crowded accommodation, with double-glazing and less exposure to infections from siblings, animals seem to be at greater risk.(Zutavern 2005) Whilst maternal diet, higher maternal age may also play a role. (Williams 1994.) Children from developed countries are twice as likely to develop eczema. (Schultz-Larsen 1986) Those who move to more developed countries quickly develop eczema at an even higher rate than the local established population, regardless of ethnicity. (Williams 1995.)
This hypothesis is supported by evidence that eczema results from an impaired TH1-TH2 cytokine imbalance. Infections induce TH1 cells, antagonise TH2 cell development and decrease the incidence and inflammatory response in eczema.(Williams 1992) TH2 cytokines. Interleukins (IL4, IL5, IL10 and IL13) are all raised and TH1 cytokines ( Interferon-y and IL2) down regulated increasing the tendency towards TH2 dominance.(Leung 2004) Children and adults with eczema have elevated serum IgE antibodies and increased activation of Type 2 T Helper cells, elevated total circulating eosinophils and mast cells which release higher amounts of histamine than normal. This imbalance of the TH2 and TH1 pathways and their associated cytokines makes individuals susceptible to inflammation. (Caitlin 2013)
The sterile immune system of newborns is TH2 dominant but normally in the first 12 months it naturally adapts and shifts towards a TH1-TH2 balance as a result of repeated exposure to diverse infectious antigens. Higher-hygiene standards, increased antibiotic exposure, vaccines and reduced contact with pathogens is favouring and allowing a TH2-mediated immune system to persist for longer than normal. (Mackie 1999)
Pathogenesis is partly hereditary. Two thirds of patients have a positive family history of allergy with either a parent or sibling/s with either eczema, hayfever or asthma. (Pizzorno 2008) When both parents are atopic their children have a 70% risk with a higher risk if their mother is atopic. (Ruzicka 1998)And Identical twins to be 85% more likely to have eczema than non-identical, 21%. (Fergusson 1982).
An array of genetic factors play a role in the immune dysregulation and epidermal barrier dysfunction in eczema (Leung 2003.)
For example, Filaggrin which is a key final protein in natural moisturising factor (NMF) of the skin and helps maintain hydration and skin PH is often absent. Children and adults with eczema display mutations in the Filaggrin gene (FLG) resulting in compromised barrier protection and susceptibility to allergens and bacterial colonisation.(O’ Regan 2008) In addition, the Leukocytes of those with eczema have also been shown to have decreased cyclic adenosine monophosphate (cAMP) levels resulting in increased histamine release and decreased bactericidal activity. (Saarinen et al 1995)
Defective cell-mediated immunity leads to increased susceptibility and overgrowth by bacterial, viral and fungal infections, particularly, herpes simplex virus (eczema herpeticum), which can be systemic and is potentially fatal; he common wart virus (papillomavirus), molluscum contagiosum and Staphylococcus aureus. Staph. A infections exacerbate eczema by acting as super antigens, stimulating an augmented T cell response and promoting increased IgE levels. (Rudikoff 1998)
Recent immunological understanding is beginning to shed new light on the role of the early establishment of the gut microflora, exposure to commensal microflora and specific bacterial species in newborns as key modulating factors in the development of eczema.
A newborn’s gastrointestinal tract(GIT) is sterile. Postnatally, a baby’s microflora is added to by repeated microbial stimulation which activates the innate and adaptive immunity. Inadequate stimulation results in a reduced intestinal surface area , alteration of enzyme patterns, mucosal barrier and mucosal IgA system – leading to a reduced oral tolerance capacity and persistence of a neonatal TH2-orientated immune response, favouring the development of allergies. (Meneghin 2012)
Functional Medicine (FM) considers eczema to be an atopic condition and looks to food allergens either IgE sensitization(Johansson 2003) and IgG food intolerances as triggers of an immune-modulated inflammatory process in genetically susceptible individuals.
It stresses the importance of improving deficiencies in the protective mechanisms of the gastro intestinal tract (GIT) and the Gut Associated Lymphoid Tissue (GALT) and sees its influence on the early development of the immune system and subsequent protection of the individual as pivotal in understanding the causes, triggers and drivers of eczema.
It accepts eczema is influenced by genetics but would argue its influence can be modulated by lifestyle and dietary change; genes can be up-regulated, as well as down regulated, and the severity and incidence of symptoms decreased by stress reduction, correct diet, supplementation and repair of gut lining.
‘Hypersensitivity’ accounts for 70-80% of cases ‘extrinsic’ eczema – in such cases immunological, usually allergic (IgE- mediated) reactions are triggered by exposure to foods, air born and topical allergens. Most sufferers test positive in skin prick tests and symptoms improve with removal of foods, elimination diets and controlled reintroduction by FM practitioners. (Pizzorno 2012)
Skin prick tests, patch tests, Total IgE Blood Tests, Specific IgE (RAST test), Component resolved IgE testing and IgE panels are tests which can be ordered to test IgE reactions.
Sensitivity to dust mites, moulds, animal dander or topical skin care and cleaning products like washing powders are all common risk triggers. Eliminating foods, removing carpets, using air purifiers, avoiding cleaning products, using hypo-allergenic bedding and clothing improves symptoms in most children and adults. (Pizzorno 2012)
A further 20-30% of people with ‘intrinsic’ eczema have no family history and pathogenesis is non IgE-mediated. In these cases, the integrity of the epithelial lining, IgA-mediated mucosal barrier and microbial actions of commensal bacteria are always addressed in FM.
A CDSA or Comprehensive Digestive Stool Analysis can check for hidden gut infections – parasites, candida and other pathogenic; intestinal flora balance, intestinal immune function and dietary fibre intake.
A child born naturally will be exposed to its mother’s microbiome in the birth canal and its immune system will be activated, or primed. Children born by C-section are denied this initial protective exposure (Bager 2008) and would be seen as a causative factor.
A recent study has taken this argument even further, a Mother’s diet, age, BMI, whether she is a smoker, how stressed she is, her socioeconomic status, the house she lives in (ie: presence of mould and other allergens), birth outcome, as well as mother’s exposure to antibiotics, have a ‘profound impact on micro biota and immunoregulation’ of the new born…early exposures impacting the intestinal micro biota are associated with the development of childhood diseases that may persist to adulthood such as asthma, atopic dermatitis, rhinitis and chronic immune-mediated inflammatory diseases, Type 1 diabetes and obesity.’ (Munyaka 2014)
A pre-term new born, exposed to medical intervention, especially repeated antibiotics would be particularly at risk. Not being breast fed is also a causative factor. Breastfeeding is known to protect against developing allergies. (Saarinen 1995) (Lucas 1990) Unless mothers are atopic and then there is a transfer of allergens in breast milk.(Cant 1986) Evidence from 5 trials involving 952 participants concluded dietary antigen avoidance by lactating mothers with atopic eczema reduces the severity of symptoms.(Kramer 2014)
The immune system of babies is exposed both negatively and positively to its mother immunity in utero, via the placenta, and during birth. If her microbiome is deficient or dysbiotic, if she has had frequent antibiotics, vaccinations, a poor diet and been exposed to chronic stress been then the quality and nature of the microbiome her baby inherits will sow the seeds of allergy.
Early weaning, before 6 months, when a baby’s immune system is immature is a risk factor. Beginning solid foods before 4 months doubles incidence of eczema.(Ferguson 1994)
The secretory IgA-rich mucous membrane of the gut is the first immunoglobulin to come into contact with food in the gut lumen – an important step in oral tolerance. It also acts as a barricade against the entry of food antigens. Many children with food allergies have lower IgA levels than normal. Low secretory IgA is also linked to infection (bacterial, yeast or parasites), aging, antibiotics, medication and stress. Chronic stress reduces IgA. (Brostoff 2000) (Breneman 1984) (King 1982)
Improvement of microflora essential to modulating the immune system’s response to potential food allergens. Supplemental probiotics and early exposure to multiple bacterial strains stimulate the intestinal immune system and increase secretory IgA levels (Sudo 1997) (Maeda 2001)
A secretory IgA (Siga) test tests saliva for imbalances and either excess or deficiency of IgA. The SIgA specifically of the gut can often be tested for as part of the CDSA test.
FM accepts that the steep rise in eczema coincides with overexposure to environmental toxins in the air, our water and food and the change from traditional, seasonal, locally grown, whole foods to mass produced, highly processed and refined foods since the 1950’s. The mass introduction of antibiotics and childhood vaccination also directly correlate to the same time period and the dysregulation of the immune system of the skin and epithelial linings of the mouth, nose, throat and gut, and the ‘atopic march’ typical of allergies.
Over-exposure to toxins progressively weakens the epithelial linings – the body’s first line of defence against toxins, bacteria and viruses. Once the barrier defences of the skin and mucosal protection of the skin is breeched and damaged it is easily overwhelmed and the antigens which should be repelled enter the blood stream raising levels of TH2 lymphocytes, promoting cytokines (IL4, IL5 and IL13) and an inflammatory cascade and increasing levels of IgE antibodies future susceptibility to more and more allergens (dust mites, grass and pollen) (Kondo 1998)
A typical Western diet low in EFAs, low in fibre and excessively high in sugar contributes to oxidative stress and the development of ‘leaky gut ‘ or increased gut permeability. (Rapin 2010) The integrity of tight junctions of the epithelial lining of the gut are compromised by chronic inflammation, pathogenic overgrowth and poor diet. (Jacobson 1981) Larger protein molecules like Gliadin from wheat and Cassein from dairy, or other partially digested molecules, and bacteria are able to pass into the blood stream and cause allergic reactions and food intolerances. ( Jalonen 1991)
Testing for IgG food intolerances, and intestinal permeability are not part of established medical practice but FM does think it is vital to assess and check for these markers. Repairing the GIT with L-glutamine and by removing pathogenic bacteria and Candida is central to FM understanding of how to resolve eczema. Elevated levels of anti-Candida antibodies are common and are a sign of active infection. Eliminating candida in those who test positive improves eczema.(Savolainen et al 1993)
Poor liver detoxification, HCL deficiency and digestive enzyme deficiency due to chronic stress (grief, fear, loneliness), PPI medication and poor diet are strong risk factors in the development of eczema in adults and especially the elderly and are addressed in FM with lifestyle and emotional support and advice as well as addition of HCL, dietary change and supplementation. Poor digestion and assimilation allows larger undigested molecules, particularly proteins to pass through the gut wall – chronic inflammation and deterioration of the villi and tight junctions of the epithelial junctions due to aging exacerbates leaky gut and enhances the risk factors.
The mainstay of pharmaceutical management is to hydrate the skin to reduce the number and severity of flare-ups, to suppress cutaneous inflammation with topical corticosteroids.
Emollients – moisturise to keep skin hydrated. Aqueous cream/Liquid and Soft Paraffin Ointments, Aveeno – a colloidal oatmeal emollient and Diprobase are commonly prescribed creams for daily use. E45, Oilatum and Dermol – an antimicrobial bath emollient are used for bathing and handwashing. are commonly prescribed for daily use.
Antihistamines – are sometimes used to suppress high levels of histamine and improve the itch-scratch cycle especially at night when children often damage the skin by itching uncontrollably in their sleep ( Eschler 1999) Non-sedating antihistamines are used during the day. Sedating anti-histamines at night.
Topical corticosteroid creams suppress the inflammatory response. 0.1-2.5% Hydrocortisone active ingredients are prescribed with strict advice to use thinly on worst areas only, twice a day, usually folds of skin at elbows, neck and backs of knees, for up to 7 days until skin is clear. Over time skin thinning, loss of pigmentation and rebound flare-ups can result from overuse. Adrenal suppression and Cushing’s Syndrome is a rare side-effect of stronger steroids. Steroid creams with added antimicrobials such as Daktacort, Fucidin and many more are prescribed for use when scratching leads to secondary skin infection.
Oral antibiotics are prescribed when skin infections have breeched the skin and become systemic. Topical antibiotic creams are prescribed to resolve bacterial infections on skin which are not yet systemic.
Systemic Corticosteroids – such as Prednisolone can be used for short duration when severe to bring symptoms ‘back under control.’ (Murray and Pizzorno 2008)
In severe cases, ultraviolet (UV) light treatments(not usually for children) and immunosuppressive medications like Methotrexate are prescribed ( Eschler 1999)
Allergy Testing – Evaluations by dermatologists and allergists including patch, skin prick and serum radioallergosorbent testing (RAST) are available by are usually only suggested in the severest cases, when there is clear IgE anaphylactic reactions or when other allergies, particularly asthma are involved. Elimination and phased reintroduction diets plus challenge tests may used in these cases under medical supervision only in hospital settings.
The negative role of pathogenic bacteria – gut dysbiosis, and the potential of intestinal permeability and its impact on the development of the immune system are addressed by medical research but not by current medical practice.
Nor are IgG food intolerances are not tested for or dietary changes suggested. In 2010 a group of researchers tried to raise the awareness of doctors to the ‘largely unrecognised’ issue of leaky. They concluded that by simply adding L-glutamine and curcumin to foods the inflammation and oxidative stress linked to tight junction opening could be inhibited and they urged further research (Rapin 2010)
Numerous studies show probiotics balance gut microbiology, restore normal intestinal permeability, improve immunological barrier function and down regulate the production of pro-inflammatory cytokines. (Meneghin 2012)
Supplementing with probiotics when a child’s immune system is still developing could positively influence the balance between TH1 and Th2 inflammatory responses and prevent eczema.
In addition, they stimulate, pattern-recognition cells in the intestinal lining called, Toll Like Receptors (TLRs). Probiotics stimulate the TLRs to recognise the difference between pathogens and friendly bacteria. These pathogen-associated molecular patterns(PAMPs) induce T cell differentiation – TH1 cellular responses versus TH2 humeral defences (Bashir 2004)
In 2014 a study in which pregnant women from 36 weeks gestation and their infants up to 6 months were given high dose 10 billion, multi strain probiotics daily. Examination and skin prick tests to milk and eggs were tests at 6 months of age and 2 years. The authors concluded atopic sensitisation and the incidence of eczema was reduced. (Allen J 2014)
However, recently published reviews, meta-analysis and a Cochrane Collaboration concluded there is still insufficient evidence to support the role of probiotics in the prevention of eczema. Similar statements are generally found on patient-centred information sites. www.cochrane.org
Despite this, in January 2015, the World Allergy Organisation recommended the use of probiotics by pregnant and lactating women to prevent the development of eczema. Recommendation was based on a meta-analysis of 29 studies in which probiotic use by pregnant women reduced incidence of AD by 9% during a 1-5 year follow-up and use by lactating women with a 16% reduction. (Johnson 2014)
The authors of an extensive review of available research concluded that many trials were of pregnant women and that studies of lactating women showed better net improvement probably because it is at this time that a baby’s immune system is developing.
Have to be high 5-10 billion daily
They also felt that more trials were needed and that most of the data collected was still too diverse may be in the process of accepting that if eczema is the first stage of the ‘atopic march’ which begins in the first few months of life by improving the microbiome of pregnant and lactating mothers can reduce the incidence not only of eczema but of all allergies.
Epidermal barrier irregularities are common in eczema and can be improved. One such, genetic deficiency of Alpha-desaturase results in decreased uptake of EFA metabolites, increased water loss and skin dryness. Linoleic and linolenic acids (EFAs) additionally provide substrates for inflammatory mediators, the prostaglandins and leukotriene, resulting in secondary deficiency of prostaglandin E1 (PGE1). (Ruzicka 1998)
Eczema sufferers may therefore require higher doses of EFAs via their diet, and/or from supplementation to be make up for defect. Doses of 1000-3000mg EPA + DHA daily have been shown to be effective against the development of allergy in several double-blind clinical trials (Teuber 2003)
A study of 145 pregnant women , with allergies, or with a husband or younger child with allergies, were given 1.6 g of EPA and 1.1g of DHA or placebo from 25 weeks gestation until newborns were 3-4 months of age. 1 out of 52 (2%) compared to 10 out of 65 (15%) in the placebo group developed food allergies while the incidence of IgE-associated eczema in the Omega 3 group was 4 out of 52 (8%) compared to 15 out of 63 (24%) in the control (Furuhjelm 2009)
Supplementation with gamma-linoleic acid (GLA) may not have the same benefit – 27 studies (1596 participants), investigating effects of Evening Primrose Oil and Borage Oil found no significant improvement in symptoms. (Bamford 2013) In contrast, 30 studies (1207 participants) found the linoleic acid(LA) and gamma-linolenic acid (GLA) in EPO did have anti-inflammatory benefits which improved itching, crusting, oedema and redness.(Hederos 1996)
Other studies of natural supplements have shown benefits, but are often small in size. A 2015 study of 72 Korean children and adults (39 adults and 33 children) and 140 healthy control subjects (0 adults and 70 children) found serum Vitamin D levels to be lower in the children with eczema, but not the adults, with eczema and concluded it may be a factor in the development of the condition. (Han 2015). A 2011, randomised control trial of 45 patients showed 64.3% improvement in symptoms in those given 1600 IU vitamin D(3) plus 600 IU A-tocopherol used together.(Javanbakht 2010)
Diets exclude egg and milk show no benefit mainly because most participants did not test positive for those foods. The authors concluded that when patients did have a suspected egg allergy, and did have positive IgE reactions to eggs, they did exhibit a 51% improvement in symptoms when eggs were excluded. (Bath-Hextall 2008)
Hypericum perforatum L. or St John’s Wort Cream has anti-inflammatory and antibacterial properties and is able to inhibit 5-lipoxygenase and COX1 pathways and can be used topically to improve eczema.(Wolfe 2014)
In a randomised placebo-controlled double-blind trial 21 patients were treated twice daily over 4 weeks with 1.5% hyperforin (verum). Skin on the side of the body treated with hypericum was better and colonisation with Staph. Reduced. The authors concluded it to was effective and suggested it be tested on larger patient numbers and compared. (Schempp 2003)
Another trial of 26 eczema patients compared the moisturising benefits of olive oil to coconut oil. They found both oils improved skin dryness but that antibacterial activity of the monolaurin in the coconut oil was superior as a proactive treatment against bacterial infections. (Verallo-Rowell 2008)
In a study of 21 children aged 6 months to 18 years old those treated with topical B12 – which has already been shown to successfully treat atopic dermatitis in adults by increasing nitric oxide production– showed significant improvement in skin condition after 2-4 weeks. The authors concluded topical Vitamin B12 should be considered as a treatment option for children with eczema (Januchowski 2009).
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