Eczematous tissue produces less fats and oils, reducing moisture retention in the skin. As dehydrated surface cells shrink, gaps appear leading to further dehydration from cells deeper down. Itching and dryness results, while infective agents or irritant substances can penetrate the skin more easily, further triggering an immunological response. Inflammation and cracked, weeping and sometimes infected skin result.1

Atopy, as in 'atopic' eczema or dermatitis, means 'without a place', and refers to the 'unusual' hypersensivity with heightened allergic IgE response. Atopy also includes asthma, allergic rhinitis and food allergy; people with AD are very likely to have one of these atopic co-morbidities at some point in their life.3 A retrospective study of 650,000 German health insurance records also found AD is a risk factor for rheumatoid arthritis and irritable bowel disease.4

Genes and the influence of environmental factors form the basis of understanding AD. The filaggrin gene (FLG), involved in epidermal keratin production, is significantly implicated in atopic responses and around 10 per cent of the Western population have filaggrin (FLG) gene defects.5

Recent AD research involving 1,300 infants looked at tap water and any potential effect on trans-epidermal water loss. Both calcium carbonate and chlorine levels €were strongly correlated€, and AD was more likely with higher concentrations than lower.6

However, €the effect estimates were greater in children carrying FLG mutations, but formal interaction testing between water quality groups and filaggrin status was not statistically significant,€ said the researchers. €High domestic water CaCO3 levels are associated with an increased risk of AD in infancy. The influence of increased total chlorine levels remains uncertain.€

Note that many AD patients do not appear to have any of the known genetic mutations associated with the condition.7