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Adapted from: The Human Gut Microbiome in Health and Disease (Part 1) and Treatments for Chronic Gastrointestinal Disease and Gut Dysbiosis (Part 2) – published in IMCJ (Integrative Medicine: A Clinician’s Journal)
Matthew J. Bull, BSc, PhD; Nigel T. Plummer, PhD
Allergic diseases, specifically those driven by type 1 hypersensitization – atopic eczema, atopic asthma, rhinitis – and type 1 food allergies have risen globally in incidence over the past 50 years, with the developed world now showing an incidence at 20% of the population, providing a considerable proportion of overall disease burden.1 Atopic sensitization occurs primarily in the first 2 years of life and can persist through a lifetime, with the expression of allergic disease typically beginning with eczema (0-2 y), asthma (>5 y), and rhinitis (>8 y) in what is referred to as the atopic march.2 In the United States, the direct costs of atopic eczema are estimated to be as high as $3.8 billion per year.3
The causes of atopic eczema are potentially numerous and are not well understood, although the method of birth (ie, vaginal vs cesarean) and a mutation in a particular human gene involved in skin-barrier function are known to be implicated.3 Characterization of the gut microbiota of sufferers of atopic eczema showed that infants at 1 month of age with the disease had a significantly lower bacterial diversity, particularly with regard to the Bacteroidetes phylum, compared with infants without atopic eczema.4 The study also highlighted decreased diversity of Bacteroidetes at 12 months of age in the atopic-eczema group, suggesting that sufferers may maintain a lower level of bacterial diversity when compare with healthy controls.
In addition, a lower number of Proteobacteria, the cell walls of which contain lipopolysaccharide molecules, was observed in infants presenting with atopic eczema. Lipopolysaccharides have the ability to elicit a host’s immune response, and low exposure to lipopolysaccharides in infancy is linked with a higher risk of atopic eczema.5
As an explanation for the marked increase in allergic disease, the concept of reduced quantitative and qualitative exposure to the microbial world during the neonatal period has been termed the hygiene hypothesis and is based on the observation of increased atopy in smaller, and particularly urbanized, families 50 from reduced exposure to microbial challenge. This underexposure to microbial antigens results in the aberrant outcome to allergen processing of immunological response rather than immunological tolerance.2 In a systematic review of 26 observational studies, it was found that C-sections were associated with a 32% increase in food allergy risk, a 23% increase in hay fever risk and an 18% increase in asthma risk in children.6
With this increase in mind, a substantial effort has occurred to assess the potential role of probiotics in the prevention and/or treatment of allergic diseases, particularly by feeding probiotics to infants. Exposure to probiotic bacteria may stimulate the immune system and train it to produce an appropriate response to allergens. When Lactobacillus rhamnosus GG was administered to high-risk infants (ie, those with at least 1 relative with atopic eczema or asthma), a 50% reduction in the incidence of atopic eczema was observed.7 Also, the skin condition of children with atopic eczema improved when they were given whey formula supplemented with the L rhamnosus or Bifidobacterium animalis subsp lactis for 2 months.8
A systematic review of the effect of nutritional supplementation on atopic dermatitis in children found that the best effects were observed when both mothers and infants were supplemented with probiotics.9


References:

1. Okada H, Kuhn C, Feillet H, Bach JF. The ‘hygiene hypothesis’ for autoimmune and allergic diseases: an update. Clin Exp Immunol. 2010; 160(1): 1-9
2. Shen CY, Lin MC, Lin HK, Lin CH, Fu LS, Fu YC. The natural course of eczema from birth to age 7 years and the association with asthma and allergic rhinitis: a population-based birth cohort study. Allergy Asthma Proc. 2013; 34(1): 78-83
3. Williams HC, Grindlay DJ. What’s new in atopic eczema? An analysis of systematic reviews published in 2007 and 2008, I: definitions, causes and consequences of eczema. Clin Exp Dermatol. 2010; 35(1): 12-15
4. Abrahamsson TR, Jakobsson HE, Andersson AF, Björkstén B, Engstrand L, Jenmalm MC. Low diversity of the gut microbiota in infants with atopic eczema. J Allergy Clin Immunol. 2012; 129(2): 434-440
5. Gehring U, Bolte G, Borte M, et al; LISA study group; Lifestyle-Related Factors on the Immune System and the Development of Allergies in Childhood. Exposure to endotoxin decreases the risk of atopic eczema in infancy: a cohort study. J Allergy Clin Immunol. 2001; 108(5): 847-854
6. Bager P, Wohlfahrt J, Westergaard T. Caesarean delivery and risk of atopy and allergic disease: meta-analyses. Clin Exp Allergy. 2008; 38(4): 634-42
7. Kalliomäki M, Salminen S, Arvilommi H, Kero P, Koskinen P, Isolauri E. Probiotics in primary prevention of atopic disease: a randomised placebocontrolled trial. Lancet. 2001; 357 (9262): 1076-1079
8. Majamaa H, Isolauri E. Probiotics: a novel approach in the management of food allergy. J Allergy Clin Immunol. 1997; 99(2): 179-185
9. Foolad N, Brezinski EA, Chase EP, Armstrong AW. Effect of nutrient supplementation on atopic dermatitis in children: a systematic review of probiotics, prebiotics, formula, and fatty acids. JAMA Dermatol. 2013; 149(3): 350-355


*These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.**This blog was written by an outside source. This blog does not necessarily reflect the views or positions of Natural Partners.