FCAAIA Notes: I guess this explains my good non-allergic fortune….I was both a finger sucker and nail biter and here I am without allergies!

But seriously, advocates of the hygiene hypothesis never claimed it was the only reason for the increase prevalence of allergies.  Even in this study, the non-sucker/biter children had a very high rate of allergic sensitization (positive allergy tests).

To boil it down, the hygiene hypothesis states that those don’t eat enough dirt and get exposed to enough microbes (or the right microbes) early in life are more likely to develop allergy.  Early exposure activates certain parts of the immune system that down-regulate the likelihood of later allergies.  Like everything else, there are multiple risks for developing allergy and it is likely a combination of things acting synergistically affects different people in different ways at different stages of life.

(Source: Dec.15, 2016. For Medscape articles: User name: FCAAIA, Password: Allergies)

The hygiene hypothesis has come under fire in recent years as being too simplistic to explain the rise in allergic disease, but two fascinating studies suggest that it is alive and well.

Children frequently stick their mucky fingers and thumbs in their mouths and in doing so expose themselves to organisms that might induce an immunological response. Researchers from Dunedin, New Zealand, sought to investigate whether those who do this more are protected from allergic disease (Lynch S et al. Pediatrics 2016. doi:10.1542/peds.2016-0443). Over 1000 children born in the 1970s joined a long-term cohort study. Parental questionnaires at ages 5–11 years identified groups of thumb-suckers, nail-biters, or neither. About 75% underwent skin-prick testing and assessments for asthma and hay-fever at ages 13 and 32 years. Amongst the 31% who had at least one of these oral habits, the prevalence of atopic sensitisation was significantly lower (38% vs 49% in those who had neither; p=0.009). Those who both thumb-sucked and nail-bit were even less likely to be atopic (31%). Logistic regression allowing for potential genetic and environmental confounders did not remove the association.

Isolated religious communities offer a valuable natural experiment. The Hutterite and Amish communities in the US are both descendants of German-speaking Europeans and genetically very similar. The prevalence of asthma amongst Hutterite children is similar to the general US population, whilst in Amish children it is much lower. Both communities are primarily agricultural, but the main difference is that the Hutterites practice modern industrial farming, while the Amish adhere to traditional practices where animals are kept in close proximity to family groups.

Researchers compared Hutterite children from South Dakota with Amish from Indiana (Stein M et al. NEJM 2016: doi:10.1056/NEJMoa1508749). As expected, atopic sensitisation was six times greater amongst the Hutterites. They took dust samples from the homes of both communities and found much higher levels of specific microbes amongst the Amish. They took blood samples from about 30 children in each community. Genetic studies confirmed their common ancestry. They found that the Amish children exhibited much more innate immunity-related cytokines, and their lymphocytes were more likely to express genes associated with immune responses to microbial products. They went further, and found that when instilled into laboratory mice, Amish household dust was more likely to suppress airway inflammation in vivo than Hutterite dust. An editorial hypothesizes that early exposure to microbes protects from asthma through a complex network that may involve both an alternative pro-inflammatory immune response and the formation of regulatory T-cells that protect at mucosal surfaces (Chatila T. doi:10.1056/NEJMe1607438). It remains unclear how much of this protection is antenatal, or whether it requires exposure to live organisms as opposed to just microbial products.

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