I agree with their view on how allergies and asthma DEVELOPE! LOSS OF HOMEOSTASIS! AIRWAYS, IMMUNE, I would answer them yes, possably with new borns, and say but this can happen at any time with environmental exposures and we do eat what we breath and swallow slavia, it's not all about ingestion, thats why with severe hypersensitives/anaphylaixis or anaphylatoid reactions triggers can cause a reaction in your gut from a inhaled re-exposure to a trigger. also inflammation from the gut to the bowel can affect the brain if that pathway threw the blood brain barrior is leaky or broke down.
lungs and sinuses different route, more direct to the brain.
2016 Apr
Allergies and Asthma: Do Atopic Disorders Result from Inadequate Immune Homeostasis arising from Infant Gut Dysbiosis?
Summary
Our global hypothesis is that atopic conditions and asthma develop because an individual’s immune system is not able to appropriately resolve inflammation resulting from allergen exposures. We propose that the failure to appropriately down-regulate inflammation and produce a toleragenic state results primarily from less robust immune homeostatic processes rather than from a tendency to over-respond to allergenic stimuli. An individual with lower immune homeostatic capacity is unable to rapidly and completely terminate, on average over time, immune responses to innocuous allergens, increasing risk of allergic disease. A lack of robust homeostasis also increases the risk of other inflammatory conditions
Immense efforts have been made to better understand the immune mechanisms responsible for allergic diseases, especially allergic asthma. These efforts have been largely based upon an assumption that a specific pattern of immune response leads to an allergic phenotype. This allergic phenotype is often described as an atopic march from early food allergen sensitization to atopic dermatitis, and subsequently to allergic asthma and allergic rhinitis.5, 6 We believe that this assumption is incorrect, leading to results difficult to reproduce or even conflicting between well done studies. Our central hypothesis is that while the immune systems of humans may vary in the strength of initial immune responses to any neo-antigen, it is more important to understand the variation in the rate and extent to which new immune responses are modified and resolved.7 We theorize that it is this capacity, or more accurately, diminished capacity, that is the underlying mechanism that leads to one or more of the “allergic march” outcomes, rather than a sequential causal pathway of one atopic condition following another.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4829075/?log$=activity
lungs and sinuses different route, more direct to the brain.
2016 Apr
Allergies and Asthma: Do Atopic Disorders Result from Inadequate Immune Homeostasis arising from Infant Gut Dysbiosis?
Summary
Our global hypothesis is that atopic conditions and asthma develop because an individual’s immune system is not able to appropriately resolve inflammation resulting from allergen exposures. We propose that the failure to appropriately down-regulate inflammation and produce a toleragenic state results primarily from less robust immune homeostatic processes rather than from a tendency to over-respond to allergenic stimuli. An individual with lower immune homeostatic capacity is unable to rapidly and completely terminate, on average over time, immune responses to innocuous allergens, increasing risk of allergic disease. A lack of robust homeostasis also increases the risk of other inflammatory conditions
Immense efforts have been made to better understand the immune mechanisms responsible for allergic diseases, especially allergic asthma. These efforts have been largely based upon an assumption that a specific pattern of immune response leads to an allergic phenotype. This allergic phenotype is often described as an atopic march from early food allergen sensitization to atopic dermatitis, and subsequently to allergic asthma and allergic rhinitis.5, 6 We believe that this assumption is incorrect, leading to results difficult to reproduce or even conflicting between well done studies. Our central hypothesis is that while the immune systems of humans may vary in the strength of initial immune responses to any neo-antigen, it is more important to understand the variation in the rate and extent to which new immune responses are modified and resolved.7 We theorize that it is this capacity, or more accurately, diminished capacity, that is the underlying mechanism that leads to one or more of the “allergic march” outcomes, rather than a sequential causal pathway of one atopic condition following another.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4829075/?log$=activity