By Dr. Larry Chiaramonte
In 1923 two allergists, Arthur Coca and Robert Cook, defined atopy as a proclivity to develop allergic rhinitis, allergic asthma, and allergic urticaria. They pointed out that these diseases were follow travelers. That is they occurred both in the same individual and in blood relatives. Patients who they considered to be atopic possessed a distinctive antibody, named by them “reagin or “skin-sensitizing antibody” because intradermal skin tests to a variety of inhalant allergens, such as trees, weeds, grasses, dust, molds, and animal danders, provoked reaction called wheals at sites of some injections. The word “atopy” is defined as “a clinical hypersensitivity state which is subject to hereditary influences; included are hay fever, asthma, and eczema”. Atopic dermatitis, allergic rhinitis, and asthma are atopic diseases that develop on a complex genetic background.
Allergy got caught up in the debate over Russian genetic teaching that what were previously thought to be acquired characteristics were in fact inherited. If the parents were sensitive to an allergen would the offspring be allergic to the same allergen or just inherit a general tendency to develop allergies? Dr. Ben Zohn from Brooklyn, and one of my mentors, settled the debate by creating a positive skin test to parasites in mothers and finding negative tests in some of their offspring after birth. Why were parasites a valid marker? Because as I said in the first segment of this series, and as you will read at entertaining length in Asthma Allergies Children: a parent’s guide, the immune mechanism that causes allergies evolved to help protect us from parasites in less-hygienic times.