Atopy is the genetic tendency to develop multiple allergic diseases including allergic rhinitis (hay fever), asthma, food allergy, and atopic dermatitis (eczema). Atopic diseases are caused by a hypersensitive immune system that overreacts to proteins in an allergen and produces a heightened immune response. These atopic diseases tend to develop at different points in life, with atopic dermatitis being highly prevalent during early childhood, but declining with age, whereas allergic rhinitis often develops during adulthood. In contrast, the incidence of both food allergy and asthma spikes during adolescence and puberty. Women tend to be more susceptible to allergic reactions than men and are likely to have more severe and more frequent allergic reactions. Similarly, while asthma has a greater prevalence in boys than girls during prepubescent ages, this tendency reverses after puberty, suggesting that sex hormones, especially estrogen, play a critical role in the pathogenesis and perpetuation of atopic diseases. Estrogen is a steroid hormone that acts primarily by binding with estrogen receptors (ERs) α and β. Besides estrogen’s essential function in the reproductive system, ERs are widely distributed in immune cells, with estrogen potentially affecting each phase of an allergic reaction. While estrogen plays an extensive role in allergic diseases, there is a critical lack of research in the intersection of the allergy and endocrinology fields. It is imperative to examine how estrogen influences the trajectory of atopy over the human lifespan, especially at pivotal stages when hormone levels change significantly, including during infanthood, preadolescence, puberty, and pre- and post-menopause. Through the examination of data from various birth cohorts, my proposed research will analyze the trajectory of allergic diseases in comparison to fluctuating estrogen levels throughout the lifetime.