Purpose of the Review <p>Early life constitutes a critical developmental window during which environmental exposures can permanently alter physiological trajectories, thereby influencing long-term susceptibility to allergic diseases. Polycystic ovary syndrome (PCOS), the most prevalent endocrine disorder in reproductive-aged women, is characterized by a constellation of metabolic and endocrine abnormalities—including obesity, insulin resistance, immune dysregulation, vitamin D deficiency, and steroid hormone dysregulation. This review aims to synthesize and evaluate the evidence for an association between these multifaceted maternal features and an increased risk of allergic diseases, particularly asthma, in offspring.</p> Recent Findings <p>Despite growing interest, the specific role of PCOS in offspring asthma remains incompletely understood. This review synthesizes current observational evidence linking maternal PCOS to offspring allergic diseases, with a focus on asthma. By integrating findings from human cohorts, animal models, and mechanistic studies, the available evidence illustrates how PCOS-associated maternal metabolic/endocrine derangements may interfere with fetal immune development and prime offspring for allergic sensitization. Recent investigations have also begun to elucidate emerging epigenetic mechanisms (e.g., DNA methylation) that may mediate these transgenerational effects, offering a framework for identifying novel biomarkers and preventive targets.</p> Summary <p>This work broadens the etiological understanding of asthma’s developmental origins by linking a common maternal endocrine disorder to offspring allergic susceptibility. Ultimately, it aims to provide actionable insights for early-life intervention strategies, emphasizing the potential to mitigate asthma risk through targeted management of PCOS-related maternal metabolic and endocrine health.</p>