Etiology and Pathophysiology of Sleep Disordered Breathing in Pregnancy (R01) | Apply Online

Opportunity Summary:

The NIH funding opportunity titled "Etiology and Pathophysiology of Sleep Disordered Breathing in Pregnancy (R01)" (Funding Opportunity Number PA-11-122) was a discretionary research grant announcement led by the National Heart, Lung, and Blood Institute (NHLBI) in collaboration with the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) and the National Institute of Nursing Research (NINR). It invited Research Project Grant (R01) applications focused on understanding why sleep disordered breathing (SDB) begins or worsens during pregnancy and how it can drive harmful biological changes for both the pregnant person and the developing fetus. The overall intent was strongly mechanistic and clinically oriented: the participating NIH institutes were looking for studies that could pin down biologically plausible, testable pathways so that future prevention and treatment strategies could be designed to reduce pregnancy and long-term health risks linked to SDB.

A central theme of the announcement was identifying the mechanisms underlying incident (new-onset) SDB in pregnancy. Pregnancy brings rapid and complex physiological changes, and this FOA specifically encouraged research that disentangles how pregnancy-related shifts in anatomy, hormones, fluid balance, respiratory control, inflammation, and metabolic regulation might trigger or aggravate obstructive sleep apnea and related breathing disturbances. Rather than simply documenting associations, the program aimed to support studies that explain causation at the level of pathophysiology, including why some pregnant individuals develop SDB while others do not, and which biological or clinical characteristics increase susceptibility.

Another major emphasis was on the pathways that connect SDB to maternal heart, lung, and blood complications. The FOA highlighted interest in mechanisms by which intermittent hypoxia, sleep fragmentation, sympathetic activation, oxidative stress, endothelial dysfunction, and coagulation changes could contribute to cardiovascular strain and other adverse maternal outcomes. In practical terms, this meant research that clarifies how SDB may influence blood pressure regulation, vascular function, cardiometabolic stress, pulmonary physiology, and hematologic or inflammatory processes during pregnancy, with an eye toward explaining clinically meaningful outcomes rather than purely laboratory findings.

The opportunity also placed strong focus on the placenta as a key biological interface. Applicants were encouraged to investigate how SDB may affect placental development, structure, and function, and how these placental effects could translate into adverse pregnancy outcomes. This includes mechanistic work on placental perfusion and oxygenation, vascular remodeling, inflammatory signaling, nutrient transport, and endocrine function, as well as how these processes may relate to outcomes such as fetal growth restriction, hypertensive disorders of pregnancy, preterm birth, or other complications. The FOA framed the placenta not merely as an outcome measure but as a mechanistic mediator that could explain downstream maternal and fetal risk.

A fourth pillar of the announcement was developmental programming, meaning how SDB-related changes in the intrauterine environment might alter fetal development in ways that increase the childs later risk of obesity, metabolic disease, and cardiovascular disease. The FOA encouraged research into how maternal SDB could shape fetal physiology through pathways such as hypoxia exposure, inflammation, stress hormones, metabolic substrate availability, and placental signaling, potentially leading to lasting changes in growth trajectories, energy balance regulation, insulin sensitivity, vascular development, or cardiometabolic set points. This long-view perspective reflects the institutes interest in identifying mechanisms that link pregnancy exposures to lifelong health risk, not just immediate birth outcomes.

Across all these areas, the stated goal of the program was to uncover clinically relevant mechanisms of SDB etiology and pathophysiology that could open new therapeutic avenues. In other words, the funders were not only seeking descriptive epidemiology but research that identifies actionable biological targets, informs screening and risk stratification, and lays groundwork for interventions that could reduce maternal and fetal harms from SDB exposure during pregnancy. The announcement explicitly encouraged multidisciplinary research teams, signaling that strong applications could benefit from collaboration among sleep medicine, obstetrics, maternal-fetal medicine, cardiology, pulmonology, physiology, placental biology, epidemiology, biostatistics, nursing research, and related fields.

Administratively, this was an R01 grant mechanism under the NIH, with no cost sharing or matching requirement listed. It was posted and created on February 14, 2011, and the final application due date was May 7, 2013, with the opportunity later archived on June 7, 2013. The CFDA numbers associated with the announcement included 93.233 (National Center on Sleep Disorders Research), 93.361 (Nursing Research), and 93.865 (Child Health and Human Development Extramural Research), reflecting the cross-institute participation and the health areas the FOA touched.

Eligibility was broad and included many types of domestic and non-domestic entities. Eligible applicants listed in the source information included state, county, and local governments; tribal governments and tribal organizations; public housing authorities; independent school districts; public and private institutions of higher education; nonprofit organizations with or without 501(c)(3) status; for-profit organizations (including small businesses and other for-profits); U.S. territories or possessions; and foreign organizations. The eligibility section also explicitly referenced institutions and organizations that often participate in NIH funding, including Historically Black Colleges and Universities (HBCUs), Hispanic-serving Institutions, Alaska Native and Native Hawaiian Serving Institutions, Tribally Controlled Colleges and Universities (TCCUs), faith-based or community-based organizations, regional organizations, and eligible federal agencies. The practical takeaway is that the FOA was designed to attract a wide range of applicants capable of conducting rigorous mechanistic research, including international contributors where appropriate.

The full announcement was hosted on the NIH grants site under PA-11-122, and contact support for access or linking issues was directed to the NIH Office of Extramural Research (OER) webmaster at FBOWebmaster@OD.NIH.GOV.

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