Childhood respiratory and atopic disease accounts for substantial morbidity and disproportionately burdens urban, poor minority children. The origins of child respiratory health begin in utero and are influenced by modifiable factors, such as maternal psychological stress and diet. While research points to the need to study both maternal diet and psychological stress together, this has not been done to date in regards to child respiratory outcomes. Also, traumatic stress is of particular importance in lower income populations given a higher prevalence of exposure. Evidence linking prenatal stress to asthma and lung function is growing; however, mechanisms remain poorly understood. Although psychological stress impacts health through numerous pathways, oxidative stress is invariably identified as a central component. Prenatal stress may disrupt placental, and consequently fetal, oxidant/antioxidant balance, which likely plays a role in stress- induced programming of wheeze/asthma risk and impaired lung growth. Conversely, higher prenatal antioxidant/anti-inflammatory intakes (e.g., vitamin E, n-3 polyunsaturated fatty acids [PUFAs]) reduce placental oxidative stress and are linked with decreased child wheezing and asthma. This will be the first prospective study to examine associations between maternal traumatic stress, oxidative stress, antioxidant status and child asthma and lung function. We will measure prenatal traumatic stress and diet to prospectively examine the novel central hypothesis that prenatal maternal traumatic stress contributes to wheeze/asthma risk and reduced lung function in childhood, that oxidative stress plays a key role, and that associations will be modified by prenatal nutritional exposures that reduce fetal vulnerability to oxidative stress. We will study associations among maternal prenatal traumatic stress, oxidative stress indexed by F2-Isoprostanes, and child asthma/wheeze (Aim 1), lung function (Aim 2), and how maternal nutritional exposures (Vitamin E, n-3 PUFAs) may modify relationships (Aim 3). The Conditions Affecting Neurocognitive Development and Learning in Early Childhood (CANDLE) cohort is a prenatal cohort of largely urban, low-income, African-American mother-child dyads, which, to our knowledge, is the only cohort with the prenatal exposure data and banked samples needed to address our aims. The study leverages existing prenatal and postpartum psychosocial assessments, prenatal dietary assessments, banked biospecimens, and proposes prospective follow-up to ascertain wheeze/asthma/atopic disease and lung function at age 9 years. This study will inform how dietary interventions may help mitigate psychosocial stress-elicited oxidant imbalance and consequent effects on developmental programming of respiratory disorders. Findings have the potential to impact clinical policy and practice and inform trials of dietary interventions to reduce stress effects on lung function.
The origins of child respiratory health begin in utero and can be influenced by modifiable factors such as maternal psychological stress and diet. Prenatal oxidant/antioxidant balance has been particularly implicated as a mechanism connecting maternal prenatal stress and child respiratory health, thus it is plausible that specific prenatal nutritional factors, such as antioxidant intake, may protect against stress-related child respiratory outcomes. This study will be the first to concurrently examine relationships among maternal prenatal traumatic stress, oxidative stress, and dietary factors on childhood respiratory and atopic disease outcomes in a largely low-income, African-American population to (1) better delineate mechanistic pathways linking prenatal stress to child respiratory health and (2) inform potential dietary interventions to help mitigate stress-induced effects.
