Ignorance is bliss: women's knowledge regarding age-related pregnancy risks.

Pregnancy risks rise with age and the average age of first time mothers is rising. This study aimed to assess women's actual knowledge and their perceived knowledge of pregnancy complications relating to advanced maternal age. A cross-sectional survey was administered to primiparous women measuring demographics, knowledge of age-related pregnancy risks, previous counselling and health literacy. Of the 218 women surveyed, the mean knowledge score was not significantly different for women <35 years of age compared to women ≥35 years of age (p = .09). Although there was no difference in knowledge between the two groups, women ≥35 years of age perceived themselves to be more knowledgeable than those under 35 (p < .01). The majority of women (67%) wanted further counselling on this topic and indicated a preference for their doctor to counsel them (76%). Women require counselling informing them of their increased risk of complications if they begin childbearing at older ages. Impact statement What is already known on this subject: The average age of first time mothers is rising worldwide. Pregnancy risks rise with age, especially in first time mothers. Previous studies have shown that knowledge of age-related pregnancy risks correlate with educational level and health literacy. What the results of this study add: This study supports those findings and also demonstrates that perceived knowledge does not correlate with measured knowledge of age-related pregnancy risks. Women ≥35 years of age (higher-risk women) are no more knowledgeable than their younger counterparts though they perceive themselves to be better informed. Greater education regarding these risks may allow women to mitigate some of these risks through lifestyle and diet alteration and will prepare women for what to expect if these risks and complications occur. The majority of women in this study seek pregnancy information on the internet, but desire further counselling from their doctors regarding age-related pregnancy risks. What the implications are of these findings for clinical practice and/or further research: Given these results, physicians must consider making greater efforts to counsel women about pregnancy risks in advanced maternal age and tailor these conversations to suit the educational level and health literacy of each individual patient.

Maternal allergen exposure reprograms the developmental lung transcriptome in atopic and normoresponsive rat pups.

The "fetal origins hypothesis" argued that physiological changes consequent to in utero exposures ultimately contribute to disease susceptibility in later life. The dramatic increase in asthma prevalence is attributed to early exposures acting on preexisting asthma-susceptible genotypes. We showed previously that distinct transcriptome signatures distinguish the developmental respiratory phenotype of atopic (Brown Norway, BN) and normoresponsive (Lewis) rats. We aimed to determine whether maternal allergen exposure would influence asthma pathogenesis by reprogramming primary patterns of developmental lung gene expression. Postnatal offspring of dams sensitized to ovalbumin before mating and challenged during pregnancy were assessed for lung function, inflammatory biomarkers, and respiratory gene expression. Although maternal ovalbumin exposure resulted in characteristic features of an allergic response (bronchoalveolar lavage neutrophils, IgE, methacholine-induced lung resistance) in offspring of both strains, substantial strain-specific differences were observed in respiratory gene expression. Of 799 probes representing the top 5% of transcriptomic variation, only 112 (14%) were affected in both strains. Strain-specific gene signatures also exhibited marked differences in enrichment for gene ontologies, with immune regulation and cell proliferation being prominent in the BN strain, cell cycle and microtubule assembly gene sets in the Lewis strain. Multiple ovalbumin-specific probes in both strains were also differentially expressed in lymphoblastoid cell lines from human asthmatic vs. nonasthmatic sibling pairs. Our data point to the existence of distinct, genetically programmed responses to maternal exposures in developing lung. These different response patterns, if recapitulated in human fetal development, can contribute to long-term pulmonary health including interindividual susceptibility to asthma.

Genetic influences on asthma susceptibility in the developing lung.

Asthma is the leading serious pediatric chronic illness in the United States, affecting 7.1 million children. The prevalence of asthma in children under 4 years of age has increased dramatically in the last 2 decades. Existing evidence suggests that this increase in prevalence derives from early environmental exposures acting on a pre-existing asthma-susceptible genotype. We studied the origins of asthma susceptibility in developing lung in rat strains that model the distinct phenotypes of airway hyperresponsiveness (Fisher rats) and atopy (brown Norway [BN] rats). Postnatal BN rat lungs showed increased epithelial proliferation and tracheal goblet cell hyperplasia. Fisher pups showed increased lung resistance at age 2 weeks, with elevated neutrophils throughout the postnatal period. Diverse transcriptomic signatures characterized the distinct respiratory phenotypes of developing lung in both rat models. Linear regression across age and strain identified developmental variation in expression of 1,376 genes, and confirmed both strain and temporal regulation of lung gene expression. Biological processes that were heavily represented included growth and development (including the T Box 1 transcription factor [Tbx5], the epidermal growth factor receptor [Egfr], the transforming growth factor beta-1-induced transcript 1 [Tgfbr1i1]), extracellular matrix and cell adhesion (including collagen and integrin genes), and immune function (including lymphocyte antigen 6 (Ly6) subunits, IL-17b, Toll-interacting protein, and Ficolin B). Genes validated by quantitative RT-PCR and protein analysis included collagen III alpha 1 Col3a1, Ly6b, glucocorticoid receptor and Importin-13 (specific to the BN rat lung), and Serpina1 and Ficolin B (specific to the Fisher lung). Innate differences in patterns of gene expression in developing lung that contribute to individual variation in respiratory phenotype are likely to contribute to the pathogenesis of asthma.