Browsing by Subject "Developmental programming"

Now showing 1 - 2 of 2
  • Thumbnail Image
    Item
    Emerging Concepts About Prenatal Genesis, Aberrant Metabolism and Treatment Paradigms in Polycystic Ovary Syndrome
    (Springer, 2012) Witchel, Selma F.; Recabarren, Sergio E.; Gonzalez, Frank; Diamanti-Kandarakis, Evanthia; Cheang, Kai I.; Duleba, Antoni J.; Legro, Richard S.; Homburg, Roy; Pasquali, Renato; Lobo, Rogerio; Zouboulis, Christos C.; Kelestimur, Fahrettin; Fruzzetti, Franca; Futterweit, Walter; Norman, Robert J.; Abbott, David H.; Obstetrics and Gynecology, School of Medicine
    The interactive nature of the 8th Annual Meeting of the Androgen Excess and PCOS Society Annual Meeting in Munich, Germany (AEPCOS 2010) and subsequent exchanges between speakers led to emerging concepts in PCOS regarding its genesis, metabolic dysfunction, and clinical treatment of inflammation, metabolic dysfunction, anovulation and hirsutism. Transition of care in congenital adrenal hyperplasia from pediatric to adult providers emerged as a potential model for care transition involving PCOS adolescents.
  • Thumbnail Image
    Item
    Increased maternal inflammation and poorer infant neurobehavioural competencies in women with a history of major depressive disorder from the psychiatry research and motherhood - Depression (PRAM-D) study
    (Elsevier, 2022) Osborne, Sarah; Biaggi, Alessandra; Hazelgrove, Katie; Du Preez, Andrea; Nikkheslat, Naghmeh; Sethna, Vaheshta; Zunszain, Patricia A.; Conroy, Susan; Pawlby, Susan; Pariante, Carmine M.; Psychiatry, School of Medicine
    Introduction: Stress in pregnancy is associated with adverse outcomes in offspring, and developmental programming is a potential mechanism. We have previously shown that depression in pregnancy is a valid and clearly defined stress paradigm, and both maternal antenatal and offspring stress-related biology is affected. This study aims to clarify whether maternal biology in pregnancy and offspring outcomes can also be influenced by a history of a prior depression, in the absence of depression in pregnancy. Our primary hypothesis is that, similarly to women with depression in pregnancy, women with a history of depression but who are not depressed in pregnancy will have increased cortisol secretion and markers of immune system function, and that their offspring will have poorer neuro-developmental competencies and increased cortisol stress response. Methods: A prospective longitudinal design was used in 59 healthy controls and 25 women with a past history of depression who were not depressed in pregnancy, named as 'history-only', and their offspring. Maternal antenatal stress-related biology (cortisol and markers of immune system function) and offspring outcomes (gestational age at birth, neonatal neurobehaviour (Neonatal Behavioural Assessment Scale, NBAS), cortisol stress response and basal cortisol at 2 and 12 months) and cognitive, language and motor development (Bayley Scales of Infant and Toddler Development (BSID)) were measured. Results: Compared with healthy pregnant women, those with a history of depression who remain free of depression in pregnancy exhibit increased markers of immune system function in pregnancy: IL-8 (d = 0.63, p = 0.030), VEGF (d = 0.40, p = 0.008) and MCP-1 (d = 0.61, p = 0.002) and have neonates with lower neurobehavioural scores in most areas, reaching statistical significance in thesocial-interactive (d = 1.26, p = 0.015) cluster. However, there were no differences in maternal or offspring HPA axis function or in infant development at 12 months. Conclusion: Our study indicates that pregnant women with a history of depression have increased markers of immune system function, and their offspring show behavioural alterations that may be the effects of in utero programming, epigenetic factors or genetic predisposition.