TY - JOUR
T1 - Antenatal maternal depression, early life inflammation and neurodevelopment in a South African birth cohort
AU - Naudé, Petrus J.W.
AU - Pariante, Carmine
AU - Hoffman, Nadia
AU - Koopowitz, Sheri Michelle
AU - Donald, Kirsten A.
AU - Zar, Heather J.
AU - Stein, Dan J.
N1 - Funding Information:
The Drakenstein Child Health Study was funded by the Bill & Melinda Gates Foundation (OPP 1017641, OPP1017579), South Africa Medical Research Council (SAMRC) and National Research Foundation South Africa, NIH, USA (U01MH115484). DJS and HJZ are supported by the SAMRC. PJWN was supported by the National Alliance for Research on Schizophrenia and Depression Young Investigator Grant (No. 25199) and Scott-Gentle Foundation. PJWN is supported by a Wellcome Trust International Intermediate Fellowship (222020/Z/20/Z). Academy of Medical Sciences Newton Advanced Fellowship (NAF002/1001), funded by the UK Government’s Newton Fund, by NIAAA via (R21AA023887) and by the US Brain and Behaviour Foundation Independent Investigator grant (24467) to KAD. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of manuscript.
Funding Information:
The Drakenstein Child Health Study was funded by the Bill & Melinda Gates Foundation (OPP 1017641, OPP1017579), South Africa Medical Research Council (SAMRC) and National Research Foundation South Africa, NIH, USA (U01MH115484). DJS and HJZ are supported by the SAMRC. PJWN was supported by the National Alliance for Research on Schizophrenia and Depression Young Investigator Grant (No. 25199) and Scott-Gentle Foundation. PJWN is supported by a Wellcome Trust International Intermediate Fellowship (222020/Z/20/Z). Academy of Medical Sciences Newton Advanced Fellowship (NAF002/1001), funded by the UK Government's Newton Fund, by NIAAA via (R21AA023887) and by the US Brain and Behaviour Foundation Independent Investigator grant (24467) to KAD. The funders had no role in the study design, data collection and analysis, decision to publish, or preparation of manuscript.
Publisher Copyright:
© 2022 The Authors
PY - 2022/10
Y1 - 2022/10
N2 - Background: Antenatal exposure to maternal psychological adversity, including depression, increases the risk of impaired neurodevelopment in children. The underlying biological mechanisms remain unclear, especially in early life during critical windows of development and maturation. This study investigated the association of antenatal maternal depression, maternal and early life inflammatory markers and neurodevelopmental outcomes in children at 2 years of age. Methods: A subgroup of mothers and their children (n = 255) that were enrolled in a South African birth cohort study, the Drakenstein Child Health Study, were followed from the antenatal period through to 2 years of child age. Maternal depressive symptoms were measured by the Beck Depression Inventory (BDI-II) at 26 weeks gestation. Serum inflammatory markers [granulocyte–macrophage colony-stimulating factor (GM-CSF), interferon-γ (IFN-γ), interleukin IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12p70, IL-13, tumour necrosis factor-α (TNF-α), neutrophil gelatinase-associated lipocalin (NGAL) and metalloproteinase-9 (MMP-9)] were measured in mothers at enrolment and in their children at 6–10 weeks and at 2 years. Neurodevelopment was assessed at 2 years using the Bayley Scales of Infant and Toddler Development III. Results: Antenatal depressive symptoms (present in 25% of the mothers) were significantly associated with higher levels of IL-7 (p = 0.008), IL-8 (p = 0.019) and TNF-α (p = 0.031) in the mothers after correcting for sociodemographic and lifestyle factors. Serum IL-1β and NGAL levels were significantly elevated over time in children born to mothers with depressive symptoms compared to those without depression, after controlling for maternal and child health and sociodemographic factors. Elevated infant IL-1β at 6–10 weeks of age partially mediated the association of maternal depressive symptoms with poorer language scores at 2 years. Conclusion: Alterations in early life immunity, as reflected by elevated IL-1β, is a potential pathway through which antenatal maternal depressive symptoms may impact language development in young children.
AB - Background: Antenatal exposure to maternal psychological adversity, including depression, increases the risk of impaired neurodevelopment in children. The underlying biological mechanisms remain unclear, especially in early life during critical windows of development and maturation. This study investigated the association of antenatal maternal depression, maternal and early life inflammatory markers and neurodevelopmental outcomes in children at 2 years of age. Methods: A subgroup of mothers and their children (n = 255) that were enrolled in a South African birth cohort study, the Drakenstein Child Health Study, were followed from the antenatal period through to 2 years of child age. Maternal depressive symptoms were measured by the Beck Depression Inventory (BDI-II) at 26 weeks gestation. Serum inflammatory markers [granulocyte–macrophage colony-stimulating factor (GM-CSF), interferon-γ (IFN-γ), interleukin IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12p70, IL-13, tumour necrosis factor-α (TNF-α), neutrophil gelatinase-associated lipocalin (NGAL) and metalloproteinase-9 (MMP-9)] were measured in mothers at enrolment and in their children at 6–10 weeks and at 2 years. Neurodevelopment was assessed at 2 years using the Bayley Scales of Infant and Toddler Development III. Results: Antenatal depressive symptoms (present in 25% of the mothers) were significantly associated with higher levels of IL-7 (p = 0.008), IL-8 (p = 0.019) and TNF-α (p = 0.031) in the mothers after correcting for sociodemographic and lifestyle factors. Serum IL-1β and NGAL levels were significantly elevated over time in children born to mothers with depressive symptoms compared to those without depression, after controlling for maternal and child health and sociodemographic factors. Elevated infant IL-1β at 6–10 weeks of age partially mediated the association of maternal depressive symptoms with poorer language scores at 2 years. Conclusion: Alterations in early life immunity, as reflected by elevated IL-1β, is a potential pathway through which antenatal maternal depressive symptoms may impact language development in young children.
KW - Cytokines
KW - Depression
KW - Inflammation
KW - Longitudinal
KW - Offspring
KW - Prenatal
UR - http://www.scopus.com/inward/record.url?scp=85134596330&partnerID=8YFLogxK
U2 - 10.1016/j.bbi.2022.07.001
DO - 10.1016/j.bbi.2022.07.001
M3 - Article
C2 - 35803482
AN - SCOPUS:85134596330
SN - 0889-1591
VL - 105
SP - 160
EP - 168
JO - Brain, Behavior, and Immunity
JF - Brain, Behavior, and Immunity
ER -