TY - JOUR
T1 - Antenatal Programming of Hypertension
T2 - Paradigms, Paradoxes, and How We Move Forward
AU - South, Andrew M.
AU - Allen, Norrina B.
N1 - Publisher Copyright:
© 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2022/12
Y1 - 2022/12
N2 - Purpose of Review: Synthesize the clinical, epidemiological, and preclinical evidence for antenatal programming of hypertension and critically appraise paradigms and paradoxes to improve translation. Recent Findings: Clinical and epidemiological studies persistently demonstrate that antenatal factors contribute to programmed hypertension under the developmental origins of health and disease framework, including lower birth weight, preterm birth, and fetal growth restriction. Preclinical mechanisms include preeclampsia, maternal diabetes, maternal undernutrition, and antenatal corticosteroid exposure. However, clinical and epidemiological studies to date have largely failed to adequately identify, discuss, and mitigate many sources and types of bias in part due to heterogeneous study designs and incomplete adherence to scientific rigor. These limitations have led to incomplete and biased paradigms as well as persistent paradoxes that have significantly limited translation into clinical and population health interventions. Summary: Improved understanding of these paradigms and paradoxes will allow us to substantially move the field forward.
AB - Purpose of Review: Synthesize the clinical, epidemiological, and preclinical evidence for antenatal programming of hypertension and critically appraise paradigms and paradoxes to improve translation. Recent Findings: Clinical and epidemiological studies persistently demonstrate that antenatal factors contribute to programmed hypertension under the developmental origins of health and disease framework, including lower birth weight, preterm birth, and fetal growth restriction. Preclinical mechanisms include preeclampsia, maternal diabetes, maternal undernutrition, and antenatal corticosteroid exposure. However, clinical and epidemiological studies to date have largely failed to adequately identify, discuss, and mitigate many sources and types of bias in part due to heterogeneous study designs and incomplete adherence to scientific rigor. These limitations have led to incomplete and biased paradigms as well as persistent paradoxes that have significantly limited translation into clinical and population health interventions. Summary: Improved understanding of these paradigms and paradoxes will allow us to substantially move the field forward.
KW - Cardiovascular disease
KW - Causal inference
KW - Developmental origins of health and disease
KW - Growth restriction
KW - Life course
KW - Low birth weight
KW - Nephron number
KW - Preterm birth
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U2 - 10.1007/s11906-022-01227-z
DO - 10.1007/s11906-022-01227-z
M3 - Review article
C2 - 36227517
AN - SCOPUS:85139771296
SN - 1522-6417
VL - 24
SP - 655
EP - 667
JO - Current hypertension reports
JF - Current hypertension reports
IS - 12
ER -