Psychoneuroendocrinology · 2026
Lifetime adversities and patterns of maternal prenatal HPA function from hair glucocorticoids.
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Orellana Dayanne, Liu Can, Avendano Sara, Tafflet Muriel, Heude Barbara, van der Waerden Judith
Аннотация
BACKGROUND: The associations between both early life and later adversities and prenatal stress physiology, particularly HPA axis function, are still largely unknown. Inconclusive previous studies highlight the necessity for adopting life-course approaches. This study examined the associations between adverse childhood experiences (ACEs), adverse prenatal life events (APEs), and patterns of maternal prenatal HPA function assessed via joint-trajectories of hair glucocorticoid concentrations (HGC). Particularly, ACEs were tested as a potential moderator.
METHODS: We analyzed data from 269 women from the French EDEN cohort. Retrospective information on maternal HGC for all pregnancy trimesters was obtained from hair samples collected after delivery. ACEs were treated as a binary exposure, and APEs were measured through a cumulative score. Inverse probability weights from propensity scores were applied to adjust for baseline sociodemographic characteristics, prenatal psychopathology, and health-related confounders.
RESULTS: Three prenatal HPA trajectories were identified: blunted (14.7%), normative (56.3%), and hyperreactive (29.0%). ACEs and APEs interacted to predict higher odds of a hyperreactive trajectory (p < 0.01) when combining blunted and normative HPA patterns as the reference category. After stratification, APEs were associated with a hyperreactive trajectory only among ACE-exposed women (aORipw =2.22 [1.28; 3.84], p < 0.01). A sensitivity analysis excluding the blunted group yielded consistent results.
CONCLUSIONS: Lifetime adversities were associated with stress dysregulation. APEs appear to heighten vulnerability to HPA function dysregulation, especially after previous exposure to ACEs. These findings provide insight into how adversities throughout the life course can interact to become embodied through maternal stress physiology.
METHODS: We analyzed data from 269 women from the French EDEN cohort. Retrospective information on maternal HGC for all pregnancy trimesters was obtained from hair samples collected after delivery. ACEs were treated as a binary exposure, and APEs were measured through a cumulative score. Inverse probability weights from propensity scores were applied to adjust for baseline sociodemographic characteristics, prenatal psychopathology, and health-related confounders.
RESULTS: Three prenatal HPA trajectories were identified: blunted (14.7%), normative (56.3%), and hyperreactive (29.0%). ACEs and APEs interacted to predict higher odds of a hyperreactive trajectory (p < 0.01) when combining blunted and normative HPA patterns as the reference category. After stratification, APEs were associated with a hyperreactive trajectory only among ACE-exposed women (aORipw =2.22 [1.28; 3.84], p < 0.01). A sensitivity analysis excluding the blunted group yielded consistent results.
CONCLUSIONS: Lifetime adversities were associated with stress dysregulation. APEs appear to heighten vulnerability to HPA function dysregulation, especially after previous exposure to ACEs. These findings provide insight into how adversities throughout the life course can interact to become embodied through maternal stress physiology.