Objective: To study in a large-scale cohort with prospective data the associations of psychosocial adversities during pregnancy with length of gestation and offspring size at birth.
Methods: We defined a priori two types of psychosocial adversity during pregnancy: life stress (perceived burdens in major areas of life) and emotional symptoms (e.g. anxiety). Measures of offspring size at birth, including body weight, body length, abdominal and head circumference, were obtained from a national medical birth registry. We included in the analyses gestational age and offspring size at birth controlled for length of gestation; the latter was calculated by gestational-age-specific z scores (ZS) reported in 10−3. We conducted multiple regression analyses adjusted for potential confounders to estimate the association between exposures and birth outcomes (n = 78017 pregnancies).
Results: Life stress (per score increase by 1; range, 0-18) was associated with shorter length of gestation (days; B, −0.14; 95% confidence interval (CI), −0.19, −0.10), increased offspring body weight (ZS; B, 9.14; 95% CI, 4.99, 13.28), body length (ZS; B, 6.58; 95% CI, 2.39, 10.77), abdominal circumference (ZS; B, 9.96; 95% CI, 5.77, 14.16), and head circumference (ZS; B, 6.13; 95% CI, 1.95, 10.30). Emotional symptoms were associated with shorter length of gestation (days; B, −0.04; 95% CI, −0.07, −0.004) and decreased body length (ZS; B, −4.44; 95% CI, −7.57, −1.32) only.
Conclusions: Life stress and emotional symptoms both predicted a shorter length of gestation, while only life stress predicted an increased offspring size at birth controlled for length of gestation; yet, the associations were rather small. The fetoplacental-maternal unit may regulate fetal growth according to the type of psychosocial adversity and even increase fetal growth in response to maternal stress in major areas of life. This potentially reflects a basic principle of intrauterine human development in response to stress.
BMI = body mass index; DNBC = Danish National Birth Cohort;IL1B = interleukin 1, beta.
From the Department of Clinical Psychology and Psychotherapy (M.T., A.H.M., G.M.), Faculty of Psychology, University of Basel, Basel, Switzerland; Department of Neurobehavioral Genetics (M.T.), Institute of Psychobiology, University of Trier, Trier, Germany; Department of Epidemiology (N.G., J.O.), School of Public Health, University of California, Los Angeles, Los Angeles, California; The Danish Epidemiology Science Centre (J.O.), Department of Epidemiology, Institute of Public Health, University of Aarhus, Aarhus, Denmark; Department of Applied Statistics in Life Sciences (A.H.M.), Faculty of Psychology, University of Basel, Basel, Switzerland; National Centre of Competence in Research “Swiss Etiological Study of Adjustment and Mental Health (sesam)” (G.M.), Basel, Switzerland.
Address correspondence and reprint requests to Gunther Meinlschmidt, PhD, University of Basel, Birmannsgasse 8, CH-4055 Basel, Switzerland. E-mail: email@example.com
Received for publication May 10, 2009; revision received December 14, 2009.
The Danish National Research Foundation has established the Danish Epidemiology Science Centre that initiated and created the Danish National Birth Cohort. The cohort is furthermore a result of a major grant from this Foundation. Additional support for the Danish National Birth Cohort is obtained from the Pharmacy Foundation, the Egmont Foundation, the March of Dimes Birth Defects Foundation, the Augustinus Foundation, and the Health Foundation. This project was financed, in part, by the German National Academic Foundation (PhD scholarship, M.T.), and the Swiss National Science Foundation (SNSF), Project 51A240-104890 (G.M.). The financial supporters had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
The authors have not disclosed any potential conflicts of interest.
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