31, 32 These measures often lack the negative valence for researchers to understand the nature of the relationship, and researchers may therefore be unable to elucidate whether a tipping point in the degree of stress exposure exists or the role of timing of exposure. divorce, job loss) may not be independent of the mother’s genetic background, psychopathology and socioeconomic status (SES) and (iii) measures of psychosocial stress during pregnancy are generally broad, frequently measured by daily problems and upheavals 30 or stressful life events from ordinary life. Human studies remain hampered by methodological restrictions, including: (i) the inability to randomize pregnant women in varying stressful condition and to systematically control for the level and timing of any exposure (ii) stressful events (i.e. ![]() stressful life events and psychological problems) is linked to long-term neurobehavioural problems in offspring, 13, 14 such as autism, 15, 16 schizophrenia 17–20 and attention deficit/hyperactivity disorder, 21–23 as well as growth-related suboptimal reproductive outcomes such as intra-uterine growth restriction (IUGR) 24–26 and obesity, 27–29 through epigenetic mechanisms. Human studies have also demonstrated that antenatal exposure to broadly defined stress (i.e. ![]() 10–12 Preclinical studies demonstrated that antenatal stress leads to dysregulated neurobehavioural functioning and problems with development, providing a solid platform for hypothesis testing in human studies. 1–6 Growing evidence 7–9 suggests that not only the genome but also the epigenome, the heritable, quasi-stable yet dynamic control of gene expression, can be modulated by the environment, and plays a vital role in defining health and disease in growing offspring. The Stress in Pregnancy (SIP) Study cohort was set up in New York City in 2009 through funding made available by the National Institute of Mental Health (NIMH), to understand the extent to which an adverse environment in utero can alter fetal growth and development, with potential lifelong impacts on health and disease, based on the theoretical framework of the ‘Developmental Origins of Health and Diseases (DoHaD) Hypothesis’.
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