Severe Maternal Stress Exposure Due to Bereavement before, during and after Pregnancy and Risk of Overweight and Obesity in Young Adult Men: A Danish National Cohort Study

Hohwü, Lena; Li, Jiong; Olsen, Jørn; Sørensen, Thorkild I. A.; Obel, Carsten

doi:10.1371/journal.pone.0097490

Cited by 43 publications

(37 citation statements)

References 34 publications

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“…It is noteworthy that our above-described finding on body composition is consistent with recent reports in large, national cohort samples linking pre-pregnancy and prenatal stress exposure related to maternal bereavement to risk of offspring overweight, obesity and risk for type-2 diabetes (Hohwu et al, 2014; Li et al., 2010; Virk et al, 2012), and our finding on immune function is consistent with another recent report linking prenatal maternal anxiety with infant illnesses and antibiotic use (Beijers et al, 2010). …”

Section: Prenatal Stress Exposure and Physical Health-related Outcsupporting

confidence: 92%

Prenatal stress, development, health and disease risk: A psychobiological perspective—2015 Curt Richter Award Paper

Entringer

Buß

Wadhwa

2015

Psychoneuroendocrinology

249

193

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The long-term consequences of exposure to excess stress, particularly during sensitive developmental windows, on the initiation and progression of many complex, common physical and mental disorders that confer a major global burden of disease are well established. The period of intrauterine life represents among the most sensitive of these windows, at which time the effects of stress may be transmitted inter-generationally from a mother to her as-yet-unborn child. As explicated by the concept of fetal, or developmental, programming of health and disease susceptibility, a growing body of evidence supports the notion that health and disease susceptibility is determined by the dynamic interplay between genetic makeup and environment, particularly during intrauterine and early postnatal life. Except in extreme cases, an adverse intrauterine exposure may not, per se, ‘cause’ disease, but, instead, may determine propensity for disease(s) in later life (by shaping phenotypic responsivity to endogenous and exogenous disease-related risk conditions). Accumulating evidence suggests that maternal psychological and social stress during pregnancy represents one such condition that may adversely affect the developing child, with important implications for a diverse range of physical and mental health outcomes. In this paper we review primarily our own contributions to the field of maternal stress during pregnancy and child mental and physical health-related outcomes. We present findings on stress-related maternal-placental-fetal endocrine and immune/inflammatory processes that may mediate the effects of various adverse conditions during pregnancy on the developing human embryo and fetus. We enunciate conceptual and methodological issues related to the assessment of stress during pregnancy and discuss potential mechanisms of intergenerational transmission of the effects of stress. Lastly, we describe on-going research and some future directions of our program.

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Section: Prenatal Stress Exposure and Physical Health-related Outcsupporting

confidence: 92%

Prenatal stress, development, health and disease risk: A psychobiological perspective—2015 Curt Richter Award Paper

Entringer

Buß

Wadhwa

2015

Psychoneuroendocrinology

249

193

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“…Childhood changes in BMI, such as the ones observed here, predict cardiovascular and pulmonary health in early adulthood (Ziyab et al, 2014) It is plausible that prenatal exposure to maternal stress signals has long-term implications for how offspring utilize and conserve energy, leading to a ‘thrifty’ phenotype associated with higher risk for obesity. Recent studies have concluded that prenatal exposure to maternal bereavement stress is associated with increased likelihood of becoming overweight as early as 10 years old (Li et al, 2010) as well as a two-fold risk of obesity at age 18 among men (Hohwü et al, 2014). The present findings indicate that fetal exposure to pCRH is a plausible mechanism underlying programming of obesity risk.…”

Section: Discussionmentioning

confidence: 99%

Fetal programming of children's obesity risk

Stout

Espel

Sandman

et al. 2015

Psychoneuroendocrinology

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OBJECTIVE Childhood obesity affects nearly 17% of children and adolescents in the United States. Increasing evidence indicates that prenatal maternal stress signals influence fetal growth, child obesity, and metabolic risk. Children exhibiting catch-up growth, a rapid and dramatic increase in body size, within the first two years of life are also at an increased risk for developing metabolic disorder and obesity. We evaluate the potential role of the maternal hypothalamic-pituitary-adrenal (HPA) and placental axis in programming risk for child obesity. METHOD This prospective longitudinal study measured placental corticotropin-releasing hormone (pCRH) and maternal plasma cortisol at 15, 19, 25, 30, and 37 gestational weeks and collected child body mass index (BMI) at birth, 3, 6, 12, and 24 months. Participants included 246 mothers and their healthy children born full term. Each child’s BMI percentile (BMIP) was determined using World Health Organization (WHO) standards based on age and sex. Child BMIP profiles from birth to two years of age were characterized using General Growth Mixture Modeling (GGMM). We evaluated whether fetal exposure to placental CRH and maternal cortisol are associated with BMIP profiles. RESULTS Placental CRH at 30 gestational weeks was highly associated with both BMIP (p <.05) and weight (p <.05) at birth when accounting for gestational age at birth and used as a predictor in modeling BMIP profiles. Maternal cortisol was not associated with child BMIP. GGMM analyses identified four distinct BMIP profiles: Typical, Rapid Increase, Delayed Increase, and Decreasing (See Figure 2). The Typical profile comprised the majority of the sample and maintained BMIP across the first two years. The Rapid and Delayed Increase profiles each exhibit a period of reduced body size followed by BMI catch-up growth. The Rapid Increase profile exhibited catch-up within the first 3 months while the Delayed group showed an initial decrease in BMIP at 3 months and a dramatic increase from 12 to 24 months The Decreasing profile exhibited normal birth weight and BMIP followed by persisting, low BMIP. The members of the Rapid and Delayed Increase profiles were exposed to the highest concentrations of placental CRH at 30 gestational weeks compared to those in the Typical profile group (Figure 3). CONCLUSIONS Exposure to elevated placental CRH concentrations during the third trimester is associated with catch up growth. An early period of small body size followed by rapid catch-up growth is a profile associated with increased metabolic risk and increased obesity risk. Our findings suggest that placental CRH exposure makes a unique contribution to fetal programming of obesity risk.

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“…Indeed, exposure to famine during pregnancy can have long-range consequences on offspring's morbidities including cardiovascular, metabolic, and mental diseases (6)(7)(8). Psychic suffering of pregnant mothers has been associated with functional alteration in the offspring's hypothalamo-pituitaryadrenal (HPA) axis (9,10) that may pave the way for psychic vulnerabilities (11), obesity (12), diabetes (13), and cardiovascular diseases (14).…”

mentioning

confidence: 99%

Prenatal loss of father during World War One is predictive of a reduced lifespan in adulthood

Todd

Valleron

Bougnères

2017

Proc. Natl. Acad. Sci. U.S.A.

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Although early-life stress is known to alter health, its long-term consequences on mortality remain largely unknown. Thanks to unique French legislation established in 1917 for war orphans and children of disabled soldiers, we were able to study the adult mortality of individuals born in 1914–1916 whose fathers were killed during World War 1. Vital information and socio-demographic characteristics were extracted manually from historical civil registers for 5,671 children born between 1 August 1914 and 31 December 1916 who were granted the status of “pupille de la Nation” (orphan of the Nation). We used a database comprising 1.4 million deceased soldiers to identify war orphans and collect information on their fathers and then paired each orphan with a nonorphan from the same birth register matched for date of birth, sex, and mother’s age at the infant’s birth. Mortality between ages 31 and 99 y was analyzed for 2,365 orphan/nonorphan pairs. The mean loss of adult lifespan of orphans who had lost their father before birth was 2.4 y (95% CI: 0.7, 3.9 y) and was the result of increased mortality before age 65 y. Adult lifespan was not reduced when the father’s death occurred after the infant’s birth. These results support the notion that intrauterine exposure to a major psychological maternal stress can affect human longevity.

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Severe Maternal Stress Exposure Due to Bereavement before, during and after Pregnancy and Risk of Overweight and Obesity in Young Adult Men: A Danish National Cohort Study

Cited by 43 publications

References 34 publications

Prenatal stress, development, health and disease risk: A psychobiological perspective—2015 Curt Richter Award Paper

Prenatal stress, development, health and disease risk: A psychobiological perspective—2015 Curt Richter Award Paper

Fetal programming of children's obesity risk

Prenatal loss of father during World War One is predictive of a reduced lifespan in adulthood

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