Preconception Stress, Birth Weight, and Birth Weight Disparities Among US Women

Strutz, Kelly L.; Hogan, Vijaya K.; Siega‐Riz, Anna Maria; Suchindran, Chirayath; Halpern, Carolyn Tucker; Hussey, Jon M.

doi:10.2105/ajph.2014.301904

Cited by 50 publications

(55 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Complications during pregnancy that include preeclampsia or diabetes, maternal obesity or excessive weight gain during pregnancy, parental smoking, maternal stress or alcohol consumption in addition to maternal age and poor prenatal care impact fetal growth and contribute to the development of increased risk for CV disease in the offspring (50, 52, 60, 69, 126, 142, 201). Some of these factors are preventable; all of these adverse early life exposures impact long-term CV health in manner that may be sex and age dependent.…”

Section: History and Etiology Of The Fetal Origins Of Cardiovascular DImentioning

confidence: 99%

Fetal Programming and Cardiovascular Pathology

Alexander

Dasinger

Intapad

2015

Comprehensive Physiology

184

144

View full text Add to dashboard Cite

Low birth weight serves as a crude proxy for impaired growth during fetal life and indicates a failure for the fetus to achieve its full growth potential. Low birth weight can occur in response to numerous etiologies that include complications during pregnancy, poor prenatal care, parental smoking, maternal alcohol consumption or stress. Numerous epidemiological and experimental studies demonstrate that birth weight is inversely associated with blood pressure and coronary heart disease. Sex and age impact the developmental programming of hypertension. In addition, impaired growth during fetal life also programs enhanced vulnerability to a secondary insult. Macrosomia, which occurs in response to maternal obesity, diabetes and excessive weight gain during gestation, is also associated with increased cardiovascular risk. Yet, the exact mechanisms that permanently change the structure, physiology and endocrine health of an individual across their lifespan following altered growth during fetal life are not entirely clear. Transmission of increased risk from one generation to the next in the absence of an additional prenatal insult indicates an important role for epigenetic processes. Experimental studies also indicate that the sympathetic nervous system, the renin angiotensin system, increased production of oxidative stress and increased endothelin play an important role in the developmental programming of blood pressure in later life. Thus, this review will highlight how adverse influences during fetal life and early development program an increased risk for cardiovascular disease including high blood pressure and provide an overview of the underlying mechanisms that contribute to the fetal origins of cardiovascular pathology.

show abstract

Section: History and Etiology Of The Fetal Origins Of Cardiovascular DImentioning

confidence: 99%

Fetal Programming and Cardiovascular Pathology

Alexander

Dasinger

Intapad

2015

Comprehensive Physiology

184

144

View full text Add to dashboard Cite

show abstract

“…Birth weight reported through maternal recall is highly correlated with medical record data into offspring adulthood (e.g., intraclass correlation [ICC] = .99 in Yawn, Suman, & Jacobsen, 1998; also see Buka, Goldstein, Spartos, & Tsuang, 2004; Jaspers, de Meer, Verhulst, Ormel, & Reijneveld, 2010; O’Sullivan, Pearce, & Parker, 2000; Rice et al, 2007). Given its sensitivity to multiple forms of prenatal stress, including prenatal exposure to trauma and violence (Hill, Pallitto, McCleary-Sills, & Garcia-Moreno, 2016), chronic stress and poverty (Bolten et al, 2010; Kayode et al, 2014; Strutz et al, 2014), cigarette smoking (Bailey, McCook, Hodge, & McGrady, 2011), and pregnancy-related stress and anxiety (Bussières et al, 2015), we interpreted lower birth weight as suggesting more prenatal stress. Children in the present study represented a full range of birth weights (from 2.6–9.8 lbs).…”

Section: Methodsmentioning

confidence: 99%

Prenatal programming of postnatal plasticity for externalizing behavior: Testing an integrated developmental model of genetic and temperamental sensitivity to the environment

Tung

Morgan

Noroña

et al. 2017

Developmental Psychobiology

View full text Add to dashboard Cite

Although both gene-environment and temperament-environment interactions contribute to the development of youth externalizing problems, it is unclear how these factors jointly affect environmental sensitivity over time. In a seven-year longitudinal study of 232 children (aged 5–10) with and without ADHD, we employed moderated mediation to test a developmentally-sensitive mechanistic model of genetic and temperamental sensitivity to prenatal and postnatal environmental factors. Birth weight, a global measure of the prenatal environment, moderated predictions of child negative emotionality from a composite of dopaminergic polymorphisms (i.e., DRD4 and DAT1), such that birth weight inversely predicted negative emotionality only for children with genetic plasticity. Negative emotionality, in turn, predicted externalizing behavior 4–5 years later, beyond genetic and postnatal parenting effects. Finally, birth weight moderated the indirect effect of dopaminergic genotypes on externalizing problems through negative emotionality, partially supporting a prenatal programming model. We discuss theoretical and empirical implications for models of environmental sensitivity.

show abstract

“…One pathway is mediated by effects on birth size: both acute and chronic maternal psychosocial stress increase the risk for intrauterine growth restriction (IUGR) and LBW (Beydoun and Saftlas 2008), including a dose/ response decrease in infant birth weight associated with serial prenatal stress events (Wadhwa et al 1993). Chronic stress has been found to explain a high proportion of birth weight disparities among Latinas, African Americans, and Caucasians (Strutz et al 2014). Specific sources of stress associated with infant size include parental job displacement (Lindo 2011), while maternal distress and depression have been linked to increased risk of LBW, as reported among both urban Brazilian (Rondo et al 2003) and rural Pakistani (Rahman et al 2007) mothers, respectively.…”

Section: Psychosocial Stressmentioning

confidence: 99%

Growth and Life Course Health Development

Mummert

Schoen

Lampl

2017

Handbook of Life Course Health Development

View full text Add to dashboard Cite

Physical growth is an emergent process integrating a complex network of social, biological, and environmental interactions. The global diversity of body shapes and sizes reflects developmental plasticity in response to environmental exposures, both advantageous and adverse, and depicts an evolutionarily robust strategy for species’ survival. Epidemiologic surveillance efforts demonstrate that early life skeletal growth and body composition trajectories are associated with and predict adult chronic disease risks. Both human and animal studies have provided an evidentiary base for the physiological mechanisms by which differences in growth processes manifest as cell- and organ-level changes that influence disease susceptibility across the life course. This chapter leverages a systems biology approach to describe macro- and micropathways affecting growth from a global perspective, reflecting on auxology’s place in theoretical frameworks that help us to understanding past, present, and future health trends. Methodological challenges that face the field are considered, and recommendations to guide future research and policy efforts are offered with the aim of advancing the science of growth biology and its contributions to life course health development.

show abstract

Preconception Stress, Birth Weight, and Birth Weight Disparities Among US Women

Cited by 50 publications

References 53 publications

Fetal Programming and Cardiovascular Pathology

Fetal Programming and Cardiovascular Pathology

Prenatal programming of postnatal plasticity for externalizing behavior: Testing an integrated developmental model of genetic and temperamental sensitivity to the environment

Growth and Life Course Health Development

Contact Info

Product

Resources

About