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Background: Previous studies have modeled the association between fetal exposure to tobacco smoke and body mass index (BMI) growth trajectories, but not the timing of catch-up growth. Research on fetal exposure to maternal secondhand smoking is limited.
Objectives: To explore the associations between fetal exposure to maternal active and secondhand smoking with body composition at birth and BMI growth trajectories through age 3 years.
Methods: We followed 630 mother-child pairs enrolled in the Healthy Start cohort through age 3 years. Maternal urinary cotinine was measured at ~ 27 weeks gestation. Neonatal body composition was measured using air displacement plethysmography. Child weight and length/height were abstracted from medical records. Linear regression models examined the association between cotinine categories (no exposure, secondhand smoke, active smoking) with weight, fat mass, fat-free mass, and percent fat mass at birth. A mixed-effects regression model estimated the association between cotinine categories and BMI.
Results: Compared to unexposed offspring, birth weight was significantly lower among offspring born to active smokers (-343-g; 95% CI: -473, -213), but not among offspring of women exposed to secondhand smoke (-47-g; 95% CI: -130, 36). There was no significant difference in the rate of BMI growth over time between offspring of active and secondhand smokers (p = 0.58). Therefore, our final model included a single growth rate parameter for the combined exposure groups of active and secondhand smokers. The rate of BMI growth for the combined exposed group was significantly more rapid (0.27 kg/m per year; 95% CI: 0.05, 0.69; p < 0.01) than the unexposed.
Conclusions: Offspring prenatally exposed to maternal active or secondhand smoking experience rapid and similar BMI growth in the first three years of life. Given the long-term consequences of rapid weight gain in early childhood, it is important to encourage pregnant women to quit smoking and limit their exposure to secondhand smoke.
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http://dx.doi.org/10.1038/s41366-018-0238-3 | DOI Listing |
Mol Cell Endocrinol
September 2025
Department of Epidemiology, University of Michigan, Ann Arbor, USA. Electronic address:
Steroid hormones are integral to pregnancy and fetal development, regulating processes such as metabolism, inflammation, and immune responses. Excessive prenatal steroid exposure, through lifestyle choices or environmental chemicals, can lead to metabolic dysfunctions in offspring. The research focuses on how exposure to testosterone (T) and bisphenol A (BPA) affects the liver's DNA methylome, a key component of the epigenome influencing long-term health.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
September 2025
Department of Pediatrics, Washington University, St. Louis, Missouri.
Excess testosterone (T) exposure from early to mid-gestation (days 30-90) leads to sexually dimorphic adverse cardiac left ventricular (LV) programming at fetal day 90 (term 147 days). Whether this sexually dimorphic impact is a direct effect of T or reprogramming that persists beyond early fetal life is unknown. We hypothesized that adverse sex-specific cardiac outcomes seen in early fetal life will persist in late gestational fetuses.
View Article and Find Full Text PDFArch Med Res
September 2025
Departamento de Biología de la Reproducción Dr. Carlos Gual Castro Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, México City, Mexico. Electronic address:
In the developmental origins of health and disease (DOHaD) paradigm, there is a clear link between an adverse prenatal environment and the development of non-hereditary diseases later in life. Exposure to intrauterine inflammation, for example, has been associated with several late-onset conditions, including neurological, cardiovascular, immune, and metabolic disorders. Moreover, maternal and fetal health are compromised under exacerbated inflammation, as it can result in spontaneous abortion, preterm delivery, or intrauterine growth restriction.
View Article and Find Full Text PDFPlacenta
September 2025
Centre for Perinatal and Neonatal Medicine, Tohoku University Hospital, Sendai, Japan; Department of Obstetrics and Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore; School of Veterinary Medicine, Murdoch University, Perth, Western Australia, Australia; Women
Introduction: Antenatal steroid (ANS) therapy accelerates preterm lung maturation. Clinical and experimental data show current regimens disrupt placental function and transport and impact fetal growth. We have previously shown that higher materno-fetal steroid exposures increase fetal glucocorticoid clearance.
View Article and Find Full Text PDFFront Hum Neurosci
August 2025
Department of Pediatrics, University of Wisconsin-Madison, Madison, WI, United States.
Amid the ongoing global substance use crisis, prenatal health research has increasingly focused on the impact of both licit and illicit substance use on fetal development, and in particular brain development. Magnetic resonance imaging (MRI) has become a critical non-invasive tool for investigating how such exposures influence the developing brain. In this review, we summarize findings from 25 peer-reviewed studies that leverage structural, functional, and diffusion MRI to examine the effects of prenatal exposure to alcohol, opioids, methamphetamines, cocaine, nicotine, or cannabis.
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