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Objective: To assess the impact of fetal exposure to cannabis on adiposity and glucose-insulin traits in early life.
Research Design And Methods: We leveraged a subsample of 103 mother-child pairs from Healthy Start, an ethnically diverse Colorado-based cohort. Twelve cannabinoids/metabolites of cannabis (including Δ9-tetrahydrocannabinol and cannabidiol) were measured in maternal urine collected at ~27 weeks' gestation. Fetal exposure to cannabis was dichotomized as exposed (any cannabinoid > limit of detection [LOD]) and not exposed (all cannabinoids < LOD). Fat mass and fat-free mass were measured via air displacement plethysmography at follow-up (mean age: 4.7 years). Glucose and insulin were obtained after an overnight fast. Generalized linear models estimated the associations between fetal exposure to cannabis with adiposity measures (fat mass [kg], fat-free mass [kg], adiposity [fat mass percentage], body mass index [BMI], and BMI z-scores) and metabolic measures (glucose [mg/dL], insulin [uIU/mL], and homeostatic model assessment of insulin resistance [HOMA-IR]).
Results: Approximately 15% of the women had detectable levels of any cannabinoid, indicating fetal exposure to cannabis. Exposed offspring had higher fat mass (1.0 kg; 95% CI, 0.3-1.7), fat-free mass (1.2 kg; 95% CI, 0.4-2.0), adiposity (2.6%; 95% CI, 0.1-5.2), and fasting glucose (5.6 mg/dL; 95% CI, 0.8-10.3) compared with nonexposed offspring. No associations were found with fasting insulin (in the fully adjusted model), HOMA-IR, BMI, or BMI z-scores.
Conclusions: We provide novel evidence to suggest an association between fetal exposure to cannabis with increased adiposity and fasting glucose in childhood, a finding that should be validated in other cohorts.
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http://dx.doi.org/10.1210/clinem/dgac101 | 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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