Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

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.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9202691PMC
http://dx.doi.org/10.1210/clinem/dgac101DOI Listing

Publication Analysis

Top Keywords

fetal exposure
24
exposure cannabis
24
fat mass
12
fat-free mass
12
healthy start
8
cannabis adiposity
8
mass
8
mass [kg]
8
mass 95%
8
fasting glucose
8

Similar Publications

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 PDF

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 PDF

Inflammation in Pregnancy: Key Drivers, Signaling Pathways and Associated Complications.

Arch 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 PDF

Perturbation of the ovine placental transcriptome occurs at sub-therapeutic exposures to antenatal steroid therapy.

Placenta

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 PDF

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.

View Article and Find Full Text PDF