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Effects of Prenatal Substance Exposure on Longitudinal Tri-Ponderal Mass Index Trajectories from Pre- to Early Adolescence in the ABCD study

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Abstract Objectives The long-term relationship between prenatal substance exposure (PSE) and obesity development remains inconclusive and poorly understood. This study aimed to explore the heterogeneity in adiposity developmental trajectories from pre- to early adolescence and investigate the influence of PSE on these patterns. Methods Five waves of data from 7 881 children enrolled in the Adolescent Brain Cognitive Development (ABCD) Study (Release 5.1) were analyzed. Tri-Ponderal Mass Index (TMI) was used to assess adiposity levels. PSE (e.g., tobacco, alcohol, caffeine, and marijuana) was collected via maternal self-report. Latent growth mixture modeling was conducted to identify TMI trajectories, followed by multinomial logistic regression to examine the role of PSE in TMI profiles, controlling for various factors. Results Three trajectories were identified: Stable TMI (86.6%), Increasing TMI (12.5%), and Decreasing TMI (0.9%). The risk of exhibiting an Increasing TMI was associated with prenatal exposure to tobacco (β = 1.53, 95% CI = 1.26–1.86, p < .001) and caffeine (daily use: β = 1.39, 95% CI = 1.16–1.68, p < .001; weekly use: β = 1.38, 95% CI = 1.13–1.69, p < .05), with dose-dependent effects. Notably, tobacco exposure both before (β = 1.55, 95% CI = 1.27–1.89, p < .001) and after awareness of pregnancy (β = 1.51, 95% CI = 1.10–2.08, p < .05) contributed to this risk, with no significant benefit from maternal cessation after pregnancy awareness. Multiple PSE substantially elevated the risk of increasing adiposity (β = 1.70, 95% CI = 1.27–2.27, p < .001). Conclusions Obesity risk can emerge long before adolescence, even during prenatal development. The findings regarding the long-term influence of prenatal substance exposure on adiposity development during adolescence highlight the importance of preconception and prenatal health interventions to mitigate the risk of obesity in offspring.
Title: Effects of Prenatal Substance Exposure on Longitudinal Tri-Ponderal Mass Index Trajectories from Pre- to Early Adolescence in the ABCD study
Description:
Abstract Objectives The long-term relationship between prenatal substance exposure (PSE) and obesity development remains inconclusive and poorly understood.
This study aimed to explore the heterogeneity in adiposity developmental trajectories from pre- to early adolescence and investigate the influence of PSE on these patterns.
Methods Five waves of data from 7 881 children enrolled in the Adolescent Brain Cognitive Development (ABCD) Study (Release 5.
1) were analyzed.
Tri-Ponderal Mass Index (TMI) was used to assess adiposity levels.
PSE (e.
g.
, tobacco, alcohol, caffeine, and marijuana) was collected via maternal self-report.
Latent growth mixture modeling was conducted to identify TMI trajectories, followed by multinomial logistic regression to examine the role of PSE in TMI profiles, controlling for various factors.
Results Three trajectories were identified: Stable TMI (86.
6%), Increasing TMI (12.
5%), and Decreasing TMI (0.
9%).
The risk of exhibiting an Increasing TMI was associated with prenatal exposure to tobacco (β = 1.
53, 95% CI = 1.
26–1.
86, p < .
001) and caffeine (daily use: β = 1.
39, 95% CI = 1.
16–1.
68, p < .
001; weekly use: β = 1.
38, 95% CI = 1.
13–1.
69, p < .
05), with dose-dependent effects.
Notably, tobacco exposure both before (β = 1.
55, 95% CI = 1.
27–1.
89, p < .
001) and after awareness of pregnancy (β = 1.
51, 95% CI = 1.
10–2.
08, p < .
05) contributed to this risk, with no significant benefit from maternal cessation after pregnancy awareness.
Multiple PSE substantially elevated the risk of increasing adiposity (β = 1.
70, 95% CI = 1.
27–2.
27, p < .
001).
Conclusions Obesity risk can emerge long before adolescence, even during prenatal development.
The findings regarding the long-term influence of prenatal substance exposure on adiposity development during adolescence highlight the importance of preconception and prenatal health interventions to mitigate the risk of obesity in offspring.

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