Family history of substance misuse and early substance initiation in adolescent frontal development
Poster No:
994
Submission Type:
Abstract Submission
Authors:
Priscila Dib Goncalves1, Ardesheer Talati2, Matthew Albaugh3
Institutions:
1Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, 2Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University, New York , NY, 3Department of Psychiatry, Larner College of Medicine, University of Vermont, Burlington, VT
First Author:
Priscila Dib Goncalves
Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University
New York, NY
Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University
New York, NY
Co-Author(s):
Ardesheer Talati
Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University
New York , NY
Department of Psychiatry, Vagelos College of Physicians and Surgeons, Columbia University
New York , NY
Matthew Albaugh
Department of Psychiatry, Larner College of Medicine, University of Vermont
Burlington, VT
Department of Psychiatry, Larner College of Medicine, University of Vermont
Burlington, VT
Introduction:
Having a positive family history of alcohol and other substances (FH+) is associated with developmental alterations particularly within the frontal cortex (Gonçalves et al, 2024; Henderson et al., 2018, Lees et al., 2021). Having a FH+ increases likelihood of early substance initiation, which has been linked to accelerated age-related thinning, particularly in prefrontal regions (McGovern et al., 2023; Volkow et al, 2018). However, little is known about the potential synergistic effects of having both a FH+ and early substance initiation (before age 15) on frontal cortical development. In this study, we extended our previous work showing more rapid thinning across the frontal cortex across ages 9-13 among those with a FH (Gonçalves et al, 2024) by (1) testing across a larger span of adolescence (till age 15), and (2) examining the extent to which group differences may be driven directly by FH versus increased offspring initiation that may result from FH.
Methods:
We used data from 8385 participants in the Adolescent Brain Cognitive Development Study (Release 5.1). FH+ was defined as having ≥1 biological parents and/or ≥2 biological grandparents with a history of alcohol/substance use problems (n=2,460). Our primary outcome was frontal cortical thickness obtained at study baseline (ages:9–11), Year 2 follow-up (ages:11–13), and Year 4 (ages:13-15). Linear mixed-effects models were fit to estimate associations between FH and the 11 bilateral frontal cortical regions. We ran two different types of models. Model A including substance use initiation (i.e., reporting having a full drink of alcohol and/or 1+ puff of cannabis) as a fixed effect, and Model B including only with participants with early substance use initiation (n=521, FH+ = 204, FH- = 307).
Our models were adjusted for sociodemographic variables (i.e., sex assigned at birth, race/ethnicity, parental marital status, household income) as fixed effects. We also included different variables for any prenatal exposure (self-report substance use at baseline for each substance separately tobacco, alcohol, cannabis and other), and a time-varying total intracranial volume as a fixed effect as well. Family relatedness, MRI scanner device and participant ID were included as random intercepts. We added a three-way interaction of FH status, age (as linear and quadratic) and average of the 11 frontal cortical regions to examine the extent to which age-related changes in specific cortical thickness was moderated by FH. We reported the results of the quadratic models as they had slight better model fit parameters.
Analyses were conducted using the 'lme4' and 'emmeans' packages in R.
Our models were adjusted for sociodemographic variables (i.e., sex assigned at birth, race/ethnicity, parental marital status, household income) as fixed effects. We also included different variables for any prenatal exposure (self-report substance use at baseline for each substance separately tobacco, alcohol, cannabis and other), and a time-varying total intracranial volume as a fixed effect as well. Family relatedness, MRI scanner device and participant ID were included as random intercepts. We added a three-way interaction of FH status, age (as linear and quadratic) and average of the 11 frontal cortical regions to examine the extent to which age-related changes in specific cortical thickness was moderated by FH. We reported the results of the quadratic models as they had slight better model fit parameters.
Analyses were conducted using the 'lme4' and 'emmeans' packages in R.
Results:
We observed significant interactions of FH with age for average frontal cortical thickness in all the models (Model A, p value = 0.007, and Model B, p value = 0.006).
In Model A (including all participants), at age 9, the overall mean of frontal cortical thickness (standardized mean) in the FH+ was 0.238, and FH- was 0.244, and at age 15, FH+ = -0.658 and FH- = -0.618 (Figure A).
In Model B, including only those with substance use initiation, at age 9, overall mean of frontal cortical thickness among those FH= + 0.021 and FH- = -0.009, and at age 15, FH+ = -0.953, and FH- = -0.894 (Figure B).
In Model A (including all participants), at age 9, the overall mean of frontal cortical thickness (standardized mean) in the FH+ was 0.238, and FH- was 0.244, and at age 15, FH+ = -0.658 and FH- = -0.618 (Figure A).
In Model B, including only those with substance use initiation, at age 9, overall mean of frontal cortical thickness among those FH= + 0.021 and FH- = -0.009, and at age 15, FH+ = -0.953, and FH- = -0.894 (Figure B).
·Figure A
·Figure B
Conclusions:
Our results suggest that a positive family history is associated with more rapid thinning of the frontal cortex during the developmental span studied. This accelerated frontal cortical thinning appears to be more pronounced among individuals with early substance initiation, indicating that those with both a positive family history and early substance use are at an increased risk for more significant changes in brain structure. Future research should explore the potential long-term implications of these changes on the development of psychopathology.
Lifespan Development:
Early life, Adolescence, Aging 1
Modeling and Analysis Methods:
Segmentation and Parcellation 2
Keywords:
Addictions
Development
STRUCTURAL MRI
Other - Substance use, Adolescence
1|2Indicates the priority used for review
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